Surgery Lecture Notebook

University
College
Ibadan
Hospital,
General Surgery
&
Specialty Surgery
Notebook/Jotter
P|
mmsmmm+imzia
Section I -
Gastro-intestinal System
1.
Upper gastrointestinal tract bleeding
2.
Lower gastrointestinal tract bleeding
3.
Acute abdomen 15
10
J Peritonitis
II - Intestinal obstruction
III - Non-surgical Causes
4.
Diseases of the large bowel
-.
29
5.
Diseases of the ano-rectum
6.
Acute appendicitis
7.
Peptic ulcer and complications (DrLadipo)
8.
Varicose veins, peripheral arterial disease (Prof. Ajao)
9.
Colostomy
10.
Bowel preparation
36
44
49
55
56
58
Section H- Hepatobiliary & Endocrine Surgery

Malignant Thyroid Neoplasm (DrAfolabi)
u.
59
Non-malignant Thyroid Diseases ( M r Akute)
12.
13.
14.
IS.
16.
Non-malignant Thyroid Diseases (DrAfolabi)
72
Thyroid Crisis (Seminar)
75
Thyroid Storm (Tutorial)
77
Hypercalcaemia ( Tutorial)
78
Thyroidectomy (Tutorial)
17.
Neck Swelling : Non-goitrous (hÂkute)
IS.
Surgical Jaundice
19.
Surgical Jaundice (DrAfolabi)
20.
84
88
1 -
92
94
Benign Breast Diseases (Dr Ogundiran)
109
Malignant Breast Disease (Dr Ogundiran)
119
Portal Hypertension (Dr Afolabi)
22.
79
II--A4
Liver, Gall Bladder, & Pancreatic Diseases

ease; -
21.
- 65
104
Section ill- Oncology ( Part I )

23.
24.
Section iv-
Paediatiic Surgery
25.
Congenital Anomalies of the GIT (Dr Ogundoyin)
26.
Surgical Jaundice in Children
130
138
27.
Undescended Testis & Hernia
142
28.
Intantile Hypertrophic Pylroric senosis
147
29.
Intussuscepion
149
30.
Congenital Anomalies of Anterior Abdominal Wall
151
31.
Childhood Malignancies
32.
Congenital Neck Masses
159
167
Section VI- Plastic & Reconstructive Surgery

33.
Wound closure, skin grafts, flaps, pedicles
34.
Wound healing & Complications
35.
Chronic Ulcers, Pressure Ulcer & Lymphoedema
36.
Burns & Scalds
187
37.
Surgical skin lesions
194
38.
Plastic surgery of the head and neck
39.
Plastic surgery of the hand
170
-
178
182
206
211
Section V- Orthopaedics
40.
Definition, Classification and PrilclplJjof Management of Fracture
218
41.
Complications of fractures and dislocation
221
42.
Fractures and dislocations of tha lowfllimbs
229
43.
Fractures and dislocations of the]upf

ipJprllimbs
44.
Pelvic fracture
242
45.
Infections of the bones and joints
245
46.
Arthritis
252
47.
Back pain, Tuberculosis of the spine
48.
Bone tumours
49.
Club Foot (Congenital talipes equinovarus)
235
257
261
267
Section XI - Neurosurgery
50.
Evaluation of the patient with neurological diseases
269
51.
Cranial congenital malformations
273
52.
Head injury -
53.
Trauma of the spinal cord
54.
Brain tumours & Tumour like Masses-1
55.
Spinal cord tumours
56.
Cervical and lumbar disc disease
^-q-f-rr"
-
282
287
295
S.
302
Chapter 1
UPPER GASTROINTESTINAL BLEEDING
Definition
-
I s bleeding from any part of the Gl tract above /proximal to the ligament of Treitz.
Causes
Common
i.
ii.
iii.
iv.
Less common
i.
ii.
iii.
iv.
v.
Rare
i.
ii.
v.
v.
vi.
Bleeding duodenal ulcer

Bleeding gastric ulcer
Stress ulcer - associated with t | | ma or stress
Gastritis
Oesophagitis
Mai lory-Weiss syndrome
Malignant gastric tumour
Benign gastric tumour
Oesophageal ulcer or tumour
Duodenal ulcer
Pancreatic tumour
Abdominal aortic aneurysm
Blood dyscrasia
Hereditary telangiectasia
Dieuolfoy's disease
Mechanism
Breach of mucosa
Inflammation
Neoplasm
Vascular malformation
Blood dyscrasia
Pathophysiology
Significant blood loss
o
> 800mls of blood
o
PCV 6 - 8% reduced or Hb concentration of 2mg/dl
Massive bleeding
o
Acute blood loss i,40%.,.. n
PCM <24% or HB ddlWgj f
Hypotension A shock
Clinical features
Symptoms
i.
Haematemesis
ii.
iii.
Malaene
Haematochezia - may be seenjili |\(Jssive
bleeding.
S
iv.
v.
Sweatung
Restlessness
vi.
Examination
1T
Coma
i.
ii.
iii.
iv.
Asymptomatic
Shock - in restlessness
Pallour
Unconsciousness
v.
Tachycardia
In Chronic liver disease

i.
Jaundice
ii.
Ascites
iii.
Spider naevi
iv.
Venous collaterals
v.
Hepatosplenomegaly
Also
i.
ii.
iii.
Epigastric tenderness - Duodenal/Gastric ulcer / Gastritis

Epigastric mass - Gastric tumour
For vascular lesion e.g Hereditary telangiectasia, check the mucous membrane of the
mouth and lips.
Management
1. Resuscitation
2. Evaluation
3. Definitive treatment
a.
Resuscitation
i.
Set up intravenous line using wide bore cannula
ii.
Take blood sample f o r PCV, Group & Crossmatch
iii.
Adminster fluid using
a.
Crystaloids e.g Ringers lactate
b.
Colloids e.g plasma substitute
iv.
Monitoring
o
Vital signs : every 15 minutes
o
Level of consciouness
o
Do urethral catheterization to monitor the urinary output - hourly
o
Do chest auscultation
o
I f available, use central venous pressure line
v.
Nasogastric tube intubation
o
Do gastric lavage - using cold saline. I t is periodically e.g every 2 hours
o
Note, the use is both diagnostic A therapeutic.
o
Clear fluid aspirate points higher G I pathology.
vi.
vii.
viii.
o
And passage of altered blood shows long duration.
o
I t is also used to decompress the stomach.
Blood transfusion
Inform Physician or surgeon
Pre-operative preparation
b. Evaluation
ii.
iii.
History
Physical examination
Digital rectal examination
iv.
Investigation
a. Endoscopy ( Oesopha-'gastro-duodenoscopy OGb) - 4 -24hrs
- To confirm the diagnosis
- For sclerotherapy
- For rubber band ligation
- For follow-up : checking f o r the size of an ulcer in
fundus or lower oesophagus
b.
Double contrast barium studies

o
Worm-like appearance - Oesophageal varices
o
Filling defects in stomach - Gastric ulcer
o
Suction in duodenal cap - Duodenal ulcer
c. Angiography
c. Definitive treatment
a. Non-operative
i. Monitor vital signs : every 30minutes and PCV every 2 hours
ii. Ensure haemodynamics stability
o
I n massive bleeding, upto 4 units of blood con be given
in 24 hours
iii. Surery
Aim
To stop the bleeding
Prevent recurrent bleeding
Treat the underlying disease e.g : shunting blood from portal to
systemic circulation
I
Indications
i. Massive bleeding
ii. Continous bleeding
iii. Recurrent bleeding
iv. Associated perforation
Depends on the cause
a. Bleeding duodenal ulcer

- The treatment depends on
i. age of the patient
ii. Severity
iii. Resources available
iv. Cardiovascular status
For young patient
o
Manage conservatively
o
Give Histamine receptor blocker e.g cimetidine
o
Do serial PCV
o
2 - 3 hourly gastric lavage : done to evacuate the clot and to see if
bleeding has stopped or not. E.g of fluids used are normal saline, cold
saline slows the clotting process.
o
Antiulcer regimen
e.g Metronidazole + Amoxicillin - to eradicate H.pylori
Elderly
o
Exploratory Laparotomy
Gastrostomy
Under run vessels
To prevent recurrence, do truncal vagotomy & pyroplasty.
Note, you scope when bleeding subsides and if not, do it under anaesthesia
b. Gastric ulcer
o
o
Fluid resuscitation
Exp. Lap : Under run vessels or partial gastrectomy f o r malignant ulcers or
bleeders.
c. Stress Ulcers/Acute gastritis

- Usually gives a diffuse pain
Treatment
i.
Histamine receptor antagonist
ii.
Proton pump inhibitors
iii.
Partial gastrectomy - if the above fails
d. Oesophageal varices
i. Fluid resuscitation
ii. Nasogastric tube
iii. Monitoring vital signs
iv. Endoscopy - to establish the diagnosis.
Treatment
a. Pharmacological e.g
o
Vasopressin, Lysopressin - to vasoconstrict splanchnic veins. I t is given

by "Rule of 20"
- 20 vasopressin
8
o
o
o
b.
- 200mls of fluids
- For 20 minutes
Nitroglycerin - to improve cardiac perfusion
Telopressin - spares cardiac vessels
Propanolol - I t reduces blood flow to splanchnic vessels and increase
peripheral flow.
Flexible Endoscopy - for

o
Rubber band ligation
o
Sclerotherapy
Sengstaken-Blakemore tube is used. I t has 4 lumen and it is passed
through the nose
First - Lower balloon : to compress the varices in the
fundus
Second - Upper balloon : to compress the varices in the
fundus
Third lumen : To aspirate the stomach
Fourth lumen : To aspirate the oesophagus
Note, the tube is not therapeutic, it only gives room to make decision f o r
treatment.
c.
Surgery
Aim To shunt blood from portal to systemic circulation
Options
1. Shunt procedures
a. Selective
o
Warren shunt - is distal spenorenal shunt
o
Transjugular Intrahepatic portosystemic
stent shunt (TIPSS)
b. Non-selective : Portocaval shunt, Splenorenal shunt. I t
diverts blood directly to the systemic circulation.
2.
Non-shunt procedures
a. Splenectomy
b. Sigura procedure
- Splenectomy
- Revascularisation of oesophagus A
stomach & fundus
- Transection A end-toend anastomosis
of lower end of oesophagus
Note, all the above procedures are PALLIATIVE !

3.
Definitive treatment
I s Liver transplantation
e. Mallory-Weiss syndrome
- Conservative: often
i. Blood transfusion
ii. Vasopressin
- Surgery: Gastrectomy
f.
Gastric tumour - Resection
g.
Blood Dyscrasias - Exclude other conditions
Chpater 2
LOWER GASTROINTESTINAL BLEEDING
Definition
- I s bleeding situated between the ligament of Treitz (duodenojejunal junction) and anus.
Or
- For practical purposes, it is any haemorrhage whose source cannot be visualized with standard
upper gastrointestinal scope.
Types
1.
2.
Occult
Overt
Causes
1. Massive Upper G I bleeding - from any cause
2. Colonic causes
Diverticulosis
i.
Carcinoma
ii.
v.
v.
vi.
vii.
viii.
ix.
x.
xi.
Amoebiasis
Angiodysplasia
Colonic polyps
Sarcoma
Lymphoma
Leukaemias
Colitis - from any cause
Intussuception
Gut infarction
Rectal and Anal

i.
Haemorrhoids - First degree
Anal Fissure
II.
10
iii.
iv.
v.
Carcinoma of rectum/ anus - Carcinoma of rectum is the commonest of bleeding per

rectum
Proctitis ( from any cause)
Stercoral Ulceration - ulceration of the mucosa from rock-like faeces
Clinical Presentation
1. Bleeding per rectum - I t may be
o
Drak tarry stool (malaena)
o
Frank blood ( haematochezia)
2. Profound anaemia
a. Chronic anaemia - is seen in patient with occult blood loss. The blood volume is intact but
there is low rbc. e.g
i.
Hookworm infestation
ii.
Carcinoma of caecum
b. Acute anaemia - seen in profuse haemaorrhage. The blood volume is reduced and the patient
be in shock e.g
i.
Angiodysplasia of colon - may present in shock. Usually there is
no
haematemesis. The patients are usually elderly,
ii.
Haemorrhoids
episodic post-defaecation bleeding - is the hallmark of haemorrhoids.
There is usually past episodes of recurrent minimal bleeding and
proplapse.
Proctoscopy will demonstrate the lesions usually at 3, 7 A 11 clock
positions.
An attempt must be made to eclude a proximal rectal tumour,
iii.
Carcinoma of caecum
iv.
Diverticulitis
- I n both iv and v, blood is mixed with stool
v.
Divertculosis - usually seen in elderly. There is history of hypertensive heart
disease. The hypertension because of high blood pressure and
atherosclerosis,
vi.
Typhoid - is associated with fever, abdominal tenderness and paralytic ileus.
11
N.B
Haemorhoids
Types
a. Primary - is idiopathic
On proctoscpy, it is seen in 3, 7,11: 00 clock positions
II
b. Secondary -as a result of

Carcinoma of rectum which should be excluded in patients >' 45years
I n pregnancy
Pelvic tumour
Investigation
a. Ancillary
II.
iii.
IV.
v.
vi.
vii.
Full blood count

o White cell count
o Platelet count
Blood grouping and crossmatching
Full Clotting profile - to exclude bleeding dyscrasias or diathesis
a. PT ( Normal = 13 - 20s)
b. PTTK (Normal = 3 0 - 4 5 s )
c. Bleeding time
Electrolytes A Urea - in preparation f o r surgery
Blood Culture - f o r typohid
Widal's test - for typhoid
Stoolm/c/s
for trophozoites of amoeba - E. histolytica is pathogenic, it engulfs blood cells
for schistosomal haemorrhage
b. Specific - I s aimed at localizing the bleeding sites

1. Rigid Proctosigmosidoscopy (18 - 20cm) - I s f o r
a. I s direct visualization of large intestine upto rectsigmoid junction,
mucosa is examined for
Colour
Texture
ii.
iii.
Mobility
Inflammation
iv.
Erosion
v.
Ulcers
vi.
Rectosigmoid
12
vii.
Adenomas
viii.
Carcinomas
ix.
Polyps
b. Biopsy or brushing for cytology - done for areas of inflammation, erosions,
polyps
c. For treatment in 1 s t and 2nd degree haemorrhoids by Injection
sclerotherapy or
Rubber band ligation
2. Flexible Fibreoptic Sigmoidoscopy ( 60cm long )
Allows for better visualization of entire sigmoid colon A rectum
I s not used for rubber band or injection sclerotherapy
I s used with diathermy
3. Flexible fibreoptic colonoscopy (160cm)
To visualize the whole colon
To identify colonic lesions that cannot sigmoidoscopes and barium enema cannot pick
Lower GI endocopy is not possible in massive lower &I haemorrhage because of
inadequate inspection, however, it is generally accepted that colonoscopy is the
investigation of choice once the bleeding has ceased.
4.
Barium enema A Air-contrast enema studies

I s useful to identify mass lesions e.g carcinomas, diverticulosis, polyps
I t would not pick smaller lesions like angiodysplasia.
5. Mesenteric Angiography ( Selective )

I t involves cannulation of superior mesenteric artery using image intensif ier and the
injection of a contrast medium
Shows blush or spillage of contrat into the lumen which points to the site of
bleeding.
For it to demonstrate the source of haemorrhage, the patient must be bleeding at
the rate of 0.5 -lml/min at the time of investigation.
Thus its disadvantage is that it does not help if bleeding is < lml/min.
6. Isotope scintinscaning
To find out the site of bleeding using Technitium 99 labelled red blood cells.
This is useful in patients who are not bleeding at the sufficient rate for
angiography to demonstrate the site of bleeding.
Management
1 . Resuscitation
To optimize the patient f o r operation
a. Airway
Position the patient in semi-prone
Extend the jaw
Digital clearing
b. Breathing
Using ventilator
c. Circulation
13
Maintain circulation by giving

i.Crystalloids e.g Normal saline, Ringers lactate
ii.
Colloids e.g Plasma, Haemacel
iii.
Blood
iv.
Ionotropic agents - is used if blood does not increase PCV e.g

dopamine, dobutamine, adrenaline. Adrenaline is used here instead of
the f i r s t 2, I t causes vasoconstriction of renal vessels leading acute
renal failure .
Monitoring
i.
Urinary output - it should be 0.5 -lml/kg/hour
ii.
Using CVP line using Swan ganz catheter- The normal is 10 15cm/H20
Limitations of CVP line
i. Restrictive lung disase
ii. Cardiac tamponade
2. Def initve treatment - Depends on the cause
i. Angiodysplasia - Resect i on
ii. Amoebiasis - Metronidazole
iii. Typhoid - Chloramphenicol, Ciprfloxacin, Ofloxacin,
iv. Diverticulosis - Resection
a. Barium enema - it coats the diverticulosis, thus stops the bleeding, thus it is both
diagnostic and therapeutic,
b.Resection - Sigmoidectomy
c.Embolisation of bleeding vessels
- I s done in developed countries.
- The Superior mesenteric artery is cannulated and the embolic material e.g
plastic gel, gel foam etc is injected through it.
- This I s Interventional radiology
v. Carcinoma of caecum
a. Give Packed red cell - Note, it is associated with chronic blood loss,
thus the blood volume is intact, but there is lack of red blood cells
b. Right hemicolectomy - involves the removal of
the distal 15cm of the terminal ileum
Caecum & appendix
Transverse colon
c. Extended hemicolectomy - is f o r tumour extension. I t involves the

removal of the above and up to the splenic flexure of the
descending colon.
vi. Carcinoma of rectum
- I s the commonest cause of bleeding per rectum
- Surgery "
i.
Abdomino-perineal resection with
Permanent Colostomy
14
Pain localization is poor.

Classification / Aetiology
i. Based on Origin
a. Primary peritonitis - the cause is from peritoneum itself. I t is NOT very common
b. Secondary peritonitis - I t arises from other causes and it is very common.
i i.
Based on Onset
a. Acute - is more common. This may also be
Aseptic /Chemical
Bacterial -is the commonest
Granulomatous
Others
b. Chronic - the commonest cause here is tuberculosis
iii. Based on extent of involvement

a. Localised - involves only a region of the peritoneum
b. Generalised - involves the entire peritoneum
I n all, the commonest peritonitis is Secondary, Acute (Bacterial) & Generalised peritonitis
Factors Limiting Peritonitis i.e causing Localised peritonitis
a.
Anatomical
i.
ii.
b.
Presence of true mesocolon - which divides abdominal cavity into supracolic and
infracolic compartments. This limits inflammation to either e.g perforated duodenal
ulcer may present with features of pelvic peritonitis
Omentum
Pathological
i.
Adhesions - is pathological
Factors Leading to Generalised Peritonitis

i.
A rapidly developing peritonitis
ii.
Presence of virulent organism
iii.
Increased peristalsis of GIT
ASEPTIC PERITONITIS
I s due to resence of chemical substances in the peritoneum e.g
i.
Gastric content - due to perforated gastric ulcer or duodenal ulcer
ii.
Pancreatic juice
iii.
Bile - from injury to biliary tract via trauma, surgery
iv.
Urine - from intraperitoneal rupture of urinary bladder
V.
Blood - is not irritant, but serves as a good culture medium for organism
vi.
Mucous
vii.
Lymph
16
ii.
Sphincter-saving procedure : is Low anterior

resection with anastomosis
vii. 4 t h Degree Haemorrhoids

i. Injection of sclerosants - the commonest used is 5% phenol in Almond. Gabriel's
synringe is made up of glass and it prevents melting by the sclerosants,
ii. Pile suturing
ACUTE ABDOMEN
Acute Abdomen I - Peritonitis
Acute Abdomen H - Intestinal Obstruction
Acute Abdomen H I - Non-Surgical Causes
Definition
Is abdominal conition of sudden onset and requires urgent evaluation and surgical treatment.
Lately, the term is not strictly related to conditions requiring surgical treatment only, but to
other conditions in which the interventions are not surgical.
Causes
a. Surgical
b. Non-surgical - i.e no operative intervention required
Acute Abdomen I
PERITONITIS
Definition
I s inflammation of the peritoneum
Anatomical Basis
Peritoneum is a semi-permeable membrane, it is well vascularized and has large surface area
There are 2 parts :
a. Parietal peritoneum
Lines the abdominal wall
I t is supplied by somatic nerves and pain is transferred via it.
b. Visceral peritoneum
Lines the viscera
I t is not supplied by the somatic nerves
15
vili.
Foreign bodies
ix.
Barium - from Barium studies
BACTERIAL PERITONITIS
- I s usually due to secondary infection of chemical peritonitis
Aetiology
- I s due bacterial invasion which may be via
a. Direct invasion
b. Local extension
c. Blood stream (septicaemia)
a. Direct invasion
- This follows
i. Perforation of a hollow viscus e.g in
Typhoid ileitis
Appendicitis
Cholecystitis
Pepti ulcer peritonitis
S I T tumour
Trauma
i
I
ii. Leakage of
abscess e.g
Liver abscess
Tubo-ovarian abscess
Malignant tumor of gut
iiii. Trauma to abdomen

b. Local extension
- This is from inflammed viscus e.g
Perforated duodenal ulcer
Salpingitis
Appendicits
Typhoid ileitis
c. Blood stream (septicaemia) / Migration through the gut wall

Note, the common causes of generalized peritonitis are
|
i.
Acute appendicitis
!
ii.
Perforated typhoid ileitis
iii.
Acute salpingitis
iv.
Perforated duodenal ulcer
Bacetrioloqy
The organisms involved are
a. Gram +ve
b. Gram -ve
a Anaerobic
d. Organisms from G i t
E.coli
i.
Streptococcus faecalis
ii. Proteus
v. Pseudomonas
v.
Anaerobes - Bacteroides
vi.
Others
Pathogenesis
The following are peritoneal reactions following the invasion of bacteria :
i.
Initial vasodilation (Hyperemia)
II.
Increased permeability
in.
Copious exudation of fluid & electrolytes - I t is initially clear, but becomes turbid and
then purulent.
IV.
There is deposition of fibrin on bowel loops. This causes matting together of the
bowel and may predispose to intestinal obstruction. This stage is called Formation od
Adhesion.
Localised peritonitis may becaome generalized.
v.
Pathophysiology
i.
There is stasis within the gut
There is a lot fluid and electrolytes moving into the peritoneum. The fluid may be upto 4
6litres in the peritneum.
iii.
Dehydration
iv.
Hypovolaemia
Hypotension
I
I
I
VI.
Shock
VII.
Consequences of shock
VIM.
Death
18
There is metabolic acidosis in the shock state

The toxins in the intestine may cause myoenteric paralysis, thus causing dilatation of the
intestine
The accumulated fluid in the abdomen causes abdominal distension. This leads to
Reduced abdominal movement with respiration
T
Impaired ventilation
I
Hypoxia
Respiratory acidosis
Proteins are lost from the perforated gut
Bowel sounds will be reduced or absent
There will be pre-renal or renal failure
Cardiovscular system may also be affected.
Clinical Features
Depends whether it is localized or generalized
a. Localised peritonitis
i.
Symptoms of causative disease e.g
Perforated appendicits
Perforated cholecystitis
i.
Pain
ii.
Fever
v.
Tachycardia
v.
Vomiting
vi.
Abdominal tenderness
vii.
Rigidity over the area of peritonitis (Guarding)
b.
r-,
vf
generalised
i.
Generalised abdominal pain - I t is constant and severe, it is made worse by movement
especially abdominal movements
ii.
Respiratory excursion of the abdomen is reduced. The patient breathes only with the
chest,
iii.
Respiration is shallow and faster
iv.
Features of Intestinal obstruction

o
Anorexia
o
Nausea
'
o
Vomiting - becomes constant when paralytic ileus is established
o
Constipation - occurs when ileus is present
v.
Diarrhoea - I s caused by pelvic abscess. I t starts with excretion of faeces to

mucous excretion
19
General examination
i.
Hippocratic fades
o
o
Ill-looking patient
Sunken eyes A temple area
o
o
o
Dry tongue
Rapid A high pulse
Dry A inelastic skin
Abdominal examination
i.
Abdominal distensipn
ii.
Little movement of abdomen with respiration
iii.
iv.
Rebound tenderness
v.
Guarding
vi.
Abdominal rigidity - is seen in generalized. I t is described as Board-like
rigidity,
vii.
Few or absent bowel sounds
Cardiovascular examination
i.
Pulse - is rapid and thready
Pelvic examination
bo not forget to examine the perineum A vagin since the cause may be from genitourinary.
Cervical excitation tenderness suggests salpingitis
Pelvic abscess is felt as anterior bulginess
Complications
1. Paralytic ileus
2. Acute intestinal obstruction
3. Septicaemia
4. Fluid & electrolytes loss
5. Residual abscess in abdominal cavity - The types are
i.
Sub-phrenic abscess
ii.
Sub-hepatic
iii.
Paracolic
iv.
v.
Pelvic
Interlobular
Investigation
Hi
l . PCV - is usually low
2. White cell count - shows leucocyosis
3. Blood culture
4. Electrolytes & urea
5. Urinalysis
6. Paracentesis abdominis ( Abdominal tap)
20
I s both diagnostic and therapeutic

I t shows the nature of fluid ( pus, blood, bile stained e t c ) .
The fluid is sent f o r m/c/s
7. Plain x-ray pf abdomen - Erect & Supine
o
Air under the diaphragm suggests perforation
o
> 3 air-fluid levels indicate stasis in the gut
8. Chest x-ray
9. Swab of vaginal discharge for m/c/s
10. Swab of urethral discharge f o r m/c/s
Differential Diagnosis
1. Acute intestinal obstruction
2. Acute haemorrhagic pancreatitis
3. Haemoperitoneum
4. Acute dysentery
5. Ruptured /Dissected aortic aneurysm
6. Basal pleurisy
7. Ureteric colic
8. Bilairy colic
9. Typhoid ileitis
10. Basal pleurisy
Treatment
Note - Whatever the cause of peritonitis, the principle of care is the same,
i.
Fluid A Electrolyte resuscitation
To improve tissue perfusion and correct electrolyte imbalance
Examples of fluid used : Ringer's lactate, Normal saline, Dextrose saline
Keep input/output chart
Monitor clinically
o Hydration status
o Dry skin
o Pulse
o JVP
Avoid circulation overload - listen to chest for crepitations
Check Electrolytes & urea frequently
Blood transfusion is given if anaemia is present
ii.
iii.
iv.
v.
vi.
Nasogastric decompression - with Nasogastric or duodenal tube. This helps to improve

respiratory movements
Broad-spectrum antibiotic therapy - to cover gram +ve, -ve & anaerobes
Potent analgesic - f o r the severe abdominal pain e.g morphine (lOOmg), pethidine (lOOmg)
Urethral catheterization - to monitor urinary ouput. Patient should void at leatst 30mls/hour.
Def initve treatment
- Ensure patient improves clinically before surgical intervention is carried out. This
makes the patient to be able withstand the stress of surgery
a.
Exploratory laparotomy - to
o
To determine the cause
21
b.
o
To clean the abdomen (Peritoneal toilette) thoroughly
o
To close perforation
Conservative treatment e.q for pelvic peritonitis (salpingitis)
o
Antibiotics
o
Analgesics
o
I V fluid
o
Monitor & Evolution
N.B
Barium enema is CONTRA-INDICATED in patients with intestinal obstruction.
Acute Abdomen I I
INTESTINAL OBSTRUCTION
Definition
Intestinal obstruction occurs when G I contents are prevented from passing distally.
Types
a. Mechanical - This can also be
i.
Simple
Mechanical
n.
b.
Paralytic
Another classification
a. Acute - usually refers to small bowel obstruction
b. Chronic - usually refers to large bowel obstruction
MECHANICAL BOWEL OBSTRUCTION

Characteristics
Acute Intestinal Obstruction
( Small bowel)
1. Colicky abdominal pain
Chronic Intestinal
obstruction
( Large bowel)
1. Obstipation
2. Vomiting
2. Abdominal distension
3. Abdominal distension
3. Abdominal pain
i4. Absolute constipation (Obstipation)
4. Vomiting - is faeculent
Note
Small bowel obstruction starts with abdominal pain while large bowel starts with
obstipation.
Vomiting is the last to occur in the large bowel obstruction because the intestinal content
travels a long distance before coming out.
22
Vomiting - from accumulation of G I contents which is due paralytic ileus

Absolute constipation (Obstipation) - it means neither solid faeces nor flatus could be
passed (constipation is difficulty in passing faeces, but flatus can be passed.
otagy
Simple Mechanical obstruction
I t means blood supply to the obstructed segment is NOT compromised.
The mechanical bowel obstruction
Accumulation of fluid and gas proximal to the point of obstruction

T
Abdominal distension
About the gas
The gas that accumulates at that point of intestine is from 3 sources :
i. Swallowed air - This is the most important because it contains
nitrogen gas which the body cannot absorb. I t
constitutes about 70%
ii. Carbondioxide
iii. Organic gases - from bacterial fermentation. Accounts f o r
20%
C02 & Organic gases can be absorbed or diffused into the body and is removed.
About the accumulated fluid
About 8 -10 litres of fluid is presented to the small bowel daily. This consists of saliva,
succus entericus, bile etc.
During intestinal obstruction, the normal absorbing strength of the intestine is lost, this
leads to fluid and electrolyte imbalance. ( Note, the fluid is not sequestrating)
Distension of the gut - if the gut is operated on, it takes time for it to return to normal.
b. Strangulation obstruction
Here, the blood supply of the gut is compromised.
The types of obstruction that easily results to strangulation are
i.
Volvulus - is twisting of the intestine along its mesentery.
Strangulation > Ischaemia Gangrene > Peritonitis
ii.
Obstructed inguinoscrotal hernia
The patient loses blood & plasma into the obstructed segment.
Toxins also escape into the circulation.
Translocation - means passage of bacteria through an intact but already compromised
intestineal wall either into the general peritoneal cavity or into the circulation.
Complications of Strangulated Intestinal obstruction

i.
Fluid loss A Electrolyte imbalance
ii.
Hypovolemic shock - from loss of blood & plasma from the
strangulated segment
iii.
Perforation - occurs if there is gangrene
iv.
Peritonitis
v.
Translocation of bacteria via compromised intestinal obtstruction.
vi.
Septicaemia - from the release of toxins into circulatio
Causes of Intestinal Obstruction
These can be grouped into :
a.
b.
Intra-luminal
Intra-mural
c.
Extra-mural
A. Intra-luminal
i.
ii.
Polypoid tumour
Intussusception
in.
Ascaris impaction - especially in children with big worm loads
iv.
v.
vi.
VII.
Large gall stones - Gallstone ileus. It usually impacts at ileoceocal junction i.e the
narrowest portion of the intestine
Foreign bodies e.g coin
Bezoars - seen especially in the mentally-retarded patients who may eat virtually
anything e.g
o
Hair - Tricho-bezoars
o
Cement - A cement bezoars
o
Tomato - Phyto-bezoars
Congenital malformations
o
Duodenal atresia & webs
o
Ileal atresia A webs
B. Intra-mural
These lesions arise from the intestinal wall
i.
Stricture - resulting from
Cancer
Radiotherapy
Chronic inflammatory lesions e.g

o Crohn's disease
o Amoebiasis
o Tuberculosis
o Actinomycosis
ii.
Iatrogenic e.g following end-to-end anastomosis
Extra-mural
i.
Adhesions ( Adhesive bands) - are fibrous bands that form after surgery
ii.
Extramural hernias e.g Inguinoscrotal hernia - it is the commonest casue of acute
intestinal obstruction in UCH.
iii.
Internal hernia
iv.
Extrinsic masses e.g
o
Tumour
o
Abscess
o
Large fibroids ( i n women)
v.
Pancreatic fibrosis
vi.
Volvulus
PARALYTIC ILEUS
I s a state in which the intestine fails to deliver or produce peristaltic wave.
or
Failure ( of normal neuromuscular mechanism ) of peristalsis to move intestinal content in an
antegrade manner
Neural
Humoral
Metabolic
Neural
i.
in.
iv.
Transection of spinal cord - causing spinal shock

Retroperitoneal lesions e.g ( Ureter, thoracolumbar spine, pancreas )
o
Acute pancreatitis
o
Ureteric stones
o
Retroperitoneal haemorrhage
Excessive handling of the gut by surgeons
Intestino-intestinal inhibitory reflex
When there is a mechanical bowel obstruction in one part of the intestine e.g
jejunum, the intestine tries to surmount the obstruction and if it fails, the
entire intestine becomes paralysed. This is mediated by a neural pathway.
Humoral
Peritonitis - Pus, urine in peritoneal cavity causes intestine to cease peristalsis. The
mediators are yet to be discovered.
Metabolic
i.
Electrolyte imbalance - is most important. The most significant is HYPOKALAEMIA !

Once there is hypokalaemia, the peristalsis stops.
1. Blockage of mesenteric arteries in patients with atherosclerosis
2. Abdominal crisis in sickle cell patients - is due to ischaemia of the vessels.
Diagnosis
I s 99% dependent on history A physical examination
Abdominal may be tympanitic
Low BP, Raised pulse rate A Reduced urinary output suggest shoch state
Investigation
j
1. Plain abdominal x-ray

a.
b.
i
Erect position - shows multiple air-fluid levels, when > 3, it suggests intestinal
obstruction
Supine position - differentiate the small A large intestines
Jejunum - Has valvulae conj (like a pile of coin )
Ileum - Has no features, it is just a hollow tube
Large bowel - Has haustrae, which do not traverse the whole diameter
Treatment
i.
Fluid resuscitation A correction of electrolyte derangement

Set up I V line with wide bore cannula
Blood transfusion - if necessary
i.
ii.
v.
v.
Nasogastric decompression
Urethral catheterization - Patient should make 30 - 50mls of urine /hour or 0.5ml/kg/hour
+ Broad-spectrum antibiotics
Exploratory laparotomy
For Strangulated hernia
o Loose the strangulation
o I f there is necrosis, do resection A join by anastomosis
o Repair the herniated part
Management of Adhesive Bowel Obstruction

Conservative treatment (Drip A Suck) is done f i r s t .
Set I V line to give I V fluid and replace the electrolyte loss - " Drip"
Pass Nasogastric tube - " Suck"
Observe closely
o When to remove NG tube
When the effluent is getting reduced
When the colour is changed
Reduction in in abdominal distension

o Patient has passed flatus, start oraffeeding with graded food i.e Water
Semi-solid > Solid
I f the conservative management fails i.e the features strangulation occur again
( Raised pulse, Low BP ),
26
Acute Abdomen I I I
NON-SURGICAL CAUSES
Introduction
These are non-surgical conditions that do not require surgery
A.
Diabetic Ketoacidosis (DKA)

I s the commonest cause of non-surgical acute abdomen
Classical features of appendicitis are seen
iv.
Abdominal rigidity
v.
Guarding
vi.
Rebound tenderness - may be localized to left lower quadrant
Note, most times, the patients are not aware that they are diabetic, so family
history is important.
I
i
li
I
!
\.
Investigation
i.
Full blood count
ii.
Urinalysis - may show
o
4+ glycosuria
o
Ketonuria
iii.
Chest x-ray
iv.
Blood sugar - is elevated
PORPHYRIA
I s not common in our environment
Clinical Feature
History of medications is important
History of urine becoming dark on standing confirms the diagnosis
C.
LYMPHOMAS
Lymphoma is a strong differential diagnosis of acute lymphoma
Clinical Feature
Classical Pel-ebstein fever
i.
Malaise
ii.
Abdominal pain
v.
Fever in every 3 days
i.
Typhoid fever
Investigation
i. Lymph node biopsy - shows Reedsternberg cells /Dorothy Reed cells
D.
LEUKAEMIAS
I s very similar to lymphoma in presentation
Blood do not clot because of the low platelets
27
SICKLE CELL DISEASE

The abdominal pain is due to thrombosis of vessels
I t is common during crisis
Diagnosis is easy because patient would have been diagnosed as a sickler.
RI6HT-SIDED PNEUMONIA
I t is found commonly in children
I t is confused with appendicitis because it occurs in the right compartment
Investigation
i.
Chest x-ray
MESENTERIC LYMPHADENITIS
Presents with upper respiratory tract infection i.e history of common cold
before presentation
I f it is diagnosed before surgery is made, it is likely to be treated surgically.
I t can be confused with appendicitis, but surgery can be done if diagnosis is not
confused.
Treatment
I s conservative
i.
Nasogastric tube
ii.
Intravenous infusion
HEPATITIS
Presents with pain in the upper quadrant. The pain is due to stretch of the capsule
I f hepatocytes are affected, the patient come down with jaundice
i.
&a\\ bladder disease
Treatment
High carbohydrate diet
PELVIC INFLAMMATORY DISEASE (PIP)
The pain is associated with menstrual period, it may be before, during or after.
Treatment
i.
Broad-spectrum antibiotics
ii.
Pus drainage - if formed
RENAL INFARCTION
Can cause low abdominal pain 6t abdominal distension.
28
DISEASES OF THE LARGE BOWEL

Consent
Mechanical
i.
ii.
Inflammatory
Volvulus
Intussuception
lesion
iii.
Diverticulitis
Neoplastic
iv.
v.
Miscellaneous
vi.
vii.
Adenocarcinoma of the Colon

Carcinoma of the rectum
Bowel Preparation
Colostomy
Section I
VOLVULUS
Definition
Is abnormal twisting of a segment of bowel on itself along its longitudinal axis.
Pa- ology
I t causes circulation compromise & closed loop obstruction
Strangulation Infarction > Gangrene
Incidence
Colonic volvulus is common in the elderly (60 - 70years)
Prtdisposing Factors
i.
Redundant segment of colon
ii.
Close approximation of point of fixation of the segment to serve as point for twisting. The
commonest site is sigmoid colon.
Aggravating Factors
i.
Chronic constipation with excessive laxative use
ii.
High residue diet leading to bulky heavy stool - this explains the increased incidence in
Bsatern Europe, Africa A Africa
Clinical Features
Abrupt onset
i.
Colicky abdominal pain
ii.
Nausea A vomiting
v.
Gross abdominal distension
Investigation
i.
Treatment
i.
ii.
Plain abdominal x-ray : shows "bent inner tube" or "sign of omega"
Fluid Resuscitation
Monitoring
- Urine output: 1 -1.5ml/kg/hr
Attempt at reduction by using lubricated rectal tube via proctoscopy if patient presents
within 24 hours when infarction will have not occurred
Or use Flexible f ibreoptic sigmoidoscopy
Surgery - Exploratory laparotomy
bo detorsion for early detorsion
Check if the gut is viable or infarcted
a. I f viable, detwist and do fixation technique.
iii.
IV.
v.
Note, viable loop

o
Flick - peristalsis
o
o
Apply warm packs - pink

100% oxygen - pink
b. I f infarcted, do the following

betwist
o
Resection
o
End-to-end anastomosis or sigmoid loop colostomy.
o
Section I I
INTUSSUSCEPTION
Definition
Is invagination of one segment of intestine into the another.
Entering segment - Intussusceptum
Receiving segment - Intussuscepiens
Epidemiology
I t is a common cause of intestinal obstruction in infants & children.
I t is relatively uncommon in adults.
Aetiology
I n infants, the aetiology is usually idiopathic, but in adults, always look for an organic cause e.g
tumour.
:|
Types
1. Entero-enteric - small bowel into small bowel
2. Ileo-caecal - the ileocaecal valve moves into the caecum
3. Ileo-colic - is the commonest in children because of the Peyer's patches especially in the f i r s t 6
months
4. Colo-colic
Thera was past history of caeco-colic intussucseption in adults in Ibadan which was called Ibadan
intussusception. However, this is rare nowadays.
Imical Features
i.
Signs of intestinal obstruction
o Colicky abdominal pain
o Vomiting
o Abdominal distension
ii.
Passage of red-currant jelly stool is seen in children - This is because of the excessive
mucous production
iii.
On examination
Sausage-shaped mass is palpated
ivestiqation
1. Barium enema
- these signs are pathognomonic
o
Claw sign - seen in incomplete intussusception
o
Coiled spring appearance - in complete
Incomplete
Complete
"flreatment
a. Early cases: < 24 hours
- Barium enema (hydrostatic) reduction in children
b. After 24 hours
Exploratory Laparotomy
a. In children - do reduction. Resect only when it is gangrenous .
b. In adults, do straight-forward resection & end-toend anastomosis.
31
Section I I I
DIVERTICULAR DISEASES OF THE COLON
Definition
Diverticulum is outpouching of the mucosa at the points where blood vessels penetrate the
colonic wall.
Causes
Most are acquired, and there is part of ageing process. (The congenital is Merkel's diverticulum
which is seen ileum.)

I t is commonest in descending A sigmoid colon.
Predisposing Factor
I s due to lack of fibre in diet ( common in Mordern American A Western Europe diet)
Clinical Features
a.
Uncomplicated diverticulosis seldom produces symptoms
b.
But in complicated, when there is obstruction of the orifice, inflammation occurs within the
diverticulum and adjacent bowel. This is known as diverticulitis.
Investigation
i. Barium enema - Uncomplicated diverticulosis shows "sawtooth appearance"
Complications
1. Recurrent periodic inflammation : Presenting with
o
Abdominal pain
o
Constipation or diarrhoea
o
Rectal bleeding
o
Fever
o
Nausea &. vomiting
2. Perforation - leading to generalized peritonitis or pericolic abscess formation if localised
3. Intestinal obstruction a.
I n colon- it is due to progressive fibrosis which causes stenosis.
b.
I n small intestine, it is due to adhesions caused by pericolitis
4. Haemorrhage - May present with profuse bleeding per rectum without clinical evidence of
inflammation.
ion
5. Fistula formation
i.
Vesico-colic - is the commonest. I t leads to pneumaturia caused by klesiella
sp , proteus sp.
ii.
Vagino-colic
Entero-colic
iii.
iv.
Colocutaneous (faecal fistula)
Nofe, diverticulosis is a cause of massive bleeding per rectum, it iccurs when the vessels are stretched
without any chemical evidence of inflammation.
Treatment
1. Elective colectomy ( Pancolectomy ) + Ileo-rectal anastomosis
2. Treatment of complications
Require emergency surgical treatment.
These complications have a high morbidity A mortality rate.
For bleeding, Barium enema is diagnostic and therapeutic.
3. High f i b r e diet
4. Follow-up
Section IV
ADENOCARCINOMA OF THE COLON
Ae iopathoqensis
1. Hereditary
i.
ii.
iii.
iv.
v.
vi.
2.
Familial adenomatous poliposis ( FAP)

Hereditary Non-polyposis Colorectal carcinoma (FNCC) - is known as Lynch
syndrome.
Peut-Jeghers
Gardener's
Turcot's
Crocite-Canada
Environmental
- There is increased incidence in Western part. I t is uncommon in West Africa.
3. Diet: I t is common in
i.
High f a t - butyric acid is carcinogenic
ii.
Low fibre - causes increase in transit time
iii.
Low f r u i t - to mop up free oxygen radicals
4. Precancerous lesions e.g
Ulcerative colitis - develops into carcinoma of colon in about 15 - 20 years later.
i.
Schistomiasis of colon
ii.
Amoebiasis
v.
Lymphogranuloma venereum.
Clinical Features
Age : usually > 50years, but it is not rare in early adult life.
II.
The symptoms depend on the site of colon involved :
a. Caecum A Ascending colon
ii.
Anaemia
33
b.
iii.
iv.
Malaise
Palpable lump
v.
Intestinal obstruction hardly ever occurs here because the luminal content is stil
liquid.
Transverse colon
i.
My be confused with Carcinoma of stomach.
ii.
Anaemia
iii.
Malaise
iv.
+ Intestinal obstruction
Descending colon

Change in bowel habit
Palpable lump
Intestinal obstruction - tooth paste caliber stool is passed
d. Sigmoid colon
II.

Intestinal obstruction
Feeling of incomplete evacuation
.-Tenesmus - is seen in low lesion. I t is thp h ^ l ^ i r k " f mrrmn*^
nf r<rtitm
Iriyestiqatton
Proctoscopy
Sigmoidoscopy : Rigid <5t Fibreoptic
Colonoscopy ( Flexible fibreoptic)- to reach the caecum
Barium enema - to check f o r synchronous tumours
Note/'iii - v are done to rule out synchronous lesions
'eatment
Pre-operative bowel preparation
Resection & End-to-end anastomosis (re-establishing bowel continuity)
Colostomy - if it is inoperable or irresectable.
Adjuvant treatment
a.
Chemotherapy
1. 5 -Fluorouracil is most common is used. I t helps to mop up micro-metastasis
o
I t reduces recurrence A increase the quality of life.
o
The dose is 500 - 750mg weekly f o r 52 weeks.
b. Imunotherapy: using Levamisole
Levamisole ( an antihelminthic ) is also used. I t stimulates the killer cells. The dose
40tid f o r 3 days, repeat every 2 weeks
o
Pre-chemotherapy requirement
PCV - > 30%
WBC- > 2,500
i.
Platelets > 150,000cells/cmm
34
c.
Radiotherapy-
external beam. I t is used in inoperable cases.
Surgical Options
1.
2.
- Right hemicolectomy
- Extended hemicolectomy
3.
4.
- Extended hemicolectomy
- Left hemicolectomy
5. Left hemicolectomy
6. Sigmoid colectomy
7. Abdominoperineal resection
Section V
CARCINOMA OF RECTUM
Predisposing Factors
Familial
Adenoma
Clinical Features
i.
Rectal bleeding - is the earliest & most common symptom. I t is usually mixed with faeces. I s
also the hallmark,
ii.
Tenesmus - is painful ineffective straining with sense of incomplete voiding,
iii.
Secondary haemorhoids - especially in patients > 45 years.
iv.
Metastasis : Liver is the commonest site, presenting with jaundice A hepatomegaly,
v.
Intestinal obstruction
vi.
Early morning diarrhea
"
Diagnosis
1. Digital rectal examination
2. Proctoscopy - f o r biopsy
3. Sigmoidoscopy
4. Colonoscopy
5. Barium enema - f o r other (synchronous) lesions which affect the course of management.
1. Tuberculosis of rectum
2. Lymphogranuloma venereum (LSV)

3. Amoeboma
35
Investigation
1. As above
2. Intravenous urogram - to know the state of the ureters
3. Ultrasound - To rule out
- Secondary metastasis to the liver
- Ascites
- Ureters involvement
4. Tumour marker - Carcino-embryonic antigen (CEA)
5. Ful blood count - f o r pre-op. prepration A adjunct treatment.
Treatment
Surgical Options
} L
o\
\
\
a.
Rectum is about 15 - 20cm long.
Proximal Third - Low anterior resection & end-to-end anastomosis (Sigmoido-retal)
b. Middle & Distal Thirds

i. Abdomino-perineal excision/resection +
ii. Sealing o f f of the anus +
iii. Permanent (Terminal) colostomy
Or I n centres with Staplers, Spincter Saving Resection can be done.
N.B Read" Anastomosis"
DISEASES OF THE ANORECTUM

RAPHA
1.
2.
3.
4.
5.
Rectal Prolapse
Proctitis
Anal Fissure ( Fissure-in-ano)
Haemorrhoids
Fistula-in-ano
36
Section I
RECTAL PROLAPSE
Definition
Is protrusion of the mucosa and submucosa outside the anus.
Types
a.
Partial
- protrusion of mucosa and submucosa of rectum outside the anus
b. Complete
- all layers of the rectal wall protrude outside the anus
- aka PROCIDENTIA
Incidence
Occurs at extremes of life : in children, 1 - 3 years and elderly individuals
Aetiology
a. Infants A Children - is due to
Undeveloped sacra\ curve which leads to direct downward course of the rectum.
Diarrhoea
iii.
Whooping cough
iv.
Malnutrition e.g marasmus
b. Adults - due to
i.
Third degree haemorrhoids
ii.
Torn perineum in females - in cases of cephalopelvic disproportion without episiotomy.
iii.
Straining from urethral obstruction
iv.
Old age - leading to laxity of anal sphincter
Treatment
a. For Infants & Children
i.
Digital repositions - by the parent. I t is done temporarily until the child gets better
and if not, Thiersch procedure is done.
ii.
Dietary nourishment
iii.
Submucosal injection of sclerosant. This elicits fibrosis to glue the mucosa.

E.g of sclerosants are
o
5% phenol in almond oil
o
Sodium tetradecylsulphate (STD)
Ethanolamine oleate
Note : Other conditions requiring sclerpsants are

i.
Oesophageal varices
ii.
Varicose veins
iv.
Thiersch 's operation
37
^
(
Using non-absorbable suture e.g silk or nylon

The stitich does cause obstruction.
I t is removed after a year
b. For Adults
Sclerosants therapy - f o r early partial proplase
Excision of prolapsed mucosa - if partial
Delome's operation
f o r complete prolapse. I t consists of
o Mucosectomy - removal of mucosa from the prolapse
o Plication of the underlying muscle - so that it is concertinaed towards
the anal canal where it is further sutured to the proximal rectal
mucosa.
IV.
V.
vi.
vii.
viii.
Thiersch's procedure
Well's operation - rectum is fixed to the sacrum by inserting a sheet of
polyvinylalcohol sponge between them.
Ripsteins operation - the rectosigmoid junction is hitched up by a Teflon sling to the
f r o n t of the sacrum.
Simple rectoplexy - Fix the rectum to sacral bone
Lahaut's operation - Hang the rectum underneath the rectus muscles
Section I I
PROCTITIS
Definition
- Inflammation of rectal mucosa only

Types
a.
Non-specific
the aetiology is unknown.
I t is believed to be a mild and limited form of ulcerative colitis
Clinical feature
i.
b.
Specific
i.
Pain during defeacation with passage of mucous and blood
Clostridium difficile - Metronidazole
38
ii.
iii.
iv.
v.
vi.
vii.
Bacillary dysentery ( Shigella) - Septrin, Metronidazole, Vancomycin

Amoeba dysentery - Metronidazole
Tuberculous proctitis - Streptomycin, Ethembutol
Gonococcal proctitis - Ofloxacin, Ciprofloxacin
Radiation - this is iatrogenic
Primary syphilis
Treatment
I s to be targeted to the various causes
The non-specific type may be ameliorated with sulphalsalazine or prednisolone enemas.
Note
Proctalgia Fugax - is anal pain of unknown origin, usually in hysteria women.
Section I I I
ANAL FISSURE
Introduction
Definition - I t is a linear ulcer situated in the longitudinal axis of the posterior anal commissure
usually in the midline. ( Anterior is common in female)
The squamous mucosa of the lower half of the anal canal is prone to superficial ulceration which
presents clinically as anal fissure.
I t is a painful condition because it involves the highly sensitive squamous epithelium of anal canal.
Types
1. Acute - when it is < 4 weeks
2. Chronic - when > 4 weeks. The base is indurated.
Clnical Features
History
i.Pain - which occurs during and after (upto 5 - 7hours) defeacation is typical,
ii.
Bleeding - is usually slight
iii.
Mucous dischrage - usually slight
iv.
There is usually sphincteric spasm which makes the fissure worse,
v.
The natural sequel of anal pain is f o r the patient to avoid def eacation which results in
anterior formation of a hard constipated stool, thus a vicious cycle is set up.
Physical Examination
i.
Sentinenel skin tag
ii.
Anal spasm
|
iii.
Intense pain on attempting to do digital rectal examination, thus DRE should only be
performed under anaesthesia i.e EUA
iv.
The fissure is usually at 6: 00 clock
1. Carcinoma of the anus
- Mostly squamous cell carcinomas
39
- There are pain and ulceration

2. Primary syphilis
3. Crohn's disease
Treatment
a. Conservative
* Aim: I s to achieve complete internal sphincter relaxation, the ulcer heals
spontaneously.
/
Options
Stool softeners e.g Agarol
Lubricants e.g Liquid paraffin
ii. Anaesthetic gel e.g Xylocaine
v. Glycerine trinitrate paste - introduce recently to relax the anal spincters.
b.
Operative
i.
Wide anal dilatation ( Anal stretch)- using 4 fingers
ii.
Lateral anal sphincterotomy
- Post-op complication is incontinence
iii.
Dorsal f issurectomy A Sphincteromy
- Involves excision of fissure leaving a gaping woung to heal by secondary
intenetion.
Section IV
HAEMORRHOIDS (PILES)
aka - Prolapsed Anal Cushion
Definition
*Are engorgement of veins in relation to the anus when the anal lining descends and is gripped by
the anal sphincter.
The mucosal lining supporting these veins are known as Anal Cushions.
Types
a. Internal - when covered by anal mucosa (appears pinkish )
b. External - when it is covered by skin (appears brownish)
c. Internoexternal - when the varieties are associated (appears pinkish brown)
Aetiology
Primary Haemorrhoids
i.Any condition predispoising to straining which cause the anal cushions to slide downwards.
ii.
Herditary
iii.
Gravity - is not seen in animals
iv.
Diarrhoea
b. Secondary Haemorhoids - associated with another condition
40
i. Carcinoma of rectum
ii. Pregnancy
iii.
iv.
v.
Straining at micturition e.g in urethral stricture, enlarged prostate

Chronic constipation
Pelvic tumours
Classification
I s based on bleeding and prolapse
a. First degree - no prolapse, but there is post-def eacation bleeding called " Splash into pan"
b. Secondary degree - There is prolapse on defaecation, but it reduces spontaneously
c. Third degree - There is prolapse on defaecation, but has to be manually reduced.
d. Fourth degree - The prolaspe remain permanently outside, it cannot be reduced manually.
Pathology
-
Internal haemorrhoids are frequently arranged in 3 groups: 3, 7, 11: 00 clock when the patient is
in lithotomy position. These are positions are in line with the blood supply of rectum.
Secondary haemorrhoids may be circumferential

Clinical Features
- " 5 Ps"
1. Bleeding ( Pallor) - is the earliest and principal symptom. May present with chronic anaemia
resulting from persistent bleeding
2. Prolapse
3. Mucoid discharge (Pus) - leading to
4. Pruritus
5. Pain - is absent unless if it is complicated by strangulation (gripped by anal sphincter) or
thrombosis.
i.
Digital Rectal Exam
- Primary haemorrhoids would not be f e l t
Investigation
f
1. Proctoscopy
'
- On the way i.e when removing the endoscope, primary haemorrhoids bulge into
view, I t is purplish.
2. Sigmoidoscopy - To exclude secondary causes
3. Barium enema - f o r those > 40 years presenting f o r the f i r s t time with haemorrhoids.
i
41
Complications
1. Haemorrhage
2. Strangulation
3. Thrombosis
4. Ulceration
5. Gangrene
6. Fibrosis
7. Pylephlebitis
Management
a. Conservative
i.
Diet - taking high fibre and avoid constipating diets
b.
ii.
Lubricants e.g Liquid paraffin to minimize straining
iii.
Sitz baths - in warm water to relax the anal sphincter.
Non-operative
i.
Elastic band ligation ( Barrons binding apparatus)
ii.
Injection sclerotherapy ( Gabriel syringe - is glass). Examples of sclerosants are
o
5% Phenol in almond oil
o
Sodium tetradecyl sulphate
o
Ethanolamine oleate
iii.
iv.
c.
Cyrotherapy - using liquid nitrogen cyroprobe at 196 C. This method is not very
popular
Infra-red ray photocoagulation - used where it is available
Operative
Indications
i.
ii.
iii.
iv.
v.
Third degree haemorrhoids

Fourth degree haemorrhoids
Fibrosed haemorrhoids
Intern-external haemorrhoids with preponderance of the external
Failure of non-operative treatment of 2 nd degree haemorrhoids
Options
- Haemorroidectomy
i.
Open technique( Milligan-Morgan)
ii.
Close technique ( Hill-Ferguson)
Post-operative Care
o
Warm baths - twice a day
o
Bulk laxative
o
Use of dilator to prevent stricture
Post-opeartive Complications
Early
i.
Acute retention of urine
ii.
Reactionary haemorrhage
42
iii.
Pain
iv.
v.
vi.
Secondary haemorrhage
Anal stricture
Anal fissure
Late
Section V
FISTULA-IN-ANO
slfini
inition
I s a track lined by granulation tissue which connects deeply in the anal canal or rectum and
superficially on the skin around the anus.
Palhogenesis
I t usually results from an anorectal abscess which burst spontaneously or was opened
inadequately.
I t continues to discharge on and off.
I t hardly ever closes permanently without surgical aid.
Classification
I s based on anorectal ring
a. Low type - Opens below the anorectal ring
b. High type - Opens above. I t has 4 sutypes
i.
ii.
v.
Supralevator
Transphincteric
Intersphnicteric
Suprasphincteric
The signicance of this classification is that a low fistula can be laid open without the fear of
permanent incontinence while a high fistula can be treated only by staged operation, it of tens
involving the use of a temporary colostomy.
SOODALL ' S RULE : states that fistula with an external opening in relation to the anterior half
of the anus tend to be of the direct type whereas those in relation to the posterior ( are more
common) of the anus tend to have curving tracks.
A
Investigation
1. Digital rectal examination - Internal opening may be felt
2. Proctoscopy - the internal opening may be seen
3. Sinogram - the anatomy of the fistula may be seen. Shows if it is high or low.
43
Treatment
o
Fistulectomy - Excision and allowing it to heal by secondary intention.
Excision + Colostomy - For High fistula
Note
Most f istulae have single opening
Multiple f istulae - think of chronic granulation :
i.
Schistosomiasis
Amoebiasis
ii.
Tuberculosis
iii.
iv.
Lymphogranuloma venereum
v.
Carcinoma of rectum
ACUTE APPENDICITIS
Anatomy
o
'
Locations
ii.
iii.
iv.
v.
vi.
o
o
o
Retrocaecal - constitutes 74%

Pelvic- 2%
Paracolic
Subcaecal
Pre-ileal
Post-ileal
Base : is identified by point of confluence of the 3 taenia coli.

Mesoappendix
Blood Supply : I s supplied by appendicular artery which is an end artery. The significance is that
its thrombosis leads to gangrene appendicitis.
Pathogenesis
Causes
Inflammation
Pinworm (Enterobium vermicularis)
Ascaris ( Ascaris lumbricoides)
Faecolith
Obstruction
Mucous accumulation
Inflammatory exudates
Increased intraluminal pressure

44
Lymphatic obstruction
Oedema A Ulceration of mucosa - I f antibiotic is given at this point, it may resolve spontaneously
Further distension causes venous obstruction
Ischaemia of the wall
Bacterial invasion
Acute appendicitis
Adherence of greater omentum A small intestinal loops to

wall off the spread
Ischaemic necrosis
Formation of appendiceal mass
I
Gangrenous appendicits
Peritonitis
Risk Factors for Perforation

1.
Extremes of age
2.
Immunosuppression
3.
Diabetes mellitus
4.
Faecolith obstruction
5.
Pelvic appendix
6.
Previous abdominal surgery
Clinical Features
There are 2 typical symptoms
i.
Pain in epigastric or peri-umbilical area - it settles down in the right lower quadrant
(right iliac fossa)
ii.
Anorexia - is a constant A useful feature
Other symptoms are
Nausea
Vomiting
iii.
Headache
45
Atypical presentation is common in the elderly who may have suprapubic discomfort and
tenesmus. (pelvic appendix)
General Examination
i.
Pyrexia
ii.
Localised tenderness in right iliac fossa
iii.
Features of peritonitis
iv.
Pointing's sign - using Mcburney's point
v.
Rovsing's sign - is elicited by pressing the side of the patient, there would be
tenderness on the right side because the of the distension of gas in the appendix,
vi.
Obturator's sign - I t involves the leg and internally rotate it, the patient feels pain.
I t is for pelvic appendix,
vii.
Psoas' sign - I t involves extending the leg. I s for retrocaecal appendix,
viii.
Pelvic appendix - may present with diarrhea and frequency of micturition.
Investigation
1. WCC - is not too elevated unless it is perforated
2. C-reactive protein - not specific. 85%
3. Plain abdominal x-ray - nil
4. Ultrasound - I f appendix is seen, it means it is inf lammed, if not, it is not inf lammed. I t shows
thickened appendix and periappendiceal fluid
5. Barium enema - I f appendix is visualized, it means it is not inf lammed. I f the whole appendix is
seen, peradventure it is obstructed by faecolith.
Complications
1. Peforation - causes generalized peritonitis which would be presenting complaint. Note, after
perforation, the pain subsides because of the relief of distension in the appendix. A f t e r few
hours, features of peritonitis set in e.g guarding, abdominal rigidity, reboud tenderness.
,
i.
Pelvic Inflammatory disease
- I s difficult to separate especially when it is on the right side.
- Ask for LMP, as it tends to occur during and just after menstrual period.
- Vaginal discharge is present
- On examination, there is tenderness in the lower abdomen.
- On vaginal examination, the cervical excitation tenderness is positive.
- WCC is very high.
- Temperature is very high
ii.
:t
iii.
iv.
v.
Mittleschmertz / Ovulation pain

- History ; Ask f o r LMP
Ruptured corpus luteum
Ectopic pregnancy
Mesenteric lymphadenitis
- I t usually occurs qfter respiratory tract infection e.g sorethroat (pharyngitis),
common cold.
- There is tenderness in right iliac fossa
- WCC - shows increased lymphocytes & neutrophils
- Treatment is conservative.
46
VI.
VII.
viii.
ix.
x.
xi.
xii.
xiii.
Right Ureteric calculus

There is severe pain A vomiting
The pain radiates to the right hemi scrotum or labial maora A right inner thigh
Investigation - shows microscopic haematuria
Treatment - involves anagelsics and good hydration
Torsion of Ovarian cysts
Ectopic pregnancy
Diabetic ketoacidosis - Urinalysis for glucose and acetone
Right-sided pneumonia
- occurs especially in children
Porphyria
Lymphoma / Leukaemia
Carcinoma of the colon
- Oschar sharen
Age -dependent Differential Diagnosis

Children
1. Gastroenteritis
2. Mesenteric lymphadenitis
3. Merkel's divericulum
4. Intussuception
5. Lobar pneumonia
Adult Female
1. Mittleschermz
2. Salpingitis
3. Pylonephritis
4. Ectopic pregnancy
5. Torsion of ovarian cyst
6. Endometriosis
Adult
1. Ureteric colic
2. Perforated duodenal ulcer
3. Testicular torsion
4. Pancreatitis
5. Cholecystitis
6. Rectus sheath haematome
Elderly
1. Diverticulitis
2. Intestinal obstruction
3. Colonic carcinoma
4. Torsion appendix epiplocical
5. Mesenteric infarction
6. Aortic aneurysm
Management
n.
Append icectomy - Open A Laparoscopy

Antibiotics - is recent
Preoperative Investigation in Appendicitis

Routine
i. Full blood count
ii. Urinalysis
Selected
Pregnancy test
Electrolyte and urea
iii. Abdominal x-ray - Supine
iv. Abdomino-pelvic ultrasound
47
Post-operative Complications
1. Wound infection
Treatment: Wound drainage A antibiotics
2. Intra-abdominal abscess
Clinical Feature
!
i.Post-op fever - 5 - 7 days after
I
ii.
Malaise
iii.
Anorexia
Investigation
i. Abdominal ultrasoun
ii. CTscan
Treatment
- Percutaneous drainage
Prevention
- Peri-operative antibiotics
3. Ileus ( adynamic)
- I s seen especially in gangrenous appendix
4. Respiratory complications
Treatment: Analgesia A physiotherapy
5. DVT
Prevention - Prophylaxis
6. Adhesive intestinal obstruction - most common late complications
Management of Appendiceal Mass

Conservative
i.
Mark the limit of the mass on the anterior abdominal wall with a skin pencil.
ii.
Nasogastric intubation
iii.
Intravenous f luidAntibiotics
iv.
Moniroting of vital signs : Temperature, Pulse rate 4hourly
Criteria For Stopping Conservative Management
1.
A rising pulse rate
2.
Increaseing or spreading abdominal pain
3.
Increaseing size of the mass
4.
Vomiting or copious gastric aspirate
48
PEPTIC ULCER DISEASE & COMPLICATIONS

linieal Anotomy of the stomach
Structures
IV.
Parietal cells : secrete Hcl A Intrinsic factor. I t is found in the body

G cells : I s found in the natrum
Antral pump : is respondible f o r gastric emptying. I t is found in the antrum and
pylorus.
Vagus nerve : is secretomotor for the stomach. Produces 60% of acid secretion
Clinical Significance
o
Drainage procedures : are
i.
Gastric jejunosotomy
ii.
Pyloroplasty
o
Truncal Vagotomy
o
Selective Vagotomy - is denervation of all stomach supply leaving other abdominal viscera
o
High Selective Vagotomy - I s also called Parietal cell vagotomy. I t does require drainage
procedures. Note, if PUD is complicated by gastric outlet obstruction, there is no need for
HSV since a drainage is necessary to relieve the obstruction.
o
Antrectomy - is removal of & cells which secrete gstrin. I t s has high morbidity and
mortality.
Blood Supply
I s by gastroduodenal artery which goes posteriorly to the f i r s t part of
duodenum. Significance of its anatomy is that ulceration into it results into
bleeding.
PEPTIC ULCER
Definition
I s ulcer caused by acid or pepsin digestion
Incidence
I s found worldwide
Male /Female ration is 9 : 1
Age : 20 - 45 years
Site of Occurrence
These are areas accessible to acid and pepsin
i.
Duodenum - is the commonest, usually the anterior portion of the f i r s t part. I f
posterior, it may extend to the pancreas. And when it is seen in both anterior and
posterior parts, it is called Kissing ulcers,
i.
Stomach
ii.
Lower oesophagus
v.
Jejunum (Gastrojejunostomy)
v.
Merkel's diverticulum - that contains ectopic gastric tissue
Pathogenesis
I s multifactorial
I t is broadly grouped into
a.
Increased gastric acid secretion
b.
Impaired Mucosal defence against acid & pepsin
c.
Acid-Induced focal gastric metaplasia
a.
Increased gastric acid secretion - both Basal Acid Output ( BAO) A Maximal Acid Output (MAO)
are increased
Cephalic - Increased stimulus of secretion e.g stress, worry, anxiety etc
i.
Humoral - Increased gastrin release e.g spices, pepper, alcohol etc.
ii.
Increased parietal cell mass
- I s commoner in mlae
- Associated with gastrinoma
- There is hyperparathyroidism
iv.
Failure of inhibition of acid
- There is disturbance of feedback mechanism between
acidity
and gastrin inhibition.
- Secretin, SIP A VIP are also involved
b. Impaired Mucosal defence against acid & pepsin

i.
Incomplete neutralization of acid and pepsin - due to
o
Inadequate alkali secretion
o
Rapid gastric emptying
ii.
Impaired resistance of duodenum mucosa

o
Ischaemia of mucosal patches
o
Decrease in the protective layer of mucous and glyoclipids e.g alcohol
50
K cxÔ [c/r~>
Q c UCc -ulOs
'
Interfenrence with the regenerative ability of duodenal epithelium.

c.
Acid-Induced focal gastric metaplasia - as in

i.
Helicobacter pylori
I s a gram -ve spiral, mobile, micro-aerophilic, flagellated, urease and
peptidase bacterium.
I t colonises alkaline mucous layer over epithelium.
Has no direct causal relationship
I s found in antral mucosa
I s seen in 90- 95% of peptic ulcer patients ( and 25 -40% of general
population)
I t s elimination leads to reduction in recurrence rate of PUD
Alcohol
II.
Smoking - Impairs ulcer'healing and promotes recurrence. I t s mechanisms are
iii.
as follows
o Impair gastroduodenal motility
o Reduced prostagladins production
o Increased production
o Reduced bicarbonate production
o Compromised blood flow
IV.
NSAIDs e.g Asprin - is toxic to surface epithelium. I t inhibits cyclooxygenase, thereby reducing prostagladins synthesis.
Cell membrane phospholipids
Phospholipase A2
T
Arachidonic acid
Cyclooxygenase
PgS2
o
o
o
PgE2
PgF2
PgD2
History
Epigastric pain
Aggravated by hunger - usually 2 -3 hours after meal
Relieved by food, alkali, milk
n.
iii.
iv.
v.
vi.
Radiation to the back - shows pancreatic involvement.

Effects of sleep, posture
Vomiting - is copious, and of stale food.
Appetite
Malaena - passage of dark tarry stools. I t is due
Fe + H2S
ê2S (is black in colour)
Haematemesis
Sudden abdominal pain - is a feature of peritonitis
o Epigastric tenderness
o Features of peritonitis
Generalized tenderness
Guarding
Rebound tenderness
o Succussion splash ( seen in GOO) - elicited 4 hours after meal
o ORE - shows malaena
Complications
1. Bleeding - is the leading cause of death in Ibadan
2. Penetration of pancreas
3. Perforation
4. Gastric Outlet Obstruction - is caused by duodenal stenosis which results from cicatrisation of
pylorus
Diagnosis
- I s basically clinical
1. Duodenal ulcer
2. Gastric ulcer
3. Gall Bladder disease
4. Reflux oesophagitis
5. Pancreatitis
6. Carcinoma of transverse colon
7. Liver Cirrhosis
8. Intestinal parasites
9. Non-ulcer dyspepsia.
Investigation
1. Oesophago-gastro-duodenoscopy (OGD) - for visualization and biopsy
2. Barium meal and Follow-through - is 90% accurate
3. Histology or bacteriology - for detection of H. pylori
4. Blood group
O - Ulcer
A - Cancer
5. Stool bacteriology and occult blood test
6. Gastric acid studies - BAO A MAO. I t is useful in Zollinger- Ellinson syndrome and Recurrent ulcer.
Treatment
A. Medical
- I s the principal mode of treatment of uncomplicated disease
Mechanism: I s to reduce free luminal protons
Aim
i.
ii.
Relieve pain - which is the main symptom

Promote healing
52
iii. Reduce or neutralize high acid secretion

iv. Eradicate H.pylori
Options
a. Parietal Cell Control
ry-^y-wvn
4
1.
2.
3.
4.
Sites
Cholinergic receptor blocker e.g Pirenzepine
H2 Receptor blocker e.g Cimetidine
Prostaglandin Analogue e.g Misoprostol
Proton pump Inihibitors e.g Omeprazole
b. Topical treatment
i. Sucralfate
ii. Colloidal Bismuth Subcitrate
c. Neutralisation of acid
d. Treatment of H. pylori - Using Triple antibiotic therapy
e. Other general measures
Rest
i.
Sedatives A Anxiolytics
ii.
Diet - Frequetn, milk avoid spoces
v.
Avoid alcohol, smoking
B. Surgical Treatment
Aim " Permanent reduction of gastric acid output
Prinicples
Neural disruption
i.
Gastric damage
ii.
Gastric resection
Indications
i.
Intractability and failed medical treatment
a. Persistent severe pain despite medical treatment
b. Non-compliance with medical treatment
c. Failed H. pylori eradication after multiple attempts
d. H. pylori ulcer that do not respond to standard treatment
Complications
a. Bleeding - when it is prolonged, recurrent or massive resulting into shock.
b. Perforation
c.
Gastric outlet obstruction - its mechanism involves

o oedema formation
o Pyloric spasm
o Cicatrisation
Options
1. Truncal Vagotoomy and Drainage (Pyloroplasty)
!
2. Selective Vagotomy and Drainage
3. High Selective Vagotomy ( Parietal cell vagotomy, Proximal gastric vagotomy)
4. Antrectomy/Partial gastrectomy
5. Vagotomy A Antrectomy
Surgical Treatment
1 . Bleeding
i.
ii.
iii.
iv.
of Complications
Haemodynamic stability
Early involvement of surgery
Early endoscopy
Suture Ligation - is a def initve ulver operation
2. Perforation - involves the general principle of treating generalized peritonitis irrespective of the
cause
i.
Resuscitation
ii.
Gastrointestinal decompression
iii.
Antibiotics - using broad spectrum
iv.
Analgesice
v.
Def initce treatment
- Closure + Omental patch
- Peritoneal toilette
- + Def initve ulcer treatment
3. Gastric Outlet Obstruction
OGD
Barium meal
Follow-through
Vagotomy A Drainage
Complications of Surgery
1.
Bleeding from anastomotic site
2.
Gastric retention - from stoma obstruction
3.
Early postprandial dumping ( Hypovolaemia)
4.
Late Postprandial dumping ( Reactive hypoglycaemia)
5.
Steatorrhoea
!j
6.
7.
8.
Enterogastric reflux
Diarrhoea
Recurrent Ulceration
9.
Iron def icience anaemia
10.
11.
Leakage of duodenal stump

Obstrution of stoma
12.
13.
14.
Acute pancreatitits
Weight loss / Failure to gain weight
Bilous vomiting
15.
16.
Megaloblastic anaemia
Osteomalacia
17. Anastomotic ulcer

18. Gastroduojejuno colic ulcer
19. Carcinoma of gastric remnant
VARICOSE VEINS A PERIPHERA ARTERIAL DISEASES

Definition
Are dilated veins of the leg
Anatomy
There are 4 groups of veins
Deep veins - has no valves
i.
Short A Long saphenous veins - has valves
ii.
Perforators - connects superficial to deep veins
v.
Intercommunicantes - connects superficial to superficial
Pathogenesis
Is due to incompetent valves
1. Posture : history long-standing (occupation)
2. Increased intrabdominal pressure e.g in pregnancy, pelvic tumour
Tests
1.
Positive cough impulse - major valve at saphenovenous junction

Technique
Ask the patient to raise the leg, the veins disappear
Then Obstruct at the saphenovenous junction
Ask the patient to cough
Feel f o r thrill
2. Positive Brodie-Trendenleburg test

Raise the leg
Obstruct at the junction
Release
The veins f i l up
3.
Double-Tredenleburg
The technique is as above
But do not release the obstruction, the veins fill up.
I t shows incompetent perforators
4. Perthe's test
Put a tornique to block the superficial veins, tell the patient to be walking about
55
Blocked deep veins

Do not operate to avoid venous gangrene
5. Venogram - is the most important
Management
i.
Venous stripping - of superficial veins
The contra-indication to this is blocked deep veins
ii.
Conservative
Raise the leg to lie above the heart
Wearing of firm elastic stockings
Complications
1. Varicose vein ulcers
2. Superficial thrombophlebitis
3. beep vein thrombosis
COLOSTOMY
Definition
I s an artificial opening made in large bowel to divert feaces and flatus to the exterior where it
can be collected in a bag.
I s also a colo-cutaneous fistula made to serve some or all the functions of the anus.
Uses
i.
ii.
May replace the anus (Permanent)

To divert faeces away from distal lesion e.g high fistula-in-ano, rectovaginal fistula
To protect distanl end-to-end anastomosis
Types
1.
Permanent
- This replaces the anus e.g in abdomino-perineal excision of the rectum ( AP resection rectum A anus are removed).
- Ideally,
i. I t should have single stoma ( which is put in the right iliac fossa )
ii. Location should be accessible to the patient f o r irrigation
iii. Pass formed faeces
2.
Temporary
Most common, it is an interim measure, pending the restoration of colonic continuity
To prevent faecal peritonitis ( f r o m anastomosis) after anterior resection.
To facilitate operative treatment of high f istula-in-ano
56
Transverse Loop colostomy
I
!
lj
is the best because of the mesentery

Sigmoid Loop colostomy is also useful in patients with Hirchsprung disease.
'
Others
3. End
n
4. Hartmann's colostomy - is a temporary end colostomy. I t s disadvantage is the difficulty in
II
subsequent r e s t o r a t i o n of bowel continuity. I t is used in Carcinoma of rectum with perforation.

5.
Devine or Divided colostomy

I s a stoma colostomy
I t is most effective method o f completely diverting t h e faecal s t r e a m f r o m a distal
lesion.
The 2 limbs of t h e colon are brought out through separate skin incisions
I!
!
!
The proximal
stoma is thus an end colostomy while distal stoma is called a mucous
fistula. I t is a completely defunctioning colostomy.
Cojlbstomv bags
I
are disposable adherent bags
Complications
|
1.
Prolapse
2.
3.
4.
5.
6.
7.
Retraction of the stoma

Necrosis of the stoma
Stenosis of the orifice
Colostomy hernia ( Parastomal) - Treatment involves closure of the lateral space.
Bleeding - from the stoma
Colostomy diarrhoea - is infective, therefore give metronidazole.
Post-op Care
i.
ii.
Inform the patient about stoma care service

Closure of colostomy - after 12 weeks
BOWEL PREPARATION
Indications
I
1. Large bowel surgery - The reasons for it are :
a.
Hard f eacal lumps cause local distension of the bowel which is already narrowed by
anastomosis. This leads to ischaemia at such sites and consequently increases the risk
of dehiscence.
b. The transiting faeces can cause mechanical disruption of anastomosis especially
during the f i r s t 4 days post-op when healing is still in the lag phase.
c. Collagenase activity is increased by local infection and this may prevent proper healing
of the anastomosis.
2. Diagnostic procedures
e.g
Barium enema
Colonoscopy
Sigmoidoscopy
Intravenous urogram
As adjunct measure in certain condtions e.g
o
Liver failure
o
Obstructive jaundice.
Methods
1. Mechanical cleansing - reduction of feed bulk using catharics, enemas
2. Antimicobial agents - to reduce the bacterial using antibiotics that act intraluminally.
UCH Methods
Diet - giving low residue diet e.g pap, Custard
Drugs - Thalazole, Metronidazole, Neomycin
Douche - using Soap & Water enema or High rectal washout. I t is usually started 5
days before the surgery.
Note, Neomycin is started 2 days before the surgery to prevent pseudomembranous colitis (
caused by Clostridium difficile)
iv.
Other techniques
a Total colonic lavage - Herculean washout
b. Oh -table lavage - done f o r emergencies
c. Oral polyethylene glycol - the trade name is Golytely
d. Oral mannitol - the disadvantage is that is the elaboration of combustible
colonic gas, methane. Thus, diathermy is not used.
MALIGNANT THYROID NEOPLASM

Introduction
ryjAes /Incidence
USA (%)
67
18
<10
1. Papillary
2. Follicular
3. Medullary
4. Anaplastic
Others
5. Lymphoma
6. Metastatic deposit
7. Teratoma
Ibadan(%)
34.48
50.58
9.2
2.3
10-15
2.3
1.15
I n iodine-deficiency areas e.g Nigeria, follicular is commoner than papillary.

Malignant goitre is rare in area with thyroxicosis
I n Nigeria,
Neoplastic goiter : 26.24%
Malignant -
.&
/ \?
... [\
. V
: 10.77
Section I
PAPILLARY CARCINOMA
Introduction
{ t is a well differentiated type of carcinoma that has a papillary form
I t occurs in solitary thyroid nodule
VT
Epidemiology
Male/Female ratio is 1 : 3 . Note, male has a greater risk of developing papillary carcinoma from
goitre, but since goitre is more common in females, the incidence is still higher in females.
Peak age : is 3 rd - 4 t h decade of life. When it occurs in the elderly, it is more aggressive.
Forms 2/3 r d of all thyroid carcinoma
3/4 t h of childhood thyroid carcinoma
^^
90% of it is post-radiation carcinoma
4|
Clinical Features
Most patients are euthyroid
i.
Young age group
ii.
Goitre
v.
Cervical mass - lymphadenopathy
v.
I n advanced stages
o
Dysphagia
o
Dyspnoea
V
C
\X
o
Pathology
o
o
o
o
o
Hoarseness of voice - is due to paresis of recurrent laryngeal nerve
Cells are arranged in papillary structures and have features of malignancy

Has Pgnflimnmq_bodies ~ these are fibromuscular which becomes calcified.
I s usually multicentric
I t metastases via lymphatics. This can lead to lateral aberrant thyroid.
I t can be occult papillary carcinoma i.e when < 1.5cm in which case, it will not be palpable.
Investigation
i.
ii.
Cytology
Thyroid scan - using 99 Technitium
o Cold nodule - shows no concentration of radio-iodine. This signifies j
malignancy
V
o Warm nodule - traps iodine, thus signifies toxic nodules
Treatment
i.
ii.
Lobectomy - may be sufficient for minimal papillary carcinoma, 1cm

L-thyroxine supplement - to suppress the TSH and prevent recurrence.
Standard
i.
treatment
Total or Near total thyroidectomy A Modified neck dissection ( i t involves removal of
cervical lymphadenopathy, but ensuring the preservation of phrenic nerve A jugular
veins.
ii.
Radioactive iodine therapy - to destroy the remaining thyroid tissue
iii.
External radiation
iv.
Thyroglobulin tumour marker
Prognosis
Criteria
a.
Low risk group - constitutes of 85% . The mortality rate is 2%
b.
High risk group - constitutes 15% and the mortality rate is 40%
a. Mavo's
('AGES")
- Depends on
i.Age : the higher the age, the worse the prognosis
ii.
Tumour grade : increases with the grade
iii.
Extent of disease
iv. ,4 Size of tumor
b. "AMES"
A - Age
M - Metastasis
E - Extent
S - Size of tumour
c.
CHICAGO
- I t considers operative findings and radioactive iodine scan for metastasis.
- Total body scan is done at 6 weeks post-operative
Section U
FOLLICULAR CARCINOMA
Introduction
Epidemiology
Constitutes < 25% of throid carcinoma
I s commoner in older age group
Is more aggressive
Peak age is 5 t h decade
Male/Female is 1 : 3
Pathology
; o
; o
o
!; o
Cells are arranged in follicular with lumen at the end of colloids.

I t is less multicentric
Has capsular or vascular invasion - This differentiates it from papillary carcinoma
I t TMôs\o^JoiJ[i^!^p^m^jô\A^Xo
skull, femur ( causing pathological fracture) A lung
Clinical Features
i.
Long history of goiter with recent history of increase in size
ii.
Chest symptoms
iii.
Bone symptoms
iv.
Late features - pain A symptoms of local invasion
v.
Lymphadenopathy - seldomly occurs
vi.
I t concentrates iodine
Treatment
There are different opinions
i.
Hemithyroidectomy + Isthmutectomy - is done in young patients with minimal capsular
invasion
ii.
Near total / Total thyroidectomy
Done for older patient
do this if there is plan of giving radio-iodine in future.
Do post-op scanning
iii.
Neck dissection - done if there is local metastasis
II'
Others
iv.
L-thyroxine - to reduce the level of TSH
v.
Radio-active iodine therapy - is given orally
vi.
External radiation
vii.
Chemotherapy - is Adriamycin-based
"t x.
N r
Hurtle cell Tumour - c ^
"
\
v
I s a variant of follicular
^
Treatment: is controversial ? total thyroidectomy \
)
Prognosis
I t is worse in follicular than papillary carcinoma.
61
10-year survival rate is 727o

o
Without invasiveness - 86%
o
With invasiveness - 44%
Section
III
MEDULLARY CARCINOMA
Intoduction
is calcitonin-producing tumour ( from C cell)
Pathology
Cell clusters
I s associated with
Types
a. Familial type is bilateral A multicentric
b.
a.
Sporadic type - has single nodule
I t spreads via lymphatic

Later, the distant may go to bone, lung, liver and adrenals
I s associated with some syndromes
MEN syndrome ( Multiple Endocrine Neoplasia)
Type I
/
Type I I - is associated with thyroid, parathyroid and adrenal.
\
I l a - is commoner. I t consists of
\
i.
Multicentric medullary carcinoma / C-cell hyperplasia
/
ii.
Phaechromocytoma
\
iii.
Primary hyperparathyroidism
\
)
l i b - Patient is tall, slender and have long extremities (like in Marfan's

syndrome). There is high blood pressure, fractures of bones etc
i.
ii.
iii.
Medullary carcinoma
Phaechromocytoma
Mucosa neuroma - of lips, tongue, conjunctiva
Clinical Features
i.
Age : between 2 - 8 0 years. The median age for familial is early 20s
ii.
No sex predilection
J
iii.
Goitre
I'
iv.
Features of hypercalcaemia e.g renal stone
v.
Diarrhoea
vi.
Hypertension - is episodic or paroxysmal. I t is due to the phaechromocytoma
Diagnosis
I s made with
i
I.
ii.
iii.
iv.
red
Treatment
i.
Thyrois mass
Serum calcitonin assay
High calcium level in serum
Urinary VMA - to assess phaechromocytoma
Total thyroidectomy
ii.
Lymph node dissection
|:
!
iii.
iV.
Adrenalectomy - removal of adrenal tumour. I n children, give replacement therapy ( ACTH)

Parathyroidectomy - removal of parathyroid gland
li
Calcium supplement
vi.
"
Prognosis
I
I
-
Thyroxine supplement
5-year survival rate is 80%

10-year survival rate is 57% with lymph node metastasis and 68% without metastasis
Nlote
Familial - is associated with chromosome 10
Treatment - Prophylactic thy?bT3ectomy ~
Section IV
ANAPLASTIC CARCINOMA
Introduction
Is undifferentiated carcinoma
Is very aggressive
Epidemiology
I s more common in the elderly
The incidence is 5 -10%
Pathology
- I t consists of sheets of undifferentiated small/giant cells
Clinical Features
i.
Patients usually presents with advanced stages in which thyroidectomy is no longer possible,
i.e with
Dysphagia
Airway obstruction
ii.
Features of metastasis to bones
63
Investigation
Trucut biopsy
Treatment
Total thyroidectomy
Modified lympho node dissection
Chemotherapy - using MAC (vincristine, Adriamycin & Cyclophosphamide)
Radiotherapy - it is radiosensitive
Prognosis
I s poor
Section V
LYMPHOMA
Ocsurs in older age groups
Diagnosis is made by FNAC
I t responds very well to chemotherapy
Use radiotherapy for regional 'spread"!
Section
VI
METASTATIC CARCINOMA
is mainly from bronchogenic carcinoma ( 20% of all)
Other sites : Breast
Treatment
I f localized - do thyroidectomy
64
THYROID DISEASES - NON-MALIGNANT

Introduction
Goitre is just swelling of thyroid gland i.e thyroid gland is said to be goitrous if the lateral lobe
are larger than the terminal phalnx of the thumb of the person being examined.
Anatomy of Thyroid gland
Location, Structure
Shape - I t is bilobed, the 2 lateral lobes are connected by isthmus. I t lies in front of
trachea and larynx.
The isthmus is between 2 nd - 4 t h ring of trachea
The lateral lobes extend to the 6 t h ring..
Weight Blood Supply
- I s very important to know
- I t is supplied by
i.
Superior thyroid artery which is from external carotid artery
ii.
Inferior thyroid artery, a branch of subclavian artery. This branch also supplies
parathyroid ans it is related to recurrent laryngeal nerve.
Venous drainage - are
a. Superior thyroid vein
b. Middle thyroid vein - drains directly into internal jugular vein. I t is a very small vein.
c. Inferior thyroid vein - - drains into brachicephalic trunk
Nerve supply
i. Recurrent laryngeal nerve - supplies all laryngeal muscles except cricopharyngeus.
ii. External laryngeal nerve - is related to superior thyroid artery, I t s transaction leads to
hoarseness of voice.
Lymphatics
Are significant to note in neoplasm of thyroid gland. I t is drained by pre-tracheal and
paratracheal^
Relations
a. Strap muscles - is anterior to thyroid gland ecept the cricothyroid.
b. Deep cervical fascia
covers and envelopes the strap muscles
I t surrounds the thyroid gland.
I t s significance is that it is separated from the thyroid gland during surgery
b. Pre-tracheal fascia
it is intimately connected to the trachea and neatly envelopes it.
I t is transparent.
I t is attached posterioly to thyroid and cricoid cartilages.
Recurrent laryngeal nerve is just behind it.
c.
I t is because of this attachment that when larynx moves, the thyroid gland
moves,
Investing Fascia
Subcutaneous
Skin
Physiology of Thyroid gland
Hypothalamus
D
Pituitary gland
D
Thyroid gland
D
Thyroid hormones - T3. T4
Note, drdw the negative feedback
Metabolism of Iodine
Iodine taken in food is converted to iodide before it is absorbed from the intestine into the
blood.
Generally, iodide is utilized by 2 organs in the body- thyroid ( uses l/3 r d ) A kidney (uses 2/3 r d )
The thyroid gland concentrates iodine to about 25 - 50 times more than any organs.
The next process is oxidation
Then, the iodide is combined with tyrosine to form mono-iodotyrosine and with another molecule
to form di-iodotyrosine.
Coupling takes place in the acini.
Trapping Q Organification D Release
Iodine
- is blocked by PotaSJum_j
I * (Iodide)
Iodine (12)
- RjrtrUpA hy r n r h i ^ n r n l ^ T h i n i i r n r i l
Mdtio- & Di-iodotyrosine
1
I
T3 A T4 ( i n colloid)
T3 & T4 bound to TSG ( i n plasma)
66
T3 ^_
T4
Reversed T3
The thyroid gland is under the influence of TSH. There are 2 basic hormones from the thyroid
gland T3 and T4. These hormones shuts o f f the TSH secretion when they are in increasing levels
( especially by the T4). TRH is weakly under the influence of T3 & T4.
At puberty, pregnancy and lactation, there is physiologic goiter.
Only 0.5% of thyroxine ( T3 A T4) is in free state
T3 is more active
T4 is synthesized more.
Pathology of Thyroid gland
These are listed in decreasing order of frequency
1. Euthyroid goiter
is goiter with no evidence of increased or decaresed thyroid hormone activity.
I t is just simple thyroid enlargement with biochemical changes
2. Hyperthyroidism - there is hyperfunctioning of the thyroid gland.
3. Neoplasm
4. Inflammatory - Because of the rich vascularity of the thyroid gland, it is exposed to pyogenic
diseases, autonomic disease ( Hashimoto's ).
5. Hypothyroidsim - I n most cases, it is iatrogenic
6. Aberration of embryology - e.g
Agenesis
Ectopic thyroid tissue
Thyroglossal cyst
EUTHYROID GLAND
Aetiology
Causes of Low levels of Production of T3 and T4
o Dietary - low level of iodine, it occurs in mountaineous areas
o Goitogens e.g Cassava (cyanide), soyabeans, gabbage
o Genetic - leading to sporadic goiter. I t is due to enzymatic deficiency (dyshormonogensis)
There is relative insufficiency of T3 A T4 in pregnancy, puberty, this leads to increased
secretion of TSH which now causes
i. Diffuse hyperplastic goiter
ii. Outpouring of colloid - if T3 & T4 are still not enough
iii. I f this persists, it causes multinodular goiter,

iv. Solitary nodule - forms if one part is affecetd
Presentation
1.
2.
3.
4.
Asymptomatic
Pressure symptoms
Toxic symptoms
Carcinomatous
Management
Hyperplastic goiter
I s seen in
i. Pregnancy
ii. At puberty
Treatment- Early introduction of L-thyroxine supplement ( I t shuts off the TSH )
Multinodular
Clinical Features
Cosmestic or aesthetic reasons

I
V*K^
Dysphagia
^r?- ,, ^"
Hoarseness of voice - is rare

ux^Treatment
- Work-up for operation
^^
- Operation
- Note. Radioactive iodine is not particularly effective
..-A c >
^'v-,.,..,,.,--\ *'
V:'
! Solitary nodule
Treatment - Operation is done in 9 out of 10 cases.
Common Investigations For Thyroid Diseases
1. Thyroid function t e s t : T3, T4 A TSH
I n most laboratories, only total T3 and T4 are checked.
Disease e.g Nephrotic syndrome, pregnancy reduce the level of globulin and thus reduce T3 & T4
TSH is the most sensitive ( i f you are to choose one), but ideally, the three should be done.
2. X-rays
a.
b.
c.
of the
Neck( Anteroposaterior A Lateral)
Chest
Thoracic inlet
3. Electrocardiogram
|! 4. Thyroid scan
j 5. Ultrasonography- I t helps to
i.
determine number of thyroid nodules i.e if multinodular
ii.
have an idea of thyroid volume before the commencement of L-thyroxine
treatment.
6. Indirect larnygoscopy - is compulsory, it is to rule out paralysis of recurrent laryngeal nerve before
thyroidectomy is done.
68
7. FNAB - done when malignancy is suspected. I t is performed under ultrasound guidiance or CT

guidiance.
TOXIC GOITRE
(Hyperthroidism / Thyrotoxicosis)
Introduction
The 2 terms are strictly not the same
Types
Primary thyrotoxicosis
- is seen in Grave's disease.
- There is diffuse hyperplastic thyroid gland with with thyrotoxic features.
- I t usually presents with a goiter and eye symptom, both occurring peripersu
- I t is usually seen in younger age group
- I t may be autoimmune or familial
a.
Secondary thyrotoxicosis e.g^Plummer's disease )

- I t is seen in Multnodular~g6lter:~
- I t usually presents with goiter with eye symptoms occurring as a complication
- The thyroxicosis is a complication.
- There are also cardiac problems
b.
Tertiary
Occurs in any age group, but usually adults
K*0
-v
^ 5
c^
Kt* ^
Clinical Features - are of sympathetic over drive
1^
Profuse sweating
Intolerance
I.
ii.
Bulging eyeballs (exophthalmos)
v.
Pre-tibial myxoedema
v.
Diarrhoea
vi.
Weight loss despite polyphagia/hyperphagia
vii.
Erratic menstruation - I t is mostly oligomenorrhoea
viii
Infertility
ix.
Cardiac features - Murmurs, high blood pressure. I t is common with Plummer's disease i.e
secondary thyrotoxicosis which is common in the elderly.
Goitre
Exophthalmos
in.
Tremulouness in handstretched and tongue
69
Wayne of Glassoow
<11
11-19
>19
Not toxic
Doubtful toxicity
Frankly toxic
I t gives values to these symptom complex. E.g > 19 is said to be toxic.

I t s function has been taken over by thyroid function test.
Treatment Modalities
i.
Antithyroid drugs
ii.
Surgery
iii.
Radioactive iodine
i. Antithyroid Drugs
a. CgrJwnazoie - is used in UCH
To prevent organification
Only about 50% responds to the drugs
Most patients (> 50%) relapse
Contraindications
i.
Complications
i. Agranulocytosis (leucopaenia )- is manifested f i r s t l y by sorethroat. I t
occurs in overdosages.
b.
B- blockers e.g propanolol - to reduce the sympathetic drive

Contra- ind icat i ons
i. Asthma
c. Anti-arrhythmic agent
d. Anxiolytic drugs
Admit the patient to the ward f o r drug monitoring.
What is "thyroid escape" Qj^jgdjne_gSgge'' ?
o
I t is given massive amount of supplemental iodine, i t inhibits
thyroxine seceretion. I t is no longer in use.
Note, none of these address the autoimmunity
ii.
Surgery
Pre-operative
i.
ii.
Check serum calcium level

Make the patigntjeutMyroid before the operation - using the above drugs. I t
takes abouijb - 8 weekaj)
Complication
iii.
i. Thyroid crisis /Thyroid storm - I t is exacerbation of

hyperthyroidism. The sympathetic overdrive at a very high
rate,
Because of the inavailability of thyroid function test, the following
parameters are used
a. Sleeping pulse rate - is marked in red pen. I t should be about 70%
b. Temperature
c. Serial weighing
d. Normal eating (3 times and not 7 times)
Operation
- Leave small amount of thyroid gland
Complications of thyroid Surgery
1. Haemorrhage
Types
a. Primary
b. Reactionary - this forms a clot and presses on the trachea causing
respiratory embarrassment ( wheeze etc)
Treatment
i. Put on oxygen
ii. Remove sutures
iii. Evacute the clot
iv. Do cricothyroidectomy - to allow patient to breathe
v. Pass endotracheal tube
vi. Manage in ICU
vii. I f there is further deterioration, do emergency
tracheostomy
2. Recurrent Layrgeal nerve injury - causes of loss of phonation
Treatment - Tracheostomy
3. External branch of recurrent laryngeal nerve injury W>Cv" <*\i\
4. Horner's syndrome - is due to injury to cervico-sympathetic nerve
5. Hypoparathyroidism - it causes
Hypocalcemia
w
I
I
Tetany
Carpopedal spasm
Treatment - Calcium gluconate
6.
Hypothyroidism
Treatment- L-thyroxine
7. Recurrence - is dreaded
71
iii.
8. Keloid scar formation

9. Hypertrophic scar formation
10. Wound infection - is rare because the area is well vascularised
11. Damage to surrounding structures e.g oesophagus, trachea
Radioactive iodine
- I t is not often used here.
Complication - Neoplasm.
THYROID DISEASES - NON-MALIGNANT

br Afolabi
WHO'S Grac ling of Goitre

Grade
I
Goitre can be felt
la
Goitre can be f e l t , but it is not visible, even with the neck
extended
lb
Goitre can be f e l t , but it is invisible with neck in normal position
II
Giotre easily visible with neck in normal position
III
Very large goitre
Classification of Goitre
1 . Simple
a.
b.
1 2. Toxic
a.
b.
c.
d.
3. Neoplastic
a.
b.
Inflammatory
4.
a.
b.
c.
d.
e.
Diffuse
Nodular
Diffuse (Grave's disease
Multinodular
Solitary nodule
Malignant
Benign
Malignant
Autoimmune
Acute Suppurative
Subacute
Riedel's
Specific e.g Tuberculosis
72
a. General
i.
ii.
Anterior neck swelling

Symptoms of pressure
Specific
i.
ii.
a.
Toxicity
Malignancy - Local, distant
Hypothyroidism - Sluggishness, poor performance in school
History
i. Biodata : Place of origin & domicile
ii. History of Aetiology/Predisposing factors
Endemic/sporadic
Familial - Grave's disease
Radiation exposure
iii.
iv.
Specific symptoms of aetiology

o Pain
o Heat intolerance
o Weight loss
o Appetite
Reasons for presentation
%
44.3
40
a. Cosmesis b. Symptoms -
c. Shame
d. Social
- 14.3
- 4.2
b. Physical Examination - follows "IPPA"

a.
b.
j
!
General examination
State of health
Acute distress
iii.
Jaundice
iv.
v.
vi.
vii.
Cyanosis
Oedema
Weight loss
Significant lymphadenopathy
Examination of the head A neck

i.
Scalp
ii.
Eyes
iii.
Ears
iv.
Nose
v.
Throat
vi.
Neck
73
c. Local examination - of the anterior neck swelling

Inspection
o Site
o Surface
Palpation
o
o
o
o
o
o
o
o
Tenderness
Temperature
Texture
Size - measure 2 dimensions
Pulsation
Setting above and below it ( i.e in the neck and abdomen)
Trachea
Lymphadenopathy
d. Systemic examination
i.
Scalp swelling
ii.
Eyes
o
o
o
o
iii.
iv.
v.
vi.
vii.
viii.
ix.
Pulse rate
Blood pressure
Apex beat
Murmurs
Skin - of palm
Finger tremors
Pre-tibial myxoedema
Deep tendon reflexes
X.
- for
Exophthalmos
Lid retraction
Lid lag
External ophthalmoplegia
Investigation
1. Serum T3, T4 4 TSH
2. Isotope scanning - lining Technitium, Radio-iodine. Cold spot indicates malignancy.
3.
4.
5.
6.
7.
8.
9.
10.
Plain Neck x-rays - AP & Lateral

'
Ultrasound : solid structure suggests malignancy
Fine Needle Aspiration Biopsy
Auotoimmune antibodies - is very important in Grave's disease
Indirect laryngoscopy
Full blood count
Urinalysis
Serum electrolyte, urea <& creatinine
11. CTscan
12. Group A Crossmatching/Autologuos donation
Drug Therapy
a. Lugol's iodine, Potassium iodice, L-thyroxine
b. Carbimazole, Methimazole, Propyl- or methyl- thiouracil

74
/
c. Diazepam, Bromazepam
d.
e.
f.
g.
Propanolol
Radioactive iodine - also used for thyrotoxicosis
Prednisolone - for thyroiditis
Antibiotics - f o r bacterial thyroiditis/abscess
Types of Thyoroidectomy
i. Lobectomy
ii. Lobectomy + Isthmusectomy
iii. Subtotal thyroidectomy
iv. Total thyroidectomy
v. Others
o Draingange of abscess
Post-op Complications
1.
Respiratory obstruction
The causes are
o Reactionary haemorrhage
Tracheomalacia
o
o
Oedema
Recurrent laryngeal nerve paralysis
2.
3.
4.
Recurrent laryngeal nerve paralysis

Hypocalcaemia
Thyroid storm
Treatment
i.
Carbimazole
ii.
Diazepam
iii.
Prednisolone
iv.
Ice packs
5.
6.
Hypothyroidism
Recurrence
THYROID CRISIS
Introduction
o Severe manifestations of thyrotoxicosis
o I t occurs in association with Grave's disease
Precipitating factors
i.
Infection
ii.
Trauma
iii.
Surgery for unrecognised or untreated thyrotoxicosis
\v-
,t-v
A?
~U^
t\
Presentation
75
Intra-operative:
o
High fever,
0
Tachycardia
o
Systolic hypertension
o
Tachyarrhythmias
o
Congestive heart failure
o
Pulmonary oedema
o
Hypotension
In Unanaesthestized patient
o
Nausea & vomiting
o
Diarrhoea
o
Jaundice
I n severe cases - convulsions, lethargy and coma
o
Pathogenesis
i.
Result of alteration in hormone binding relat

increase in free thyroid hormone levels, rather than an increase in thyroid hormone
release; except in case caused by thyroid surgery when there is also an increase in
thyroid hormone release.
Management
II.
in.
Treat the inciting event

Large doses of propyj-thjoj.
il 250 - 400mg Q4h via N/G tube or orally to inhibit the
synthesis of thyroid hormonre and peripheral conversion of T4 to T3.
Saturatedjsolution of potassiumjodide (SSKI) 8 drops 6hrly orally or via N/G
IV.
Or 1 gram sodium ipodate I V daily to inhibit further hormone release from the
g\and. (Propylthiouracil should be started before iodine administration to prevent
subsequent iodine-induced increases in glandular hormone stores)
B-adrenergic receptor antagonist to block the peripheral adrenergic effects of TH.
VI.
EG Continuous infusion of short acting agent such as Esmolol 0.25 to 0.5mg/Kg loading
dose followed by a continuous infusion of 0.05 to O.lmg/Kg/min.
VII.
bexamethasone large doses I V to inhibit both the release of thyroid hormone and the
peripheral conversion of T4 to T3.
VIII.
Other supportive measures

o Oxygen
o
I V hydration
o Acetaminophen
o Cooling blanket to reduce fever.
Mortality
o Without treatment = 100%
o With treatment = 20%
76
THYROID STORM
( Tutorial)
Definition
^
I s an exacerbation of thyroid symptoms in a poorly treated patient
- Causes
,-.
|
1. Surgery
2. Stress
3. Infection
r4. Emotional upset
Aft
Clinical Features
i.
Hyperpyrexia
|
ii.
I r r i t a b i l i t y /Restlessness
iii.
Heart failure
iv.
Excessive sweating
Wayne's Index
I s an index that numerical values to various symptoms 4 signs which sums up the thyroid
symptoms
Parameters
i.
ii:
iii.
IV.
v.
vi.
Palpitations
Heart failure
Weight loss
Eye signs
Appetite
Excessive sweating
Grade
<10
10-19
>20
Euthyroid
Equivocal
Toxic
Precautions f o r Thyroid Storm (Infra-operative)

I V propanolol
i.
I V diazepam
ii.
I V hydrocortisol +
v.
Lugol's iodine +
v.
I V infusion with normal saline
HYPOCALCAEMIA
Reference Range of Calcium
9-llmg/dl or 2.2 - 2.5mmol/L

Clinical features
i.
Trousseau sign - is carpal spasm following the application of blood pressure cuff above the
systolic pressure,
ii.
Chvostek's sign - I s facial muscle twitches following the tapping of the facial nerve at the
angle of the jaw
Investigation
1. Serum calcium A albumin

2. ECS - shows
o Delayed Q T interval
o Broadened QRS complex
Classification
i.
ii.
Mild
Severe
Management
a. Mild
i.
ii.
Oral supplements - oral calcium lactate tabs

I V calcium - as I V calcium gluconate or chloride. Give slowly to protect the heart
b. Severe
i.
Oral Vitamin D
ii.
Oral calcium lactate
iii.
I V calcium
THYROIDECTOMY
Types
Indications
Pre-operative Care
Postoperative Care
Complications
Thyrotoxic Strom
Types
1.
Subtotal thyroidectomy
Old Definition Removal of thyroid gland leaving an equivalent of the thumb of the patient on
either side.
-~.
New Definition: About (4g)s left behind on either side.
2. Near total thyroidectomy - Removal of the gland leaving about 2g or a rim of tissue on either
side
3. Total thyroidectomy - I s removal of bilateral lobes. There is risk more damage to surrounding
structures e.g parotid, external superior branch of laryngeal nerve. L-thyroxine is required for
life.
4. Partial thyroidectomy - Removal of part of the thyroid gland
5. Lobectomy - Removal o f one lobe
Indications
v
1. Goitre
a. Benign - Subtotal /Total
Simple diffused disease - Endemic goiter
Simple toxic - Grave's disease
in.
Solitary nodular goiter
iv.
Multinodular goiter
v.
Dominant thyroid nodule
b.
Malignant
i.
ii.
v.
v.
Follicular adenocarcinoma
Papillary
Medullary
Anaplastic carcinoma of the thyroid - is not a common indication for
thyroidectomy. Isthmusectomy /chemotherapy /Radiotherapy is done.
Isthmusectomy helps to relieve the upper airway obstruction
Lymphoma
Treatment - Chemotherapy
79
Pre- operative Care

1. Full blood count
a. PCV - for anaemia which might be due to malignancy
b. WCC - to rule out thyroiditis
c. Platelet
2. Electrolyte & Urea - to ascertain renal function
3. Chest X-ray - To assess the lung state. I t is more indicated in patients > 40 years. I t is
compulsory for Grave's disease and malignancy
4. ECG - especially in patient > 40 years
5. Blood group & crossmatching
6. Indirect laryngoscopy i.
To assess for paralysis of vocal cord
ii.
Also for medico-legal implications.
I t is done pre-operatively A post-operatively, though direct laryndoscopy can
be done during extubation.
7. Fine Needle Aspiration Cytology
8. Thyroid Function test - for patient with subclinical thyroid function
Others- depend on mode of presentation
9. Soft tissue neck x-ray - To show
i.
Tracheal deviation
ii.
State of cervical spine/spondylosis
iii.
Metastasis
iv.
Calcification
10. X-ray of thoracic inlet - To show retrosternal extension of the thyroid gland. During surgery, it
is approach from the neck. I n 1 - 3% of patients, the vessels come from the anterior
mediastinum,.
11. Serum Calcium A Albumin
,s
Correction factor
For every lg/l drop in albumin, there is an equivalent 0.8/dl (.4/5) rise in calcium e.g
o if albumin drops by 1.5g/l, you add 1.2 to get the correct value
o if albumin drops by 0.5g/dl, you add 0.4
Note, in medullary carcinoma of the thyroid gland, there is hypercalcaemia, instead of
hypocalcaemia. I t is due to high level of calcitonin.
I n MEN I l a , there is excess parathyroid hormone
While MEN l i b = MEN I l a + Neurocutaneous syndrome
,i,i
ijj
12. Ultrasound of the neck - may show

o Cystic or solid mass
o Enlarged cervical lymphadenopathy not clinically palpable
13. Informed consent - Inform the patient about
i.
Anaesthesia
ii.
Damage to recurrent laryngeal nerve - resulting into loss of voice
80
III.
IV.
Damage to superior laryngeal nerve - resulting into change in voice. This is

very important if the patient is an actress or a singer
Total thyroidectomy - which requires the use of thyroxine f o r life.
Procedure
a. Position
Lie supine and extend the neck to draw the neck vessels
Put sand bag beneath the head and place head on a headlift
b. Incision
- A collar incision is made at about 2 fingers breadth above the jugular notch
c. Spare
the recurrent laryngeal nerve
Parathyroid gland
Superior and Inferior laryngeal artery - Ligate the superior laryngeal artery twice i.e
double ligature.
Post-operative Care
Steam inhalation - to reduce laryngeal oedema
i.
Nutrition - Change to oral on 1st day post-op
ii.
Analgesia
v.
Intravenous fluid
v.
brain - remove 2nd day post-op
vi.
Suture - remove 3 - 5 th day post-op
Thyroxine Dose
2 - 3ug/kg/day
\pt !"[/'200ug daily
Complications
1.
Respiratory d stress from airway obstruction - this is caused by the following

Damage to recurrent laryngeal nerve
i.
Compressive haematoma
ii.
Larygeal spasm
Treatment'- Re-pass NS tube and give corticosteroid
iv.
Laryngeal oedema
Treatment - as for iii
v.
Floating trachea
Treatment - Endotracheal intubation
Prevention - By plicating the strap muscle, thus reduce the space for
trachea to float
vi.
Tracheomalacia
Treatment & Prevention - as for Floating trachea
- I t could be due to infiltration by metastasis, thus-in management,
you leave the enotracheal tube f o r few days post-op.
81
vii.
Injury to the trachea i.e not closed up
Common clinical feature - Stridor

General Treatment For All
i.
Re-intubation
ii.
Tracheostomy
iii.
Oxygen therapy
2. Damage to recurrent laryngeal nerve
o
One side leads to hoarseness of voice while bilateral involvement causes paralysis.
o
Note, initially, it causes stridor and later hoarseness of voice
Treatment - Tracheostomy
3. Damage to external laryngeal branch of superior laryngeal nerve
4.
Damage to inferior thyroid artery which supplies parathyroid gland. This leads to ischaemia and
profound hypocalcaemia.
5. Hypoparathyroidism - is manifested by
o
Paraesthesia (tingling oral sensation)
o
Cramps
o
Tetany
o
Carpopedalspasms
6. Reactionary haemorrhage - is the commonest
Prevention
o Maintain good haemostasis during surgery
Complication
i.
Respiratory distress from haematoma & contraction of strap muscles.
7. Recurrent thyrotoxicosis
8. Horner's syndrome - is due to damage sympathetic chain
9. Wound infection - is now rare
10. Damage to surrounding structures e.g oesophagus
11. Thyrotoxic storm
12.
Stitch granuloma
13.
Stitch sinus
Treatment - Excise
14. Keloid formation

Treatment
i.
ii.
iii.
Excision
Radiotherapy
I M triamcinolone
82
15. Hypothyroidism
Classification of Post-op complications
a.
Infra-operative
Thyroid storm
b. Early
i.
ii.
v.
v.
vi.
c.
Delayed
i.
ii.
Airway obstruction
Damage to recurrent laryngeal nerve
Damage to external branch of superior laryngeal nerve
Damage to inferior thyroid artery
Reactionary haemorrhage
Stitch granuloma
keloid formation
Hypothyroidism
Complications of Total A Subtotal Thyroidectomy

Total
II.
Subtotal
i.
Risk of damage to surrounding structures is more

Hypothyroidism
Recurrence
Note
Tracheostomy : > 14 days
Endotrachealtube : Between 7 - 1 4 days
83
NECK SWELLING NON GOITROUS
Anatomy of the neck
Lymphatic drainage
First classification
a. Midline
b. Lateral
Midline
1.
Thyroglossal duct cyst
2.
Median sublingual dermoid cyst
3.
Laryngocoele
4.
Zenker's diverticulum
5.
Subhyoid bursa
6.
Plunging rannula
Lateral
1.
Parotitis
2. Pleomorphic adenoma
3. Calculi
4. Branchial cyst
5. Cystic hygroma
6. Sternocleidomastoid tumour
7. Lymphadenopathy
8. Cervical rib
Second classification - ( According to Mr Akute)

a.
Congenital abnormalities
i.Thyroglossal tract abnormalities
ii.
Branchial cyst
iii.
Cystic hygroma
iv.
Cervical rib
b.
Tumour (Benign & Malignant)

i.
Thyroid tumours
ii.
Salivary gland tumours
iii.
Sarcoma, Lipoma, Neuroma A Fibroma
iv.
Chemodectoma - tumour of the chemoreceptors on the carotid
bodies
c.
Traumatic
i. Sternocleidomastoid tumour
d.
Diverticular
i.
ii.
Laryngocoele
Pharnygeal pouch
84
e.
A.
Lymphadenopathy
Midline
I t involves unpaired structures
Thyroglossal Cyst
I s a congenital anomaly of thyroid gland
I t is common in children, it occurs in l $ t decade of life. 40% are teenagers. But it can also
occur in adults.
Most are related to hyoid bone either infra- or suprahyoid, but it is sub-hyoid.
I t is a midline swelling, though can be a bit displaced to the left because of its relationship
to the hyoid.
I t is usually enucleated
Treatment
i. Surgery - Excision. I t involves the
o Dissection of t h r entire tract
o Removal of about 1cm of the hyoid bone - to prevent
recurrence
Laryngocoele
I s common in wind instruments blowers
I t occurs between the thyrohyoid muscle
Zenker's diverticulum / Pharyngeal pouch
I s a diverticulum from pharynx
I t is through the dehiscence ( of Kilian) between thyropharyngeal and cricothyroid parts of
inferior constrictor
Median Sublingual Dermoid Cyst
I t can be misplaced for suprahyoid thyroglossal cyst
Plunging Rannula
I s a mucoid degeneration of salivary tissue
I t usually sublingual
I t trasnilluminates
Treatment- Deroofing
B.
Lateral
a. Salivary gland
i.
Parotitis
Viral ( Mumps) - Post-pubertal infection also affect the testes
Bacterial
Autoimmune ( dear's syndrome) - dryness and sialectasis

ii.
Tumours
a.Pleomorphic adenoma (of the Parotid gland)
I s the commonest
Although it is benign, it is very prone to recurrence
85
I t usually occurs in 5 th decade, but young girls in this environment do have it.
I t is not common with submandibular gland, instead carcinoma is more common
with it
Treatment = Superficial parotidectomy
Note
Malignant mucodermal syndrome
During treatment the gland is not removed because of the branches of facial
nerve (TZ BMC)
The cervical branch is very small
The facio-venous plane divided the parotid gland into superficial and deep.
iii.
b.
b.
Monomorphic adenoma
c.
d.
e.
Squamous cell carcinoma

Frank Malignant
Undifferentiated
Calculi
- I s common with sumandibular gland
- Ask the patient to open mouth and check the ducts.
Branchial Cyst
is abnormality of 2 nd branchial cleft
I t occurs at upper l / 3 t h of sternocleidomastoid muscle . I t usually lies under
it
I t occurs infrequently in the young adults ( 20 - 40years). I t is congenital, but
rarely occurs before 20 years
I t is found in the lateral neck
I t is highly recurrent
When it becomes a fistula, it moves to lower l / 3 t h .
Treatment: Surgery - Excision
- I t is very difficult to remove.
c.
Cystic
- Is
- It
- It
- It
hygroma
a carvernous lymphagioma i.e harmatomatous formation.
is seen in small children (neonates A infants)
transilluminates brilliantly
is f uound in suprclavicular region
Treatment- Excision.
d.
Sternocleidomastid tumour
I s not really a tumour
I t is due to trauma during delivery which causes ischaemic fibrosis
Treatment
Physiotherapy (massage) at early stage
86
e. Cervical rib - rib is attached to t h e 7 t h cervical vertebra
f.
Lymphadenopathy - is the commonest lesion in the neck
Causes
a. Primary malignancy
i.
ii.
b. Metastatic
i.
Melanoma
ii.
Sqamous cell carcinoma.
'
c. Inflammatory
pecificusually
involves acu
a. Non-s
Tonsillitis
ii. Pharyngitis
iii. Histiocytic
iv. Necrotising
v. Infected scalp
r
r
r
r
r
r
r
r
b. Specific - is usually granulomatous

Tuberculosis
ii. Atypical tuberculosis
iii. HIV
iv. Sarcoidosis
v. Toxoplasmosis
vi. Trypanosomiasis
vii Leishmaniasis
Management
a. History
b. Physical Examination
c. Investigation
Full blood count
,
i.
Chest x-ray
ii.
Neck x-ray
v.
FNAC / Excision biopsy
v.
Mammography /Ultraspund of breast
vi.
Indirect laryngoscopy
vii.
Direct laryngoscopy
viii.
Bronchoscopy
ix.
06b - to view A biopsy.
X.
j~~
f
Lymphoma (Hodgkin's A Non-hodgkin's )

Leukaemia
Mammography
Treatment
Most - Surgical excision
Note
Incisional biopsy of a lymph node in the neck is worrisome because
the scar formed make it difficult to examine later
i.
the scar also makes life diffilcult f o r the patient
ii.
spread of the tumour
v.
makes radiotherapy difficult
v.
may loose follow-up to patient
SURGICAL JAUNDICE
o
o
o
o
o
o
o
o
Definition
Epidemiology
Aetiology
Pathogenesis
Clinical Features
Management
Complications
Prognosis
Definition
I s jaundice that is amenable to surgical intervention
Epidemiology
i.
ii.
Aetiology
1.
2.
3.
^.
5.
6.
7.
8.
Geographical
Age
Gender
Gall stones ( Cholelithiasis) - is the commonest

Malignancy
i.Carcinoma of pancreas - is the commonest in this group
ii.
Cholangiocarcinoma ( of common bile duct)
iii.
Primary liver cell carcinoma
iv.
Carcinoma of the stomach with metastasis to porta hepati
v.
Peri-ampullary carcinoma
vi.
Carcinoma of the duodenum
Sclerosing cholangitis
Biliary atresia A other biliary anatomical variations
Choledochal cyst
Lymphadenopathy of porta hepatis
Post-transfusion jaundice
Traumatic - Post-cholecystectomy
GALL STONES (CHOLELITHIASIS)

Definition
I s the term applied to the presence of gall stones in the gall bladder and biliary passages.
Anatomy
CTD
Types
1.
Mixed stones - accounts f o r 80% . I t contains cholesterol, bilirubin, calcium.

- I s described as multiple, multifaceted and laminated.
2. Metabolic stones - I t accounts for 10% and consists cholesterol mainly

3. Pure pigment stones - I t accounts f o r 10%. I t is seen in sickle cell, thalassemias .
4. Calcium carbonate stone - This is very rare.
Clinical Features
Depends on the site of the stone
There are 6 modes of presentation
i.
Asymptomatic - I n U.S, out of 30% of people who have stones, only 20% show the
symptoms
i.
Mucocoele - i.e mucosal oedema
ii.
Hydrops of gall bladder
v.
Cholescystitis
v.
Empyema - when it is infected
vi.
Strangulation - forming gangrene. This is rare.
Based on the site of the stone
a. Soil Bladder
Dyspepsia
i.
Occasional vague pain - in right hypochondrium. I t may radiate to right shoulder,
ii.
Fat intolerance
v.
Femal, Obese, Fertile, Flabby
v.
Tenderness in the right hypochondrium
b. Common bile duct
i.
Biliary colic
89
ii.
iii.
Cholangitis
Biliary cirrhosis
c. Ampulla
i.
Recurrent acute pancreatitis - presents right hypochondrium radiating to the back.

And vomiting.
CHOLECYSTITIS
Types
a.
b.
Acute
Chronic
i.
I s usually acute presentation of chronic existing cholecystitis i.e acute alone is rare.
ii.
The patient is female, fertile, f o r t y and flabby
iii.
Abdominal pain - Recurrent attacks of pain in right hypochondrium or epigastrum. I t is
referred to the right shoulder associated with dyspepsia A anorexia,
iv.
Fever
v.
History of f a t intolerance
On examination
vi.
vii.
Postive Murphy's sign - is catch of respiration at the height of inspiration. The "catch " is due
to pain.
Investigation
1. Routine & basic
i.
Full blood count
ii.
Chest x-ray
iii.
Stool microscopy
iv.
Urinalysis
2.
3.
4.
5.
6.
Liver function test

Plain abdominal x-ray - shows opacity
Ultrasonography - is the gold standard
Oral cholecystogram
Intravenous cholangiogram
- The last 2 methods are outdated.
Treatment
a. Resuscitation
Rest
ii.
Intravenous fluids
iii.
Glucose
iv.
Analgesics e.g pethidine
90
v.
vi.
vii.
viii.
Nasogastric intubation
Antibiotics e.g cefuroxime
Antispasmodics - if the stone is in common bile duct
Vitamin K - lOmg intravenously
b. Operative - The options are

i.
Cholecystectomy - There are 2 types

Open - is done here
- After removing the stone during the surgery, a stent is
placed in the common bile duct to dilate the obstructed common bile duct.
Laparoscopy -
ii.
iii.
Choledochotomy - I s no longer uSed

ERCP - is used to remove stone from common bile duct, pancreatic duct or ampulla.
MALIGNANT JAUNDICE
Causes
1.
2.
3.
4.
Carcinoma of head of pancreas

Cholangiocarcinoma
Hepatoma
Hepatic secondaries - from colon, stomach, breast etc.
Clinical Features
Deep and progressive jaundice
Constitutional symptoms and signs
Abdominal mass
Investigation
a. Basic & Routine - as above
b. Ultrasound
c. CT scan
d. Biochemical markers
e. Biopsy
Pre-operative preparation of Jaundiced Patient
i.
Correct bleeding disthesis - by giving vit.K lOmg intramuscular for 5- 7 days
ii.
Rehydration - that may result from hepatorenal syndrome
iiii.
Electrolyte A Urea
iv.
Serum creatinine
v.
Antibiotics - to treat the infection resulting from bile stasis
vi.
High carbohydrate diet
91
Treatment
a.
Surgery
a. Whipple's operation - Carcinoma of head of pancreas
b. Hepatectomy - f o r one lobe involvement e.g secondaries
c. Cholecystojejunostomy - is a palliative by-pass
b. Chemotherapy - e.g 5-f luoracil
c. Radiotherapy - its use is very limited
d. Hepatic transplantation - if the lesion is only confined to liver i.e no metastasis
Prognosis
I t is poor because of late presentation
SURGICAL JAUNDICE
(OrAfolabi)
m
Definition - as above
Epidemiology - as above
Aetiology - as above
Pathoqensis
o The aetiological factor e.g calculus, neoplastic
o Biliary tree
o Stasis
o Hepatocellular dysfunction
o Cholangitis
o Malabsorption
Clinical Features
With respect to aetiology and the effects, of obstruction
Symptoms
i.
Jaundice
ii.
Vomiting
iii.
Anorexia
iv.
Weight loss
v.
vi.
Abdominal swelling
vii.
Pruritus
viii.
bark urine
ix.
Pale stool
Signs
x.
xi.
Hepatomegaly
Ascites
92
xii.
Management
i.
ii.
iii.
Gall bladder distension
Confirm the clinical diagnosis

Assess physiological status
Investigate f o r surgery
Investigations
1. Abdominal ultrasound
2. Abdominal CT scan
3. Endoscopic Retrograde Cholangiopancreatography ( ERCP )
4. Liver Function Test
a. Serum bilirubin
b. Alkaline phosphatase
c. AST
d. ALT
5. Serum albumin - reduced
6. Globulin
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
Treatment
a.
b.
v
Cholesterol
Urinalysis
Serum electrolytes A urea
Serum creatinine
Full blood count
Blood group & Crossmatching
Haemoglobin electrophoresis
Blood culture
Chest X-ray
Abdominal X-ray
Transhepatic cholangiography
Oral cholecystography - is NOT used for patient with obstructive jaundice
Optimise
i.
ii.
iii.
iv.
v.
vi.
vii.
the patient
Rehydrate
Correct anaemia
Correct electrolyte derangement
Give vitamin K - for bleeding disorders
Nutritional support - carbohydrate, protein
Bowel preparation
Peri-operative antibiotics
Specific
i. Choledocholithiasis
Intra-operative cholangiography
Cholecystectomy : There are 2 types
a. Open
b. Laparoscopic
Exploration of the common bile duct
Insertion of T-tube
Management of T-tube
Endoscopic sphincterotomy
ii. Carcinoma
- Endoscopic insertion of biliary stent
- By-pass surgery
i.
Chole-cysto-jejunostomy - for Carcinoma of pancreas
ii.
Chole-docho-jejunostomy - for Common bile disease
iii.
Gastrojejunostomy
iv.
Jejuno-jejunostomy - side to side OR Roux-en-Y
Complications of Treatment
1. Bleeding
2. Septicaemia
3. Renal failure
4. Anastomic dehiscence
5. Others
Proqnosis
Depends on aetiology and the stage of presentation
Conclusion
" Do it right the f i r s t time, because life is not a dress rehearsal"
Bob Gas
LIVER, GALL BLADDER <& PANCREATIC DISEASES

Content
i.
ii.
iii.
Gall Bladder
i.
ii.
,,
iii.
I
iv.
Primary Liver cell carcinoma

Amoebic liver Abscess
Pyogenic abscess
Conegnital anomalies
Gall stones (Cholelithiasis)
Gall bladder carcinoma- Read up
Gall bladder disease in children - Read up
Pancreas
Carcinoma of the head of pancreas
Acute pancreatitis - Read up
DISEASES OF LIVER
PRIMARY LIVER CELL CARCINOMA

Introduction
I s common in blacks and far East
I t is commoner in male
Arguably the commonest malignant carcinoma of liver in the world
Age incidence is about 40years
Predisposinq Factors
Chronic HBV or HCV infection ii.
Chronic liver disease
- Both are associated with > 90% of cases
- Active hepatitis D Cirrhosis D PLCC
- 10% is non-cirrhotic (and these listed below)
iii.
iv.
v.
vi.
vii.
viii.
xi.
Af latoxin - is a my
Haemochromatosis
Venous obstruction
Androgens
Oral contraceptives
Irradiation
Carcinogenic substances e.g Arsenic
Schistosomiasis
Clonorchis sinensis - causes more of cholangiosarcoma
PathoDhvsiolo
Chronic HBC / HCV infection
Liver cirrhosis
Primary liver cell carcinoma
Massive
Nodular
Diffuse
The f i r s t 2 accounts f o r 90%
Soread
Hepatic vein : to IVC D Systemic circulation D secondaries to lungs
Lymphatics - accounts for 25%
Adjacent structures
r
V/<o>
Adenocarcinoma
Clinical Features
i.
Hepatomegaly
ii.
Abdominal pain
iii.
Weight loss
iv.
Anorexia
v.
Jaundice
vi.
Haemoperitoneum
Clinical types
1. Frank cancer - account for 60%. There is cachexia, hepatomegaly, ascites
2. Occult cancer - accounts 16%. Here, the liver is not markedly enlarged.
3. Acute abdominal cancer - accounts for 8%. I t presents with haemoperitoneum, without any
history of trauma sxcept leiomyosarcoma of lesser omentum. ( Acute abdomen), 1 fj\-vsv< ri< eP\
* 4. Febrile cancer - presents like tropical liver abscess
;r >' \-,A. <;W" -? '-'9'" t V i ; ; *\\\\<>\\ i ^ i W A
5. Metastatic cancer - secondaries in lungs, bones
Vv-.vîow 0 a,Yvy)oc
6. Bleeding varices presentation
Investigation
1.
Full blood count : shows
o
Marginal anaemia
o
Hypochromia
o
Anisocytosis
o
Leucocytosis
j
|
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
Serum bilirubin
Plasma protein
Liver function test i.e enrymes
Clotting profile : PT, PTTK
Ultrasound - shows multiple deposits &. extrahepatic spread.
Tumour marker - Alpha-f etoprotein : I t is raised in 95% of patients V
Contrast-enhanced CT scan - is more diagnostic
MRI - has more resolution than CT scan.
Angiography - to detect minute cancer cells. I t is also needed f o r the surgery
Percutaneous liver biopsy - has 97% accuracy
Laparoscopy + biopsy
FNAB - the cytology shows cancer cells. /
Pre-op : Ensure good clotting profile and available FFP
Scintiscaning
ERCP
- For 12,13 A 15, ensure normal haematological values before the procedures
Complications of Primary tumour

1. Haemoperitoneum
- D ^ d
2. Obstructive jaundice
3. Bleeding varices
. ' ^
, L
V> c k ^ OQVA t *
VVW
^
^v^/ayV;
_ S C A W A ^
\H> s $<i , C L b " - W ^ , > m 7 c v K
Treatment
i.
- Surgery
Liver resection - done if the tumour is confined to a particular site. I t s mortality rate is 25
30%
ii.
Radiation - is poor
^
iii.
Hepatic artery ligation A Embolisation U c ^ q g A ^ c w ) f c Gooses VStW^'C f\.oov^ c^~
iv.
Direct alcohol intralesional injection
<^W a ^ v A Y-o c-><op V>V*c\w.cx
v.
Heat treatment
vi.
Injection of cytokine
vii.
Chemotherapy - using adriamycin Utfxfc V ^ W ^ - c M ^ c d l ^ - W ^ ^ c ^'
viii.
Liver transplant
Post-operative complications
1. Bleeding (Haemoperitoneum) - embolise the vessels, cannulate the hepatic
AMOEBIC LIVER ABSCESS

Pathogenesis
- Read up the life cycle of Entamoeba histolytica
Faeco-oral
1
1
Colon
Portal circulation V* *A>c*~*vh\
Liver
Clinical Features
I s similar to that pyogenic liver abscess which is usually multiple.
i.
Right upper quandrant syndrome - it consists

o
Abdominal pain - which is constant and aching. I t is due to stretching of the
Glisson capsule
o
Fever
o
Jaundice
ii.
iii.
Wasting
Hepatomegaly
97
iv.
Anorexia
v.
Night sweats
vi.
Malaise
vii.
viii.
Nauses A vomiting
Pleurisy
ix.
Cough
N <^
.^
^t*'
Note, usually amoebic ruptures into surrounding structures, buM>yogenic abscess does not. I t ruptures into
peritoneal cavity, gut or lungs.
i.
Ascending cholangitis i C k ^ W o ^ S , U ^ U
CO*A*> P U D *
Investigations
1. Full blood count - shows anaemia, leucocytosis
(
2. Ultrasound - shows area of hypoechoic zone >t t r-<\.^ c Wytyfcxc) O^s
3. CT scan
4. Serology - Indirect haemaglutination \ '. ^>\*2_ <Xx wy\^c\ <5. ELISA
6. Stool microscopy - for cysts and trophoizoites (which is infective). I t is seen only 30% of
patients.
7. Diagnostic aspiration - reveals classical anchovy sauce (cholocate) sputum
Diagnosis
By haemaglutination or Widal's test
4^ 1 ^ |p <Ywv
l)
Treatment
Medical
iii.
Metronidazole - 800mg t i d f o r 1 week

Chloroquine / ^</y^l
Gentamicin & Pencillin
Surgery
Done if medical treatment fails. I t involves
i.
Percutaneous drainage
ii.
Open drainage- is controversial tWoQ>u Cwtos. (^YcyAYu<, C V ^ o X p
v^c ^ J ^ ^ ,
- Tube drainage is done under ultrasound or CT guidance
98
PYOGENIC LIVER ABSCESS

Introduction
I s a poly-bacterial infection
I s usually multiple
Aetiology
Ascending cholangitis
Apendicitis - via portal vein
Hepatic artery infection
Postraumatic
Direct extension
i.
ii.
v.
v.
'
Organisms
i.
ii.
\*.\
- v.- -
E. COli \y
C -iWiV
.. c s-<-V o y * r ' - *
&-*
( S^(P u- a c ^ ScPhcov.
Klebsiella
Clinical Features
as above
But, rupture into chest is unusual
Investigation
Blood culture Diagnostic aspirate + culture - yields better T C..S
Ultrasound
CT scan
^,0,-V
\.v>,u
V.'.VO.H
rU\ \o\A C a t W
Treatment
Drainage + antibiotics
Drainage can be
a. Tube drainage under Ultrasound or CT guidance or
b. Open drainage
All these are controversial!
99
GALL BLADDER DISEASES

Investigation Of Gall Bladder A Biliary Tract
(Inflammation, Obstruction, Neoplasm)
1.
Plain Abdominal X-ray - shows

- Only 10% of gall stones are radio-opaque
- Air in biliary tree : seen in emphysematous cholecystitis A biliary enteric fistula
(choledochoduodenal fistula)
2.
Ultrasound
I t is gold standard.
I t is used for initial investigation (as f i r s t line) of biliary tract disease. I t is deifinite
in > 92%
I t does not use radiation, and can detect gall stones A gall bladder carcinoma.
Hyperechoic stones are seen in dependent portion of the gall bladder casting acoustic
shadow ( a radiolucency)
I t shows wall thickening
I t does not pass through gases (A bone), hence does not show the loer part of
common bile duct under the duodenum.
3. Computer tomography scan

I s good in retroperitoneal part i.e lower part of common bile duct
I t is more expensive
4.
Endoscopic Retrograde Cholangiopacreaticoduodenography (ERCP)

delineate common bile duct, pancreatic duct of Wirsung
I t is done by passing down the endoscope to cannulate the Ampulla of Vater, the dye is then
injected
Uses
i. Useful in jaundice patient
ii. To see the cause/level of obstruction
iii. To biopsy - for Carcinoma of head of pancreas or cholangiocarcinoma.
5. Percutaneous Transhepatic Cholangiogram (PTC)

- I t is complementary to ERCP and used for biopsy and therapeutic purpose.
- A dye is injected into the liver to outline the biliary tree.
- Ensure normal haematological values to prevent bleeding
6. Magnetic Resonance Cholangiopancreatography (AARCP)
- is now almost replacing ERCP.
7. Scinitigraphy - f o r acute cholecystitis A sickle cell disease. I t is a radionuclide scan after injection
of 99 Technitium-labelled derivative og IDA.
8. Oral cholecystogram
- Cholecystitis not secondary to gall bladder stones (10%)
100
9. Intravenous cholangiogram
**Note - the last 2 methods are rarely used now because of the advent of ultrasound
10. Radionuclide scan - I s injection of Technitium 99m labeled derivative of IDA.
I t is used to diagnose acute chloecystitis (acalculus, calculus type)
Inject dye, if common bile duct is obstructed, no dye is seen.
11.
CONGENITAL ANOMALIES
Introduction
- I s very common
Types
1.
2.
3.
4.
5.
6.
Agensis or Rudimentary
Situs invertus
Double or triple
Complete septal division
Direct communication with liver
Cystic duct - short, ultrashort, ultralong
7. Moneyam's hump
8. Aberrant vessels
GALL STONES ( Cholelithiasis)

Incidence
o 35% of it occurs in women and 15% in men
o Affects 20 milion in USA
o Commonest surgery in Europe & North America, 10 - 20%
o 48% in Pina, India

o
o
I n Africa, it is < 1%
I n Ibadan, it 0.007% and 2.17o in pregnant women. Recently, 19 cases seen in 3 years
1. Age - I t increases with advancing age, common in 30 - 40years in Blacks
2. Sex - commoner in women
3. Obesity
4. Pregnancy
( - I t is common in " f a t , fertile, flat, female f o r t y or f i f t y year")
Note
- Most patients in Africa are asymptomatic and it is common in slim women
5.
6.
7.
8.
9.
10.
11.
12.
13.
Diet - common in those eating refined food

Infection
Chronic liver disease
Hyperglyceridaemia
Ileal dysfunction
Oral contraceptives
Biliary infections
Intravenous hyperalimentation
Haemolytic disorders - Sickle cell disorder
Types of Stones
a. Mixed - commonest worldwide. I t consists of cholesterol, bilirubin, calcium. I t is
brown and multifaceted.
b. Pigment stone - is common here especially in hemolytic disease e.g Sickle cell dieseas
c. Pure Cholesterol stones - is not common here. The stone is pale white
Clinicopathological syndromes
i.
Asymptomatic - in most patients, 10 - 90% depending on series
ii.
Dyspepsia - is indigestion
iii.
Biliary colic - a colicky pain in the right hypochondrial region. I t is defined as acute
cholecystitis without systemic symptoms
iv.
Acute calculus cholecystitis - biliary colic + constitutional /systemic symptoms
v.
Emphysematous cholescystitis - due to gas-forming organism, Clostridium welchii
vi.
Empyema of gall bladder - pus in gall bladder
vii.
Mucocoele of gall bladder - due to excessive secretion of mucous which is not infected. The
bile is absorbed,
viii.
Perforation - causing peritonitis or choledo-anteric fistula
ix.
Chronic calculous cholecystitis
x.
Mirizzi syndrome
- Type I, II, I I I
xi.
xii.
Acalculus cholecystitis
Adenomatosis
Treatment
a. Medical
Aim To dissolve gall stone with bile salts e.g deoxycholate ( Dissolution therapy)
Criteria
iii. Pure cholesterol stone
iv. Must not be > 2cm
v. Sail bladder must be functioning
Recurrence rate: 50%
b.
Surgical
i.
ii.
Extracoporeal short-wave lithotripsy (ESWL)

Cholecystectomy - done by laparoscopy or open (in laparotomy cholecystectomy,
the risk of biliary injury is high)
111.
IV.
Complications of Cholecystectomy
i.Bile duct injury
ii.
Bleeding - from a branc^vof the cystic artery
iii.
Bilioma
iv.
W / W syndrome ( Wattran Water syndrome)
v.
Post-cholecystectomy syndrome Bile duct Exploration
- Choledochotomy - Sump syndrome
Cholecystostomy
- to drain the gall bladder with a needle & syringe
PANCREATIC DISEASES
Carcinoma of the head of pancreas
Acute pancreatitis
CARCINOMA OF HEAD OF HEAD PANCREAS

Embryology
Pancraes develops from ventral and dorsal pouches of the duodenum. The ventral pouch forms the
head of pancreas whil the dorsal froms body and tail.
Introduction
- Is the commonest cause of surgical jaundice in old people (> 60 years)
Incidence
Male/female ratio is 3 : 2
Occurs in elderly group
1. Diabetes mellitus
2. Smoking
3. Alcohol
Cliinical features
I t is non-specific
i.
Back pain - is central. I t radiates to the back
ii.
Weight loss
v.
Carcinoma of the head of pancreas presents with
o Surgical jaundice - obeys Courvoisier's law .
o Weight loss
o Distended gall bladder

o Pan radiating to the back
Investigations
1. Barium meal - shows widening of the C -loop
2. Ultrasound
3. CI scan
4. PTC
5. ERCP - shows "double duct sign". I t is pancreatic and common bile duct
6. Arteriography
7. FNAB - I t is not allowed as seedling of the carcinoma can result to the other parts
Differential Diagnosis of Ca of head of pancreas
1. Lymphadenopathy
2. Carcinoma metastazing to the ampulla
3. Chronic pancreatitis
Treatment
Surgery
i.
ii.
iii.
Whipple's procedure - done for simple non-metastatic tumour. I t s success rate is

25%.
Biliary by-pass : Cholecysto-jejunostomy + Gastrojejunostomy
Triple by-pass
- Roux en-Y + Entero-enterostomy
Chemotherapy- is poor
PORTAL HYPERTENSION
Introduction
I s hypertension within the portal vein and its tributaries which include the superior mesenteric,
inferior mesenteric vein d the splenic vein.
The porta vein is located in the hepatoduodenal ligament at the free edge of the lesser omentum.
I t accompanies hepatic disease in 90% of cases
There is a disturbance of extrahepatic vascular system
The increased pressure can be due to
a. Increased blood flow
b. Obstruction to flow
Aetiology
1.
Increased Hepato-portal flow without obstruction

- Fistula between the splenic vein and splenic artery
2. Extra-hepatic outflow obstruction (_ P%V - v^
, ,
cîAeÔ-v10,
. .
Vv
C^N-J^*
<A\ c ^
104
Blockage at the level of the 3 hepatic veins preventing blood from leaving the liver to
the IVC e.g Budd Chiari syndrome (thrombophlebitis of the portal vein causing
obstructions
,\ V 3 Y . . .
A K ^ ^ ^ W P ^ C
V^ c c\ *-*<** ^ôt^-A
n
3. Obstruction to extra-hepatic portal venous system ( n
- by lymph node, carcinoma of pancreas
x \
4. Intrahepatic obstruction e.g liver cirrhosis <ÂhUj-^<; cW> f\<>AVe oicoUoV L i v ^ r c i v

I t is the commonest cause of portal hypertension, accounts for > 90% of causes
There is destruction of normal liver architecture
Pathophysiology
o
The normal pressure is < 250mmH20 ( mean is 215mmH20 ) or < 25mmHg
o
Measurement can be done by
Omental /portal vein cannula
Splenic pulp manometry
iii. Splenography
iv. Umbilical venography
Pathology
a.
There are 2 groups of functional collaterals

Hepatopetal flow - consists of
I.
Hepato-colic veins
r
ii.
Hepato-renal v.
in.
Epiploic v.
iv.
Diaphragm v.
.
*, -' . s ôA \
Ay ^ -Q
' a\<A' A -pch
rin$H
\ , v'v^ /-Ay J ~
:
b. Hepatofuqal flow
- out of the liver
i.
Coronary /Oesophageal v. - Oesophageal varices
ii.
Superior rectal veins ( haemorrhoidal v.)
iii.
Umbilical v.
iv.
Retroperitoneal v.
Manifestations of Portal Hypertension
a. Oesophageal varices
b. Ascites
c. Hypersplenism
d. Encephalopathy & Coma
a.
OESOPHAGEAL VARICES
These are dilated and engorged veins in the submucosal plexus of oesophagus, stomach ( cardiac,
fundus, lesser curvature ) duodenum A ileum.
Rupture can occur from oesophagitis causing massive upper &I bleeding.
105
I n these patients, > 90% of them have intra-hepatic disease especially liver cirrhosis.
In children, the obstruction to venous flow could be extra-hepatic.
Natural Course of Oesophageal varices
About 30% of patients of cirrhotics with varices bleed
The time between diagnosis and bleed is 1 -187weeks (within 2 years of diagnosis.)
Extra-hepatic has low mortality while Cirrhotic varices has high mortality
60% of cirrhotics re-bleed within a year
Prophylactic treatment is unhelpful except in childaafcr types A & B ( a classification of O&M that
is based on albumin ) who have good hepatic functions
ACUTE BLEEDING
I t is usually the manifestation in children
70% occurs before 7 years and 90% before 10 years
I n adult, 25 -33% of massive upper G I haemorrhage
The cause of bleeding
i.
Varices - accounts for 50%
Rule out other causes of upper S I bleeding
ii.
Gastritis - for 30%
iii.
Duodenal ulcers - 9%
\ ^
V>T>
fycvv
^CAM
^
,v
*{'* V ^ '
Diagnosis 4 Investigation
CIM^'
i.
Stigmata of cirrhosis
o
Finger clubbing
o
Palmar erythema
o
Asterexis
ii.
Splenomegaly - is suggestive portal hypertension
iii.
Liver function test - is UNRELIABLE I I t may be normal or minimally raised,
iv.
Barium swallow - I t shows longitudinal worm-like defect in the oesophagus. I t gives
high false negative result.
v.
vi.
Coeliac A Superior mesenteric artery angiography

Oesophageal balloon tamponade
Using S t ^ s V ^ \ > ^ j b e
- I t is diagnostic and therapeutic (short term)

- A third tube ( Minessota tube) is used to drain the blood
vii.
Oesophagoscopy - is most reliable, but may miss varices due/to observer variation.
i I
Treatment
a.
Non-operative
i. Direct control - using tamponade
i i . Indirect - aims at reducing the pressure in the splanchnic circulation e.g
Somatostatin analogue ( Octreotide )
Propanol (IV) - e.g propanolol, it reduces blood flow in intestine <&

varices
i i i . Transjugular Intrahepatic portosystemic stent shunt (TTPPS)
b.
Operative
i. Direct control
o
DEVASC - Revascularisation of the oesophageal veins ( e.g
QHassap_[Sjiprocedure)
o
Ligation
o
Gastro-oesophageal resection, then applying stapler
o
Resection A Suture back - thereby discontinue the varices
ii.
Indirect control - by creating Porto-systemic shunt e.g
Superiorvena cava to superior mesenteric vein
Splenic vein and adrenal vein
Prevention of Recurrent Bleeding

1
1.
Sclerotherapy somatostatin
,. ^ s ^ 0 tl t - < -llv^r- Inject intra- or perivariceally using phenol, tetracedylacetate f A\crr.*< I f f l - ^ 0 0 " *
2.
Surgery - especially in children
o
Presinusoidal - has good outcome of surgery
o
Post-sinusoidal - has post-operative outcome
3.
2 - year survival same - shunt v sclerotherapy
4.
End-stage liver disease - TTPSS/ Sclerotherapy, then liver transplantation
b.
ASCITES
Pathophysiology
is complex and incompletely understood
The portal hypertension is a minor factor i.e the degree of ascite does not correlate with the
degree of pressure in the portal vein
Lymphatic / Arterial / Venous
Hypoalbuminaemia
- There is sodium and water retention ( Urinary ADH level is elevated)
Treatment
i.
Rest
ii.
Diet
High carbohydrate
Protein
Vitamins
Potassium supplement
Low sodium
107
iii.
iv.
v.
vi.
Diuretics e.g Aldactone, chlorthiazine & K supplement

Paracentesis abdominis - is indicated only whenjthere is respiratory distress
Porto-caval shunt
~
Peritonovenous shunt - DENVER, LEVEEN.
c.
HYPERSPLENISM
I s due to sequestration of blood by spleen
Note, splenomegaly is NOT equivalent to portal hypertension
There are
Anaemia
Leukopaenia - WBC < 4,000/cmm
Thromboctopaenia - < 100,000 /cmm
Treatment
Treat the cause of the portal hypertension, as splenectomy is rarely indicated
Porto-caval and distal splenorenal shunt ( Warren) to correct hypersplenism in 2/3 r d
of patients.
d.
ENCEPHALOPATHY A COMA
This is Child C classification
I t is Porto-system encephalopathy, a neuro-psychiatric syndrome
I t is associated with liver cirrhosis and hepatic failure
I t is rare in extra-hepatic involvement^ ^
A
Coma occurs when the hyper<ammonaemiaj2j^5g_/dl/
Treatment of Porto-systemic EncepFalopathy
i.
Reduction of dietary protein
ii.
iii.
iv.
v.
vi.
vii.
Give glucose - to maintain rbc and help the liver

Control S I bleeding
Give K+ supplement
Give carthatics and enemas - to increase f eacal load by increasing bowel movement
Give non-absorbable antibiotics e.g neomycin to reduce the micro-floral which aids
ammonia production
Give lactulose - it breaks down to lactic acid which reduces the pH of the intestine and
thus reduces the transfer of ammonia into blood, \~\ \\i \-\, ^\ \ \ ] \ - 0 c -<", W ^ W A
Surgery for Portal Hypertension

- First and foremost, control the manifestations
e.g
.
Bleeding : Ligation, transaction, oesophagoscopy, jejunal
interposition
Ascites
108
Reduction of Portal pressure flow

i.
Splenectomy
ii.
Porto-caval shunt
o
End-to-end
o
Side-to-side
o
H-graft
iii.
Spleno-renal shunt
o
End-toend
o
Side-to-side
iv.
SMV -IVC
o
o
-Mesocaval shunt
Side-to-side
H-graft
BENIGN BREAST DISEASES

( Or Ogundiran)
Anatomy of the Breast
Embryology
The breast develops in the thickened portion of the ectodermal tissue known as Milk
steak line arising from the pubis to the axilla in early foetal life.
I t is a dermally derived organ lying with the subcutaneous tissue.
Post-natal ly,
Male breast - the buds become rudimentary
Female breast - development correlates with age. I t is regulated by hormones.
Location
I t extends from 2 nd to 6 t h rib in the midline to the posterior axillary line.
BENIGN DISORDERS OF THE BREAST

Congenital
i.
ii.
iii.
Anomalies
Amastia /amazia
Polymastia
Polythelia!
Developmental
i.
ii.
v.
Nipple retraction
Under-developed breast
Mammary hypertrophy - Virginal hypertrophy
^
Abberation of Normal Development and Involution ( ANDI)
109
c. Inflammatory
Infantile mastitis
Acute (bacterial) mastitis
Tuberculous Mastitis
AAondor's disease
Duct Ectasia
i.
ii.
v.
v.
d. Lumps
Fibroadenoma
Fibroadenosis
Cysto-sarcoma phylloides
Traumatic f a t necrosis
Ductal papilloma
Cysts of the breast
Galactocoele
i.
ii.
v.
v.
vi.
vii.
e. Nipple disorders
f. Gynaecomastia
Section I
a.
Amastia /Amazia - is absence of breast.lt is commoner in men. I t is associated with absent

pectoralis muscle
b.
Polymazia /Polymastia - There are accessory breast tissue developed along with the normal
breast
c.
Athelial - is absence of nipple, especially in men
d.
Polythelial
-
Consists of supernumerary or accessory nipples.

I t may be unilateral or bilateral.
I t may be functional or non-functional, but it is usually non-functional
Sect/on I I
DEVELOPMENTAL DISORDERS
a.
Nipple Retraction
I t usually occurs at puberty as the nipple does not grow in syncytium with breast
and i t is flattened
I t is prone to ulceration especially during breasfeeding.
Receny history of nipple retraction in middle aged woman may suggest an underlying
breast malignancy
b.
Underedeveloped breast
110
The breast is out of syncytium with the rest of the body mass. Patient may require
oestrogen treatment or even augmentation mammoplasty.
c.
Mammary Hypertrophy
- Virginal hypertrophy - is an enlargement of breast after an abortion or f i r s t
pregnancy.
Treatment - Reduction mammoplasty
d.
Aberration of Normal Development and Involution ( ANDI) - is deviation from normal due to
cyclical changes from menarche to menopause.
Section III
NIPPLE DISORDERS
I t may be from one or more lactiferous duct.
Types /Classification
a.
Based on the number of breast involved
o
Unilateral - the cause is local to the breast
o
Bilateral - it is systemic
b.
Based on the nature of the discharge

i.
Clear /serous - the causes are
o
Physiological
o
Parous
o
Papilloma
o
Fibroadenoma
Bloody
II.
0
Ductal papilloma
o
Carcinoma (Intraductal )
in.
Milky
o
o
o
Lactation
Duct ectasia - abnormal dilatation
Prolactinoma
IV.
Purulent
v.
Abscess
o
Duct ectasia
Brownish/Breenish
o
Duct ectasia
o
Fibroadenosis
o
Clinjical Presentation
!
- Determined whether
o it is unilateral or bilateral
o Coming from one or more orifices
Colour of discharge
Associated lump especially in nipple areolar
111
Invest iqot ion

1. Discharge sample for cytology - to rule out carcinoma
2. Discrage sample f o r m/c/s - to rule out infection
3. Ultrasound of the breast - detects papilloma
4. Mammography
Note, both 3 and 4 are not specific
5. CTscan of brain - if it is bilateral to rule out prolactinoma ( and brain tumour)
Treatment
a. Infection
i.
Antibiotics - I n most cases, the discharge stops
ii.
Excision of the duct
b. Ductal papilloma or duct ectasia - Microduchectomy i.e excision of a single duct.
Section IV
INFLAMMATORY DISORDERS
a.
M A S T I T I S OF INFANTS
o
I t occurs in newborn
o
I t is equal in both male and female
Aetiology
I t is due transfer of maternal oestrogen in utero, this stimulates breast development and
prolactin stimulating milk production.
i.
Swollen breast - may be unilateral of bilateral
ii.
Tenderness
iii.
Discharge - is referred to as "Witches' milk "
Treatment
Do nothing, it usualy resolves after few days of life. Just reassure the mother.
b. ACUTE MASTITIS /LACTATION M A S T I T I S

definition
I t is an inflammatory disease of the breast.
Incidence
70% occurs in late pregnancy and during lactation period
Aetiology
- Staphylococcua aureus - is commonest
Pathogenesis
n:
o
o
o
I t starts with cracking of nipples caused by the sucking infants.

Then, infection sets in by the normal flora
The organisms ascend through the lactiferous duct into breast lobules.
Uniformly swollen breast
i.
Breast pain - in late pregnancy
ii.
Purulent nipple discahrge
v.
Consitutional symptoms - Fever, malaise etc
On examination
i. Fever
ii.
Uniformly swollen part or all the breast tissue
iii.
Tenderness
iv.
Shiny skin
v.
vi.
Hyperaemia
Ipsilateral lymphadenopathy
Investigation
i. Full blood count - shows leucocytosis
Treatment
i.Stop sucking from the affected breast
ii.
Give antibiotics - is given for 14 days
iii.
Give analgesics
iv.
Give antipyretics
v.
Incision & drainage - if has formed abscess
vi.
Excision - for antibioma
Complications
1. Breast abcesss - if left untreated for a long time. I t is a fluctuant mass
Treatment - Incision A Drainage.
o
Drain early before antibiotics treatment to prevent sterile pus formation which resolves
to form antibioma which presents as a lump in the breast.
2. Antibioma
-
is formed after abscess formation & cold abscess.

I t is firm .
There is history of previous inflammation.
I t is difficult to differentiate from neoplasm until excision biopsy is done.
TUBERCULOUS M A S T I T I S
I s chronic inflammatory lesion
I t is difficult to differentiate from advanced disease of breast carcinoma because there are
Peaud'orange & significant lymphadenopathy ( ? axillary )
MONDOR's DISEASE
I s seuperficial thrombophlebitis of the superficial veins of the breast
113
Presentation
o Cord-like swelling of the breast
o I t is confused with occult malignancy
Treatment
o
I t is self-limiting, re-assure the patient
o
Give anti-inflammatory and analgesics
e- DUCT ECTASIA
Definition
I s abnormal dilatation of lactiferous duct usually due to periductal inflammation
Aetiology
There are theories
i.
ii.
I t may be due stagnant secretions which can be as a result of blockade or

inflammation and consequent fibrosis,
I t can result from ageing
Clinical Presenatation
i.
ii.
iii.
iv.
v.
Breast pain
Nipple discharge - serous or brownish
Nipple retraction - is due to fibrosis
Swelling in the sub-areolar region
Areola fistula - between the duct and nipple
Treatment
Excision of the duct
Cytology
M/C/S
114
Section V
LUMPS / TUMOURS
Results from disorders of cyclical changes from menarche to menopause.
The lumps arise from ducts, connective tissue or both
a. FIBROADENOMA
Introduction
- I s a benign tumour of the breast
Incidence
I t forms about 70% of benign breast disease or lumps. I t is the commonest in Ibadan
I t occurs between 14 - 30 years. Intra-canaliculi is common between 30 - 50 years.
Pathology
I t is usually the pericanalicular type
Pathogenesis
I t results from hyperplasia of a lobule.
I t is a combination of fibrosis ( connective tissue) & glandular tissue
I t is usually well encapsulated especially the peri-canaliculi, making it separated from the
surrounding tissue.
Note, Intra-canalicular type is common between 30 - 50 years. I t is not as hard as peri-canaliculi.
Clinical Features
History
i.
Lump in young women- is usually painless, but may become painful during
menstruation
Examination - I t is
ii.
Firm
iii.
Roundish
iv.
Well encapsulated
v.
Freely mobile within the breast tissue. I t is called "Breast Mouse"
Variant
1.
Treatment
o
o
o
Giant fibroadenoma
it usually occurs a f t e r puberty
I t grows rapidly to becaome a big lump. I t fill the whole breast
FNAC - to rule out malignancy

I f there catamenial increase in size and FNAC shows benign lesion, just WATCH
Do excision - I f there is increase in tumour size + tenderness even if FNAC is benign
115
b. C/STA-SARCOMA PHYLLOIDES
Introduction
I t may be benign or malignant
I t is a serocystic disease of Brodie
Incidence
I t is common above 40 years
Clinical Features
i.Huge uneven bosselated tumour
ii.
Has sarcomatous component
iii.
Malignant type may metastasize to lungs, liver, skin with ulcerations
Diagnosis
o Establish diagnosis with FNAB or Trucut biopsy
Treatment
a. Excision - I f it is small-sized
b. Mastectomy - For large size and late presentation
c. FIBROADENOSIS
Introduction
- I t is also called by any of the following names
i.Fibrocystic disease
ii.
Chronic mastitis
iii.
Chronic mastopathy
iv.
Cystic disease of breast
v.
Mammary dysplasia
Incidence
Peak age is 35 - 45 years. Note, this is also the peak age incidence for carcinoma of breast in
this environment.
Pathogenesis
I t is due hormonal dysfunction. I t is an aberration of normal development and evolution.
Clinical Features
i.
Age - is typical
ii.
Breast pain - I t is
Diffuse
Cyclical : waxes and wanes
Worst with menses - it is wosre during or just before
iii.
Breast fullness
iv.
Discrete lump in the breast - which may be tender, coarse or granular. I t is described
as nodular "pebble" or "stones" or "rice" grain within the breast
v.
Young woman, old nulliparous woman, non-lactating, common in Caussians
116
Investigation
1.
2.
3.
4.
Fine Needle Aspiration Biospy - to exclude malignancy ( due to similar peak age)
Excisional biopsy - is the gold standard. I t establishes the diagnosis
Ultrasound - to differentiate between solid and cystic lesion
Mammaography - I t is not done in this environment as best results are achieved in
above 50 years. Most of patients here are < 50years and false positive result does
occur.
Treatment
a. General
Advise - Firm brazier to support fuller breast and prevent pain
Analgesics
Vitamin B Complex
Diuretics
b. Specific ( Drugs )
Diuretics - to reduce the fluid in the breast
Anti-prolactin hormone e.g bromocriptine
i.
Anti-oestrogen e.g Tamixifen
ii.
Anti-gonadotrophic drugs e.g danazol
v.
Evening Primrose oil ( Gamma- Linoleic acid) is used to stabilize the epitheial cells via
v.
prostaglandins
d POST- TRAUMATIC FAT NECROSIS

The trauma may an inconsequential violent contraction of pectoralis muscle. The lesion
organizes and becomes chalky which then turns to lump.
o
Destruction of f a t component of breast
Necrosis
Healing by fibrosis
Differentia/ Diagnosis
1. Breast carcinoma
z. 6ALACTOCOELE
Introduction
o
I s cystic accumulation of breat milk in surrounding tissue.
Pathogenesis
I s due to obstruction of main ducts during lactation, thus the duct becomes distended with
milk
History
Lump in the breast, with history of recent lactation
Treatment
i. Aspiration with a wide bore needle
ii. Excision
f. DUCT PAPILLOMA
o
o
I s proliferation of ductal tissue which manifest as either a lump of nipple discharge which is
brownish or bloody
Malignancy is a differential
Investigation
o Discharge sample f o r m/c/s
o Ductography - x-ray of contrast filled ducts. Helps to rule out filling defects
Treatment
Excision - Open micro-ductectomy
g. C/STS OF THE BREAST

May be solitary or multiple
Majority are due to fibrocystic diseases
May be palpable or not
Aspiration/Excision for m/c/s A Cytology
h. GYNECOMASTIA
I s abnormally enlargement of male breast
I t is usually at the nipple-areolar complex
Causes
1.
Physiological
-
Usually at puberty.
I t may be unilateral or bilateral
I t is usually painful and tender
May require analgesics and anti-inflammatory
I t may persist
2. Liver Cirrhosis - because of the inactivation of oestrogens in the liver

3. Iatrogenic - Oestrogenic treatment
4. Testicular atrophy
5. Drugs
differential Oiaanosis
i. Breast carcinoma - it causes unilateral enlargement and usually in outer quadrants
118
Treatment
Subcutaneous mastectomy
Chapter 24
MALIGNANT BREAST DISEASES

( Or Ogundiran)
Introduction
Malignant breast diseases are not restricted to carcinoma of the breast which constitue the
majority, it also the diseases listed below.
Types
a. Carcinoma - accounts f o r 97% of all malignant breast diseases
b. Sarcoma - accounts for 0.5%
c. Osteogenic Sarcoma
i. Cystosarcoma phylloides ( Malignant phylloides tumour)
ii. Serocystic disease of Brodie
d. Lymphoma - Burkitt
e. Metastatic breast disease
f. Diseases of skin - e.g Basal cell carcinoma, Kaposi sarcoma
CARCINOMA OF THE BREAST

Introduction
I t constitutes the bulk of malignant disease of the breast
I s the commonest malignancy in the female (apart from skin cancers)
I s a major cause of death
I t arises mainly from the ductal cells
Epidemiology
Most lumps in the breast are benign
I n Western world, breast carcinoma occurs in 1 : 10 women
I n Nigeria, the incidence is 116 / 100,000. About 15 years ago, it was about 33/100,000.
The peak age in Nigeria is 35 - 45years and 55 - 65years in Caucassian.
Women aged < 30years constitute > 12% in Nigeria and < 5% in Caucassians
Peak age (years)

Course
Prognosis
Aetiology
Africans
35-45
More aggressive
Caucasians
55 - 65 ( post-menopausal)
Better
Combination of both genetic
Likely to be genetic
and environmental factor
Average age is 42.5 years i.e premenopausal women
119
i.
Age - the risk increases with age
.
ii.
Sex - Females are 99% more affected. I n male, the incidence is 0.5 - 1% ( Nigeria - 5%)
iii.
Geography - as above
iv.
Family history - 1st degree relatives with BRCA have more probability
"'
v.
Prolonged exposure to oestrogen I t is not necessarily an initiator but a promoter. I t is seen i
women with
a. Prolonged menstrual lifespan - Early menarche & Late menopause
"""
b.
vi.
vii.
viii.
ix.
x.
xi.
xii.
Exogenous oestrogen therapy - OCP, HRT ( HRT is common among the

Caucasians)
Nulliparity or late age of f i r s t pregnancy i.e > 30years

Obesity in Postmenopausal women A because f a t cells metabolise androgens to oestrogen, t h n
raising the level of oestradiol. Also obesity lowers the serum level of hormone-binding globul i
which should bind oestradiol, hence f r e e oestradiol is increased,
Atypical Epithelial Hyperplasia "^
Irradiation - especially girls who in their childhood were treated with irradiation for
Hodgkin's lymphoma or leukaemia
Oovorectomy
"^
Non-breastfeeding
Genetic mutations - BRCA I & I I - is only seen in 5 - 10% of cases. Other associated genes
are Tumour suppressor genes e.g ATM gene, Li-Fraumeni syndrome ( BRCA, Ovarian,
Colorectal) & P53
Peculiar Negative Characteristics in this Environment

1.
Early age of onset
2.
Aggressive disease pattern
3.
Bulky scissous (fibrous) tumour
4.
Late presentation
Risk Identification
There are 2 models
a.
Gayl's model
b.
Samus model
The Parameters taken account are
1. Age
2. Race
3. Number of hyperplastic breast disease
4. Family history
5. Age of f i r s t full term pregnancy
Pathology
Breast carcinoma can develop from duct or lobular unit.
Types
a.
In-situ
i.
Lobular carcinoma
120
ii.
Ductal
Invasive - accounts for 80%

i. Lobular carcinoma
ii. Ductal carcinoma
In-stiu means a cancerous process that is limited by the basement while" invasive" means
infiltrating
Site
Upper outer quadrant has the highest incidence (as it contains more glandular tissue)
History- Can be grouped into 3
a. Symptoms in the breast - seen in 90%
b.
Associated with axillary pathology - seen in 5%
c.
Symptoms of distant metastasis - seen in 5%
a. Symptoms in the breast

i.
Lump in breast - is usually painless, but progressively increase in size,
ii.
Skin involvement
o Puckering of the skin
o Tethering of the skin
o Ulceration
iii.
iv.
v.
vi.
vii.
viii.
ix.
Mastalgia - breast pain

Paget's disease of the breast
Nipple discharge - brownish, purulent or blood-stained. Note, in some cases, bloody
discharge is the primary symptom,
Nipple abnormality - may be flattening or eversion/recent nipple retraction ( rule out
congenital, i.e is it from childhood)
Big breast - with no lump
Shrunken breast
Satellite lesion e.g multiple lesions
b. Features of axillary pathology

Axillary swelling - due to lymphadenopathy
Ulceration of the lymph node in axilla
Ipsilateral arm swelling called lymphoedema ( with involvement of the other breast, it
is a feature of advanced disease )
121
c. Symptoms of distant metastasis

i.
Supraclavicular lymphadenopathy
ii.
Brain - presents with features of space occupying lesions :
o Seizures spells
o Lateralising signs
o Paralysis
o Features of raised ICP
o Coma
Spine
m.
Back pain - is chronic and persistent
Features of spinal cord compression
Paraparesis / paraplegia
Unstable gait
Sphincteric disturbance - faecal A urinary incontinence

IV.
Chest Pleural effusion
Lung parenchymal involvement - there are 2 types
a. Diffuse - Lymphangitis carcinomatosis
b. Discrete - Canon-ball opacities
Respiratory distress
Bones
Bone pain + tenderness
Pathological fracture especially long bones (proximal part of humerus
and f emus) and also to short bones.
Liver
VI.
o Ascites (abdominal swelling)
o Jaundice
a. Examination of the breast (lump)
I t is hard, craggy or irregular
i.
Skin ulceration
ii.
Non-tender
v.
I t may be fixed to the underlying structures
v.
Paeud'orange
vi.
Eversion /flattening of nipple
vii.
Lymphoedema of arm
viii. Axillary lymphadenopathy
b. Systemic examination - f o r evidence of metastasis
Chest
i.
Abdomen
ii.
Skull
v.
Spine
v.
Arm
122
1.
2.
3.
4.
5.
6.
7.
8.
Fibroadenoma
Fibroadenosis
Galactocoele
Traumatic fat Necrosis
Chronic breast abscess
Burkitt lymphoma
Lipoma
Sebaceous cyst
Staqinq
I t helps to plan treatment and determine the prognosis
The methods are
a. Manchester classification - is clinical. I t may not be accurate.
b. TNAA classification - is pathological. I t should be more accuraie
a.
Manchester Staging - I s clinical

Lump without axillary involvement
II
Lump + discrete axillary lymphadenopathy
III
Lump + Matted axillary lymphadenopathy OR

Lump + skin involvement or attachment to chest +
Axillary LN
Evidence of distant metastasis :
Supraclavicular lymph node
Chest
Abdomen
IV
Investigation
These are grouped into three
a. To confirm the diagnosis
i. Biopsy
Needle biopsy- there are 2 types

o
FNAB/FNAC
o
Trucut biopsy - is core tissue biopsy
Surgical biopsy
o
Incisional - when the tumour is big, usually > 5cm
o
Excisional - when it is 2 - 3cm
o
Wedge biopsy
Interpretation
i.To know the histologic type
ii.
To determine the histologic grading
iii.
For biological studies - to determine the treatment
iv.
To determine the hormonal receptor activity of the tumor
a.
Eft +ve and PR +ve : Has better prognosis
b.
ER -ve and PR +ve
Note,
ER - Estrogen receptor
PR - Progesterone receptor
b. To determine the extent of the disease i.e to stage
i.
Chest x-ray - it shows
o
Evidence of pleural effusion
o
Solitary nodular deposits - seen as canon ball opacities
o
Diffuse lung parenchymal involvement
o
Osteolytic changes in the ribs - this takes 2 week to show
ii.
iii.
iv.
v.
vi.
Spine x-ray - Thoracolumbar or Lumbosacral

X-ray of proximal long bones & pelvis
Abdominal ultrasound
- To see liver & peritoneal cavity f o r ascites
Bone scan - shows early osteolytic changes as " hot spots"
Brain CT scan- done when suspecting brain metastasis
c. To prepare the patient for definitve treatment

i.
Blood
o Full blood count - is mandatory
o Electrolytes 4 urea - may be necessary
o Group & crossmatching
ii.
Liver function test - it consists of
iii.
iv.
o
Bilirubin-Total A direct
o
Protein - Total & albumin
o
Aspartate transainase (AST)
o
Alanine transaminase (ALT)
o
Alkaline phosphatase (ALP)
ECS - f o r adult or elderly patient
Echo - f o r elderly patient
Treatment
I t depends on
Age
i.
Menopausal status -i.e- pre- or postii.
Parity
v.
Stage of the disease
Aim- To cure or offer palliative treatment
Modalities
a. Surgery
b. Chemotherapy
c. Radiotherapy
d. Hormonal
e. Immunotherapy / Biological therapy
a.
Surgery - the options are

Diagnostic
o Excisional biopsy
o Incisional biopsy
Therapeutic
- Done to achieve control of the tumour
i.
Radical mastectomy (Extended)

- I t was used in the past. I t involves removal of
o
Whole breast
o
Some muscle
o
Lymph node - Axillary, Internal mammary
-
I t is NOT good
ii.
Modified Radical mastectomy

- I t is good f o r early stage disease
- I t involves
o
Removal of whole brest
o
With or without removal of Pectoralis minor
o
Axillary clearance - removal of axillary lymph node A
fat
iii.
Breast Conserving surgery

- I t is a recent technique. I t involves
Simple lump excision ( f o r tuours ~ 2cm diameter)
Segmental resection of breast - ( Quadrectomy or
Lumpectomy) - f o r tumour < 5cm
Adjuvant treatment- Radiotherapy
- I t is used f o r stage I & I I
- I t is good f o r young ladies
iv.
Toilet Mastectomy
I s used for locally advanced breast cancer with ulcer which is
f ungating & malodourous
I t is done with
o Chemotherapy
o Antimicrobial
o Wound dressing
b. Radiotherapy - I t is used as
Neo-adjuvant (before surgery) - to downstage the tumour
Adjuvant (after surgery) - to mop up micro cells left after surgery

The indications are
i.
Localised secondary in spine, brain
ii.
c.
Palliation - for pain A bleeding ulcerated cancer ( where haemostatic

dose is given)
Combination chemotherapy - CMFV. CAF

Can also be given as
a. Neoadjuvant - to shrink the tumor and make it amenable to
surgery
b. Adjuvant
Requirement
c. PCV - not < 30%
d. W B C - n o t < 3 , 0 0 0 / m m 3
e. Platelets.-.not < 100,000/mm 3
Aoents used
('.Cyclophosphamide
Methotrexate
ii.
iii.
5 Fluorouracil
iv.
Adriamycin
v.
Prednisolone
Docitaxel
vi.
vii.
Mitomycin C
Complications
i.
ii.
v.
Ulceration of GIT - Abdominal pain, bloody diarrhea

Mucositis
Alopecia
Bone marrow depression - Infection, Anaemia, Thrombocytopaenia )
Treatment
i.
Stop the drugs
ii.
Good nursing
iii. Blood transfusion
iv. Give CSF to stimulate blood cells * x p f i .^, ? r
d.
Hormonal / Endocrine Manipulation

^
i.Oovorectomy - via radiation or surgery
ii.
Drugs - using antioestrogen e.g tamoxifen. I t is given to women who rejects
oovorectomy.
Note, removal of adrenal orpituitary gland is OBSOLETE !
e. Immunotherapy / Biological therapy

i. Agents stimulating host response
BCG
Thymosin
Levamisole
Corynbacterium parvum
ii. Non-specific immunotherapy
Human epidermal growth factor (EGF) receptor - as some

tumours have been known to elaborate the antigen of EGF
Monoclonal antibodies e.g trastuzimab ( @ Herceptin) - used

against the kind of tumour expressing the antigen.
Treatment Of Advanced Disease
i.
Control pain
ii.
Blood transfusion
iii.
Control bleeding
iv.
Give definitive treatment
Malignant Pleural Effusion

v.
CTTD
vi.
Pleuridesis
vii.
Definitive treatment
b.
Lung Parenchymal disease

i.Bronchodilators
ii.
Steroids
Supplemental oxygen
HI.
Brain Metastasis
i.
Steroids + Antacids
d.
e.
Spine Cord Compression

Steroids + Radiotherapy
- Regular turning
- Bladder training
- Anticoagulant
Funqatinq Disease
f. Wound dressing with honey
iii.
Antibiotics
iv.
Anti-tetanus
v.
Analgesics
Age - the younger the age, the more aggressive the disease
I t worsens with the increasing stage
Stage I ' s 10-year survival is about 90%
For all stages with no treatment, the survival is within 2 years
Clinical Types of Breast Cancers

a.
PAGETS DISEASE OF NIPPLE

o I t is seen in 3% of breast cancers
Clinical Features
i.
The lesion is localized to nipple area. I n the early phase, there is e
rash at the nipple
ii.
The rash is itching, and bleeds on scratching
iii.
Blood nipple discharge
iv.
Lump may be absent - Note, palpable lump has good prognosis
v.
There is history of treatment with antifungal with no relief
Diagnosis
- Biopsy of the nipple
b. M A S T I T I S CARCINOMATOSIS ( Inflammatory )
Introduction
I t is a terrible fast growing killer diseae
I t is seen in 2% of breast cancer patients
I t is generalized
i.Redness of breast
ii.
Oedema
iii.
Warmth
iv.
Pain
v.
Other features of inflammation : fever, tachycardia, raised wbc are absent.
1. Mastitis ( Acute/Bacterial)
Treatment
Early - Modified Radical Mastectomy +
Prognosis
- I s bad. Most patients die within 6 months
SAkCOfoA
ypes
a. Cystosarcoma phylloides (Malignant phylloildes tumour)- is commoner
b. Serocystic disease of Brodie
is a sarcomatous disease i.e a connective disease
I t can be benign or malignant
I t is higly vascularised
The malignant type metastasizes via blood to lung, liver etc. I t is not infiltrating
Treatment
a. Surgery
b. Radiotherapy
c. Chemotherapy - is not useful
OSTEOGENIC SARCQMA OF BREAST

Is
Is
Is
It
It
a form of non-osseous osteogenis sarcoma

similar to cystosarcoma phylloides
vascularised and well circumscribed
is not infiltrating
may start spontaneously of from pre-existing lesions :
i.
Fibroadenoma
ii.
Treatment
i.
ii.
Phylloides tumour
Surgery
Radiotherapy
BURKITTS LYMPHOMA
I t occurs as part generalized burkitt's lymphoma involving the ovary, CNS, breast ect
Treatment
- Chemotherapy
METASTATIC BREAST DISEASE

is very rare
The commonest site is "the other breast"
BREAST CANCER I N PREGNANCY

About 12% in our environment
In the past, the treatment involves termination of the pregnancy
Consider the gestational age
CONGENITAL ANOMALIES OF THE GASTRO

INTESTINAL TRACT.
Introduction
Commonest congenital anomalies seen in children.
They cause obstruction to the flow of intestinal content.
Has world wide occurrence
Has no sex, racial or geographical predilection
Commonest anomalies
1. Duodenal atresia
2. Malrotation of the gut
3. Intestinal atresias
4. Hirschsprung's Disease
5. Anorectal malformation
Embryology of the GIT
- GIT appears as a straight tube at 3rd week of I.U
- Divided into Foregut, midgut and hindgut
Foregut
Rapid epithelial proliferation
Vacuolization and recanalisation
May fail
Midgut
Rapid growth.
Physiological herniation.
Anticlockwise rotation over 270 with fixation.
May also get arrested.
Hindgut
Appears as the cloaca
Divided into urogenital sinus (UGS which is anterior) and anorectal canal (ARC which is posterior)
by urorectal septum
Proctodaeum and cloacal membrane disintegrate and invaginate to join the ARC
130
Section I
DUODENAL ATRESIA.
Epidemiology
Failure of recanalization
Incidence: 1 in 10,000 LB in Europe ( 1 - 2 cases /year is seen here)
No familial incidence
Associated anomalies -50%
Down's syndrome- commonest chromosomal anomaly
Pathology
-
Atresia/stenosis - 2nd p a r t 85%.

Rest
-15%
Clinical Features
Polyhydramnios - 50%
Prematurity
Bilious vomiting - is the main presentation
No abdominal distension - because it involves the upper GIT
Diagnosis
i.
ii.
Prenatal abdominal USS - shows dilated fluid filled stomach and duodenum
Plain abdominal x-ray - shows
- Double Bubble sign ( i n stomach &. duodenum)
- Absent gas in distal part of GIT
iii.
Abdominal USS- To rule out any other associated anomalies
Types/ Classification.
I
: Stenosis or Diaphragm.
II
: Atresia with a fibrous cord joining the two ends and intact mesentery
HI
Atresia, no connecting fibrous cord but has a V - shaped defect in the mesentery
Treatment.
Not an emergency
Resuscitate
Surgery - Duodenoduodenostomy
Treatment Steps
Resuscitation
jjj Sj|||| \
1. Nil per oram
"VI'
2. Pass Nasogastric tube - to prevent aspiration
3. I V fluid - to correct dehydration
4. Correct Electrolyte abnomalities
5. Monitor urinary output - using Paul's tubing
131
6. Intramuscular Vit. Kl injection for 1 we,ek - to avoid haemorrhagic disease of the newborn
(HDN)
7. Intravenous broad apectrum antibiotics
8. Group and Cross match blood
10. Blood sample f o r electrolytes & urea, creatinine
9. Incubator care
Section I I
JEJUNOILEAL ATRESIA.
Introduction
I s a major cause of intestinal obstruction
1: 330 LB
Equal sex incidence
Aetiology - Vascular accident to a segment of bowel
Associated Anomalies.
1.
Sastroschisis - is the commonest, is due to premature atrophy of right umbilical vessel
2.
Intestinal Malrotation
3.
Exomphalos / Omphalocoele
Clinical Features
i.
ii.
iii.
iv.
v.
vi.
vii.
Maternal polyhydramnios
Persistent bilious vomiting
Abd distension
Failure to pass meconium
Visible peristalsis
Dehydration
Failure to thrive
Types / classification
I
: Stenosis or Diaphragm.
II
: Fibrous cord connection. No mesenteric defect
I I I a : Atresia + V-shaped defect

b : Atresia + apple peel/xmas tree appearance
IV
: Multiple atresias
Investigations
1.
2.
Plain abdominal X-ray - show multiple air fluid levels

Barium Enema
- micro colon - due to disuse atrophy
- associated malrotation.
Treatment
Resuscitate
Surgery
- Entero-enterostotny.
Section I I I
MALROTATION OF THE GUT
Abnormalities
1.
Non rotation
2.
Incomplete rotation
3.
4.
Reversed rotation
Incomplete Fixation
*'
Clinical features
i.
Worldwide incidence
ii.
Occurs at any age
iii.
iv.
v.
vi.
vii.
viii.
ix.
Equal sex incidence

Persistence bilious vomiting
t Abdominal distension
+ Constipation
Failure to thrive
t Abdominal mass
Features of peritonitis - due t o perforation. There is fever A abdominal pain
Investigations
1.
Abdominal Ultrasound (Doppler)
- Fluid filled dilated Duodenum
- Whirlpool Effect - is due to the twisting of the bowel ( midgut volvulus)
2.
Barium meal and follow through

- Abnormal positioning of the ligament of Treitz ( becomes right-sided)
- Duodenal obstruction - especially in association with midgut volvulus
- Jejunal loops filled on the Right of SMV
Treatment
1.
2.
Resuscitate acute cases

Surgery
Ladd's operation ( Reason f o r prophylactic appendicectomy)
Section IV
HIRSCHSPRUNG'S DISEASE
Introduction
aka Congenital aganglionic megacolon
Epidemiology
1: 4/400LB to 1:7,000LB
M:F = 4:1
No racial predilection
Runs in families
Pathophysiology
- Normal Bowel Control
Extrinsic
Parasympathetic - has excitatory effect on bowel
Sympathetic - has inhibitory ( more) A excitatory effects
in.
Non cholinergic, non adrenergic - is supplied by Nitric oxide synthetic enzyme
Intrinsic
Meissners plexus
Auerbachs plexus
I n Hirschprung disease, there is deficiency of Nitric oxide transmitter, thus, there's persistent
excitatory effect on the bowel, resulting into spastic bowel.
Pathology
a.
Neonate
Normal colon
b. Older children
- collapsed Rectum
- dilated colon
Clinical Features
ii.
v.
v.
vi.
vii.
viii.
ix.
Delayed passage of meconium

Chronic intermittent constipation
Progressive abdominal distension
Refusal of feeds
Failure to thrive
Vomiting
Fever
Occasional diarrhoea
Empty Rectum
Investigations
1.
Barium Enema - shows funnel shape appearance
2.
Rectal Biopsy
a.
Suction biopsy - done in neonates
b. Open rectal biopsy - in older children
i|, ,
Histoloov
- I t shows excessive actylcholinesterase enzyme/activity
3.
Rectal manometry
To measure intrarectal pressure
The receptive relaxation of the rectum is lost due to increased pressure.
Associated Anomalies
1.
Down's Syndrome
2.
Anorectal malformations
3.
Intestinal Atresias
4.
Von Recklinghausen's disease
Treatment
1.
2.
3.
Stabilize acute cases /Resuscitation

Initial colostomy
i.
To divert stream of f eaces
ii.
The dilated part shrink for use in definitive surgey
iii.
Allows the baby to grow/thrive
Surgery - Pull through operation
Pull Through Operation.

- The components are
i.
Rectosigmoidectomy
ii.
Pull through
iii.
Colo anal anastomosis
Types are
i.
ii.
iii.
Swenson's pull through

Duhamel pull through
Soave pull through
135
Section V
ANORECTAL MALFORMATIONS
Introduction
Commonest anomaly of t h e hindgut
Aetiology is unknown
-
1: 5 0 0 0 LB
No racial predilection
A f f e c t males more slightly
May be familial
Classification
a.
+ Fistula - Using pelvic diaphragm as t h e anatomical landmark

. High
Intermediate
Low
ii.
b.
Supralevator
c.
i.
High
ii.
Intermediate
Infralevator
i.
Low
Seen in 5 0 % of cases
Commonly seen with High ARM
SIT
Hirschprung disease
i.
Duodenal atresia
ii.
Malrotation
GUS
i.
Cryptorchidism
Hypospadias
ii.
Vesico-ureteric r e f l u x
v.
Bicornuate uterus
VACTERL
V - V e r t e b r a l anomalies e.g kyphosis, scoliosis
A - Anorectal anomalies
C -
Cardie (congenital) anomalies e.g VSD, TOF, occasionally PDA
TE - Tracheo-oesophageal anomaly - Tracheooesophageal f i s t u l a

R
- Renal anomaly - Polycystic kidney disease, Horseshoe, cross

ectopia
L -
Limb d e f o r m i t y
Radial dysplasia - is the commonest limb defect

Pes planus (flat foot)
Talipes equinovarus ( Club f o o t )
Talipes-calcaenous deformity
Clinical features
a. Without fistula
'
r
r*
iii.
iv.
v.
vi.
vii.
viii.
b. With Fistula
ii.
Absent anus
Failure to pass meconium
Progressive abdominal distension
Visible peristalsis
Refusal of feeds
Fever
Vomiting
iv.
v.
vi.
Abnormal anal opening

Passage of meconium stained urine
Fever
Refusal of feeds
Vomiting
UTI - due to ascending infections into 6US
Investigations
1. Lateral Prone Transtrochanteric x-ray. ( formerly called
D
>2
High
Intermediate
1-1.5
<1
Low
Invertogram)
" D " = is the distance from rectal pouch to the level of radio-opaque metal object at the anal opening.
2. Loopogram/colostogram
3. Abdominal ultrasound
Treatment
i. Stabilize
ii. Surgery
a. Low malformations
- Anaplasty
b. Intermediate <S High

i. Initial colostomy
ii. Posterior Sagittal Anorectoplasty
(PSARP)
137
SURGICAL JAUNDICE I N CHILDREN

- Or Ogundoyin
Introduction
Jaundice can be medical or surgical
Aetiology
a. Medical
i.
ii.
v.
v.
vi.
Surgical
i.
Physiological
Hypothyroidism
Alpha-1-antitrypsin deficiency
Gilbert's syndrome
Rotor's stndrome
Infantile hepatitis
Biliary atresia
Choledochal cyst
BILIARY ATRESIA
Introduction
I s failure to develop patency of whole or part of the extrahepatic bile duct leading to
obstruction of bile flow.
Epidemiology
I t varies worldwide
1 in 10,000 to 12,000 LB
No racial preponderance
I t is NOT genetic
Male/Female ratio is 0.64 : 1
I t is not commonly associated with other congenital defects.
Are not common
1. Congenital heart disease
2. Multiple spleens
3. Pre-duodenal portal vein
Classification
Atresia of Common bile duct
Atresia of common bile duct & hepatic duct
Atresia of extrahepatic duct
r
i
C.T3
Aetiology
Is unknown
1.
2.
3.
Viral infection : coxsackie virus is mostly implicated. Also EBV.

Vascular accident
Pancreatic biliary mal -junction
Pathology
I s panductal
The intrahepatic duct is narrowed, distorted and irregular
There is bile stasis, distortion of liver cells, giant cell transformation, focal necrosis and
intralobular fibrosis.
_
Clinical Features
Jaundice
i.
Passage of clay-coloured stools
ii.
Passage of yellowisn coloured urine
v.
Hepatosplenomegaly
v.
Failure to thrive
vi.
Intracranial bleeding - due to impaired absorption of f a t soluble vitamins A.D.E.K which leads
to mal-coagulation.
vii.
Liver cirrhosis
viii.
Portal hypertension
Investigations
a. Specific
1.
2.
3.
4.
5.
6.
7.
b.
Others
i.
Abdomninal ultrasound - shows gall bladder

Contrast-enhanced CT scan - to outline the biliary tree and other structures that
USS can not shows
Duodenal aspiration - from the 2 nd part of duodenum
Endoscopic Retrograde Cholangiopancreatography (ERCP)
Laparoscopy - to view extrahepatic tree
Liver scan - DISIDA
Intra-operative cholangiography - done if all the above methods cannot make the
diagnosis.
Stool examination
139
ii.
iii.
iv.
v.
vi.
vii.
Urinalysis
Liver function test
Clotting prfile : PT, PTTK
Full blood count
Electrolyte &. Urea
Group & cross-match - for fresh whole blood
1. Neonatal hepatitis
2. Choledochal cyst
Complications
i.
ii.
iii.
iv.
Failure to thrive
Bleeding diathesis
Liver cirrhosis
Liver cell carcinoma
Treatment
I t depends on the clinical state of the patient on presentation
a.
b.
c.
Stabilise
i.
ii.
iii.
iv.
v.
the patient
Nil per oral (NPO)
Intravenous fluid - preferably 10% dextrose
Intravenous antibiotics
Bowel preparation
Vitamin Kl injection - lmg daily for I week
Kasai operation - is Porto-enterostomy

Liver transplantation - if liver cirrhosis has occurred
Prognosis
Is very good if the presentation is before the age of 8 weeks
I t is fair a f t e r 10 weeks
I t is poor afterwards, as features of cirrhosis has set in.
The amount of fibrous tissue present, as these biliary ductules
ductules.
Prognosis is good if there are no complications.
r
CHOLEDOCHAL CYST
Introduction
J
I s f u s i f o r m or cystic dilatation of t h e e x t r a h e p a t i c duct.
Aetiology
!
~
I s due t o anomalous arrangement of t h e pancreaticobiliary ductal system.
Classification
Grade
Description
Saccular / d i f f u s e f u s i f r o m dilatation o f EBD
II
Diverticulum o f EBD
III
Choledochocoele
IV
Multiple cysts ( I n t r a / e x t r a or b o t h )
f~
Pathology
Single /multiple intrahepatic cyst (Caroli's disease)
Thick-walled, f i b r o t i c cysts
There is t h e inflammation o f t h e bile ducts
The liver findings vary w i t h age
i.
Neonate',
ii.
Older
nil
Children
o
Round cell i n f i l t r a t i o n
Bile duct p r o l i f e r a t i o n
Liver f i b r o s i s
Clinical Features
a.
In Infants
r
b.
Older
( 1 -
3months)
i.
O b s t r u c t i v e jaundice
ii.
Acholic stools
iii.
Hepatomegaly
iv.
Low grade f e v e r
v.
No abdominal pain
vi.
No mass
children
i.
Seen a t > 2 yaers with a classical t r i a d
Jaundice
Abdominal pain
Abdominal mass
ii.
Hepatomegaly
iii.
Liver cirrhosis
iv.
Portal hypertension
hi t .i.ijjj;
HHy
Investigation
i.
Abdominal ultrasound - shows cysts, liver state, dilatation of veins & ascites
ii.
DISDA scan
iii.
ERCP
iv.
Intraoperative cholangiography
Treatment
s
i.
Stabilization
ii.
Surgery
a.
Roux-en-Y-cystojejunostomy
b.
Hepaticojejunostomy
Complications
i.
Ascending cholangitis
ii.
Others
i
i
"
UNDESCENDED TESTIS <& HERNIA

- Dr Ogundoyin
Embryology
Induction of the gonadal ridge D Undescended testis
Abdominal phase- is passive i.e testis is stationary
Canaliculi phase- is active and it is controlled by
i.
Hormonal factor - from testosterone which aids testis descent and FSH. Postnatally,
none of these aids the descent of testis,
ii.
Mechanical - due to traction pull exerted by the gubernaculums and torsion force by
the abdomen.
During the canaliculi descent, if the testis comes across a lot of fibrous tissue in the inguinal
cana\, it will be trapped.
I f the testis is able to get out of the external ring of inguinal canal, a finger like projection
springs out to determine the ectopic site of testis.
Hernia
I s a result of failure of processes vaginalis to close.
Types
1.
2.
3.
4.
Undescended testis - in which the testis is normal path of descent

Ectopic testis - testis is away from the normal path of descent
Cryptoorchisdism - hidden testis
Retractile testis - The testis is already in the scrotum but get out of the scrotum most time.
142
Section I
UNDESCENDED TESTIS
r
c
[
Introduction
I s seen worldwide
No geographical or racial barrier
Note, usually, left testis descends f i r s t before the right, hence right undescended testis is
commoner
Premturity
i.
Inguinal hernia - seen in 70% of cases
ii.
Hypospadias
v.
Prune Belly syndrome
v.
Hunter-Hurler syndrome
vi.
Anorectal alformation
vii.
Spinal bifida
viii.
Exomphalos
Persistent absence of testis from scrotum since birth
Persistent
abdominal pain - in Torsion of testis
II.
On examination
Swellings aroud the inguinal ring
i.
Scanty ruggae on the affected side
ii.
Attempt to bring down testis if found in the path of descent.
Diagnosis
Is clinical
Complications
1. Degenerative changes - only affects the sex cells. I f it is bilateral, it leads to infertility while
unilateral causes subfertility.
2. Trauma to the ectopic site
3. Torsion of the testis
4. Malignant transformation
Investigation
1. Abdomino-pelvic ultrasound - to trace the location of testis
2. Doppler ultrasound - to identify testicular artery and trace to its termination
3. Arteriography of the testicular artery
4.
Laparoscopy
5.
Others
i.
ii.
<
Haemoglobin concentration
Haemoglobin electrophoresis
143
Treatment
Surgical
-
Orchidoplexy
I t is better before 2 years.
Follow-up is f o r life
Intimate the parents about the possibility of malignant change.
Section I I
ECTOPICS OF T E S T I S
Possible Sites
1. Superficial pouch
2. Lower part of the anterior abdominal wall
3. Femoral triangle
4. Perineum
5. Contralateral scrotum
Diagnosis, Investigation A Treatment- same as in undescended testis
Section I I I
CRYPTOORCHIDISM
The scrotal sac and ruggae are well developed
Section I V
HERNIAS
Introduction
I s commonest surgical presentation in children seen in Surgical Outpatient.
Epidemiology
NO racial or geographical predilection
Male/Female ratio is 9 : 1
Undescended testis
i.
Hypospadias
ii.
Hunter-Hurler's syndrome
v.
Exomphalos
v.
Types
Indirect inguinal hernia - is the commonest in children
Clinical presentation
A swelling which continues to protrude out of the anterior abdominal wall.
On examination
Positive silk glove sign - if the hernia is not obvious
Diagnosis
I s clinical
Complications of hernia
i.
Irreducibility
ii.
Obstruction
iii.
Strangulation : The history of strangulated inguinoscrotal swelling is similar to that of
obstruction.
'
Investigation
i.
ii.
Haemoglobin concentration
Haemoglobin genotype
Treatment
Surgery - Herniotomy : I t does not include the repair of posterior wall.
Section V
STRANGULATED INGUINO-SCROTAL HERNIA
Clinical Features
The history of strangulated inguinoscrotal swelling is similar to that of obstruction.
i.
ii.
v.
v.
vi.
vii.
viii.
Swelling
Intermittent cry
Abdominal pain - is colicky
Vomiting
Refusal of feeds
Fever
Constipation - occurs later
Gradual abdominal distension.
On examination
i.
Features of dehydration or shock
o
Fast thready puls^||(|( | | j U
i.
ii.
v.
Tachycardia
Low blood pressure
Jaundice - if septicaemic
Hyperaemic & oedematous swelling
Tenderness - very much
v.
Bowel sounds is hyperactive
Diagnosis
Is clinical
Investigation
1. Abdominal X-ray : shows
o Dilated loops of bowel
o Multiple air-fluid level
o Gas\esser\ess
Treatment
a.
Resuscitation
i.
ii.
iii.
>
e.
d.
e.
I V infusion - using Normal saline to ensure urine output. Cal

deficit and add with the maintenance
Nasogastric tube - NPO, to control vomiting
Urine output - Paul's tubing
Broad spectrum antibiotics

Potent analgesics & Sedatives ( using I V diazepam)
Attempt to reduce the hernia.
Surgery - when the reduction fails.
Section VI
HYDROCOELE
Definition
I s accumulation of fluid in the scrotum.
Types / Aetiology
a. Primary
is
It
It
It
b.
idiopathic
is congenital
is also known as Communicating hydrocoele
is commonest in children
Secondary- is due to an underlying pathology e.g

i.
Schistosomiasis
ii.
Trauma
I
iii.
Tumours of the testis
iv.
Filar iasis
f v.
Chronic granulomatous disease
c. Other types
o Infantile Hydrocoele
o Hydrocoele of the gut
o Vaginal hydrocoele - is the commonest in adults
I
Same as that of hernia in children.
I s painless
Is fluctuant
I t transilluminates brilliantly
You may(not) palpate testis
Investigation
As in hernia
Treatment
I n the f i r s t year of life, you just assure the parents and if after 1 year it does not resolve, then
intervene.
Ligation of Patent processus vagnialis in children.
INFANTILE HYPERTROPHIC PYLORIC STENSOIS

Introduction
I s a congenital anomaly seen in f i r s t 2 weeks of life.
Is a cause of upper 61 obstruction
Aetiology
Unknown
Predisposing factors
i.
First bron male infant
ii.
Blood group A
iii.
Milk cord syndrome - is due to hypersensivitity reaction to breast milk
Pathology
\
There is hypertrophy of circular muscle of pylorus
There is characteristic olive-shape of the pylorus
\\
\
Clinical features
\
Persistent projectile vomiting in f i r s t 2 weeks of life following breastfeeding, it is non-bilous
I t contains recently ingested food and subsequently clear fluid.

\
Constipation
No abdominal distension
Complications
i.
Severe dehydration
ii.
Electrolytes imbalance
Hypokalemia
Hyponatraemia
Hypochloraemia
Metabolic acidosis
iii.
iv.
Malnutrition
Jaundice -unconjugated hyperbilirubinaemia is characteristic. The cause is unknown. I t
disappears sponatenously
Features of malnutrition
Features of severe dehydration - depressed fontanelle, sunken eyes, loss of skin turgor
Abdomen
Flat
Palpable mass
'"
Hyper-reactive bowel sound
The mass is more appreciated when the baby is feeding because the baby will
be more relaxed. Use the left hand to palpate and do it from the back.
Investigation
1.
Abdominal ultrasound scan - done especially if the mass is not palpable. For
- Location
-Origin
-Site
- Size - (total) total length of pylorus A thickness of circumference, it is diagnostic of
IHPS if the following are seen
s Length > 16mm
s Thickness > 4mm
S Whole size > 12mm
2. Barium meal and Follow through - done if ultrasound scan is not available. 2 signs to check for are
S Rail track signs
S Rat tail appearance
3. Others
i.
PCM
ii.
Blood group and cross-matching
-.
iii.
Serum electrolytes
i
Treatment
i.
ii.
v.
Fluid & Electrolytes resuscitation

- 5% dextrose in 0.45 ( Half normal saline ) - it supplies the Na, Chloride & hydrogen
ion
- Give potassium hypochloride ( <cl") - for the hypokalemia, after calculating the
deficit and normal requirement. I t is given slowly.
Passage of Nasogastric tube
Urethral catheterisation - to monitor urinary output. Adequate should be l-2ml/kg/hour
Definitive treatment - Surgery ( Ramstedt pyloromyotomy ). Note, it is done after
resuscitation.
148
INTUSSUSCEPTION
Definition
-Telescoping or Prolapse
2 VARIANTS
Idiopathic
Enteroenteral
IDIOPATHIC INTUSSUSCEPTION:
> 9 0 % of cases
> M ostly Ileocolic
A" Affects infants and toddlers
V
ENTEROENTERAL INTUSSUSCEPTION:
',
^ O c c u r s in older children and neonates

r* Jejunojejunal,jejunoileal
ileoileal,etc
^ Assoc, with PLP-Pathological Lead Points
,"
Pathological Lead Points

1. Meckel's Diverticulum
2. Enlarged Mesenteric Lymph Node
3. Mesenteric or Intestinal Tumoursa. Lymphomas
b. Polyps
4.
5.
6.
7.
8.
9.
10.
c. Harmatomas(Peutz-Jeghers Syndrome)
Mesenteric or Duplication Cysts
Submucosal Haematomas -Henoch-Schonlein Purpura,Coagulation dyscrasias
Ectopic Pancreatic and Gastric rests
t'
Inverted Appendiceal stumps
I lull
"
Ascaris lumbricoides
"
Sutures and Staples along anastomoses
Ileus in the post operative period
11. Indwelling Jejunal catheters

12. Cystic fibrosis
(I
I
PREDISPOSING FACTORS
^Recent Dietary Change
1 Ifl 11 < >
^ Acute Coryza
^Seasonal Variation-peak in summer and mid winter
^Rotavirus vaccine
^Familial
PATHOGENESIS
Imbalance in longitudinal forces
. .
Pathological lead point
Disorganised pattern of peristalsis
> Invagination of intestinal wall into lumen
Invaginating- Intussusceptum
Receiving - Intussuscipiens
-Progression
-Prolapse out of anal car\a\
-Invagination of mesentery - Intestinal Obstuction
%
-Impedance of lymphatic return
^ R i s e in intussusceptal intramural pressure
r^Rise in hydrostatic pressure
-Impedance of venous return
-Obstruction of arterial inflow
Înfarction
l>
Mucosa -most sensitive to ischaemia

Currani jelly stools -sloughed mucosa
blood
mucus
^Transmural gangrene
^Perforation
ll
CONGENITAL ANOMALIES OF ANTERIOR ABDOMINAL WALL

Introduction
I s defect of any part of the anterior abdomimll wall involving the whole or part of the layers.
E.g
i
Exomphalos or Omphalocoele(
i.
Gastroschisis
\
ii.
Embrology
Anterior abdominal wall develop segmentdlly of metamerically, thus the innervation and blood
supply.
Is formed by convergence of the cephalic, caudal, lateral and medial folds at the centre.
There is failure of fusion of folds
,
Groups
a.
|
Early stage : Primary thoracoabdominoschisis becauses it may extend to involve the thorax.
Omphalocoele (/4mer/<:<j/7)/Exomphalos {British)
Body wall dysplasia
Gastroschisis
b. Late stage
i.
Patent urachus
Patent Omphalomesenteric duct
ii.
Umbilical hernia
v.
v.
vi.
Exstrophy of the Cloaca

Prune Belly Syndrome/Congenital deficiency of abdominal musculature
Gastroschisis - has many theories for its origin.
Section I
EXOMPHALOS or'DMPHALOCOELE
Introduction
I t is protrusion of the abdominal viscera into the base of the umbilical cord and it is always
covered by a translucent membrane. Note, umbilical hernia is covered with skin.
Epidemiology
The combined incidence is 1 in 2000 LB
Male/Female is 2 : 1
No racial difference
Aetiology
I s due to defect in the midline of the anterior abdominal wall at the umbilica area as a result of
failure of development of abdominal folds and non-rotation or incomplete return of the bowel.
Persistence of the body stalk
151
"|i
Pathology
- ' - . . ' .
The covering membrane is avascu\ar and it comprises of
i.
Peritoneum
ii.
Wharton's jelly
iii.
Amnion
The sac contains abdominal viscera
Types
a.
b.
Omphalomesenteric major : when the defect is > 4cm

"
minor : when < 4cm
Clinical Features
i.
Protrusion through an abdominal wall defect
ii.
Intact or ruptured covering membrane
iii.
I s located on any part of the anterior abdominal wall along the midline.
iv.
Features of associated anomalies i
Associated anomalies
1
rd
About 2/3 ( 80%) are associated with other disorders. These are divided into
a.
b.
Syndromic
i.
ii.
I
Chromosomal anomilies e.g Trisomies 13,18, & 21
Beckwith-Wiedmatms syndrome (EMS)
Omphalocoele
o
o
o
o
Macroglossia
Macrosomia
Hypoglycemia - due to pancreatic islet hyperplasia
Gigantism - visceral & somatic
iii.
Upper Midline
o
o
o
o
o
Syndrome ( Pentalogy of Cantrell)

Epigastric exomphalos
Anterior.diaphragmatic defect
Sternal defect
Ectopia cardia
Intracardiac defect - is usually ventricular septal defect
(VSD) '
iv.
Lower Midline
o
o
o
o
o
o
Syndroma
Bladder Sr cloaca exstrophy
Anorectal malformation
Colonic atresia
Vesicointestinal anomalies
Sacral vertebral anomalies
Meningomyelocele
Non-syndromic
o
Congenital heart defect - seen in 30%
o
Intestinal malrotation I, ,
o
o
Undescended testis
S I T abnormalities
Diagnosis
Is clinical
.
Prenatal diagnosis is possible with
i.
Maternal abdominal ultrasound
ii.
Maternal serum A fetal amniotic fluid alpha-f eto protein. I t is not very specific
because it is also seen hepatoblastoma & spina bifida.
;
'''f
Investigation
i.
ii.
v.
v.
vi.
vii.
Full blood count

Group & crossmatch
Electrolytes & Urea
Serum protein
Chest x-ray
Random blood sugar - to rule out hypoglycaemia.
Treatment
This depends on
i.
Intact membranes
ii.
iii.
Size of the defects
a. Conservative management
Antibiotic therapy - per oral
Painting with agent which hapJeJ larotic & antimicrobial properties
e.g
70 % alcohol - is'lfcommonly used here
o
2.5% Formal saline
is% - used in the absence of alcohol
o
2% Silver su phaJjjazine cream
o
Mercurochrc
me * j s nephrotoxic
o
Lugol's iodine - may cause goiter in some patient
o
GV - messy <S predisposes to infection
N.B
Involves covering the membrane with normal saline-soaked gauze
Immediate return of the whole bowel is not advisable to avoid abdominal hypertension and
respiratory failure from upward displacemeftf of the diaphragm
Painting with diluted mercurochrome which encourages epithelisation of the membrane. This is
indicated if the patient has other abnormalities.
b. Surgery
The aim is to convert the exomphjalos to ventral hernia.
I s a 2-stage repair
First, for Ruptured Exomphahs
Resuscitate the patient
i.
Incubator care
153
'}:
'
iii.
iv.
v.
vi.
vii.
IV fluids
I V antibiotics
Nasogastric tube + Nil pt ore
Monitor urinary output
Injection of Vitamin Kl
Cover with intestinal bag to reduce contamination and heat loss
N.B
Procedure of Surgery
Primary closure
i.
Skin closure
ii.
Silo
3
1
Serial returning of the viscera

Silastic material can be used to form a silo pouch to cover the protrusion. I t
prevents dehydration of the bowel and provides temporary coverage.
Then start to reduce the silo pouch gradually to return the bowel and prevent - i
intrabdominal hypertension.
f
b.
Wound repair
Complications of Packing under Tension

1. Respiratory distress - due to impaired movement of diaphragm
2. Compression of great vessels e.g Inferior vena cava
3. Impaired renal function - due to compression on renal artery
4. Bowel ischaemia - due to compression on mesenteric vessels
]
]
]
Prognosis
I s poor because of
Sepsis
in.
Heat loss
iv.
Fluid & Electrolytes imbalance
1
Section H
GASTROSCHISIS
Introduction
.
I t is extra-umbilical localization of anterior abdominal wall defect.
I t was initially thought to be ruptured omphalocoele.
Aetiology
i.
ii.
Pathology
I'"1'
I Mill
Vascular accidents
Prenatal ruptured of an exomphalos
1
1
I s due to defect at the junction of umbilicus and normal skin.
154
The location is the right edge of umbilicus. The umbilicus is still held in place by the vessels.
The exposed bowel has oedematous wall.which is coloured and has exudates ( due to exposure to
amniotic fluid)
i l l
I'
Diagnosis
Can be made in-utero with ultrasound
i.
Bowel thickening and dilatation
ii.
Smoking
Clinical Features
i.
Full thickness defect
ii.
Small defect usually to the right of the umbilicus
iii.
Smooth edge with no covering sac
iv.
Eviscerated organs - exclude liver. The eviscerated bowel becomes dilated, inf lammed,
oedematuos, thickened, leathery and shorter than normal,
v.
The patient is usually premature
- I s rare
i. Intestinal atresia - is the commonest
i i . Mal-rotatio of the gut
i i i . Cryptoorchidism
i v . Ventricular septal defect (VSD)
Diagnosis
Is clinical
May be made by prenatal diagnosis
Investigation
1.
Prenatal diagnosis - to rule out other congenital abnormalities
2.
Others
Treatment
i.
ii.
v.
v.
Stabilise the patient

Use of slio pouch
Give total parenteral nutrition - is central venous feeding
Surgery - primary closure
Exploration of the bowel - to exclude intestinal atresia. This has increased the survival rate to
90% because they have fewer congenital anomalies.
N.B - The defect is usually < 4cm in diameter

Post-op Care
i.
Ventilation
155
i"
Prognosis
I t is good in developed coutries, the child may live a completely normal life, but it is poor in
developing countries due to
i.
Infection
ii.
Severe dehydration
iii.
Hypothermia
DIFFERENCES BETWEEN EXOMPHALOS <& GASTROSCHISIS
1.
2.
3.
4.
5.
6.
7.
8.
9.
Location
Defect
Sac
Cord attachment
Intestinal appearance
Liver
Abdominal cavity
Bowel atresia
Exomphalos
Umbilical r i n g .
Varies ( 4 - l ] ) l n j |
Intact /rupturedjmembrane
Onto the sac
"
Normal
i *
Often preser t |
Small
Common ( 4 0 - 80%)
Rare
Gastroschisis
Lateral
Usually < 4cm
Absent
Normal
Abnormal
Rare
Normal
Rare
Common
m^
(
-
Section H I
UMBILICAL HERNIA
I s due to deficiency of tiely closure of unmbilical ring, causing defect at linea alba.
At birth, the size is < 1cm and complete closure is achieved by 3years.
Obstruction of umbilica hernia is rare because the ring is definite.
I n contrast, paraumbilical hernia is beside the umbilical defect and it has no definite ring.
Treatment
Herniorrhaphy ( repair of hernia): I t is Maybr
aybr repair which involves making infra-hernia incision
and double breasting of the fascia.
1
1
n
n
156
Section I V
PATENT URACHUS
I t is vesico-cutaneous
The Location :
Clinical Features
i.
Wetness airound the umbili
Investigation
i.
Injection of urograffin at umbilicus, then take a lateral x-ray.
Treatment
- Excision & Closure of defect at abdominal.
Section V
PATENT OMPHALOMESENTERIC DUCT
I s tubular attachment between ileum (antimesenteric border) and umbilicus.
MerkePs divericulum
Clinical feature
i.
Faecal discharge
Investigation
ii.
Contrast studies to delineate
Treatment
- Elective abdominal exploration with closure of the fistula
Complications
1. Volvulus - by forming .an axis for it
2. External intussusception
Section V I
EXSTROPHY OF CLOACA
Pathology
Is due to imperfect closure of abdominal wall to pelvis.
Major components A Treatment
i.
Omphalocoele - primary closure
ii.
Exstrophy of the bladder - anterior bladder is not formed - repair. Closure of the bladder
depends on the patient,
iii.
Fistula between bowel & bladder ( Vesico-intestinal) - Resection & anastomosis
157
IV.
V.
Epispadias ( i s on the dorsal surface)

Absence of bones of the foot ( Talipes equinovarus)
]
]
Section V I I
PRUNE- BELLY SUNDROME
aka : Eagle Barret / Congenital Deficiency of the Abdominal Musculature

Incidence
1 : 40,000 of deliveries
Occurs almost exclusively in males
.
I
I
Aetiopathogenesis : Due to defect in development in tF
]
]
]
]
]
]
]
]
^mesodermal layer.
Narrowed Vesicoureteric junctions

!
Megaloureter
our
Megacystitis
Hydronephrosis
Pathology
Deficient anterior abdominal wall musculature
Large urinary bladder
Cryptoorchidism
Treatment
ii.
Divert urinary stream

Urethroplasty
Reconstruction of the anterior abdominal |/all.
1
]
Section V I I I
INGUINAL HERNIA
Introduction
r
Is due failure of closure of processus vaginalis which usually obliterates in males by 2 nd & 33rd
month life.
There is increased risk of bowel obstruction jh infants which causes strangulation and eventually
ischaemic necrosis.
i.
Hydrocoele - which is fluid in the processus vaginalis, they may not be herniation.
Double silk sign : is positive for inguinal hernia
1
1
158
1
Hydrocoele transi I luminates. ôte, inguinal hernia may also transi I lunate because of
the skin.
Treatment
Herniotomy - excision of the hernial sac.
I n adults : herniorrhaphy + herniotomy
Complications
1.
Recurrence - if the deep ring is wide. The indl: ince is < 1% after herniotomy.
CHILDHOOD MALIGNANCIES
Introduction
I s uncommon, it represents 2% of all cancers
I s between 0 - 1 5 years
I s 2nd most common cause of death in children > 1 year
Leukaemia is the commonest
Brain tumours - commonest solid tumours
Incidence
I s highest among the infants. I t declines to the 9 years and then rises again.
I t is commoner in male
Types
Are derived from embronal tissue.
Leukaemia
i.
CNS tumours e.g Medulloblastoma, gliomas
ii.
Lymphomas
v.
Neuroblastoma
v.
Wilm's tumour
vi.
Bone tumours
vii.
Soft tissue tumours - Rhabdomyosarcoma
viii.
Teratomas - Sacrococcygeal teratoma
ix.
Liver tumour
x.
Brain tumours - is the commonest solid tumour
Clinical Features
Fever : Leukaemias ( because of reduced wbc), Lymphoma
i.
Vomiting - especially in brain tumour, as feature of raised ICP
ii.
Constipation - in Abdominal masses
v.
Cough - seen in mediastinal tumours
v.
Bone pain - Neuroblastoma
vi.
Headache - in brain tumour
vii.
Lymphadenopathy - in Leukaemia & Lymphoma, and Metastasis
viii.
Haematuria - seen in Wilm's tumour, Rhabdomyosarcoma
X
"
159
Investigations
1. Full blood count & differentials - for tliose, presenting with fever, lymphadenpathy
2. Abdominal CT - f o r vomiting
3. Brain CT - for vomiting
4. Chest X-ray - f o r cough
5. Plain X-ray of the bone - for bone pai i
6. CT scan - f o r headache
7. Abdominal ultrasound - for haematuri i
8. Intravenous urogram - for Wilm's tutr [>ur
NEUROBLASTOMA
Introduction
Is
It
It
It
an embryonal tumour of adrenal gland.

develops from neural crest cells - Adrenal medulla & Sympathetic chain
may regress spontaneously or becomes mature and benign
is usually progressive
Epidemiology
The incidence is 1 in 8,000 - 10,000 childrt i below < 15 years
907o is seen in children below < 7 - 8 years
Peak age incidence is < 2 years ( 50%)
Male /Female ratio is 1.2 : 1
Is the commonest intra-abdominal tumour in children below < 1 year
Aetiology
I t is familial, it is seen in twins
Sites
i.
N.
iii.
iv.
v.
vi.
Adrenal medulla - 50%

Retroperitoneal ]
25 %
Paraspinal
]
Mediastinal - 20%
Pelvis
]_5%
Neck
]
Pathology
Grossly
I s highly vascular
; ;;
I s a purple grey mass with significant haema
May be solid or cystic
Is easily ruptured, is friable pseudocapsule, often necrotic
Microscopic
Small round cells - ( Matured/ Differentiated )
Closely packed small spheroidal cells - I n ma L 'e/Und

Rosette formation
Mode of Spread
i.Direct
ii.
Haematogenous
iii.
Lymphatic
Secondary sites
i.Regional lymph nodes
ii.
Bone cortex
Liver
iii.
iv.
Brain
v.
Bone tumour
vi.
Spinal cord
vii.
Lungs
Pathogenesis
I t may regress spontaneously
I t may become mature % benign
I t is usually progressive
1. Beckwith-Wiedmann's syndrome
2. Hirchsprung disease
3. Fetal alcohol syndrome
4. Fetal hydantoin syndrome
5. von Recklinghausen disease
6. Smith-Lemli Opitz syndrome
CI nical Features
Is related to site of the mass
Prsence of metastasis
Production of certain metabolic tumour by-products
i.
ii.
v.
v.
vi.
vii.
Abdominal mass - is seen 50 - 75%

Abdominal pain & distension
Weight loss
Failure to thrive
Fever
Anaemia
Hypertension
In the Neck <S Mediastinum

Horner's syndrome
i.
Proptosis or bilateral orbital ecchytftjsis
ii.
v.
Dysphagia
v.
Paraplegia - Dumb bell tumour
Flushing, sweating & irritability

Acute cerebellar ataxia - causing Ddnci g eye syndrome
Diarrhoea - due to secretion of vasiictflve intestinalpolypeptide (VIP)
VI.
vii.
viii.
Investigation
i.
in.
IV.
v.
vi.
vii.
viii.
IX.
x.
Plain abdominal x-ray : shows

mass lesion
stippled calcification
Chest x-ray : shows
Mediastinal widening
Metastasis to the chest
CT scan : shows
tumour origin
calcification.
MRI - for intraspinal lesion
Intravenous urogram
Serum catecholamines
24 -hour urinary collection - for
Vanyllic Mandelic Acid (VMA)
Homo Vanyllic Acid (HVA)

Bone marrow biopsy
Radionuclide bone scan
The last 2 investigations are used to stage.

Staging
Evans syst em
Grade
I
II
III
IV
IVs
Description
Tumour is confined to organ of origin

Tumour is extracapsular but has not crossed the midline with
unilateral lymphadenopathy
Tumour has crossed the midline exluding overhanging tumour &
bilateral lymphadenopathy
Distant metastasis
I or I I + with involvement pfjbone.mqrrow or subcutaneous
tissue or liver
Treatment
Surgery
Chemotherapy - for advanced disease
Radiotherapy - not effective
Combination is MAC
The tumour is not very sensitive to chemotherapy.
Prognosis
Depends on
i.
Age
ii.
Stage of the tumor
iii.
Site of the tumour
WILM'S TUMOUR
Introduction
Is an embryonal neoplasm
I s the commonest renal tumour in children
Epidemiology
Vc^f'
The age range is # - 9years
r-*^
The incidence is 8 in 100,000Cchildren < 15 years
No racial difference
Male/Female is 1.1: 1
I t may be unilateral or bilateral
Aetiology
It is familial i.e autosomal dominant

Associated Conditions
i.
Aniridia - is absence of iris
ii.
Beckwith-Wiedmann syndrome
iii.
Hemihypertrophy
iv.
Genitourinary anomalies
v.
Denys-Drash syndrome
o
Pseudohermaphroditism
o
Wilm's tumour
o
Degenerative renal disease
vi.
Hypertrophy - limbs
Pathogenesis
Absence of tumour suppressor gene W"J 1 A 2
Pathology
Gross
Large, bulk & encapsulated
Grayish white with fibrous septa
Focal areas of necrosis & haemorFha
163
Microscopically
Contains stromal & epithelial elements
I s well differentiated
Anaplastic
o
o
o
Staging
II
III
Limited to organ of origin, no lymphadenpathy

Beyond the kidney i.e extra-renal and no lymphadenopathy
Spread to adjacent structures <& lymphadenopathy (beyond the
kidney and the
tumour cannot be resected)
IV
Distant metastasis
-
Bilateral kidney involvei|vent
Clinical Features
i.
Healthy thriving pre-scholer
ii.
Hypertension
iii.
Haematuria - is a late sign
iv.
Occasional abdominal pain
v.
Fever
vi.
Non-tender, large, smooth abdominal mass
vii.
viii.
ix.
x.
xi.
xii.
xiii.
xiv.
xv.
Anaemia
Acute abdomen - due to tumour rupture
Cardiac murmur
Hepatosplenomegaly
Ascites
Varicocoele
Cough
Haemoptysis
Chest pain
The last 3 features are signs of metastasis to the chest.
t
]
]
]
]
]
]
]
]
]
]
]
]
1
]
1. Neuroblastoma
2. Lymphoma
3. Rhabdomyosarcoma
Investigation
i.
ii.
iii.
iv.
v.
Abdominal ultrasound - to see mas

scites etc
Plain abdominal x-ray - shows linea fa cif ication ( ? stippled in neuroblastoma)
Contrast-enhanced CT scan
Chest X-ray - shows cannon ball s|jn,|leural effusion
Bone marrow aspiration
164
]
]
]
]
i
1
vi.
General: FBC, Urinalysis
Treatment
I AII:
Surgery - Partial or total nephrectomy
I I I - V : Chemotherapy + Radiotherapy
r
r
The combination chemotherapy consists of ( VAC) Actinomycin D + Vincristine

For the advanced stage, use adriamycin + Cyclophosphamide
LEUKAF/V :AS
Introduction
Most common
3 rd commonest cancer in < 15 years
Types
i.
ii.
Acute lymphoblastic tumour ( ALL)

Acute myeloid leukaemia ( AML)
Acute lymphoblastic tumour ( ALL)

is commoner, it constitutes 75% of all childhood leukaemias
Common between 2 -3 years
Is commoner in male
Investigation
i. FBC : - shows leukocytosis with immature cells
- and left shift of wbc
Prognosis
- 5-year survival rate is about 807o

Acute myeloid leukaemia ( AMD
I t constitutes 25% of all
Incidence
- I s highest in f i r s t 2 years and later in childhood.
Prognosis
5-year -survival rate has improved, but it is still less ( 40%)

Treatment
,,.;..!{. ,,. i^jj,
Chemotherapy: CHOP , MOVP
' '
H
Intrathecal chemotherapy - f o r CNS involvement
II
1
3
3
3
3
]
]
3
]
3
1
3
1
LYA Ph 5MAS
I s the 3 most common childhood malig an les

Hodgkin's lymphoma is slightly commone in USA.
Burkitt's lymphoma is commoner than HL. I t is seen malaria endemic area.
Treatment is chemotherapy.
RHABDOMYOSARCOMA
Introudction
I t is a soft tissue sarcoma derived from mesoderm of embryo
I t can affect any part of the body but it is common in head and neck region.
I t also affects the genitourinary system ( called Sarcoma botyroides) and extremities.
Treatment
Excision
Chemotherapy : Adriamycin- based
SACROCCY6EAL TERATOMA
I s located in sacral region

I t may be malignant
Treatment
Excision
Consult to Neurosurgeon
LIVER TUMOURS
1.
Hepatoblastoma
is malignant
3 j
Treatment: Excision ( Lobectomy)
2. Hepatoma (PbCC)..
I s more aggressive than Hepatoblastoma.
3;
31
3
16
3
1
CONGENITAL NECK MASSES

Branchial cleft defects
Thyroglossal duct cyst
Cystic hygroma
Section I
BRANCHIAL CLEFT DEFECTS
( Branchial fistula - Saliva discharge)
r
r
Introduction
I t usually develops from 2 nd branchial cleft.
The 3 r d branchial cleft can also give
e to a sinus,
I t is located at anterior border of lc
third sternocleidomastoid muscle.
I t is linked to tonsillar fossa.
I t passes through the carotid bif urdati n
I t rarely results in remnant cartilag >, &uyst.
Investigation
ii.
Fistulogram - by injecting methylene! bli 2 to outline the tract

Sinogram
Treatment
Excision of the cyst/sinus
Section I I
THYROGLOSSAL DUCT CYST
Introduction
I s remant of embyronal defect along the course of descent
I t is one of the commonest congenital midline neck masses
Embryology
o
o
o
o
o
Thyroid diverticulum foramen caecum is formed at 4 -7 t h week of intrauterine life

The diverticulum descends
Hyoid bone is formed from 2nd branchial t r c h
Tract or duct is closely related to the bc|ie during descent before obliteration
I t is due to failure of obliteration
Epidemiology
I t is rare in newborn
I t is seen in pre-school A young adolescent
167
Clinical Features
It
i.
It
ii.
It
iii.
It
It
iv.
is a midline, soft, cystic mass above or below hyoid bone

is smooth, soft and non-tender
_
moves with tongue protrusion <& swelling. ( Note, thyroid gland only moves with swallowing.). J j
is immobile while the tongue stays protruded.
F
mostly transilluminates - containng yellowish fluid
,
Complications
II.
Recurrent infection
Abscess formation
Fistula
]
]
]
]
]
]
]
]
Investigation
Ultrasound - f o r thyroid gland
Chest x-ray
Indirect laryngoscopy - if it is big
Treatment
Antibiotics
Drainage of abscess
Excision of the thyroglossal du<
Surgery - "Sis trunk operation!
stula. You excise up to the base of the tongue,

excise the middle portion of the hyoid bone.
Complications of Treahne
Recurrtice
i.
Infecti n
ii.
Section I I I
CYSTIC HYGROMA
Introduction
I s a multiloculated cystic space lined by endothelial cells resulting from mal-development of

the lymphatic sacs with subsequent failure to achieve connection of these sacs.
H
s a lymphangioma caused by sequestration or obstruction of lymphatics.
J
I s a true cyst
Incidence
- 1 in 12,000 LB
Sites
i.
ii.
v.
V.
Neck (Posterior
Axilla - 20%
Mediastinum
Inguinal region
Mediastinum
triangle of the) - 75%

I
]
I
] - 5%
]
]
]
]
]
\
Clinical Features
A cystic mass which is large soft & fluctuant, associated with distortion of the adjacent
II.
iii.
anatomy.
Dyspnoea - when it is big

I s often multilocular
I
"
Diagnosis
Is mostly clinical
I t transilluminates brilliantly
Can be diagnosed prenatally before 30weeks of gestation
Commonest cause of intrauterine death mortality
Investigation
Ultrasound - multilocular, cystic mass
CT scan
MRI
r
r
Complications
1. Increase in size
2. Infections
3. Respiratory obstruction
4. Dysphagia
5. Haemorrhage
6. Nerve compression
Treatment
a.
b.
Treat infections f i r s t
Surgery - Excision, is the treatment of choice
Complication
i.
II.
iii.
c.
of Surgery
Damage to carotid \lls4fcls & nerves
Infection
'
Fistula
iv.
Recurrence
v.
Cosmetic deformity
Sclerotherapy : using bleomycin, C f4\ I
169
WOUND
CLASSIFICATION
WOUND CLOSURE
SKIN
GRAFTS
FLAPS & PEDICLES
i
i
Section A
WOUND CLASSIFICATION
Definition
A wound is a breach in integrity of tissues.
I t can a f f e c t all tissues of the body as opposed to ulcer which involves only the epithelial
surface.
]
3
]
Classification
Criteria
i.
ii.
iii.
iv.
v.
a.
Appearance
Velocity of infiltrating object
Involvement of underlying viscera
Part of tissue involved
Degree of inf ectivity
Based on /Appearance - is the commonest met

i.
Puncture
I t occurs from a tiny slender object, it results into a closed flap injury in
which the skin is closed because of the elasticity.
I t is important to known there can anaerobic contamination of the wound
especially clostridiumjêjuni. 4 r _ _ ^ - " "
Contusion - occurs when t ; ;ue is subjected to blunt trauma, the skin remainsjntact.
I t is recognized by hypen i m a &. swelling( due to haematoma which mat^become
secondarily infecte abd fc n pn abscess.
in.
Abrasion - is when only a \ r1 of the overlying skin is lost
iv.
Incision - is produced by c ve '/ sharp object e.g surgical incision. The edge is neat
and the injury is only alon; th path of the object.
1
n
Laceration - is produced t / o ject that is not sharp like that of incision. The edges
are neat, but ragged. Excise Ipe; tissue adjacent to the line of trauma because it can
become necrotic
VI.
Avulsion - occurs when a part of the body is sheared from the underlying structures. _
There are 2 types
i
a. Partial- not completely removed
~~
b. Complete
VII.
viii.
Degloving - occurs when part of th^sjînjs removed circumf erentiqJiy,

Amputation > ^<^,nCfe U^V?
3
i
170
Based on velocity of infiltrating

object
The dividing line is speed of sound ( 340m/s)
i.
Low velocity wound
ii.
High velocity wound
Involvement of underlying viscera
a.
Penetrating
b.
Non-penetrating
Part of tissue involved
' *i.
Skin
Mucosa
ii.
Muscle
iii.
iv.
Tendon
Degree of infectivity
i.
Clean : is produced under! epfric condtion and there is no penetration of viscera e.g
removal of lipoq ; thyroidectomy. I t does not require the use of
antibiotics bee ;e i t has a low very risk of becoming infected,
The wound can I
iosed primarily i.e immediately.
ii.
Clean-contaminated : O c a s ijhen there isyiojatipn L of hollow yjscus which has sterile

ontents e.g gall bladder with no organism in urine (i.e
n urine m/c/s
eri-operative antibiotics can be used.
in.
Contaminated : I s entering of 1 hollow viscus with infected content e.g
Cholecystitis
Traumatic wounds with presentation within 6 -8 hours of

incidence
Operations of prepared bowel

I t requires delayed primary wound closure
iv.
Dirty wound : I s entering into a viscus containing pus, faeces e.g operation on
unprepared bowel.
171
Section B
WOUND CLOUSRE
Timing of Wound Closure

a.
Primary closure - I s done when the wound is
o clean
o clean-contaminated
o contaminated - after doing some procedures & giving
antibiotics
b.
Delayed closure - is done for

o Contaminated wound
o Dirty wound
- I t involves NOT closing the wound immediately, the wound is observed f o r features of
infections.
- The wound is closed before healing starts, usually within 3 r d - 5 t h day before the formation
of granulation tissue.
c.
Secondary closure
,
- I t involves revising the wound before closure
- Infection is treated
- Granulation formation would have starred bef Qre-ihexlosiire
- E.g wound dehiscence
Preparation f o r closure - " AER. EAT. AWDR "

Assess the patient f i r s t - ABC of resuscitation
Evaluate the wound - to determine the type, risk of infection & exclude other injuries
Rest - to prevent further injury
Elevate the limb - to prevent haemorrhage
Analgesics
Tetanus prophylaxis
Antibiotics - only given when indicated
viii.
Anaesthetics
ix.
Wound irrigation - is done for all t j u ds. Jet lavage is used.

Debridement - removal of dead tis: fie
1.
Re-evaluation - to determine the typ of closure using the reconstructive ladder.
The Reconstructive Ladder (aka Plastic Surgeon [oMbox)
172
a. Do Nothing
No surgical intervention
Treat conservatively i.e as a[
IV<
b. Direct closure
I s done if the skin edges are close and c n : ! ill be brought together.
Materials used are
Sutures
Skin tapes -'
Skin clips
Sutures f means " to sew")
- Sutures are materials used to appose two surfaces, when used to occlude blood
vessel, it is called Ligature
Types
a. Abosrbable & Non-absorbable
The process of absorption involves
i. Hydrolysis- which is commoner e.g dexon
//*. Enzymatic digestion e.g catgut
b.
c.
Based on the origin - NalLral

NaAr & Synthetic
Based on the nature of
t | e suture - Monofilament &.
rft|e
Multifilament ( which is usually brqdfd or twisted)
Examples
Absorbable
1. Catgut - is natural. I t is derived from intestine of sheep
2. Polyglycolic acid ( Dexon)
3. Polyglactin acid (.Vicryl)
4. Polydioxanone (PDS)
Non-absorbable
1. Silk - is natural. I t is from silk worm larva.
2. Cotton - is natural, from cotton plant.
3. Stainless steel - is natural
4. Nylon
5. Polypropylene (Prolene)
- Naûrdlôcc^
because of the proteins they contain.
Sizes
Appropiate size of sutures should be used.
The lesser the number of Os, the thicker the suture.
Site
Head & Neck
Size
5/0 non-absorbable
Face
6/0 non-absorbable
Tendon
4 / 0 non-absorbable
Nerves
5/0 non-absorbable
Fasicles
8 / 0 - 10/0 non-absorbable
Circumferential stitch
6/0 non-absorbable
Q : What size of suture is mostly used?

A : 3/0 non-absorbable
Removal of Stitch
Site
Limbs
Trunk
Face
Time in days
7-10
7
5
Note
- Stitch match - occurs when stitch : hys too long
- Subcutaneous sutures are often us 'ul
Precautions for Suturing
ii.
Handle the tissues
iii.
Sutures should not
1
s I j f t for prolonged period
c. Skin graft
d. Flap
SecTôn C
SKIN GRAFTS
Definition
I s a piece of skin transferred from one part of the part of the body to another, it is completely
detached from its blood supply or donor site attachment.
Types
i.
ii.
iii.
iv.
Autografts : is the commonest. I t means from the same person.

Isografts : I t means from an individual with the same HLA or genetic make-up e.h identical
twin,
Allografts {Homografts) - From inidindual with different genetic make-up, but the same
species
Xenografts {Heterografts) - from different species
]
]
]
]
]
1
1
]
1
]
5
]
3
]
3
1
1
Types
a.
Partial thickness skin graft (STSG ) - pka " Thiersch"
b.
Full thickness skin graft ( FTSG ) aka Wolfe graft
Characteristics
STS6
1. Epidermis + Part of dermis
2. Take is better
3. Contracts more, therefore not used for
over joints
4. Pigmentation is worse
5. I s more susceptible to trauma
^
FTSG
Epidermis + Whole dermis ( without subcutaneous
tissue)
Take is less
Contracts less
I s better
Is more pliable
a. Split Thickness Skin Graft ( STS)

- There must be adequate vascular bed.
Donor Sites - Any part can be used.
i.
Thigh - is the commonest
ii.
Scalp
iii.
iv.
Arm
Buttock/Sluteal region
Graft Procurement
The instruments used are
i.
Humby's knr|| - is used in UCH
ii.
Electric der jrtome
iii.
Pneumatic d j;tr|iitome
iv.
brum derma j
Graft Processing
i.
Lay on Vaseline gauz
; sofratulle. Allow the rough surface to face upwards
ii.
Fenstrate
iii.
Avoid dessication
i c :vering it with saline-soaked swab
iv.
The graft may be m* >h d - by passing it into Mesher machine. This is done to
increase the size of Ih skin.
Transfer to recipier \ s e, the rough surface should be on the bed.
v.
Graft Dressing
i.
Layered dressing - I t may be 3- or 4-layered dressing.
4-layered is commoner.
FirstNon-adherent layer e.g sofratulle
V
Second- Antimicrobial agent e.g honey. This absent in /
3- layered dressing.
ThirdAbsorbent layer e.g gamgee
Fourth - To secure the dressing e.g Crepe bandage
175
ii.
Tie-over dressing
- I t is to put
- Put stitch c
*"
- I t is more i
applied.
iii.
frsure over the area

area
I in congruous areas where crepe bandage cannot
be
Open dressing
- I t is NO" o1 en done.
Monitoring
o
Review the wound appr
o
There may be a need t<
tely to assess take,

nt the grafted area
b. Full Thichness Skin Graft (FTSG )

Donor Sites
Post-auricular - fo face
Supra-clavicular - for larger amount of graft
Groin
II.
Upper eyelid
v.
Antecubital fossa
v.
Dressings
i.
Tie-over dressing - is the commonst f o r FTSG
Instruments
i.
ii.
Scalpel
Forceps
jl
]
]
Factors Affecting Skin Graft Take

a. Local - these are more important
i.
ii.
iii.
iv.
v.
Haematoma
Seroma
Infection
Trauma
Movement
UppYXS*Xvv\.<*Wv 0{
C^rc^t
3
]
telaeA'
b. Generalised
Infection
Systemic disease e.g diabetes mellitus,
Malnutrition
Other types of Grafts & Sources
1. Cartilage - Costochondral junction
2. Bone - Iliac crest
3. Nerve - Sural nerve
4. Tendon - Palmaris tendon
176
3
3
3
]
Si'rt onb
FLAPS MEDICLES
Definition
I s a mass of tissue transferred from on z p r t of the bdoy to another with its blood supply intact
I s used when the full thickness of the skin is involved and the recipient bed is NOT vascular e.g
Bare bone (when periosteum is eroded)
Bare tendon
Cartilage
Major nerves & vessels

Classification
I t is based on
a. Proximity to defect
i.
Local- it shares aboundary with the recipientjsije
ii.
Regional- it does not, but the flap is from the same region of the body
111.
Distant
b. Tissue contained
\.Skin flap- only skin + subcutaneous. I t is thinnest
c.
ii.
Fasciocutaneous - above + deep fascia
Mi.
Musculocutaneous
iv.
Muscle flap-
v.
Fascial flap- fascial<ilone
or Myoflap - above + muscle
muscle alone
Geometry of the transfer

ii.
Rotational
Hi.
Advancement
iv.
Transpositional
FREE FLAPS
For microvascular surgery
PEDICLES
Is when the donor and recipient sites are left together for 2 weeks
TISSUE EXPANDERS
177
WOUND HEALIN
5i
.1
COMPLICATIONS
on A
WOUN b IIEALING
Wound Healing
Wound healing is a process by which the bo >y repairs damaged or injured tissue with living
tissues.
I
Many times, the replacement is with fibrous tissue, but in few cases, there is regeneration e.g
liver, abrasion
I t occurs in skin (taken as the prototype ), bone etc
Phases
I t is actually a continous process, but a r t f icialy divided into 3 phases
a. Inflammation bay 1 - 4
I t involves
i.
Vasoconstriction, platelets aggregation & coagulation
The vasoconstriction helps to limit blood lost, the stasis of blood also
helps to ease the formation of platelet plug.
ii.
Vasodilatation - to recruit cells. Neutrophils arrive within 3- 6 hours while
monocytes & tissue macrophages take about 4 -5 days. This is therefore
called phase of demolition. - ^ r A f t c ^ W y
Increased vascular permeability
in.
b. Proliferation: Day 5 - 2 1
- There is fibroblasts formation which produce collagen and ground substance (amorphous
matrix).
- This results in
/.
Wound contraction
- Is produced by the contractility ability of fibroblast (called myofibroblast).
This brings the edges of the wound together.
//'.
]
]
1
3
]
1
1
1
]
]
]
1
1
Granulation tissue formation

- I s a mixture of collagen & blood vessels
- There is increased epitheliasation
Note
The proliferative phase can be subdivided into the following
a. Epitheliasation
Basal cells are mobilized to the wound area and proliferate by mitosis.
Contact inhibition makes the cells to stop dividing.
The cells then differentiate into keratinocytes.
178
0
1
1
I n well apposed wounds, epitheliasation is complete in 48 hours. I t is healing

by primary intention i.e without excessive scarring.
I n secondary intention healing, the migration of cell required a bed of
granulation tissue ( which appears reddish & granular appearance. I t occurs in
wide gap healing.
b. Granulation tissue formation
c.
Contraction
d. Fibroplasia
There is formation of scar tissue from collagen deposition by fibroblast
Secretion of procollagen
Hydroxylation of proline ( requires ferrous iron, vitamin C & Ketoglutamate.
Capillary in growth (ref. qxygen) via budding of the cut edge of the vessels.
c.
Maturation (Remodelling) : Beyond day 21. There is

Collagen organization into regular fashion. There is balance between formation and
removal of collagen.
Increasing tensile strength. I t increases to maximum in 3 - 6 months ^
q SVv . f
There is maturation of scar in 6 - 12months.
Types of Healing
a. Healing by First Intention
I t occurs in
o clean wounds
o wounds with narrow gflps
I t occurs within 3 - 1 4 days

There is practically no granu ti( ;i tissue formation
b. Healing by Second Intention
- I t occurs in
o
dirty or infected wouVid;
o
Wound with wide gap
- There is prolonged wound healing
^
- There is granulation tissue formation. This is the hallmark.
- There is abnormal scar formation - Hypertrophic, keloid or unstable
Factors Affecting Wound Healing
a. Local
1. Local infection
2. Tissue handling
3. Wound cleansing
4. Debridement
5. Haemostasis - a drain is used to contol it
6. Spillage - of toxic materials
7. Local blood supply e.g facial wound heals faster than lower limb wounds
179
8.
9.
1
1
1
Foreign bodies e.g cotton wool

Types of tissue involved - labile or p 'K inent cells
b. General
1.
2.
3.
Growth factors - FDF, EGF etc

Nutrition e.g vitamin C, zinc, methionine
Oxygen - is neede f o r hydroxylation of ollagen to form tropocollagen
4. Oxygen radicals
5. Age
6. Systemic disease e.g diabetes mellitus, haemoglobinopathies, chronic liver failure, uraemia
7. Systemic infections
8. Drugs e.g NSAIDs, steroids, cytotoxics
9. Smoking
10. Radiation
11. Carcinomas
"
Section B
W O U N D COMPLICATIONS
2. Wound infection
2. Wound dehiscence
3. Pigmentary changes - hypo- or hyper-
1
1
4. Septicaemia
5. Chronicity - chronic wounds are the types that do not heal after 6 weeks
6. Abnormal scars e.g
o
Keloid
o
Hypertrophic scar
o
Hypotrophic scar
i
o
Painful scar
7.
8.
9.
10.
Contractures
Dyschromias - is abnormal of pigmentation ' hyper- & hypo-pigmentation
Implantation cyst - by "epidermal elements
Neoplasia e.g Marjolin's ulcer may result into squamous cells carcinoma
1
t
]
3
ABNORMAL SCARS
Types
Keloids
Hypertrophic scars
180
^fe
Differences
.1
Keloids
Hypertrophic
Not obvious
5. Aetiology
6. Course
Familial
Common in Black;
Common among f tmaj e in child
bearing age
Adolesecent & early adult age, 10 3Oyears
Unknown (? Wound)
I t continues to increase in size
7.
I t extends beyond the original
1. Genetic
2. Race
3. Sex
J 4,
Age
Borders
wound
8. Location
Similarities
i.
scars
I s also commoner in females

Children
Is related to tension
Increased initially, but after
6month - 1 year, it becomes static,
the size may even start reducing.
'-'}
I s common in parts exposed to

severe friction & tension e.g
Sternal, deltoid,back, lower back,
ear lobe.
Both tend to occur in wound that heal by second intention. Note, keloid can also occur after
f i r s t intention.
Treatment
a. Hypertrophic scar
- Excision 6\ approximation of the edges together to allow healing by f i r s t intention.
b. Keloid
Treatment modalities are.
i.Surgery - Excision &. closure, with the following
ii.
Injection of triamcinolone which is a f luoriniaTe^^t^r^[q)injected into keloid.
I t anhances the action of collaenase. I t is given every 2 weeks
iii.
Superficial low voltage radiotherapy
-
r
r
Other
^y
Modalities
iv.
Silastic gel and cream - I s used for about 3 months. I t is sticked on the scar
for about 12 hours/day
v.
Pressure application - using pressure garment or Gobsct for at least 23
hours/day for about 6 months. I t helps to mature a healing wound faster
VI.
The 3 modalities are called ' TRIPLE REGIME
Silicon gel
181
]
]
]
CONTRACTURES
Definition
Is excessive fibrosis across joints or flexural surfaces of the body, limiting movement e.g
phallux. t > q
3
1
Treatment
i. Surgical release & wound closure with
o
Z-plasty technique
o
Skin graft
o
Flap
Prevention
i.
ii.
iii.
Physiotherapy
Appropiate spliniting - for an adult. > ght splint can also be used.
Early wound closure - latest 2 week;;
CHRONIC
ULCERS
1
1
1
LYMPHOEDEMA
PRESSURE
ULCERATIC M
Section A
1
1
1
1
CHRONIC ULCERS
Definition
are wounds that do not heal after 6 weeks
Causes
1. Trauma - is the commonest

2. Infection
a.
Non-specific e.g diabetes mellitus
b.
Specific e.g Tuberculosis, Syphilis, Buruli ulcer
3. Vascular
a. Arterial
b.
Venous
'
:.!]*,.
; .^j.
c. Lymphatic
4. Haemoglobinopathy
5. Neurotrophic e.g
/.
Diabetes mellitus
ii.
Syphilis
182
,1
Hi.
iv.
v.
VI.
vii.
Leprosy
Spinal cord injury
Spical cord compression
Syringomyelia
Tabes dorsalis
6. Pressure /decubitus ulcer - it is commonest in the buttock/gluteatl region

7. Malignancy e.g
i. Basal cell carcinoma
ii.
iii. Malignant melanoma
iv. Kaposi sarcoma
v.
Infiltrating tumour e.g breast disease
Painical Presentation
a.
History
- the duration ?
- How it started?
,t
.*,
b. General <& Systemic examination
,r
>5
''-
c. Examination of ulcer
i.
Edge- the following are descriptions with what they suggest
Shelving- healing wound
o
Undermined- Tuberculosis
o
Punched out- Syphilis
o
Raised - Malignant
o
Floor - is the part
o
o
o
seen. I t may b
Granulations
Discharge - pi
Slough
nt/serous /bloody
in.
may be hard, f i r m or soft. The following are

Base - is what is f e l t by palpatio.
ckecked for
o
Induration
o
Attachement to one
Unusual tendi m ss: an example of non-tender ulcer is neurotrophic
o
(syphilitic) ul< er.
IV.
Surrounding skin o
o
o
o
7
T
for
Oedema
Healthy skin
Pigmentation- hyêr-rlor hypoVaricosity
Regional lymph node - for

o
Firm, tender LN - suggests infective lesion
o
HardLhi - suggests carcinoma
183
o
o
Soft
Discrete, matted or tender
vi. Regional Vascularisation
Investigation
1. Full blood count
2. Genotype
3. X-ray - of the ulcers and bony areas. For osteomyelitis
4. Angiography
5. Wound swab or biopsy f o r m/c/s Indications
i.To rule out infection
ii.
Before closure of all wounds
' ,
3
.1
Signs of Infection
The wound is not healing
i.
There is copiius discharge
ii.
Tenderness
v.
Reddish
v.
Surrounding skin is oedematous, warm, tender
Treatment
Bed rest
Treat underlying causes e.g
o
Malignancy
o
Varicose veins - Venous surg y
o
Tuberculosis - anti-tb drugs
o
Diabetes mellitus - Arterial fr- lass
in.
iv.
v.
Skin graft - is done granulation tissue i: |hîlthy

Anti-tetanus
Antibiotics - given as necessary becausf it s not required in all cases especially if it is not
infected
Complications of Ulcer
1. Infection - Local &. systemic
2. Abnormal scars
3. Contractures
4. Lymphoedema
5. Bone complication - Osteitis, Osteomyelitis
6. MarJohn's ulcer
7. Tetanus
!l
184
r
r
r
r
Section B
PRESSURE ULCERATION
Introduction
I t is called Decubitus ulcer when it occurs in bed-ridden patients
Aetiology
a. Extrinsic
i. Pressure
ii. Friction
iii. Shear forces
b.
Intrinsic
i.
ii.
iii.
Infection
Hypoproteinaemia
Anaemia
iv.
Sensory loss
v.
Impaired mobility
vi.
Faecal & urinary incontinence
Clinical Staging
I :
Limited to epidermis & superif icial der his
II:
Full thickness skin damage
I I I : Muscle involvement
IV " Bone or joint involvement

Treatment
Grades I. U &
III
- Conservative treatmentwhich includes

Control of infection
i.
Debridement
ii.
Avoidance of pressure - using fenestrated foam, Roho cushioc or special beds e.g air
iii.
f luridised or low air loss
iv.
Regular turning of patient - done 2-hourly
v.
Ensure no soilage of beddings
vi.
Ensure that the bed is smooth
Grade IV
i. Surgery
- Wide excision of the ulcer with bone resection
- Padding of residual bone
- Closure with flap
il"
185
s4
tion C
LYMP C EDEMA
Definition swelling particularly of the limbs due to
:c mulation of lymphatic fluid
Aetiology
a. Primary (unknown)
i.
Lymphoedema congenita - ha | e< ly onsent
ii.
Lymphoedema praecox - has fuv nile onset
iii.
Lymphoedema tarda - has Ia11 o set
b. Secondary
i.
Recurrent infection particularly.^ bare footed e.g recjjrxsnt-lymphgngjtis - is the
commonest cause.
i.
Filar iasis
ii.
Surgical trauma - including resection of lymph nodes.
v.
Infiltrating tumours
Clinical features
i.
Limb, and scrotal swelling
ii.
Other features of filariasis
iii.
Scar of previous surgery
1
\
Investigations
i.
For evidence of filariasis
ii.
Lymphanigogram
3
1
Complications
a. Early stage
1. Recurrent limb swelling - which pits initially
b. Intermediate stage
12. Established non-pitting swelling - caused by protein accumulation in the interstitium &
fibrosis
13. Early skm changes of keratoses
c.
Late stage
4. Filiform or nodular hyperkeratosis
5. Recurrent ulcers - sometimes with copious discharge
6. Malignant transformation to Lymphagiosarcoma
7. Infections of ulcers - occurring later
Treatment
i.
Treat the pre-existing disease
ii.
Early physiotherapy
iii.
Elasticated stocking - for early stage
]
]
]
]
1
1
1
]
]
/
iv.
Physiological operations
a. Early stage
o Thompson's swiss rolh is excision of skin &. bury it under fascia
o Re-anastomosis of lymphatic channels
b. Late Stage
o
Excisional surgery e.g Charles operation
BURN INJURY
Definition
I t is a coagulative necrosis of skin due to the causes listed below
Aetiology
1. Moist heat - is scald injury
2. Dry heat e.g in explosion of adulterated kerosene
3. Chemicals e.g acid, alkali, phophates
4. Electricity
5. Friction
6. Others (abroad):
i. Ultraviolet radiation
ii. Cold
Epidemiology
- Age and sex incidence (Ibadan, 1992-199
o
o
38% of patients were under 11 y ars

Overall:
Males = 53%
Females = 47%
- The commonest cause ( i n abroad) is moisl\he$t
Mediators of the burn response
Local
i.
Cytokines
ii.
Oxygen radicals
iii.
Arachidonic acid metabolites
iv.
Endotoxins
Systemic
i.
Catecholamines
187
i.
ii.
v.
v.
vi.
vii.
viii.
ix.
x.
Aldosterone
Growth hormone
Antidiuretic hormone
5HT
Histamine
Thyroxin
Adrenocortical steroids
Glucagon
Insulin
Inflammatory mediators
o
Repressed production in healthy individuals
o
Production continues, no negative feedback
o
Activate release of others and pottdntiate their action
o
Acute exaggerated response can cause cardiovascular collapse
a. Cytokines
Types
o
o
o
o
o
Tumour necrosis factor ( TNF)

Interleukin-1
Interleukin-2
Interleukin-6
Interferon gamma
Effects
i.Increase in vascular permeability
ii.
Catabolism of muscle
iii.
Production of anaemia
iv.
Initiate wound healing
v.
Produce fever
b. Oxygen radicals
Examples
o
Super oxides
o
Hydrogen peroxide
Effects
II.
Alter vascular permeability

Cause RBC haemolysis
Disrupt interstitial matrix
c. Arachidonic acid metabolites

a. Cyclooxygenase pathway
o
Prostaglandins - the effects are vasodilation, pain, erythema
b. Lipoxygenase pathway.
o
Leukotrienes -C4, D4 - ari l/asoconstrictors
1
1
1
1
Systemic Changes in a Burns Patient

a. Skin
o Coagulative necrosis
o Disruption of basement membrane
o Blistering
o Vascular changes
o 3 zones (Janzekovic)
i.
ii.
Hi.
Coagulation
Stasis
Hyperaemia
See Fig 1
'
b. Cardiovascular
o
Vascular and RBC damage
.
o
Increased vascular porosity
o
Cathecholamines cause peripheral and splanchnic vasoconstriction
o
Cardiac muscle damage from mediators, fluid overload, drugs, sepsis
]
]
]
c. Renal
Oliguria- this can be pre-renal, renal or post-renal. I t is due to
]
]
]
Pre-renal
i. Splanchnic vasoconstriction
ii. Reduced GFR
Renal
iii.Reduced parenchymatous flow, causing iscahemia
Post-renal
iv. Myoglobin, haemoglobin precipitates in tubules
d. Gastrointestinal tract
o Curling's ulceration - results from ischaemia
o Gastric dilatation
o Ileus
o Gut barrier disruption and bacterial translocation. This, with ileus, results into bloated abdomen
e. Respiratory system
Upper
o Upper airway oedema from heat component of smoke
o Upper airway oedema from chemicals (noxious gasses)
1
1
1
1
Lower
o Restricted chest expansion
o Interstitial damage and pulmonary oedema
o Carbon monoxide and cyanide poisoning
- Treatment involves anticipating it and by passing endottacheal tube.
1
^. i
189
Ik
1
1
Management Of Acute Burn Injury

'.>::..
"FFH. IAAAM. WWP"
1.
First aid and ABC of resuscitation - disconnect the patient from the cause
2.
Fluid administration - after passing wide bore cannula into large vein
3.
History and examination
4.
Initial investigation - Electrylotes & ureas
5.
Anaelgesic, antitetanus, antibiotics
Give intravenous narcotics ( I V morphine & chlorpheramine). Don't use novagine or
paracetamol.
Giving antibiotics is not routine, but is given prophylactically for patient with
inhalational injury.
6.
7.
8.
9.
10.
11.
12.
2.
E.g Penicicclin or cloxac in

Antiulcer drugs
- using H2 -blockers e.g ra ti ine
Anticoagulants - prophylactically
Management of inhalation
Wound debridement and dressin
Wound excision and skin graft
Physiotherapy - of chest
Measurment of vital signs
Fluid administration
a.
Parkland formula
I n the 1 st 24
b.
c.
Colloids : Watson's modification of Muir and Barclay's formula

Hypertonic saline
Evans' formula
Brooke's formula
Monitor patient by:

i.Clinical
ii.
iii.
iv.
3a.
ho rs, 4ml/kg/% of Hartman's solution
response
Ensure urine output of at least 30ml/hr in adult.
PCV - 6-hourly, 12 hourly
Pulse oximetry
History
Time of occurrence
Part of body involved
Associated injuries
Accident site
Premorbid status e.g seizure
Treatment received so far - f i r s t aid measure
Risk of renal failure
> > <>-'
3b.
General examination
Wallace's rule of 9
190
T-.
3c.
Clinical
o
o
o
examination
Wallaces rule of 9 in patients aged >12 yrs.
Berkow's modification of Lund and Browder chart in children < 12 years,
Depth of burn
Table 1.1 Classification of burns
Type oi burn Blistering
Appearance Pinprick test
Superficial
dermal
Bright red
Sensitive to
pain
Deep derma! Blisters

Creamy
are broken coloured/
mottled
Dullness to
pain,
sensitive to
touch
Full
thickness
No
Present
Absent
Grey/white
or brown
sensation
classification.jpg
8. Wound dressings
o
Debridement
o
Meshed gauze
o
Cotton gauze
o
Cotton wool
o
Bandage
Treatment by exposure
Areas that are difficult to dress: fa< |e, lenitalia and perineum
191
Minimally discharging wound
To allow for frequent monitoring: finger tips
To allow f o r joint movement (polythene bag on the hand)
Note, partial skin burns can regenerate skin while full thickness skin burns require
graft
Treatment of full thickness burn wound

i. Early wound excision
ii. Partial thickness skin graft
Treatment of partial thickness burn

'
o
Change dressing 5 days after or as necessary
o
Wound heals in 14 days

- See Fig. 4
Management of burn wound / donor site discrepancy

o
Temporary skin graft: allograft, porcine skin
o
Staged skin grafting
Meshed skin grafting
Cultured keratinocytes (skin culture)
Skin substitutes: integra, biobrane

- See Fig. 5
Management of inhalation injury

See Fig. 6
1.
Clinical suspicion
2.
Escharotomy - is a circumferenti dpt to reduce the restriction of dead tissue )skin)
3.
Bronchoscopy and intubation - to is alize ulcers, erythema
4.
Blood oximetry
5.
Oxygen and oxygen tent
6.
Antidotes - to mop up cyanides
7.
Positive pressure ventilation (art rit 102 40kpa)
Clinical indications for intubation
Absolute
1.
Burn of the palate, t|>ng je and pharynx
2.
Oedema of the posterior pharynx and upper glottis
3.
Burn of vocal cords
Relative:
1.
2.
3.
Hoarseness
Facial burn
Sooty sputum
/
Management in the subacute phase
1.
Blood transf ussion
2.
Early wound cover-, tangential / fascial excision
3.
Delayed wound cover (on granulation tissue after escharectomy)
4.
Treatment of fever
5.
Treatment of psychiatric manifestations
6.
Physiotherapy
7.
Nutrition
7. Nutrition
6. Early
and Metabolism
i.Early burn wound cover
ii.
Carbohydrate:
Protein
i
iii.
Vitamins
v.
Electrolytes
v.
- vi.
Oral
Nasogastric: elemental feeds
vii.
Parenteral
viii.
physiotherapy
Chest
Hand
ii.
iii.
Early ambulation
iv.
Other joints
Prevent pressure sores
v.
Infection in Burns
a. Wound infection
a.
Bacterial
b.
Klebsiella
|
Pseudomonas
Staphylococcus aun
Streptococcus
Fungal
Candida
Actinomyces
Phytomycosis
c. Viral
Herpes simpk x
b. Chest infection
c. UTI
d.
e.
Thrombophlebitis
Deep vein thrombosis
193
Prevention
1.
2.
3.
4.
5.
6.
First aid period patient's bed

Isolation e.g Burn unit
Sterile procedures
Early definitive wound cover
Antibiotics
Selective gut decontamination
Chronic complications of burns

1. Skin
Dyspigmentation
Abnormal scars: hypertrophy, keloid
Contractures
'
Chronic ulcers
Marjolin's ulcer
2
3.
4.
5.
if.
iii.
iv.
v.
Anaemia
Chronic pu Imonary insufficiency
Psychiatric : disturbances
Tetanus
SURGICAL KJIN LESIONS

(Tumours 6 mphoedema).
Content
1.
2.
3.
4.
5.
Cysts
Skin infections
Hematomas
Benign neoplasia
Malignant neoplasia
Sect on I
CYSTS
Introduction
Cysts can be congenital or acquired
Types
a.
b.
Sebaceous cyst
Dermoid cyst
a. Sebaceous cyst
Pathogenesis
- Occurs when there is occlusion of the duct from sebaceous gland to the skin.
Pathology
- I t contains keratin and its breakdown products lined by squamous epithelium
I t contains a cheese-like material that is yellowish to brownish colour
- I t is recognized by a punctum (pin point) on the surface of the swelling
- I t is commoner on the face and the scalp
b. Dermoid cyst
Introduction
- I s often congenital
- I t is lined by epithelium
Pathogenesis
- I s due to implanatation of dermal tissue or epidermal into deeper tissue
Types
a.
External angular dermoid
eye
b. Midqi dermoid - Can oca j

c. Implantation dermoid - I:
driven subdermally. I t is i
I t is cystic
i.
Occurs on the face ii.
seen on the face (lateral to lateral canthus of the

the neck or between 2 eyebrows
quired, it occurs when parts of epidermooid gets
lly secondary to tumours.
>u ;lly lateral to the lateral canthus of the eye
Treatment
Excision
Complications
1. Recurrence
2. Infection - makes it painful
3. Compression of adjacent structures
195
]
]
]
]
]
SKIN] SECTIONS
Classification
Non necrotising
Localised
Diffuse
. Furuncle (boil)
i. Cellulitis
ii. Actinomycosis
. Carbuncle
i. Cellulitis
iii. Hidradenitis
Necrc j si ng
i.
F jr lier's gangrene (scrotum ) - is due to

endarteritis
ii. C ihcfum oris
i.
Aleleney's synergistic gangrene
cc jrs on abdominal wall, usually after a
gi<
al procedure
su
as gangrene
ii
Types
Furuncle
- is usually caused by Staphylococcus aureus
Treatment- Oxacillin
]
]
Cellulitis - is caused streptococcus

Treatment- Penicillin
Extensive cellulitis
Treatment
i.
ii.
iii.
iv.
v.
1
Admit
Rehydrate
Treat the constitutional symptoms: Fever
Antibiotics
drainage
]
]
(antipyretics)
Hidradenitis
- The commonest site for hidradenitis is axilla, also occurs in groin. Theses areas contain apocrine
glands. I t usually suppurates
Treatment
a. Early stage- antibiotics
b. Late stage- Drainage & excision of the affected tissue. Cover wound with
flap
Fournier's gangrene
I s caused by aerobic and synergistic anaerobic organisms.
I t affects the scrotum mainly ( especially the subdermal layer)
Treatment
Supportive therapy
i.Antipyretics
ii.
Antibiotics - to cover Gram +ve & -ve
b. Excision of dead tissue
c. Wound closure with flap
a.
196
j
-*
I
]
3
]
]
,1
]
1-
Cancrum oris
Treatment- as above
Gas gangrene
- I t causes myonecrosis
Clinical features
Pain
Swelling
ii.
Constitutional symptoms
iii.
Tocaemia
iv.
v.
Blister formation
Investigation
i.
Treatment
i.
n.
iii.
iv.
X-ray - shows gas in the muscle plane
Aggressive treatment with antibiotics - using

High dose of penicillin
o
Ciprofloxacin
o
Cephalosporin
o
Metronidazole
o
Debridement
Hyperbaric oxygenation - because the organism is anaerobic.
Amputation - if it is severe
Section I V
HARMATOMAS
Definition
- A lesion resulting from disproportionate gHwlth of structures local to the area
Types
a.
Melanomatous naevi
b.
Vascular aberrations
Haemangiomas
Lymphangiomas
C.
Neurofibromas
d.
Sebaceous naevi
a. MELANOMATOUS NAEVI
Types
Epidermal - there is aggregation of melanocytes. I t is confined in the epidermis.
Junctional - there is projection into the dermis ( i n between the epidermis & dermis)
Intradermal - is toally confined to the dermis
iv. Compound - Involves the epidermis, junction and dermis
Features that Suggest Malignant Transformation
Change in size
i.
Change in pigmentation - is getting darker or lighter
ii.
Weeping - i.e forming blister & discharging serous fluids
v.
Bleeding
v.
Encrustation
vi.
Satellitism
vii.
VariegationClinical Features
- I s seen as flat spots that are black or brown.
Treatment
Excisional biopsy - ONLY if malignant change is suspected
b.
HAEMANGIOMA /ANGIOMAS
Clinial Features
I t may present soon after bifth, grows for about 6 months to one year and then start
regressing.
I t is associated von-Hippel L l l d i u syndrome - which is
L laucoma
o
/
increatic disease
o
c erebellar angiomas
o
Complications
i.
ii.
v.
Treatment
i.
ii.
iii.
Infection
Ulceration
Bleeding
Embolisation
Re-assure the parents 50 - 60% of the cases regress spontaneously

Steroids e.g prednisolone A triamcinolone are injected into the lesion.
[Prednisolone is short-term(l - 2weeks),using low dose]
Excisional biopsy surgery- is indicated ONLY if there are complications like
bleeding; embolization.
198
c.
LYMPHANGIOMA
Treatment
I t hardly regresses, hence excisional surgery is required
d.
NEUROFIBROMA
Types
a. Local
b. Generalised ( von-Recklinghausen's disease )
Aetiology
- Has familial tendency
'
Clinical Features
i.
Cafe-au-lait spots - hyperpigmentated areas
ii.
Lysch nodules on the iris
Treatment
i.
Excisional biopsy - done ONLY if malignant change is suspected.
Note, curettage or shaved biopsy is discouraged !!!
e.
f.
SEBACEOUS NAEVI
I t is congenital
I s more common on the scalp J>f face

Has malignant potential /;
Treatment
Excision
199
BENIGN SKIN LESIONS

i.
a.
Hi.
iv.
v.
il
1
Lipoma
Papilloma
Fibroma
Desmoid tumour
Dermatofibroma
Dermatofibroma
I s a kind of fibroma that occurs in the deeper part of dermis but presents as a hyperpigmented
area on the skin, hence causing confusion in making diagnosis.
tion V
MALIGNAN SKIN LESIONS
Types
i.
a.
Hi.
iv.
v.
vi.

Malignant melanoma
Basal cell carcinoma
Kaposi sarcoma
Merkel cell carcinoma
Soft tissue sarcoma
]
]
3
1
]
1
]
I. SQUAMOUS CELL CARCINOMA

Definition
Arises from epidermis
1
1
Aetiology
Arises usually from premalignant lesions via
i. Sun damaged skin - is seen in Caucassian
ii.
Actinic keratoses
iii. Leukoplakia - these are white patches on the skin or mucous membrane
iv. Radiation dermatitis
v. Chronic ulcers e.g Marjolin's
vi.
Sinuses
vii. Scars
Clinical features
Commonest in head and neck worldwide
i.
But, common around the ankles in Nigeria,
ii.
Sometimes starts as a slowly enlarging erythematous patch with sharp irregular edges called
Bowen's diseasejMore typically it is papillomatous or ulcerative.
200
1
1
IV.
Raised everted edge
Investigations
- Because many patients present late, evidei
of metastases should be sought,
X-ray of the underlying bone fc" its involvement
CT scan - for the above reasot
it.
Incisional / Excisional biopsy
"ule out other lesions
iii.
Investigation for managemen
iv.
Full blood coun
Wound swab f <J| rtj/c/s

Preparation for surgery
ECS
Chest x-ray
Treatment
Surgery
i.
iiiii.
iv.
v.
Wide local excision ( mostly 2cm off the edge) + skin cover
Dissection of involved regional lymph nodes - if there is significant
lymphadenopathy
Radiotherapy : only the poorly differentiated lesions are reasonably
sensitive. For patients not f i t surgery.
Crotherapy
Amputation
Prognosis
Predictors of tumour recurrence are1. Degree of differentiation
- Poorly differentiated lesions are more likely to recur
2. Depth of tumour invasion
3. Perineural invasion by tumour
I I . MALIGNANT MELANOMA
Introduction
- Is the Z"1 commonest malignancy in this environment
Epidemiology
Age - is rare before puberty ( 3 0 - 6 0 years)
Sex- male/female ratio is 1 : 2
Aetiology
Precursors are :
i.
Dysplastic naevus
ii.
Melanoma in situ
Others
\
iii.
Albinism
iv.
Xeroderma pigmentosum
Pathogenesis
- Malignant melanoma arises either as a change in preexisting naevus or de novo.
Clinicopatholoqical varieties
a. Lentigo maligna
I s commonest in Caucassians.
I t is common in elderly and on the face.
I t has bad prognosis
b. Superficial spreading melanoma

occurs as a patch on the trunk and limb.
I t is common in young people *
c. Nodular melanoma
Occurs as a nodule
Has the worst prognosis
1
1
1
d. Acrolentiginous melanoma
Is the commonest in this environment
Occurs on the feet, around the nail and nail bed
I t s prognosis is poor
e. Amelanotic melanoma
N.B
Affects commonly head and neck and exposed area: in light skinned individuals (e.g. Caucasians). I n Nigeria,
and in other blacks, affects mainly heel, ankle and{ vie of the foot. Also found in oral mucosa and
anorectum. Very rare in Albinos.
Investigation
Incisional biopsy is not allowed.
Histologically Clarke's level is less prognltt eating than Breslow's thickness.
Classification
a. Clarke's Level of invasion - is a pathologi i\ taging
Clarke's
level
Within epidermis
Within papillary derm
n
At junction of papillary aid reticular dermis
HI
Within reticular dermis
IV
Beyond skin
b. Breslow's thickness
Thin
Thickness ( mm)
<0.76
202
1
1
1
1
1
1
1
"I
1
1
Thick
0.76 - 1.5
>1.5
Local lesions alone
Moderate
r
Clinica Staqinq
Ha
Stage I + Satellite lesions /in transit
lib
Stage I + Regional lymph node
III
"*Cesions beyond regional lymphatic drainage"*'*
Note, some patients can have both I l a & b

Treatment
1.
2.
3.
Wide excision with reasonable margin ( 2 -5cm) often + skin graft

Ray digital amputation only in cases with involvement of digit.
Adjuncts
i.
Immunotherapy - usif recombinant a-interf eron (TILS - Tumour
infiltrating Lymphomono-clonal antibody + Cytotoxic). Intralesional
BCG has been used.
//.
Chemotherapy
For stc ce l l l .
The ag itis used are dacarbazine (DTIC),
Mel
an
///.
Isolated
iv.
Limb ?e-fusion
For st< e I l a and l i b after excision
I t invc e cannulation of an artery & vein in the groin through
thedr h (Welphalan) is injected
Radiotherapy
Prognosis
I s based on
i. Staging
ii.
Sex - female
iii.
Age
iv.
Size of tumour
v.
Pre-existing naevus
203
III.
1
1
1
1
BASAL CELL CARCINOMA
Aetioloqical factors
Ultraviolet rays - UVB component

Predisposing lesions
1. Naevus sebaceous
2. Albinos and patients with xeroderma pigmentosum are
susceptible to sun change.
Epidemiology
I t is commoner in Caucassian because of lack of protective melanin. I t is uncommon in blacks
About 85% occur on the face, majority occur above the imapginary line drawn from angle of the
mouth to tragus.
Clinicohistologic types
a.
Superficial
b.
Nodular - Is circumscribed & nodular
c.
Nodulo-ulcerative
d.
Cystic
e.
Morphoeic - I s difficult to diagnose and treat because it appears as arease of dermatitis
Course
I t is often locally malignant i.e. does not often metastasise.
Treatment
1.
2.
3.
4.
Excision - offers best prognosis

Cryosurgery,
Radiotherapy
Chemotherapy - 5-Flourouracil cream is only for early lesions
1
1
Inform the patient to avoid sun exposure and wear protective material
IV. KAPOSI SARCOMA

Introduction
I t is not a real tumour of skin. I t is a t/cj|^4/ar tumour (. multifocal )arising from mid-dermis.
I t may be solitary or widespread.
Some of them are AIDS-related
Histologic Types
II
III
1
1
1
1
1
Mixed ( Spindle cells & vascula; I d annels)

I s most sensitive to chemotl- arcpy
Monomorphic ( Only spindle eels)
Anaplastic (pelomorphic cells)
- Has poorest prognosis
204
1
1
1
1
1
1
r
r
Types /Clinical Features

1. Classic type
Occurs in 50 - 80 years
Common in lower extremities
I t s course is indolent
2. African Nodular florid
is the commonest in adult ( 25-40 years)
Male/female ratio is 1.3 : 1
I t is characterized by nodules which are often fungating
I t s course is indolent, but locally aggressive.
3. Lymphadenopathic
Occurs in 2 - 13years
'
I t is characterized by generalized lymphadenopathy
I t s course is rapidly progressive.
4.
_.
-i
Visceral ( Therapy-related)
- Those at risk are
i. Patients on renal transplant
ii. Autoimune disease
- I t is local or widespread
Course - I t may stop when the drug is used.
AIDS-Related Kaposi Sarcoma

I t is in 19 - 64 years
I t is characterized by involvement of mucocutaneous, lymph node & viscera
I t s corse is variable
Investigation
1. Chest X-ray - shows canon ball opacities
2. Bone X-ray
3. HIV Antibody test
4. Stool
5. Biopsy
r~ Treatment:
Chemotherapy. Using
- Vinblastine
- Etoposide
- Bleomycine
- Adriamycine
- Methotrexate
n
b.
c.
d.
Immunotherapy
Radiotherapy
Local therapy
i.
Recombinant alpha
fe' feron
Excision
Curettage
205
iii.
iv.
Cryotherapy
Electrodessicatidh
V. SOFT TISSUE SARCOMA

Liposarcoma
Malignant fibrous histiosarcoma
Leiomyosarcoma
Fibrosarcoma
Synovial sarcoma
Rhabdomyosarcoma
bermatofibrosarcoma
Neurofibrosarcoma
3
1
PLASTIC SURGERY OF THE HEAD AND THE NECK

1. Congenital Anomalies
2. Infections
3. Tumours
4. Trauma
5. Cosmetic Surgery
Sect/on I
Types
Broadly, there are three groups of craniofacial anomaly. These are
1.
Clefts
2.
3.
Dysplasias or Hypoplasias
Craniosyostoses - Small head syndromes
a.
Pathogenesis
CLEFTS
Are due to failure of fusion of the 5 t rqcesses that constitute the face (Classical theory of
His) or
Failure of merging of mesodermal mc
m the region of the face (Mesodermal penetration
theory).
Epidemiology
!
Incidence of cleft lip varies among racei
I n Caucasians 1:600 - 1400 live births.
- I n Nigeria, 1:1,100 - 1: 2800 live births
206
'l
Aetioloqical factors
1. Intrauterine infections (TORCH)
2. Heredity
3. Use of folic acid and vit B6 in early pregnane}! n duces incidence
Nomenclature
a.
Cleft of primary palate - if it is found pn erior to foramen incissura
b.
Cleft of secondary palate - if posteric \
Clinical findings
There are several in combination.
a. In the nose, the features are
i.
Deviation of the columella and the tip of the nose
ii.
Flaring of alae nasi
iii.
Hypoplastic alar
iv.
Absent sill of nostril and nostril floor
v.
Deviated nasal septum
b. In the lip, they are
Cleft
Protruding prolabium in bilateral cleft.
Abnormal insertion of orbicularis oris
c. In the alveolus
i.
ii.
Forward displacement and outward rotation of the medial segment

A collapsed lateral segment.
d. In cleft palate.
i.Cleft in uvula, hard and soft palate
ii.
Abnormal insertion of palatal muscles.
Treatment
a. Cleft lip
- Flap repair at 3 months.
- Rule of 10 i.e. at 10 weeks, when Hb is 10%, and the weight.is 101b.
Method- Rotational advancement flap repair ( Millard)
b. Cleft palate
- Flap repair from 6 months upward.
Method
i. Langenbeck's repair]
ij
ii. Advancement flap
iii. Furlow
.hi
- There may be need to treat respiratory tract infecton prior.

- Also fitting of grommets for ear
207
Follow up
Revise any deformity when necessary
Nasoendoscopy as required
Speech therapy
b.
CRANIOSYNOSTOSES
Small head
I s when birth circumference of the head is <33cm
is due to premature fusion of sutures.
This leads to
Intracranial hypertension
Visual impairment
Neuropsychiatry disorder
The resulting shape of the head is due to compensatory over growth parallel to the abnormal fusion
Skull shape
Abnormally closed suture
Trigonocephaly
Triangular
Metopic
Scaphocephaly
Boat shaped
Sagittal
Turricephaly
Skull height
Basal
Oxycephaly
Pointed head
Coronal
Section I I
INFECTIONS
1.
2.
3.
Cancrus Oris
Gingivitis
Periapical abscess
1 CANCRUM ORIS
Definition
- I s an infective spreading gangrene
the oral cavity.
Predisposing conditions
Malnutrition
Poor oral hygiene
A debilitating disease e.g., m is
f
r
Aetiopathogenesis
- I t starts as a gingivitis
- The infective organisms are
i.
Bacteroides melaninogenicus
ii.
Borellia vincenti
iii.
Fusiform fusiformis
Stages
- There are two stages:
Pathologic process
Stage
Acute
Chronic
Treatment
Inflammation, Gangrene,
Demarcation
j Defects, Fibrosis,
j Contracture, Trismus
Fluid replacement
Correction of anaemia
Release of trismus, contractures
Closure of defects
ii. Gingivitis
iii. Periapical abscess
Section III
TUMOURS
1. Soft
tissue
Tissue involved
Skin
Parotid
Gingival
Tumour Type
SCCBCCMM
Mixed parotid tumour
Adenocarcinoma, Epulis
Excision and graft or flap

Superficial parotidectomy
Radical parotidectomy Excision and
curettage
2. Odontogenic tissue
(tissue capable of
forming teeth)
cyst
Enucleation
Ameloblatoma
3. Bony tissue
Fibrous dysplasia
Excision with margin

and bone graft
Excise after bone growth.
Wide excision Chemotherapy
(cyclophosphamide)
Wide excision
Osteosarcoma. Burkitt's
lyphoma
Treatment
Fibrosarcoma
209
Section
IV
TRAUMA
Aetiology
i.
ii.
iii.
iv.
v.
RTA
Sports
Burns
Human and animal bite
Gunshot
Clinical features
- Look for
Associated head injury
Airway compromise
Lacerations
Bone fractures
Investigations
1. Appropriate X-ray
2. CTscan
/
Complications
/. Wound infection
2. Nerve conduction
3. Ocular problems
4. Brain damage
5. CSF rhinorrhoea
Treatment
i.
ii.
iii.
iv.
v.
disorders
Airway maintenance
Treatreatment shock
Antitetanus
Antibiotics
Specific
a.
For soft tissue

6/0 nylon or prolene for skin.
Remove stitches in 5 days.
I f mucosa is involved stitch with catgut.
b.
Flap should be transferred if bone is exposed.
c.
For fractures use closed or internal fixation as necessary.
Section V
COSMETIC SURGERY
Procedure
Brow lift
Blepharoplasty
Face lift
(meloplasty)
Indication
Baggy eyelids
Excess facial folds particularly
nasolabial
Trichloroaceric acid Jessner's solution
Lip furrows
Dermabrasion
Shallow facial pits (scars) e.g.,

from pimples
Abdominoplasty
Liposuction
Scalp flap transfer
instrument
-Abnormal sagging frontal furrows
Chemical peel
Rhinoplasty
Special
Dermabrading machine
Nasal hump, saddle nose post

traumatic deformity
Baggy or drooping abdomen; f a t t y
apron
Fatty abdomen, upper thigh,
buttocks, f a t t y gynaecomastia
Baldness
Special suction apparatus

Tissue expander
(sometimes after tissue
expansion)
i^Â&tftB&&&&..<
HAND SURGERY
L
2.
&
<L
fr
Z_
&
Congenital Anomalies
Hand Infections
Hand Trauma
Nerve Injuries - Classification <5 Treatment
Replantation
Hand Tumour
Inflammatory / Oegenerative Disease
Microsurgery
r
211
Section
]
]
Classification of congenital anomalies (modified from Swanson)
Class
i. Arresi of development
Example
Absence of part of the limb e.g.
phocomelia where the hand is
attached to the trunk with absence
of the rest of the upper limb
Treatment
transfer in the case of an absent
thumb
ii. Failure of
differentiation of parts
Syndactyly- joined fingers

Camptodactyly- Flexion contracture
Clinodactyly - Sideway deviation
Separate fingers and graft raw

surfaces between the fingers in
syndactyly
iii. Duplication
Polydactyly
Triphalangism - 3 phalanges in
thumb, mirror hand
Excise extra digit
I iv. Overgrowth
Macrodactyly - large finger
Reduce bone and soft tissue
j v. Undergrowth
Hypoplastic finger
1
1
1
Pollicization or toe to hand
'
| vi. Constriction band

j syndrome
Amniotic band syndrome
Z plasties to release constriction
| vii. Generalised skeletal

! anomalies
Modelling deformityf fO\</<</vrC ^s^Jk'
N.B
Types of Syndactyly
a. i. Simple - i.e only soft tissue is bridging the finger together. There is no bony components in
the fusion
ii. Complex - there is bony component
b.
i. Complete - when it extends to the tip of fingers

ii. Incomplete - when it does not.
c.
Complicated Syndactyly - when there is a combination of clinodactyly or camptodactyly.

Treatment involves separating the fingers especially when it involves 2 fingers of different
length.
1
1
]
]
1
3
]
Causes of Hypoplastic Fingers

1. Neurofibroma
2. Arteriovenous malformation
Aetioloqicol factors
i. Genetic transmission
i i . Chromosomal aberration
i i i . Environmental causes
Radiation- N uclear, Therapeutic
Infection. TORCH syndromes
212
1
1

Drugs, thalidomide
iv. Unknown - constitutes a large group. I t is a subject of exclusion.
Section I I
HAND INFECTIONS
Aetiology
Bacteria and fungi enterihe hand through hair follicles, abrasions, hangnails, lacerations,
burns, avulsions etc.
Most hand infections tent to be localised'but when not adequately treated they get
generalised.
Examples of Organisms are
Bacterial
i.
staphylococcus aureus - Gram positive organisms particularly staph aureus
are mostly involved,
i.
Staphylococcus albus
ii.
Streptococci
v.
Gram -ve organisms
v.
Eikenella corrodens is frequently associated with human bite infections.
Fungi
Candida albicans
Virus
i. Herpes
,Bfi^
Clinical features and treatment:
V
i. Paronychia
,
Infection of eponychium i.e., nail foldjs is the most frequent. ~^>
I t can affect the germinal disc of nail bed
^
I t usually starts with a minor injury or simple hangnail.

Chronicity may be noticed in people whose hands constantly get wet e.g., launderers, and
dishwashers.
Candida albicans is cultured from most of these.
Treatment
o Treatment of the acute infection consists of frequent soaking for 15 minutes in
warm soapy water and lifting the nail fold to promote drainage under digital nerve
block with antibiotic cover.
\
Ai-
ii. Felon or distal pulp infection
I s a high lateral or volar longitudinal incision over the fluctuant area is required
I t can lead to destruction of the nail bed and even to osteomyelitis.
The pain is localized in the pulp.
213
i i i . Suppurative tenosynovitis
I s due usually to spread from adjacent infection.
I t presents with tenderness ++ over tendon and fixation of finger in flexion.

fowiavel sign V is pathognomonic
Treatment - Irrigation of the tendon
iv. Deep palmar space Infections

v. Infection of Space of Parona
Principles of management of hand infection

i. Rest, elevation and immobilisation
i i . Antibiotics after culture and sensitivity
i i i . Incision and drainage
iv. Tetanus prophylaxis
1
]
Section
III
H A N D TRAUMA
Aetiology
/.
2.
3.
4.
5.
Afeedle puncture,
Blade, knife cut, broken glass or edge of metal
Burn,
Boxing and allied sports
Machine parts e.g., fan belt, grinding mechanism, guillotine, hot press machine like those used in
Ct>n\\v\r\ wrappers
\k\r*r\r\r\ar*G
/ i n n those
+ \nr\e*o used
\\<*r>A in
in plastic
t- inc+ir- manufacturing
vnrtm i T / i r + i ir*\r\/~> industries,
iiriAi iO+ritf road
r*r\nA t+rna
n -fff+i c
i/* accidents,
nrr\Ac>Y\+C
r\Y\A
sealing
and
and
explosion.
Clinical features
The wound may be classified unto tidy and untidy.
Those caused by machines and gunshots are common and usually untidy. They therefore get
easily infected unless treated promptly.
The injury may involve nerves, tendons, intrinsic hand muscles as well as bone and joint.
Examination should therefore be towards detecting this.
Investigations
1. X-ray is useful to confirm bone fractures and joint malpositioning
Principles of treatment hand injury
1.
Early debridement - within the 6 hours of trauma
2.
Proper Irrigation
2U
]
]
T
"
]
_
1
'I
]
0
]
3.
4.
5.
Primary repairof damaged structures including soft tissue cover. Occasionally a delayed primary
closure is necessitated.
_.., ,.
Elevation and early mobilization based on one of the several regimens e.g., Kleinert traction to
prevent stiffness after tendon repair
Antitetanus and Antibiotic cover as well as Analgesics
Note, position for immobilization is very important. I t is in Salute posture of police hand.
Section IV
CLASSIFICATION OF AND TREATMENT OF NERVE INJURIES
Seddon
Neuropraxia
Axonotmesis
Neurotmesis
Sunderland
1 st degree
2 nd degree
3' d degree
Disrupted
Minimal axonal
Total axonal
Axon,
endoneurium
Neurotmesis
4 t h degree
Neurotmesis
5 t h degree
Axon,
endoneurium,
perineurium
All structures
Treatment
Conservative
Conservative
Explore and
repair if no
recovery
Repair
Prognosis
Complete days/months
Complete in months
Moderate reduction of
function
Repair
Mixed reduction
Moderate reduction of
functon
Methods of nerve repair

a. Direct repair:
Use of fine sutures, 8/10 - 10/0, particularly synthetic non absorbable. Healing is very slow
lmm/day. Immobilise the hand for 3 weeks.
Any form of repair may be performed by applying sutures to:
i. Epineurium (epineural repair)
i i . Perineurium (fascicular repair)
iii. Groups of fascicles (group fascicular repair)
'..
b. If direct repair is not possible

i. Nerve grafting e.g., using sural nerve
ii. Free vascularised nerve graft where the gap in large or surrounding tissue is scarred
iii. With caution
a. Mobilizing both nerve ends and devascularize and jeopardise nerve union
b. Transportation of nerve from original track
c. Slightly flexing the joint to expediate nerve end contact b and c are not
recommended
215
Section V
REPLANTATION
Introduction
I t is the restoration of continuity and the relative anatomical position of completely
Survival of replanted tissues have improved since the 1 s t reports in the 60s.
Tissues that have been successfully replanted include limbs, scalp, ear, nose.
Best results are obtained from clean, guillotine cut.

Contraindications to replantation are
1.
Concomitant life threatening injury
2.
Severe crushing of parts
3.
Prior surgery to amputated part precluding.replantation
4.
Inhibiting systemic illness
Relative
5.
6.
7.
8.
9.
Contraindications
Psycological disturbance
Avulsion injury
Single digit amputation
Prolonged warm ischaemia time
Extreme contamination
Care of amputated part

While awaiting replantation, do the following
i.
Wrap in saline moist gauze,
ii.
Put in polythene bag or container,
iii.
Then put container in mixture of ice and water
Steps to undertake, after induction of anesthaesia
i.
Bone shortening and fixation
ii.
Arterial repair
iii.
Venous anastomosis
iv.
Nerve and tendon repair
v.
Skin closure.
Section
VI
HAND TUMOURS
1.
Ganglion - is the commonest
2.
Haemangiomas
3.
Neurofibroma
4.
Exostoses
5.
6.
Giant cell tumour

Skin tumours like- SCO, BCC, MM (see chapter on surgical skin lesions).
7.
Soft tissue sarcomas -
Section VII
INFLAMMATORY /DEGENERATIVE DISEASE
Rheumatoid arthritis
i.
Swan neck deformity - fexion of proximal interphalangeal joint and extension of
interphalangeal joint. I t is due to rupture of tendons,
ii.
Boutonoises deformity - flexion of proximal interphalangeal joint hyper-extension of distal
interphalangeal joint.
fruptyren's contracture
I s due to shortening of the palmar fascia, subcutaneous nodules of palmar fascia and also formation
of cords deep to the skin.
: - . , . .
Sometimes, there could be history of trauma.
Treatment
Divide areas of fibrous bands by doing a fasciotomy but in extensive case, do a Fasciectomy.
Section VIII
MICROSURGERY
I t involves the use of a magnification provided by an operating microscope or a magnifying loupe in
performing surgery.
Indications
1.
Anastomosis of small vessels of about 1 -3mm calibers as done in the following situations
Replantation of amputated digits
Revascularisation of near complete amputated
in.
Free flap transfer
Nerve anastomosis using interfascicular repair.
217
J
1
I
OSSIFICATION <& PRINCIPLE OF MANAGEMENT OR FRACTURE
Definition
Fracture is any break or loss of continuity of bone
I n children, it may just be a bend ( called fireenstick fracture)
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Structure of Bone
I s made up of organic and inorganic components
a. Organic- is purely collagen. I t is more in children, thus make them to have
greenstick fracture.
b. Inorganic - is calcium, it gives strength to the bone
These 2 components vary in different individual according to their age.

Collagen is protein portion and it forms the framework for bone formation.
Periosteum : is the bone covering. I t is extremely thin in adults but thick during the younger age.
Types of Bone
a. Cortical bone - I s the part in between the ends of bone, it is hard.
b. Cancellous bone - This is soft, resilience and well vascularised
Mechanism of Fracture
1. Fracture arising in a normal healthy bone - This requires a very strong impact.
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2. Stress Fracture - This arises in healthy bone, repeated trauma or forces is required. I t is
common in metatarsals. For 2nd metatarsal, it is called March facture.
3. Pathological fracture - This fracture arising from a diseased bone. I t requires minimum force to
occur. E.g
Osteomyelitis
Paget disease
i.
Rnno /-vc+c
ii.
Bone
cysts
v.
Bone tumour
v.
Bone infection
vi.
Osteoporosis
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Characteristics of Fractures
This determines the management line of a fracture
a.
Open or Closed
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Open
it means the fracture communicates with the exterior or epithelial lining e.g
o
fracture of mandible communicating with the mouth
o
fracture of pelvis into urethra, vagina or rectum
I t is likely to be infected or contaminated. Note, wounds after
is regarded to be infected.
6 hours
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Closed
- There is no communication with the exterior or epithelial lining.
- Potentially, it is non-lethal. Plaster of Paris can just be applied.
b. Displacement or Non-displacment
nn
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Management varies with age. I n a child, upto 70% o f f ended can re-align itself while adults do
have the ability of remodeling. > 50% off endedness must be religned.
c.
Angulation of fracture
May be lateral or medial as shown below
VN
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V\
The point of direction is important because of the surrounding structures.

Medial angulation in tibia can easily become open.
d.
Fracture line orientation

Transverse
Oblique
Spiral oblique
e. Components of the fracture - Communited & Non-communited

i.
Communited - when fractures break into pieces or fragments, i.e Has > 2
components,
ii.
Non-communited - is just a fracture without breakage into pieces or
fragments.
Principles of Fracture Management
I t can be divided into
a.
Non-operative
i.
Plaster immobilization
ii.
Skin traction - to establish a confer traction
iii.
b.
Skeletal traction - this is used for muscular people. A pin is passed.
Operative
i.
Open reduction and Internal Fixation (ORIF)
ii.
Intramedullary nailing
Principles of
i.
ii.
iii.
iv.
v.
vi.
vii.
viii.
ix.
x.
Treatment of Open Fracture

Admit the patient
,
Sketch the wound or picture it
Soak gauze inside iodide and place it on the wound and bandage it.
Give parenteral antibiotics - to mop up organisms that have entered the circulation.
Tetanu prophylxis
Parenteral analgesia - preferably narcotic e.g pethidine except if contraindicated
Reduce the bone and allow the bone to be covered by tissue
Splint the fracture
Def initve treatment
o
Extensive debridement
o
Stabilize the bone.
Rehabilitation
Note
i.
ii.
iii.
iv.
Prohpylaxis
Analgesics
Splinting
Debridement
COMMON FRACTURES
In Children
1. Fractures of distal radius
I t is usually Sreenstick fracture which occurs because of of high amount of organic &
little inorganic components. This makes the bones NOT to be brittle, it only bends.
They also have strong/thick periosteum
2.
Buckle fracture
- e.g Fracture of distal radius
3. Supracondylar fracture of the humerus

Occurs when a child falls on outstretched hands
. The reaction depends on the weight A age of the child
There is a risk of damage to nerve & brachila artery
In Adults
1. Co lie's fracture
Found in the elderly
220
Is the commonest fracture of the upper limb

Is due to osteoporosis
Results in Dinner fork fracture r
COMPLICATIONS OF FRACTURES <& DISLOCATION

Introduction
Are grouped into general and specific
a. General
1.
2.
3.
4.
5.
6.
Complications
Shock
*
Crush syndrome
Deep venous thrombosis & Pulmonary thromboembolism
Tetanus
Fat embolism
Delirium tremens
Local / Specific complications

1. Skin complications
2. Muscle
3. Tendon
4. Nerve "
"
5. Arterial
6. Compartment syndrome
7. Volksman ischaemic contracture
8. Bone complications
9. Joint complications
GENERAL COMPLICATIONS
1. Shock
Resulting from hypovolaemia. The bleeding is usually hidden and may lead to acute renal
failure. About 3 - 4L may be lost in pelvic fracture and 1 - 1.5L in femoral shaft fracture.
2. Crush syndrome
I t results from crush injuries. There is damage to muscle which leads to myoglobinuria ( dary
coloured urine) and eventually acute renal failure. To prevent, give adequate fluid.
3. Venous thrombosis and Pulmonary thromboembolism :
- The thrombosis is due to release of thromboplastin which stimulates the coagulopathy.
Therefore note, venous thrombosis is not due to prolonged bed rest.
- Give DVT prophylaxis - Low molecular weight heparin (Clexane) is used here.
- Also do PT, PTTK to monitor it.
4.
Tetanus
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5. FAT EMBOLISM
Introduction
-Usually occurs in multiple long fracture with intramedullary nailing.
- 9 8 % manifest within 48 hours and 100% within 72 hours.
- W i t h i n 12 hours, 25% show symptoms :
Restlessness
i.
Incoherence
ii.
Disorientation
v.
Tachycardia
v.
Tachypnoea
vi.
Petechial haemorrhages - seen inlight skin people of front and
back.
Cerebral hypoxia
VII.
Diagnosis
o
o
o
o
o
Differential
i.
ii.
Deterioration in cerebral function

ABG shows severe hypoxia ( P02 < 60mmHg) and hypercapnia ( PC02 is very
high)
Examination of clot blood - shows f a t globules
Urine - f a t globules are also seen
ECS - shows right ventricular strain.
Diagnosis
Adult respiratory distress syndrome
Pulmonary thromboembolism
ii.
v.
v.
vi.
vii.
Prevention
i.
ii.
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Treatment
i.
]
]
Transfer to Intensive care unit or High dependence unit (HDU)

Correct anaemia
Assisted ventilation
Heparinisation - to cause lipolysis
Fluid resuscitation
Dextran - to improve capillary flow
Clofibrate - to reduce plasma lipids
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Gentle fracture manipulation

Early stabilization
6. DELIRIUM TREMENS
I s seen in alcoholics. I t is a withdrawal symptom
Treatment
i.
Careful nursing
ii.
Rehydration
iii.
Pian relief
iv.
Sedation
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v.
I f severe, give haloperidol 10 -60mg/day. First dose is I M 2 -lOmg if

necessary.
B. LOCAL COMPLICATIONS
1. Skin complications
i.
Fracture blisters
I s common around ankles.
Treatment involves puncturing it with sterile needle and dress with sofratulle.
Any patient with fracture blisters should not have ORIF until the blister is
healed.
ii.
Plaster sores - is due to undue pressure from plaster
iii.
Open fractures
Soft tissue necrosis is common with ankle dislocations
2. Muscle complications
i.
Torn muscle fibres
ii.
Disuse atrophy
Treatment
o
Excision of the muscle
o
Start exercise early
3. Tendon omplications
i.
Torn tendon - To recognize it, tell the patient to do active movement of the joint, he
would be unable to do so.
ii.
Avulsion fracture - Tendon + tiny bone attached to it are sheared o f f e.g

o
Olecranon fracture
o
Patella fracture
Treatment K wire fixation
iii.
Late rupture e.g extensor pollicis longus.

I t is commonly due to Colle's fracture
I t occurs after 6 - 8 hours of injury.
Mechanism:
I s due to haematoma which lifts up the tendon and cuts o f f its blood supply (
Vinculo longus and brevis)
Treatment: Replace with extensor longus.
iv. Tendinitis - inflammation around tendon.

4. Nerve complications
i.
Nerve injury - Neuropraxia is common in closed fracture injury e.g
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ii.
Humeral shaft fracture - is the commonest. I t affects the radial nerve

especially in the mid shaft.
Nerve compression - is due to callous formation
Arterial complications
I s different from Compartment syndrome
I t means there is arterial inury at the time of injury.
Clinical Features
i.
Large amount of blood loss if it is open injury
ii.
Early loss of distal pulse or may just be weak,
iii.
Pal lour
iv.
Cold extremities
Compartment syndrome
Definition
I s a condition in which there is a build up of pressure within closed or
unyielding osseo-facial compartment sufficient to reduce capillary blood
perfusion.
I t occurs when the pressure is> 40mmHg_3
I t can occur without fracture
I t is commoner in lower limb, commoner in tibia than thigh.
(Note, the compartments in .leg are
a. Anterior
b. Lateral
c. Posterior - has superficial & deep
I t is rare in arm
I t can occur without fracture
Clinical
Feature
i.
Pain - is the f i r s t and most constant symptom. I t persists despite splinting. I t
is unrelieved by position and unresponsive to narcotic agents. I t is out of
proportion to what is expected
i.
Swelling, i t is hard on examination. I t is tense and shiny
ii.
Passive flexion of the digits cause severe pain
v.
Tenderness
v.
Pulselessness - is a late sign.
I n summary, the 5Ps are
o
Pain
o
Parasthesia
o
Paralysis
o
Pulselessness
o
Pallor
Diagnosis
Measurement of pressure using catheter
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i. Arterial injury
ii. Neuropraxia
iii. Fracture
iv. Deep vein thrombosis
Complications
i.
ii.
iii.
iv.
v.
Muscle ischaemia
Nerve ischaemia
Volkmann ischaemic contracture
Acute renal failure
Metabolic - hyperkalemia
Treatment
Is surgical. The procedure is called Open fasciotomy. I f it is leg, it is cut on
both media and lateral sides.
7. Volkmann's Ischaemic contracture
I t usually the result of missed compartment syndrome.
The flexor muscle are affected
Patient develops severe contracture of digit.
Treatment
Is difficult to treat
8. Bone complications
^
i.
Avascular necrosis e.g Talus, Scaphoid, Fracture head of femur
Mecahnism: is due to the end arteries
ii.
Delayed union - said t o occur when a f r a c t u r e is united a t expected t i m e t h a t union should

occur
iii.
Non-union : Here, the bones would unite except by surgical intervation.

Types
i.
Atrophic
There is no callous formation. The bone ends become rounded.
I t requires bone graft.
ii.
Hypertrophic
I s described as elephant foot.
Treatment: Internal fixation.
iv.
Mal-union including synostosis

Treatment - Corrective Osteotomy
v.
Growth disturbance - is seen in children e.g Fracture femur ( Note, it grows faster than
the normal femur)
Treatment: Allow 1 - 2cm overriding to compensate for the overgrowth.
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vi.
Infection - Osteomyelitis ( usually caused by Staph, aureus)
9. Joint complications
i.
ii.
iii.
iv.
Joint instability - is commonest with shoulder joint

Joint stiffness - is due to
o
Capsule thichening
o
Fibrosis tissue formation in joint
Myositis ossificans - is common with elbow dislocation
Treatment
o
Rest
o
Indomethacin
o
Excision of calcified mass
Sudeck's atrophy / Reflex sympathetic
I s common in hand and feet
Associated with soft tissue
Occurs 6 - 10th weeks after
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dystrophy
fractures.
injury
injury
Mechansim is due to abnormal response to trauma at the site

Clinical Features
Severe pain
i.
Swelling
ii.
Warmth
v.
Sweating
Diagnosis
X-ray - shows diffuse disuse atrophy & osteopaenia of bone
Treatment
iii.
Analgesic
Suanethidine block
Physiotherapy
v. Secondary osteoarthritis - common with ankles -
vi. Unrelieved dislocation.

For Comparison
Misconceptions
i.
Fractures do not involve bone alone, but with tissue also
ii.
Fracture causes not only head problem, but systemic too.
Classification of complications of fractures
a. General
1. Hypovolaemic /haemorrhaqic shock - occurs in multiple long bone fracture & pelvic fracture
Treatment
i.
Set Intravenous line with wide bore cannula [ 16(5 or 14G (this is white) ] in the
antecubital vein.
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3
0
]
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II.
Before line is set up, withdraw 20mls of blood for

o
Blood group & crossmatch
o
Electrolytes A urea
III.
Monitor vital signs

o
Pulse
o
Blood pressure
o
Urine output - the normal should be
A d u l t : 3 - 5 /50m/hour
Children : 1 - 2ml/kg/hour
Central
venous pressure
o
Pulmonary wedge pressure - using Shawn ganze catheter
o
..:
Crush syndrome
I t causes the release of myoglobin which precipitates in kidneys as crystals,
resulting into acute renal failure with passage of coca-colour urine.
Treatment
ii.
iii.
Early recognition
Give intravenous fluids
Alkalinisation of urine
using Ringer's lactate
3. Fat embolism
I t usually occurs in multiple long bone fracture.
The f a t released into circulation gets deposited at lungs resulting into
respiratory insufficiency.
i.
I t usually manifests within 72hours. 70 - 80% presents within 24 - 48hours
ii.
I t j s rare before 12 hours and beyond
iii.
Restlessness
iv.
Tachypnoea
v.
Petechial haemorrhage in anterior chest wall
Diagnosis
High index of suspicion is required.
I s made with ventilation perfusion
Investigation
Arterial blood gases : shows
Reduced oxygen tension, < 60mmHg

Increased PC02
Treatment
Correct anaemia
Ventilatory support
Heparin - to stimulate lipolysis
4. beep vein thrombosis
Introduction
227
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- Following trauma, there is increased coagulability of blood.

- This depends on site e.g calf f
o
Pain
o
Swelling
o
Homan's slgrTJ tenderness on palplation of calf
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Investigation
,
1.
Deep venogram - using a tornique
bisadvantape
i. Difficulty in finding vein if there is oedema
ii. The contrast is irritative
2.
Doppler Ultrasound - to detect clot. I t is not invasive and has high

yield for pelvic veins DVT, but low yield for calf veins.
3. Radioactive I - 121 + Fibrinogen - Has high yield f o r calf DVT but low
for pelic DVT.
Treatment
i. Restriction to bed - to prevent
dislodgement
ii. Heparin pump - giving 24,000 i.u
iii. Warfarin
Day 1 - lOmg
Day 2 - lOmg
Use INR-standardized value of PT.
]
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Maintain between 2 - 2.5^1
I f INR is > 4, give warfarin
I f patient is high risk, warfarin is used for 6

months, low risk is for 3 months
^l
Maintenance dose is 2.5 -5mg
Prevention
i. Low molecular weight (LMW) heparin -
]
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is obtained by fractionalization by enzymatic means.

-
I t causes minimal disruption of clotting system.

I t is given subcutaneously ( on anterior abdominal wall)
1
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E.g Enoxaprim (Clexnae @), at 40 i.u daily
Gas gangrene
I s infection with Clostridium welchii.
The patient toxaemic (septic)
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FRACTURES <& DISLOCATION OF THE LOWER LIMBS

Content
i.
ii.
v.
v.
Hip Dislocation
Fracture of the Neck of the Femur
Fracture of the Femur
Fracture of Tibia
Ankle fracture
HIP DISLOCATION
Cause
Is mostly due to dashboard injuries
Types
a. Posterior dislocation - constitutes about 90%
b. Anterior
"
tt
c. Central
( referred to as Stove in pelvis)
Diagnosis
i.
ii.
iii.
iv.
Severe pain
Hip is flexed, adducted and internally rotated
Radiograph
Exclude sciatic nerve involvement - ask the patient to move the great toe.
Treatment
a. Closed reduction - is done under general anaesthesia and muscle relaxation using suxamethoinum
b. Open reduction - is indicated when closed reduction fails.
Complications
1. Irreducible dislocation
2. Scaitic nerve injury
3. Avascular necrosis - the longer the duration between the dislocation and reduction, the greater
the risk.
4. Secondary osteoarthritis - due to a known cause
5. Recurrent dislocations
6. Myosistis ossificans - it usually involves the hip and elbow dislocation.
Treatment
Avoid excessive use of exercise / Rest
Use indomethacin
7. Late undiagnosed dislocation
1. Fracture of femur - may also occur simulatneously
FRACTURE OF THE NECK OF FEMUR
Incidence
o
o
Below 60 years, it is commoner in males and is due to trauma.

Above 60 years, it is commoner in females as a result of osteoprosis & osteomalacia
Depends on the level of fracture
Classification
a.
Intracapsular - Note, the capsule covers the anterior part of the neck completely
i.
Subcapsular
ii.
Transcervical
b. Extracapsular - I s prone to myositis ossificans, but this is not due to poor blood supply.
i.
Basal
ii.
Pertrochanteric
iii.
Subtrochanteric
Clinical Features
i.
Inability to bear weight - occur immediately or a few days after a fall
ii.
Pain in the hip or groin
iii.
Shortened and externally rotated hip
iv.
On examination, there is tenderness and the patient is unable to raise the leg.
v.
X-ray:
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Garden's Classification
o
Applies only to the intracapsular fracture
Grades
I
II
Description
o Incomplete fracture of the cortex
o ( I n f e r i o r cortex is not broken)
o No displacement
o Fracture line is complete, but no displacement
III
o Complete fracture line with slight displacement
IV
o Complete fracture & complete displacement i.e no contact at all
Type I I I & I V have 90 - 95% possibility of avascular necrosis.
Because of intercurrent disease processes
1
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0
1
1
Investigation
Treatment
i.
ii.
iii.
Preliminary skin traction

Physiotherapy
Antiobiotics
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]
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iv.
Analgesics
v.
Surgical treatment
a.
Intracapsular fracture
i. Young patient
Garden 1 & 2: Fixation with 2 or 3 screws
Garden 3 <St 4: - Reduction (to convert it to 1 or 2)
. - Fixation with 2 or 3 screw
- There is a risk of failure if avascular necrosis
should occur. ( Explain this to the patient)
ii. Middle age

Garden 1 d 2: Fixation with 2 or 3 screws
Garden 3 & 4: Total hip replacement

iii. Elderly
Garden 1-4:
b.
Hemiarthroplasty - ( t h e y are not so active)
Extracapsular fracture
o
Surgical fixation with hip sliding screw ( Dynamic hip screw) at angle 135'o
Complications of Surgery
1. Avascular necrosis
2. Non-union
3. Screw penetration into joints
4. Mal-union
5. Dislocation - in Total Hip Replacement ( THR).
FRACTURE OF FEMUR
Aetiology
I t almost always result from high energy injury e.g
Road t r a f f i c accident
Fall from height
iii.
Crush Injury
iv.
Pathological fracture e.g due to breast or kidney cancers
Levels of Fracture
Upper third
Middle third
ii.
Lower third
iii.
iv.
Supracondylar
v.
Intercondylar
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Blood loss
About 0.5 - 1 litre may be lost into the thigh (as fracture haematoma)
Diagnosis
ii.
iii.
iv.
Inability to bear weight - the patient could not get up following the injury.
Abnormal mobility of the site
Pain at the site
Shortened and externally rotated leg
Treatment
ii.
iii.
iv.
ABC of resuscitation
Trauma care
Conservative
Surgical fixation
o
I n advanced countrie, all fractures of femur are repaired surgically with closed
intramedullary nailing ( i n adults). I n children, the treatment is conservative and it
depends on the age.
For Adults
Upper and Middle Third
Lower Third
Supracondylar
For Children
Age in years
<2
2 -10
10-15
o Intramedullary nail fixation

o
Kuntcher nail is no longer used in developed
countries, but it is still used here.
o
There is limitation of rotation & vertical force.
o Locked intramedullary nail
o
Plates & Screws
- 95% angle blade plate
i
i
o Sallow's traction
o Hip spiker
Skin traction and Thomas
- Skeletal traction
""
Indications for Internal Fixation

i.
Associated head injury
ii.
I n the absence of satisfactory region, intramedullary nailing is not used so
that epiphyses would not be damaged and thus preventing normal bone growth,
use plate and screws.
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FRACTURE OF TIBIA
Introduction
o
I s the commonest open fracture because of the subcutaneous location of tibia.
Aetiology
1. Torsional stress e.g sporting injuries, domestic accidents
2. Violence transmitted through the feet e.g fall from height, RTA
3. Direct blows e.g RTA
/
'
Clinical Feature
i.
History of trauma
ii.
Pain
iii.
Swelling
iv.
Deformity
v.
Tenderness along the subcutaneous surface of tibia.
vi.
Examine for
o
Laceration
o
o
Neurovascular defect/injury
Diagnosis
Plain radiograph
Treatment
a. Conservative
Children
o Manipulation under anaesthesia
o Above knee POP
Adults
o
o
o
o
b. Operative
i.
ii.
Manipulation under anaesthesia

Above knee POP
Convert to Samiento POP after 3 weeks
Below knee
Intramedullary nailing
Plates <& Screws
iii.
Application of External Fixator
ANKLE FRACTURE
Introduction
Synovia joint ( Diarhrosis)
Saddle ( Seller joint) - Biaxial surfaces are concavo convex, compared with Mortise & Tenon
joints of wood workers
,S\
:1
Aetiology
>
1. Torsional injuries e.g Sports injuries, domestic accidents
2. Compresseion injuries e.g Fall from heigt, Rapid deceleration ( car accident)
Clossfication
1
Pott's Fracture - ankle fracture

- There are 3 degrees
a. First degree : Fracture involving 1 malleolus
b. Secondary degree : " involving 2 malleoli
c. Third degree :
" involving 3 malleoli
Lange Hansen
Supination/Lateral rotation - is the 'commonest
Pronation/ above
ii.
Pronatio/ Lateral
iii.
Suppination / Adduction
iv.
Suppination/ Dorsif lexion
v.
i
1
1
1
1
1
1
1
1
Webers
A
B
C
Fracture of lateral malleolus below the syndesmosis

Fracture within the syndesmosis
Fracture above the syndesmosis
A l : Just below the lateral malleoli

B2 : Involving medial malleolus
C2 : Involving
Clinical Feature
i.
ii.
v.
v.
History of trauma
Pain
Swelling
Tenderness over the left and medial malleoli or collateral ligament.
Deformity
Diagnosis
Plain radiograph of the ankle
Principle of treatment
- Stability of the ankle is based on the lateral malleoli
Treatment
a. I f Undisplaced : Below knee POP
b. I f Displaced :
i.
MUA + Below knee POP
i
ii.
Internal Fixation using Plates & Screws on the lateral malleolus/fibula, Kirsher wire
on the medial malleolus.
234
1
1
iii.
ORIF - Indicated if there is presence of diastasis ( wide separation of tibia and

fibula.
FRACTURES <& DISLOCATION OF THE UPPER LIMB

Content
-
i.
ii.
iii.
iv.
v.
vi.
vii.
Clavicular fracture
Shoulder dislocation
Humeral Fractures
Supracondylar fracture
Elbow Dislocation
Forearm Fractures
Carpal &. Hand Injuries
CLAVICULAR FRACTURE
Introduction
The incidence is 10 - 16% of all fractures
I t most frequrnlty seen in childhood
I s twice commoner in males
80% occurs in the middle third because muscles are only attached to the lateral and medial ends.
Mechanism of injury
i.
Fall on shoulder
ii.
Breech delivery
iii.
Motor bike accidents
.
;
Associated Injuries
i.
First rib fracture - may cause rupture of the subclavian vessels,
ii.
Scapula fracture
iii.
Pneumothorax
iv.
Subclavian vessel injury
v.
Brachial plexus injury - affects the medial cord
'
Clinical Features
i.
Pain - caused by the nerves in the periosteum
ii.
Deformity
iii.
Swelling
iv.
Loss of function
~~ Treatment
I f it is not severe, use a sling or triangular bandage.
Figure 8 bandage is used to be used for severe fracture, but it is no longer in use.
For babies, apply no bandage.
235
Indications For Surgery i.e ORIF

1. Open fractures
2. Secondary injury
3. Skin laceration
4. Severe displacement
SHOULDER DISLOCATION
Introduction
Shoulder joint is most ununstable joint in the body
I t accounts f o r 50% of all dislocation
Stability of Shoulder Joint
i.
Glenoid labrum - it articulates with l / 4 t h of the head of humerus
ii.
Glenohumeral ligament
iii.
Rotator cuff muscles - These are
a.
Supraspinal
b.
Infraspinalis
c.
Subscapulars
d.
Tere minor
iv.
Long head of biceps - playa a role
Classification
a. Based on direction
i.
Anterior
- is the commonest type.
- The mechanism involves slight abduction and external rotation.
- Axillary view of X-ray shows "empty sulcus sign "
ii.
iii.
iv.
Posterior
- Is more painful
- The upper limb is adducted and internally rotated
- There is posterior prominence at the back
- Prominent coracoid process is suggestive of posterior dislocation
Inferior
Superior
b.
Based on cause
i.
Traumatic
ii.
Atraumatic
c.
Based on time of occurrence

i.
Acute
ii.
Chronic
III.
Recurrent - also called Habitual dislocation. ( e.g seeen in someone called Alewi who
was using it to collect money from people). Note, this type is not supposed to be
operated upon.
History
History of fall
Road t r a f f i c accident
History of epilepsy
Pain
Deformity
Loss of function ( Pseudoparalysis)
i.
ii.
v.
v.
vi.
Investigation
Axillary or Lateral thoracic view.
Note, Anteroposterior view may appear normal
Treatment
i.
ii.
v.
v.
Rest the patient

Analgesics
Consult to Orthopaedic surgeon
Manipulation under anaesthesia (MUA)
Posterior dislocation usually needs open reduction.
Complications
1. Recurrence - is due to
>
.
>
Anterior glenoid erosion
Capsular lesions
in.
Bankarts lesion - is detachment of glenoid labrum which actually deepens the socket
iv.
Rotator damage
2. Vascular injury - to axiallry vessels
'
3. Neural injury - to Brachial plexus
N.B
Luxatic eurate - inferior dislocatures
HUMERAL FRACTURES
a.
Fracture of mid-shaft affects radial nerve which gives most its supplies early in the course, thus
it can be managed conservative.
- U-slab, Full arm cast
b.
Fracture of surgical neck of humerus causes damage to the axillary nerves and vessels, thereby
causing avascular necrosis.
SUPRACONDYLAR FRACTURE
Introduction
Occurs in the f i r s t decade
Is twice commoner in male
I t accouts f o r 15 - 35% of fractures
]
]
]
Mechan sm
Fall on outstretched arm
Flexed elbow
i.
Types
1.
Flexion
- accounts for 2 - 5%
Mechanism: Fall on a flexed elbow, the distal segment moves
1
1
1
1
1
1
1
2.
Extension
Mechanism Fallon outstretched arm, the distal segment moves upwards and
backwards
GARTLAND Classification
Type
I
II
III
Description
o Break, but no displacement
o Periosteum is intact
o There are swelling &. "fat pad sign"
o There is slight contact between the 2 bones with angulation
o
Total displacement i.e no contact at all
Clinical Features
Pain
Swelling
Deformity
Loss of function
Radial pulse - because of the risk of damaging brachial vessels
i.
Assess for medial & radial nerve injury
ii.
Examine the neuromuscular status
238
1
1
Treatment
Put the patient to sleep
Reduce the fracture under image intensif ier
Flex the elbow as much as radial pulse is f e l t
Options are
a. Immobilisation with POP cast - the elbow should be > 90
b. Percutaneous K wire - is used if the fracture in unstable
c. ORIF
Indications for ORIF
o
Type I I I
o
Failed close reduction
o
Neurologic deficit
o
Vascular insufficiency
i.
ii.
v.
Complications
1. Cubitus varus / Sun's stock - is the most common mal -union
Treatment
- Corrective supracondylar valgus osteotomy
2. Loss of motion
3. Hyperextension
4. Acute compartment syndrome - there is severe on dorsif lexion
5. Nerve injury - The order of occurrence is as follows
Radial nerve - commonest it is the closest nerve to the elbow

Median nerve injury - 2nd
Ulnar nerve injury - 3 rd

6. Vascular injury - Brachial vessels
7. Volkmann Iscahemic contracture - is the most serious complication. The pathogensis is depicted
below
Ischaemia D NecrosisD Fibrosis
8.
Avascular necrosis of trochlea
9.
Myositis ossificans
10. Pin site infection
ELBOW DISLOCATION
Classification
a. Anterior
b. Posterior - May be lateral or medial
Mechanism
Fall on Flexed elbow or Outstretched arm
Differential
i.
I t may be confused with supracondylar fracture which forms triangular pattern.
239
Clinical Feature
I n dislocated elbow, there is loss of triangular pattern.
Olecranon process is more proximal
Beware of nerve entrapment e.g of median nerve and at times ulnar nerve.
Treatment
Posterior reduction
FOREARM FRACTURES
galleazi Fracture
I s fracture of distal radius with dislocation distal radioulnar joint
Monteggia Fracture
I s fracture of proximal ulna with dislocation of radial head i.e the proximal end.
Midshaft Fracture in Children
There is damage to the radial nerve
Treatment
- Manipulation under anaesthesia
- Immobilisation with POP
COLLE'S FRACTURE
Definition
I s fracture of distal (linch or 2.5cm) radius
I t usually occurs in elderly and in osteoporotic bone
I t is also referred to as Dinner Fork Deformity
Clinical Feature
i.
Problem with climbing siaircase
ii.
The typical features are
o
Dorsal angulation
o
Dorsal displacement
o
Radial angulation
o
Radial shortening
iii.
I t may be accompanied by fracture of ulnar &. styloid process
Treatment
Manipulation under anaesthesia
Below elbow plaster
ii.
SMITH FRACTURE
Definition
Compared with Colle's fracture
There is volar (anterior) angulation or displacement
I t is a reversed Colle's fracture
r
r
Treatment
i.
ii.
Manipulation under anaesthesia and

Above elbow plaster
Complications
a. Acute
i.
ii.
v.
r
r
b.
Acute Carpal tunnel syndrome - causes damage to median nerve

Tendon damage
Carpal injury - There is injury to carpal bone.
Late
i.
ii.
v.
v.
vi.
S t i f f hand
Shoulder hand syndrome - is common in the elderly
Mal-union
Non-uinon
'
,
Rupture of extensor pollicis longus
Sudeck's atrophy - is a reflex sympathetic dystrophy. The X-ray reveals osteopaenic
features
Clinical Features
i.
Pain
ii.
Stiffness
iii.
Loss of hair
. .
,
iv.
Blueness
CARPAL /HAND INJURIES

1. Scaphoid fracture
Pain is localized in the anatomical snuff box
Sometime, the break does not show on x-ray until after 2 weeks
I t is notorious i.e does not heal. I t undergoes avascular necrosis.
Like Colle's fracture but incorporates the thumb
Scaphoid receives its blood supply from distal
Treatment
- Scaphoid plaster
241
2. Lunate Fracture
Avascular necrosis of Lunate bone is called Kienbock's disease
I t can damage the median nerve
3. Boxer's injury
Is a common injury
I s injury or fracture of neck or head of 5 th metacarpal.

Treatment
Back slab ( 2 fingers strapping)
POP f o r 3 weeks
PELVIC FRACTURES
Introduction
I t is the most common life threatening fracture because of the major vessels in the pelvis.
Also, because pelvis is hidden, it can contain 2/3 r d of the whole blood.
Anatomy
o
o
o
o
Right hemipelvis
Left hemipelvis
Sacrum
Pubic bone
Stability of the Pelvis

.
I s posteriorly as anterior sacroiliac joint is very slimsy.
The main structures involved in stability are listed below
Posterior sacroiliac ligament - prevents rotational instability
i.
Sacrotuberous ligament - prevents vertical shearing
ii.
Sacrospinous ligament - prevents torsion and rotational movement,
v.
Pelvic floor - contains the viscera
v.
Capsule of the Sacroiliac joint
vi.
Sacroiliac ligament interossei
Prognosis
10% of patients usually die .
Out of this, 4% is due to haemorrhage. I t is usually retroperitoneal i.e not seen. And this is the
reason for doing CT scan in this group of patients. Laparotomy is also not done for associated
abdominal injury is because the negative pressure stopping the haemorrge. You use conservative
management.
The mortality increases exponentially with other viscera damage (i.e associated injuries) e.g
i.
Colonic injury
ii.
Urethral injury
iii.
Damage to the pelvic floor
242
iv.
v.
Damage to nerves
Avulsion to sacral plexus
Classification
I s based on prognosis and instability
I t is given by MARVIN TILE (1988)
No disruption of the pelvic ring

Pelvic joints are stable in both horizontal & vertical planes
Mecahnism:
i.
Anteroposterior injury
ii.
Avulsion injury of iliac spines or ischial tuberosities
Disruption in the horizontal stability of pelvis
But vertical plane is stable
Mechanism
i.
Lateral compression injury
- Is called Closed Block Injury
ii.
Anteroposterior force e.g fall on buttock
- diastasis of pubic symphysis
- the gap is > 2cm
- I t is also called Open Book Injury
Mechanism: Vertical shear e.q Fall from heiqht on lea. The fracture
line is through the foraminae
,
Complications
1. Nerve injuries - examine the nerves for every type C fracture.
- You check for sensation and muscular movement.
2. Visceral damage - is common
Investigation
1. Full blood count
2. Group and crossmatch
3. X-rays
i.
Pelvic inlet - Type A injury
ii.
Pelvic outlet - Vertical displacement and rotation
iii.
Anteroposterior
4. CT scan
Treatment
Type A : ORIF - using plates
Type B : I f it is not displaced, there is no need for operative treatment, but offer bed rest.
Type C :
Conservative
Definitve
243
a.
External fixator + Skeletal traction - to reduce proximal shift for hemipelvis.

The weight used is 10% of body weight.
b. ORIF - to prevent mal-union & non-union. Also helps to restore the stability.
Management
1. Resuscitation
.
? ,
o
ABC or resuscitation
Fluid replacement using 2 widebore cannulae for I V lines
Other techniques are
Pneumatic antishock garment
Embolization of pelvic vessels
iii.
Surgery
For Open book injury, stabilize the pelvis. *

2.
Definitive
Pre-operative
i.
CT scan - to define the pattern
ii.
Delay the operation for about 5 - 7 days to allow patient's general condition to
improve.
Indications For OIRF
a.
b.
Anterior
.To
i.
ii.
v.
improve pelvic stability

I n association with laparotomy
Tilt fracture ( bone protrusion into pelvis)
Associated acetabular fracture
Poster or
i.
ii.
Inadequate reduction
Presence of open posterioir wound
Associated acetabular fracture
Management of Complications
1.
Haemorrhage
i.
ii.
iii.
iv.
v.
Fluid replacement/ blood transfusion

Monitoring of
vital signs
Urinary output
Central venous pressure
Application of external fixator - to reduce the pelvic volume and consequently the
caesation of pelvic haemorrhage
Arteriography & Embolisation
Laparotomy - is rarely done
2. Lower urinary tract injury

*
Diagnosis - is made by seeing at the meatus of haematuria
244
Investigation
i.Retrograde urethrography
ii.
Cystoscopy
3. Neurologic injury
- Sciatic nerve is most frequently damaged
4. Intraabdominal visceral injury e.g to uterus, vagina, rectum
Investigation - Diagnostic peritoneal Lavage
5. Pulmonary complications e.g
i.
Pulmonary embolism
ii.
Prevention
a. Early embolisation
b. Anticoagulant mobilisation
6.
Arthritis
Treatment
i. Osteotomy
i.
Fusion
ii.
Arthroplasty
INFECTIONS OF BONES <& JOINTS

Content
Acute Osteomyelitis
Chronic osteomyelitis
Chronic Osteomyelitis of Insiduous Onset
Acute Suppurative/Septic Arthritis
Brodies Abscess
ACUTE OSTEOMYELITIS
Aetiology
1. Staphylococcus aureus - is the commonest organism in all age groups and conditions
2. Streptococcus - is seen in youg children < 3 years
3. Salmonella species - accounts for 25% in sickle cell patient. Note, 60 - 65% is due to
staphylococcus aureus in this group of patients, i.e Staph, aureus is the commonest cause o
osteomylitis in sickle cell patient and NOT salmonella.
4. Pseudomonas sp. - is seen in drug addict.
5. Others - these are occasional
i.
Pneumococci
ii.
Haemophilus
iii.
Brucella
Sites of Infection
Varies with age group
a.
Childreni.
ii.
iii.
iv.
the site is metaphysic because of the following reasons

More blood flow to the growing end
Rapid growing cells are unduly susceptible
The delicate vessels are easily injured and haematoma is a suitable medium for
bacterial growth.
The hairpin arrangement of capillaries slows down the rate of blood flow, thus
allowing organisms to settle
b. Young infants - the very end of the bone mdy be involved.

c. Adults - the midshaft may be attacked.
d. Sickle cell patients - the diaphysis is usually involved. I t is commoner than metaphysis.
Soucres of Infection
Haematogenous
Always commonly from minor skin abrasion
Rarely from boil
Bone may be infected from wound
Pathogenesis
Infection
Cellulitic phase - there is acute inflammation resulting in accumulation of neutrophils, oedema or

exudates.
Suppurative phase - This formation of abscess occurs if there is no intervention
J
Bone necrosis - resulting from shortage of blood supply to a high number of cells
New bone formation / Involucrum

the periosteum in children is thick. I t moves away from the bone
Results into new bone formation
Clinical Features
History
Malaise
i.
ii.
Fever
Pain - is localized, it is severe and unrelieved by rest
v.
Toxaemia
v.
vi.
History of preceding skin infections

Skin infections
vii.
Sorethroat
I n young children, the symptoms may be mild or even absent in neonates.
Signs
i.
ii.
v.
v.
vi.
vii.
Limb is held still - occur initially, then

Swelling
Redness
Localised finger-tip tenderness
Warmth
Oedema
Neighbouring joints - at least few degree of painless movement
Investigations
"
1. Full blood count - shows leucocytosis, there is shift to the left
2. Erythrocte sedimentation rate (ESR) - is high. I t may be normal in children. The normal range is 0 lOmm/hr. The methods are Westergreen & Wintrope.
3. Blood culture : is positive in 50% cases
4.
Bone Aspirate for m/c/s : Is 90% positive. I t is not always positive especially in fulminanat infection.
I t has been replaced by ultrasound.
5. X-ray of suspected bone

- For the f i r s t 10 - 14 days, it shows no abnormality i.e no bone changes because 507o of
calcium should be lost before x-ray shows any abnormality.
- The changes are
Patchy rarefraction of metaphysic
Periostitis - thin line which is parallel to shaft. I t shows new bone formation.
Sclerosis - is new periosteal bone
Sequestra - is sometimes seen
6. Bone scan using Technitium 99 - shows increased uptake
I n summary, the diagnosis is made by
Full blood count: Anaemia & Leucocytosis
ESR - High > 15mm/hr
HI.
Blood aspirate - +ve
?c^"'
1. Acute suppurative arthritis/Septic arthritis
- There is pain & joint swelling
2. Acute rheumatism ( Still disease)
3. Juvenile rheumatoid arthritis- There is
o
Fever
x
o
Pain - is multiple i.e more joints
247
o
o
o
The child is ill-looking

ESR - is raised
Leucocytosis - not marked
4.
Sickle cell crisis - due to infarction of bone. The dignosis is based on Technitium 99 in which there is
reduced uptake.
5. Gaucher 's disease - there is cellular infiltration. The liver is enlarged.
Treatment
ALL patients must be admitted.
1.
o Staphylococcus - Combination of 2nd or 3 rd generation cephalosporins e.g Zincef,
Rocephin + Erythromycin to avoid resistence.
o Convert to oral antiobitcs when temperature becomes normal for 72hours. The criteria to
observe are
- Oral drugs must be available
- Good absorption
- No vomiting or diarrhoea
o Continue antibiotic for a total of 6 weeks (minimum) - to have good serum level of
antibotic
2. Analgesics
3. Splintage - to reduce the risk of pathological fracture
4. Surgical drainange and drilling - for abscess
Complications
1. Chronic osteomyelitis
2. Metastatic infections
Empyeme thoracis
Pyopericardium
iii.
Lung abscess
3. Suppurative arthritis - especially in the hip and kness
4. Altered length of the bone.
CHRONIC OSTEOMYLEITIS
Introduction
I s very common here
Aetiology
1. Post-traumatic & Post-operative - commonest
2. Sequel to acute osteomyelitis
3. Chronic osteomyelitis of insidious onset - by low virulent organism e.g Stapylococcus albus Brodie's abscess.
Clinical Features
i.
History of trauma, surgery or previous acute osteomyelitis
248
ii.
iii.
iv.
v.
vi.
Pain - occurs when the sinus is blocked

Swelling - is localized
Discharge - occurs later
Single or multiple sinuses
Skin hyperpigmentation
Invest iqat on
1. Full blood count - no anaemia
2. ESR - is normal
Except for the acute flare up of infection
3. Wound swab -the commonest organism is still staphylococcu aureus. Note, polymicrobial organism
is NOT common.
Diagnosis
X-ray : Shows
i. Generalised sclerosis - loss of corticomedullary differentiation
ii. Bone-in-bone appearance
iii. Irregular bone expansion
iv. Sequestrum & Cloaca
Treatment
a.
Belfast procedure - is a 2-stage procedure

First stage
Excision of all non-viable tissue until bleeding tissue is reached.
Excise dead bone as well to bleeding bone.
Raise a flap or use bone cement as a filler, introduce antibotics
Put drainage tube
Second stage
Is done after 6 weeks
Involves removal of the bone cement
Then fill the defect with bone graft ( usually from iliac crest)
Papineau technique
Is a 3 - 4
Use more
Excise all
Excise all
stage procedure
instead of bone cement
dead bone
non-viable tissue
249
CHRONIC OSTEOMyELITIS OF INSIDUOUS ONSET

e.g Brodie's abscess
Introduction
There are 5 different groups
I t is small and located in metaphysic.
]
]
]
3
1
]
]
]
3
3
3
3
3
Clinically
I t may be asymptomatic for years
Bur may present with recurrent attacks of pain
The commonest site is the distal metaphysic of tibia.
Tenderness
Swelling - usually little
Investigation
X-ray : shows translucent area with a well-defined margin and surrouding sclerosis
Treatment
i.
As above
ii.
iii.
Surgical under antibiotic cover

Drainage under ultrasound guidance - to identify the organism.
ACUTE SUPPURATIVE/SEPTIC ARTHRITIS

Aetiology
Staphylococcal aureus
Ocassionally, streptococcus
Sources of Infection
i.
Penetrating wound
ii.
Eruption of bone abscess into joint
iii.
Blood stream
Pathology
Synovial infection
Neutrophils infiltration
I
Release of Lysozymes
Destruction of articular cartilage by Lysozymes
^1
Accumulation of pus - if it is not drained
i
i
i.
I
Abscess & Sinuses
250
Healing - opposing surfaces may adhere causing Fibrosos ankylosis or often, trabeculae grow across
joint forming Bone ankylosis
Clinical Features
Are very similar to osteomyelitis
Symptoms
i. Fever
ii.
Ill-looking
iii.
Toxaemia
iv.
v.
Throbbing pain in joint

Joint swelling
Signs
- Vary, it depends on the joint affected e.g knee
i.
Skin - warm, reddened, swollen and joint held flexed.
ii.
Patella tap - reveals fluctuant joint
iii.
All movements are grossly restricted
For Deep joints e.g Hip
i.
I t is warm
ii.
Hip is flexed
iii.
All movements are abolished
Investigation
i.
ii.
iii.
iv.
v.
Full blood count - Leucocytosis

ESR - is rased
Joint aspirate - For Gram stain, cultrure & sensitivity
Blood culture
X-ray of the joint - shows osteopaenia and reduction in joint space
1. Acute osteomyelitis
2. Rheumatic fever - Thers is fleeting joint pains and associated cardiac lesions
3. Acute non-suppurative arthritis e.g cystal-induced e.g gouty arthritis . I t is diagnosed by looiking
at the joint under polarized light, the crystals are seen.
4. Reiter's syndrome - I t consists of "UAC"
a. Arthritis
b. Conjunctivitis
c. Urethritis - is usually gonococcal
5. Haemarthrosis - following trauma or in haemophilia. I n haemophilic patients, you don't put needle
into the jopint, 60% of the Factor V I I I must be present before any procedure.
Treatment
1. Joint aspiration - Surgical drainage & Wasout under arthroscopy especially f o r the knee. This is
to remove all red blood cells, enzymes & Lysozymes.
Note, Washout is the hallmark of the treatment. I n the hip, remove the capsule.
2. Antibiotics - for 6 weeks
251
3. Analgesics
4. Splintage - to avoid septic dislocation especially the hip joint in children.
5. Mobilise - once the local symptoms subside. Start with non-bearing-weight bones to bearing
weight bones.
6. Splint the joint - done in position of function if articular cartilage is destroyed.
o Knee : 10 - 15 flexion
o Hip :
10 Abduction, 15 Flexion
o Elbow : 90 Flexion
o W r i s t : 30 borsif lexion
ARTHRITIS
Content
i.
ii.
iii.
Arthritis/Osteoarthritis
Rheumatoid Arthritis
Cervical Spondylosis
ARTHRITIS / OSTEOARTHRITIS
Introduction
Arthritis = Arthros- (joint) + -itis (inflammation)
I t is al ubiquitous disease i.e affects all ages, all social dasses and all facets of patient's life
Osteoarhtritis is defined as inflammation of joint that is associated with new bone formation
unlike in Rheumatoid or Gout (secondary osteoarthritis)
Aetiology/Types
There are > 100
1.
Infective : via
a. Haematogenous seeding
b. Extension of adjacent osteomyleitis
c. Penetrating wounds or injury to the joint
Occurs in low immunity states ( from septicaemia)
Viral infection
is common in children and those from low socio-economic group
Inflammatory e.q gouty arthritis.
I t usually affects big toe, knees.
I t is common among the Caucaussians
Rheumatoid arthritis ( a component of rheumatoid disease) is both inflammatory &
autoimmune. There is thickening and hyperplasia of synovium, it is described as "
weep"D Pannus
Psoriatic arthritis ( a complication of psoriasis) is associated with skin lesions. I t is
not common here.
3. Metabolic e.q
o
o
o
o
o
Rickets
vitamin bone disease
gouty arthritis - is due to accumulation of uric acid
Pseudogout - due to pyrophosphate
homocystinuria
4. Autoimmune e.q Rheumatoid arthritis

There is antibody against synovium
Pannus
E.g SLE - Antinuclear antibody.
Treatment
- Anticancer drugs
'
l
5. Wear & Tear

-
Theory
The cartilage wears off with old age or jumping up & down
Laminar splanus covers the cartilage of children but with aging, it wears out.
Genetic factors are implicated.
Pathogenesis of Osteoarthritis
I s failure of an organ
i.
Cartilage - is affected mainly because it is the one resoonsible f o r frictionless movement The
other features are :
o
I t is smooth
o
I t is a shock absorber
*
o
I t is also responsible for load transmission
ii.
Subchondral bone - is extremely thick, cuts off blood supply.
iii.
Synovium - the hyaluronic in synovial fluid helps in maintaining the integrity of the joint but
fails as a result of hyperplastic synovium. Hyaluronic acid is now as a treatment for
osteoarthritis.
iv.
v.
Muscle
Ligaments - though, there is no change is size, it can rupture.
I n whole, a vicious cycle is set up. The reduction in cartilage encourages bone growth to
compensate which consequently shuts off the nutrition to the cartilage.
Irritation of the synovium makes it to "weep" i.e producing effusion.
Pathology
i.
ii.
Loss of articular cartilage

Synovitis
253
iii.
iv.
Debris or loose bodies

Osteophytes formation
]
]
]
]
1
1
1
1
1
1
1
1
3
01
Clinical Features
Joint pain
Tenderness
ii.
Hoint creptius
iii.
iv.
Limitation of movement
X-ray Findintjs
i.
ii.
iii.
iv.
Subchondral cyst formation

Subchondral sclerosis
Disc narrowing
Osteophytes formation
Biomechanical
Altered tensile strength
Altered compressive stiffness
Altered shear compression
Cartilage permeability - it imbibes fluid
Subchondral bone stiffness
Biochemical
i.
ii.
v.
v.
Reduced proteoglycan concentration

Altered aggregation of prostaglandins
Collagen fibre size is increased and wea
Matrix molecule homeostasis
Cartilage turnover is increased
Histology
Cloning of chondrocytes
Violation of tide mark
Clefts in cartilage mantle
Risk Factors For Osteoarthritis
1. Age - increases with age
2. Gender - commoner in female especially the osteoarthritis of the knee where the ratio
Male/Female is 1 : 10. I t is due to peculiar deposition of f a t along the waist line and oestrogen
withdrawal at menopause. Oestrogen is chondroprotective.
3. Race - commoner in blacks
4. Trauma - both major and minor
5. Occupation - is due to over-use e.g
Kneeling - as in Clergyman's knee, Housemaid's knee
Elite
athlete
o
Football
Q
Farming
O
6. Obesity
7. Genetic affecting the matric & collagen
8. Bone density - DEXA : Dual Energy X-ray Apsoptiometre is used to measure bone density
254
ft
9. Oestrogen deficiency
10. Nutritional deficiency - i.e reduced protein intake.
Epidemiology /Scope
80% of people affected (with radiological evidence) are > 55years
I t affects l / 4 t h of older people in the world
I t is a main indication for joint replacement surgery
I t is the 4 t h highest impact condition in women and 8 th in men.
I n UCH, From May 1996 to Dec. 2001, 3,982 cases were seen.
The ratio of Knee osteoarthritis/hip osteoarthritis is 3 : 1
Average age (years)

Male/Femal ratio
Knee Osteoarthritis
59.1
1.3 : 1
Hip Osteoarthritis
49.5
1: 1
Clinical Features
i.
Joint pain
is deep dull ache
is initially intermittent
is localized or referred
is aggravated by movement
Origin of the Joint Pain

i. Subchondral bone - medullary hypertension
ii. Osteophytes - stretching of nerve ending in periosteum
iii. Ligaments - due to stretch
iv. Euthesis
ii.
Emotional pain - due to

o
Progressive deformity
o
Reduced productivity
o
Frustration/negative feelings
o
Anxiety
o
Family problems
iii.
iv.
v.
vi.
Joint stiffness - worse in the morning and relieved in the afternoon

Crepitus - noisy joint
Abnormal joint shape
Functional impairment
Management
a. Non-medical
i.
Exercises - I t helps to
o Increase the range of motion
o For muscle s+i*enq+heninq
o For gait normalization
Low impact aerobies
Patella tapping
i. Wedge in sole - for bowleg

ii. Patient education
v. Custom made devices
b. Pharmacological
i.
ii.
Systemic e.g Analgesic using NSAIDs

Local therapy e.g topical gels, intra-articular injection.
3
1
]
]
]
]
]
1
]
1
]
1
]
1
"1
Disease Modifying Osteoarthritis Drugs (DMOAD)

- these are chondroprotective
i.
Tamoxifen
ii.
Chloroqune
iii.
Glucosamine sulphate
iv.
Chondroitin sulphate
v.
Tetracycline
c.
Surgical Mangement - The options are

1. Soft tissue release
2. Osteotomy
3. Arthrodesis = for joint effusion
4. Arthroplasty - THA & TKA
- using stainless steel or plastic prosthesis
RHEUMATOID ARTHRITIS
Is ar\ autoimmnune disease
I s rare in Nigeria
Is symmetrical in manifestation
Systemic symptoms e.g
o Painful eye
o Irritable bowe syndrome
Affects 25 - 50 years
Has gender bias
CERVICAL SPONDYLOSIS
I s occupational hazard
Features
o unexplained shoulder pain
o paraesthesia in fingers
o dropped thumb
o dizzy spells
o occipital headaches
Prevention
i.
ii.
iii.
Geriatric medicine
Health education
NGO
256
iv.
Social amenities
BACK PAIN <& TUBERCULOSIS OF THE SPINE

BACK PAIN
Definition
j- '
'
Is pain that originates from the spine.
History
i.
ii.
iii.
iv.
v.
vi.
Present history
Past medical history
Childhood history - of severe injury e.g fracture of pedicle in children
Family history - of rheumatoid arthritis, ankylosing spondylitis
Occupational history - weight lifting
Obstetric history - uterine prolapse
a. General - outlook, gait as the patient enters
b. Specific
i.
Deformity
ii.
Spinal mobility - forward & backward
iii.
Straight leg raising test ( SLR)
iv.
Reflexes
v.
Sensation
..'.
Investigation
>
i.
Full blood count
Anaemia suggests multiple myeloma
Leucocytosis - infections
ii.
ESR - is
o
High in ankylosing spondylitis, infection ( Tuberculosis ) of the spine
o
Normal - mechanical disease
iii.
iv.
v.
vi.
vii.
viii.
ix.
x.
xi.
xii.
xiii.
Plain radiograph : AP & Lateral - Shows

o soft tissue shadow
o disc proplase
Serum Calcium & phosphate
Alkaline phosphatase
Serum protein electrophoresis
Myelogram - for mechanical lesions
CTscan
MRI
Discography
Nerve conduction studies
Spine scintigraphy
Genotype
1
Causes
a.
Non-spinal
i.
Gynaecological
o
o
o
Vaginal prolapse
Endometriosis
Fibroids
ii.
iii.
Renal
Other retroperitoneal pathologies e.g
o
Carcinoma of the head on pancreas - is common in the elderly
iv.
v.
vi.
Vascular lesions - Abdominal aortic aneurysm

Peripheral nerve entrapment
Gullain-Barre syndrome ( i s Acute infective polyneuritis)
'
1
.
1
1
b. Spine &, associated structures

i.
Bone
o Fractue
o Primary bone tumours
o Metastasis / secondary deposits
o Blood dyscrasia
ii.
Bone & Joint - infection & inflammatory
iii.
Soft tissue pathologies
o
Ankylosing spondylitis - described as Bamboo spine
iv.
v.
vi.
vii.
viii.
ii
Segmental Mechanical derangement

o
Disc degeneration /Degenrative spine lesion
o
Spondylosis - leading to osteoarthritis. I t is graded I to I V
o
Sponylolisthesis - break in pedicle. Vertebral body moves forward
o
Spinal deformity
- Infantile : 1 - 3years
- Juvenile : 3 - Puberty
- Adolescence : Puberty - Epiphyseal closure
- Adult
o
Disc prolapse
j
_
j
' '
Inflammatory
o
Neurological spine
Disc protrusion - least occurs in the thoracic. I t is more in Lumbar ( L5, SI) followed
by cervical (C5,6,7)
Root entrapment from degenerative changes
Neurogenic claudication - spinal cord stenosis
Management
Indications for Surgery
i.
Onset of neurological deficit despite conservative treatment
ii.
Onset of bladder dysfunction - Neurogenic bladder.
Procedure: Discectomy ( Fenestration)
258
1
0
1
1
i
"1
TUBERCULOSIS OF THE SPINE
r
IntroductionI s usually secondary to primary focus
I t spreads to spine via haematogenous route
The common site is thoracolumar spine
Incidence
Age : I t increases with age
Sex : Is almost equal
Pathology
r
r
r
the organism is acid fast bacilli

I t causes caeseating granuloma with surrounding pus.
The tubercles composed of monpcytes & epithelial cells forming minute masses with central
caesation in the present on Langerhans type giant cells.
The abscess expand following path of least resistance.
Skin sinuses amy form.
The bone reaction to the infection varies form none to severe
The infection spares the intervertebral discs initially (unlike staph, aureus). Their involvement is
a late sign.
The infection beneath the anterior and posterior longitudinal ligaments.
Clinical Features
Non-specific
Early stage
i.
Malaise
iii.
iv.
v.
Night sweats
Fever
Weight loss
Late stage
vi.
vii.
viii.
Wekaness
ii.
Back pain - due to bone collapse

Paralysis - due to pressure effect & vascular compromise. Spastic type is commonest.
Cervical involvement shows :
o
Hoarseness - due to recurrent laryngeal nerve paralysis
o
Dysphagia
o
Respiratory stridor - Mi lor's asthma
Investigation
1. Full blood count - anaemia
2. ESR - mild elevation
3. Serum protein - is low
4. Mantoux test
5. Spine X-ray
Early Features
i. Subtle decrease in one or more die spaces
ii. Localised osteopaenia
259
1
1
1
1
1
1
1
1
Late
i.
ii.
v.
Vertebral collapse - called Concertina collapse

Soft tissue swelling
Calcification
Absent vertebral body
6. CT scan - shows more bony destruction

7. MRI - shows more of soft tissue involvement
8. Biopsy and culture
1. Pyogenic infection - by Staph, aureus, Salmonella typhi ( i n sickle cell patient)
2. Fungal infection e.g histoplasmosis duboisii
3. Secondary metastatic disease e.g Ca prostate '
4. Primary tumours of bone e.g Osteosarcoma, Chondrosarcoma, Myeloma, Eosinophilc granuloma &
Aneurysmbone cyst
5. Sarcoidosis
6. Giant cell tumour of bone
7. Bone deformities e.g
Scheuermann's disease - is due to anterior collapse of mant vertebrae.
Treament
Medical
Anti-tuberculous drugs
i.
ii.
v.
v.
Isoniazid : 300mg daily

Rifampicin
Ethambutol - not recommended for use in children because it affects visual acuity
Thiacetazone - is mainly used for children
Pyrazinamdie
Surgery
a. Costotransversectomy - to drain the abscess

b. Radical debridements Arthrodesis - using iliac graft or ribs or fibular. This should be done under
anti-tb drugs cover.
Indications for surgery
Involvement of > 1 vertebra
i.
Resistance to chemotherapy
ii.
Recurrence of disease
v.
Severe kyphosis with active disease
v.
Signs & Symptoms or cord compression
vi.
Progressive impairment of pulmonary function
vii.
Progression of kyphotic deformity.
Contraindications to Surgery
i.
Cardiac failure
ii.
Respiratoryfailure
260
1
1
1
1
1
1
1
1
TUMORS OF THE BONE

MALIGNANT & SOFT TISSUE TUMOURS
1. Osteosarcoma
2. Chondrosarcoma
3. Myeloma
4. Lymphoma
5. Ewong's sarcoma
6. Synovial sarcoma
7. Fibrosarcoma
8. Liposarcoma
9. Metastatic bone tumours
~~
Introduction
I s rare
I s 1% of all tumours
- The treatment requires a multidisciplinary approach
You regard all soft tissue tumours as malignant until proven otherwise.
Classification of Malignant bone tumours
i.
ii.
v.
v.
vi.
vii.
viii.
ix.
x.
Osteogenic - Osteosarcoma
Chondrogenic - Chondrosarcoma
Fibrogenic - Fibrosarcoma
Haematopietic - Myeloma. Lymphoma
Vascular - Angiosarcoma
Fibrous - Malignant Fibro Histo Sarcoma (MFH), Fibrosarcoma
Fat - Liposarcoma
Muscle - Leiomyosarcoma (smooth muscle), Rhabdomyosarcoma (skeletal muscle)
Synovial - Synovial sarcoma
Lymphatic - Lymphosarcoma
Clinical Features
Pain - this makes majority seek attention
i.
History of trauma in a child
ii.
Firm fixed masses
v.
Duration of symptoms is usually long, may be weeks or years.
v.
25% of them are subcutaneous
vi.
They are frequently vascular
Prognosis
I s based on size
r
261
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1
1
1
1
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1
OSTEOSARCOMA
Introduction
I s the most common primary malignancy of the bone in children.
Incidence
I t occurs in 2 nd - 3 r d decade ( Secondary is 6 - 7 t h decade)
30%> occur outside the paediatric age group. A consistent number of cases occur after 35 years.
Male/Female ratio is 1.5 : 1

I s characterized by production of osteoid directly from malignant spindle cell stroma.
...,....._,.
Paget's disease
Chondrosarcoma
iii.
Radiation - Radiatio-induced tumour tends to re-occur often
Common Sites
I t affects long bones mostly
90% originate from metaphyseal end because of its rich vascularisation and it is also soft.
The bones affected are
i.
Distal femur - commonest
ii.
Proximal tibia
iii.
Proximal humerus
]
1
1
1
Clinical Features
Increasing painful swelling
i.
Swelling
ii.
Tenderness
v.
Warm
v.
Overlying skin is stretched
vi.
Limitation of movement
VII.
Pathological fracture
X-ray Finding
i. Codman's triangle
ii. Sunr rays or sunburst appearance
iii. Cortex erosion
iv. Radiolucent (lytic)
Treatment
Neoadjuvant chemotherapy & Limb salvage surgery
( Adriamycin, high dose methtrexate )
Prognosis
They survive or die from local disease.
Jaw tumours in adults mainly 80% disease for
,_
1
1
1
1
1
T
1
262
1
~i
CHONDROSARCOMA
Introduction
Majority are of the central type
Sites
i.
ii.
Pelvis
Shoulder
Proximal femur
Incidence
Occurs in the middle age
The risk increases with age
There is high risk of local recurrence
Pathology
Low grade lesion is confused with Enchondromas (i.e cartilage lesion within the bone)
There is calcification within the medullary canal.
Metastatic rate
a. High grade - 75%
b. Moderate grade - 15 - 40%
Note
On X-ray, the difference between Enchondroma & Calcification is that in calcification, there is
thining of the cortex.
Investigation
1. X-ray : shows calcification
2. CTscan
3. MRI
MYELOMA
Introduction
Is the most common primary malignant tumour in adults
Incidence
Occurs 5 - 6 years
Male/Female ratio is 2: 1
Aetiolgy
Is due to proliferation of marrow plasma cells
Clinical Features
Bone pains
i.
Features of anaemia - fatigue
ii.
Fever
v.
Malaise
v.
Weight loss
'
263
Investigation
1. X-ray ( Skull, Limb, c h e s t ) : shows
Punched out multiple osteolytic lesion
Pepper-salt appearance
2. Chest x-ray : multiple punched out lesion in the ribs
1. Plasmacytoma - is when multiple myeloma is localized
2. Burkitt's Lymphoma
3. Hodgkin's lymphoma
Complications
1. Kyphosis
2. Cord compression
3. Patholgica fractureAnaemia
4. Thrombocytopaenia
5. Leucopaenia
LYMPHOMA
I s usually secondary
Occurs in 5 -6 t h decades
I s mostly diaphyseal
X-ray shows pathological fracture
Prognosis is poor.
EWINS'S SAkCOMA
Introduction
I s a higly malignant round cells tumour
I t is seen in children & adolescents, 907o of patients
I t is rare in blacks
Has male predominance
I t usually affects many bones
i.
Osteomyelitis
ii.
Metastatic neuroblastoma
X-ray
: Snows
i. Loss of corticomedullary differentiation
ii. Onion skin appearance
SYNOVIAL SAkCOMA
Rarely arises from joint
I t resembles syn
There is soft tissue calcification within the mass
FIBROSARCOMA
Is rare
Can be seen anywhere
LIPOSARCOMA
Is relatively common
Occurs in the middle age
Has wide range of malignant potential
METASTATIC BONE TUMOURS

Introduction
Is the commonest malignant bone tumours
Is usually multiple
Spine is the most frequently affected site
Primary sites
- Are usually paired organs
i.Breast
ii.
Renal
iii.
Prostate - is bilobed and crosses midline
iv.
Thyroid
v.
Lung
vi.
Stomach - because it crosses the midline
Pathology
- Most are lytic lesions except
i. Prostate
ii. Hodgkin's disease
iii. Carcinoid tumours
Investigation
1. Plain X-ray
- The sites are metaphyseal <& diaphyseal
- The border is callous
- Type of matrix involvement : Osteoblastic or osteolytic or pepper salt
appearance
- Type of bone destruction
- Periosteal response
- Soft tissue extension
X-ray of pelvis : shows osteo
(radio-opaque) metastasis from the prostate
- Pathological fracture from osteolytic lesion
Humerus - shows osteolytic (radiolucent) metastasis
J
]
]
2. Chest X-ray - canon ball metastasis

3. Bone scan
There is increased uptake intensity of radioactive material. I t is not
predictive of malignancy
Myeloma presents with cold spot
I n osteomyelitis, the hot areas are not necessarily malignant.
Staging
Prognosis is related to stage of the disease
Helps to monitor treatment
American staging involves TNM A Histological grade.
ENNEKING - based on surgical grade,'site &. metastasis. Grade measure the biological
behaviour of a lesion
4.
Biopsy
Open biopsy is preferred and not FNAB or FN AC
The location and orientation are crucial
Pre-op assessment of CT, MRI to determine the most direct route.
Peripheral portions are preferred
Wedge of tissue (1cm) is taken
i. Intralesional excision
ii. Marginal excision
iii. Wide excision
iv. Radical excision

Beware of satellite and skip lesion
IN
5. CT scan - Shows loss of corticomedullary differentiation and extraosseus involvement.

6. MRI - for tissue masses. Shows the extraosseous involvement and medullary canal.
7. Angiography - Vessels appear intralesional. I t can be used for pre-operative embolisation or f o r
inarterial infusion of cytotxic drugs.
Treatment Options
1.
Surgical - most important
Excision
i.
Resection & Bone transplant
ii.
Limb Salvage Resection
Has helped to improve the quantity & quality of life
Has 5 - 15% of local recurrence
Contra-indications
i. Major neurovascular involvement
ii. Pathological fracture
iii. Inappropiate biopsies
iv. Infection
1
1
1
1
1
1
1
]
1
1
]
]
T
1
266
1
v. Extensive muscle involvement

vi. Skeletal immaturity
2.
3.
4.
5.
Chemotherapy - as neoadjuvant & adjuvant

Radiotherapy - as neoadjuvant & adjuvant. Thjp use is controversial
Immunotherapy - for experimenta studies I
Molecular biology - to type people prone to have bone tumour
CLUB FOOT
(aka Congenital talipes equinovarus)
Epidemiology
Incidence is about 50 - 60% of all congenital malformations in UCH and other parts of Africa
Is commoner among low socio-economic people
Male > Female - 2 : 1
I s not common in advanced countries again because of frequent termination of such pregnancy.
Aetiology of Talipes equinovarus
a. Congenital
b. Idiopatthic
c. Others
Trauma
Poliomyelitis
Hypothesis & Predisposing factors
I s probably due to lack space in -utero for the child (as shown by the factors below ) or to
excessive myoepithelial cells.
Predispoisng factors
! 1 i
First child
j ,,
Oligohydramnios
i.
Multiple pregnancy
ii.
Breech delivery
v.
Diabetic
patient
v.
' i
Components/ Features
Tibial torsion
i.
Shortened tendo-achilles <& hypodevelopraent of calf muscles
ii.
Contracture of "Thomas Heart Muscles"
T - Tibialis posterior
D - Flexor digitorum longus
H - Flexor hallucis longus
iv.
v.
vi.
vii.
Contracture of posterior capsue of ankle joint

Medial inclination of talonavicular joint - leads to the varus deformity of hind foot
Contracture of subtalar joint (talo-calcaneous j o i n t )
Fore-foot adduction - is the deformity in the mild form
267
"
History
"J
1
Usually taken from the mother

Pregnancy history
.
o Duration of pregnancy
o Illness during pregnancy
o Drugs ingestion
Delivery
I
o Mode
o Did the child cry immediately afteribirth - for associated syndromes
o Passage of meconium - for Hirchsprung disease
Treatment
s
S
S
S
S
S
S
J
~
1
t
1
Re-assure the parents

Teach the mother on manipulation of the legs
,
A f t e r 2 weeks, use tapes to start the correction. ( Tape is preferred to elastoplast because
the child's skin is still delicate
'
After 2 weeks, start serial cast immobilization using above knee P.O.P ( Above-knee P.O.P is
used to relax the tendoachilles so as to give room f o r adequate dorsif lexion.The P.O.P is
changed every 2 weeks for the next 3 months
Then do x-ray to see the ossification centres
Follow-up with Denysban shoes
I f there is no improvement, do surgery at when the child is 1 year old.

i
Procedure
Elongate the tendoachilles

Elongate the above 3 muscles
Do posterior athrotomy of the ankle joint - to relax it
Do arthrotomy of the subtalar join
Re-alignment of talonavicular joint - The side effect of this is damage to
posterior tibial nerve & vessels
Post-operative
S
Put above-knee P.O.P for 3 months
S
Then place on corrective shoes for at least 5 years
3
1
3
3
3
3
j
I
~
3
1
3
Complications of treatment
1. Skin ulceration
'
2. Rocker-bottom foot
3. Avascu\ar necrosis of the small bones of the foot
4. Soft tissue loss
5. Recurrence
Prognosis
I s wosre if presentation is made after 1 ydor, by which it will require bony re-alignment (
osteotomy)
Note
Triple athrodesis - fusion of subtalar, talonavicular & calcaneocuboid joints

Or
Medial tarsectomy
*
268
1
]
i.
BASIC CONCEPTS <& EVALUATION OF PATIENTS WITH NEUROLOGICAL DISEASES

Introduction
I n management of brain-related illnesses, other parts of the body should not be neglected.
The disorders of the brain can be grouped f # o
a. Intrinsic CNS disease
b. Disorders that have impaclflon the brain primarily.
Neurological Assessment
Good general evaluation
a.
History
b.
General examination
c.
Systemic examination
II.
Neurological evaluation
Basic Concepts of CNS

A. Intracranial volume / Pressure Relationship
I n adults, the intracranial volume has fixed capacity of 1,800ml. At 1 year, 60% of this volume
has been formed. The volume is achieved at'the age of 5 years.
The constituents are
Constituents
mis
1. Brain
J.400
a. Brain substance
%200
b. Interstitial
200
200
2. CSF
200
3. Blood
Total
i;800
When there is introduction of an extraneous substance, the volume increases and to avoid
increase in pressure, some of the CSF or blood are displaced i.e the pressure remains constant
for a while.
Later in the presence of foreign material, the pressure rises.
Normal pressure is 10 - 20mmHg
I - Low resistance
I I - Moderate resistance
I I I - High resistance
269
Monro-Kelly Hypothesis
I
The addition of increased volume into the intracranial space is often compensated for by CSF and
blood displacement up to the point that I C l increases or begins to rise.
I n other words, ICP will be normal as long as there is compensation and it begins to rise as soon
as the limiting compensation is reached.
Note, nutrient's delivery to the brain is driven by perfusion pressure.
This is calculated as below

Perfusion pressure = Mean ABP - ICP
Mean ABP = Diastolic p r e s s u r e - l / 3 r d of Pulse pressure
Pulse pressure = Systolic pressure - Diastolic pressure
1
1
1
1
Thus, keeping ICP normal means keeping diastolic

and systolic pressure normal
iilsl
IF
Three Mechanisms of Compensation in Raised ifcP

i.
Displacement of CSF into the soinal tract
Displacement of blood into venous circulation
II.
Shifting of brain structures
iii.
B. Cerebral Blood Flow
!
Normal is 50 /100g tissue
|
Cortex receives 70ml/100g ( 70%'mnd White matter receives
C. Brain Oedema
Differences between
Brain Capillaries
1.
2.
3.
4.
]
]
]
]
]
]
Systemic capillaries
Fenestrations are present

No tight junctions
The epithelium has vesicles
No astrocyte foot processes
Absent
Present
Does not
These abut on the brain epithelium, together they
form brain blood barrier
Type of Oedema
a. Vasogenic oedema
\
Under certain conditions, the EBB breaks down ( due to separation of intercellular
junctions) to result into cerebral oedema.
b. Cytotoxic oedema
This has 2 causes
]
'i.
Water intoxication
ii.
Hypoxia
i
I t is due to injury and damage to cells in the nervous system i.e all cells e.g Neurons,
glial cells & epithelial cells ) in qNS are affected.
'
270
]
]
]
]
1
""j
J
1
1
~
c. Interstitial oedema
Is caused by obstruction in the flow of CSF.
The oedema increases the intracranial volume, thus causing raised intracranial
pressure.
I t also affects the concentration of electrolytes
'
Cytotoxic
Vasogenic
Mechanism
Cellular injury
Water
intoxication
Vascular
Trauma
Infection
Interstitial
CSF
transudation
CSF flow
obstruction
Treatment
Dexamethasone
Mannitol
CSF Drainage
Used
Used
NO
Not effective
Mannitol
NO
Not used
Not used
YES
Principles of Treatment of Raised Intracranial Pressure

Remove the cause
i.
Treat oedema
ii.
Drain CSF
v.
Hypothermia
v.
High dose barbiturate
Evaluation
a.
b.
c.
d.
e.
f.
History
Examination
Tests
Clinical diagnosis - is made based on the aetiology and location.
Structural & Functional diagnosis - is made from history & examination
Pathological diagnosis
i.
Congenital
ii.
Traumatic
iii. '
Inflammation
iv.
Neoplastic
v.
Vascular
vi.
Degenerative
vii.
Metabolic
viii.
Toxic
Patholoqy
- Are groupec into
a. Brain
b. Spinal cord
c. Peripheral nerves
d. Neuromuscular junction
e. Muscles
271
J
]
The history-taking should reflect this order
i.
General well being
ii.
Language
iii.
Memory
.
iv.
Affect
v.
Ability to concentrate
vi.
Cranial nerves
o Smell abnormalities (ansomia, parosmia)- suggess lesion at the base of the brain
o Vision
o Facial symmetry
o Chewing / Swallowing/taste - suggest lower brainstem lesion
o Breathing difficulty - suggests'lower brainstem lesion
o Tongue movement - suggests pathology in the medulla
vii.
Spinal cord
o
Power
o
Sensation
o
Co-ordination
o
Gait - suggests cerebellar lesion
I
~~
]
]
]
1
1
1
,,"*'
Investigation
1. Skull x-ray : is a primitive test, but it is still very important to detect
o
Fractures
o
Raised intracranial pressure
o
Osteomyelitis
2. Spine x - r a y : done f o r trauma cases

3. CT scan
a. Brain
b. Spine
c. Myelography
4.
5.
6.
7.
8.
9.
Magnetic Resonance Imaging

U l t r a s o n o g r a p h y - u s e d in children
Electroencephalogram (EEG) - t o classify seizures
Electromyography ( E M S )
N e r v e Conduction studies
Evoked Potential
a. Somatosensory
b. Visual-evoked
c. Brainstem-evoked
I
~
_
1
~~
~
1
' ' '
-''"'
Note,
Fibrillation - is muscle contraction not visible to naked eye.
Fasciculation - is visible,but there is loss of efferent nerve
i
-'
<-
J
""]
j
272
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10. Lumbar puncture for CSF - for

Chemistry
o
Cytology
o
Bacteriology
o
Virology
o
o
Immunology
11. Angiography
CRANIAL CONGENITAL MALFORMATION
i.
ii.
v.
v.
vi.
vii.
Hydrocephalus
Encephalocoele
Craniosynostosis
Congenital dermoid cyst
Anencephaly
Chiari malformation
Sub-galeal inclusion cyst
Introduction
Congenital: means 'present at birth'
"Congenital defects" are different from "genetic defect" e.g
i.
HbSS - is genetic, but not congenital i.e does not manifest at birth
ii.
Rubella infection in mother causing hydrocephalus - the hydrocepha
birth, but it is not a genetic disease.
Aetiology
a. Genetic - accounts for l / 3 r d
b. Environmental - accounts for l / 3 r d
c. Both - for l / 3 r d
Most congenital malformations are combinations of environment &. genes.
Note, environmental factor is seen in 2/3 r d of all cases.
Examples of environmental causes
Nutritional
i.
Infective
ii.
Chemical
v.
Radiation
v.
Physical defect
Types
1.
2.
3.
4.
Hydrocephalus
Encephalocoele
Craniosynostosis
Congenital dermoid cyst ( over anterior fontanelle )
5. Chiari m a l f o r m a t i o n
-'-''.-
6. Others
i.
Cranial bifida ( Rachischis )
ii.
Congenital cyst of third ventricle
iii.
Congenital absence of corpus callosum ( Agenesis ) - is common in spina bifida. I t may be
partial or complete.
Note, the f i r s t 5 are COMMON !!!
HYDROCEPHALUS
Introduction
CSF is produced at the rate of
0.3ml/min ( 0.15ml/min in infants )

20ml/hour
540ml/day
Definition
i
1
1
3
]
]
I t is accumulation of CSF in the intracranial space, which may be

a. Epidural hydrocephalus - this is not practical
b. Subdural hydrocephalus - is also practically non-existing
_
1
c. Subarachnoid d. Ventricles - occurs more easily. Occasionally, it involves subarachnoid space

There is production - absorption mismatch
RememberMonro-Kelly hypothesis
CPP = MAP-ICP
]
]
3
1
]
Incidence
Occurs in < 1/10,000 live births
I t may be congenital or acquired
^Pathophysiology
CSF is an ultrafiltrate of plasma
I t is produced at the following sites
i.
Choroid plexus of lateral & 3 r d ventricles
|
ii.
4 t h ventricle
iii.
Ependyma
4 t h ventricle and ependymoma contribute slightly
The circulation is shown below
Choroid plexus
]
]
rd
Latera & 3 ventricles
1
I
Foramen of Monro
274
1
n
ventricle
t
Aqueduct
4 t h ventricle
1
1
Subarachnoid space - including the cisterns ( which are pockets )
Arachnoid granulations
occurs via pressure mechanism & bulk transport
For CSF to move into venous system, intravenous pressure must be lower.
Veins
|
Causes of Obstruction
Ischaemia of the brain - causes absent myelination of axons and the child presents with aphasia
1.
Excessive production of CSF - I t is a rare condition and is due to choroids plexus pathology e.g
i.
Choroid hyperplasia
ii.
Choroid papilloma
2. Obtsruction - Practically, this is the cause of hydrocephalus

Common sites
i.
Foramen of Monro
ii.
Aqueduct of Sylvius - Aqueductal stenosis or septations
iii.
Foramen of Magendie & Luschka
iv.
Arachnoid granulations
Types / Classification
a. Obstructive & Non-obstructive - This method is pref f ered by Neurosurgeons
b. Communicating & Non-communicating
Communicating - means the CSF can pass through the entire ventricular system e.g aqueductal
stenosis
Non-communicating - There is extra-venricular blockage
Causes of Hydrocephalus
a. Foraminal obstruction ( of Monro)
Colloid cyst of 3 r d ventricle
Arachnoid cyst of 3 rd ventricle
iii.
Lipoma
iv.
Hypothalamic/Thalamic lesion
1
b. Aqueductal lesions - is the most frequent cause of hydrocaphalus
i.
Aqueductal stenosis - is congenital, it may be isolated or occurs with
myelomeningocoele. I t causes Childhood hydrocephalus.
ii.
Aqueductal septations - is congenital
iii.
Aqueductal bifurcation - is congenital
IV.
Tumor at the base e.g
o
Craniopharyngiom
o
P i t u i t a r y adenoma
o
Ependymomas
o
Astrocytoma
o
Medulloblastoma
o
Pineal tumour
o
Glioma
-*
i
_
I
~~
h-
Iatrogenic e.g stent obstruction

c. 4 t h Ventricular / Exit foramen
i.
Chiari malformation
/
I s descent of brainstem and part of cerebellum (tosils) into foramen magnum.
I t may occur without hydrocephalus
I s diagnonsed by CTscan or MRI
Predisposing factors
o
PROM A Amnionitis
o
Prenatal infection - CMV
o
Herpes simplex
o
Bacterial, viral .parasite
'
o
Congenital brain tumours
ii.
Dandy-Walker malformation
I s a congenital posterior fossa cyst
Note, CSF circulation is established by 8 th week of intrauterine life by
opening of the Foramina of Magendie & Luschka, thus failure of this causes
dilatation of the 4 t h ventricle resulting into cystic formation - Infantile
hydrocephalus.
I t consists of
V
Hyoplasia of veins of cerebellum
S
Distension of 4 t h ventricles
s
Failure of opening of 4 t h ventricle
There is a variant where the 4

d.
ventricle is NOT distended, it is called Vermian hydrocephalus.
Subarachnoid space
i.
Post-haemorrhagic hydrocephalus
o Intra-ventricular - is associated with prematurity & distress
o Ruptured cerebral aneurysm
o Head trauma
e. Arachnoid granulations - due to infections

i.
Rubella infection
276
]
]
1
3
1
1
^J
-*
1
~
_
I
1
1
1
1
0
1
r
~s
ii.
iii.
iv.
Cytomegalovirus
Toxoplasmosis
Bacterial meningitis - occurring at any age
The f i r s t three cause inflammation of the arachnoid granulations which heals with fibrosis.
f.
Superior vena cava compression by mediastinal tumours
Common causes
1.
2.
3.
4.
Aqueductal stenosis - causes childhood hydrocephalus

Dandy-Walker malformation - causes infantile hydrocephalus
I n t r a - & Post-natal infection
Chiari malformation
I s age-dependent
I t may be present at birth and not detected if the head of the baby is not measured. This can
then be present in later in life.
/~
May be a sign of underlying disease
a.
I n Newborn - Infantile Hydrocephalus

Here, because the sutures & fontanelle are still open, the ventricular distension is not
measured accompanied by rapid enlargement. There is mild to moderate head
enlargement because the. cortex thins out as the ventricular size is increasing.
I t s peculiar ways of presentation are
i.Apnoeic spells
ii.
Irritability
iii.
Vomiting
iv.
Bradycardia
v.
Poor feeding
vi.
Tense anterior fontanelle
vii.
Rapid head enlargement
Distended scalp veins
viii.
ix.
Seizures
Early detection is made by serial measurement of head circumference
Investigation
i.
Skull x-ray - is of no use, because it cannot differentiate between the ventricles &
subarachnoid space,
ii.
Ultrasound - is very good
*
iii. CT scan
,
iv. MRI - is least valuable
Infants
i.
ii.
Increased occipito-frontal circumference (OFC) - to > 97%

Wide anterior fontanelle
Sutural diathesis
277
#
iv.
v.
vi.
vii.
viii.
Distended scalp veins

"<-.
Failure of upward gaze - because superior colliculi responsible for it is affected
Sunsetting sign - is due to brainstem compression
Cranio-facial disproportion
Neuromuscular delay
ix.
Cognitive delay
These features can also in neonate ( i n late phase)

Monro-Kelly hypothesis is not applicable because sutures are still open.
c. Toddlers or Older Children
Headache
Lethargy
ii.
Drwosiness
iii.
iv.
Vomiting
Papilloedma
v.
6 t h Nerve palsy ( Lateral rectus)
vi.
vii.
Hypertonia & hyperref lexia
Manaqement
Depends
o
o
o
on
How the patients present
When the patients present
Severity
Prinicples of Tretment
i.
Clinical evaluation
o
o
ii.
iii.
iv.
Careful history - including prentatl & family history

Examination - including OFC
Confirm the diagnosis

Establish the level of severity
Establish the progression (tempo) of the disease - because patient with mild hydrocephalus
may not require treatment
Indications for Treatment

i.
Rapid rise in ICP
ii.
Progressive neurological deficit
iii.
Moderate/severe static deficit
Modes of Treatment
a. Medical / Non-surgical
i.
Carbonic anhyrdase inhibitors e.g actetazolamide or diamox. I t is used for mild
infantile hydrocephalus. I t provides transient relief.
b. Intermittent CSF aspiration - useful in neonates
c.
Surgical - there are 2 cateogories
Endoscopic
.--.. -. I s used for older infants and children
- No implant is left behind
Indications
Obstruction above the level of Aqueduct Sylvius e.g aqueductal

stenosis. Endoscopic Third Ventriculostomy is done. I t involves
puncturing a hole at the floor of the 3 rd ventricle.
Dandy-Walker malformation - where the 3 r d and 4 t h are enlarged. A

hole is made in the wall of 4 t h ventricle.
Azoidance of shunt complications
Complications
i.
Recurrence
Implant/Shunts - is left to by-pass the CSF into venous circulation. E.g

o
Ventriculo-peritoneal - is now in use
o
Ventriculo-pleural
o
Ventriculo-atrial
o
Ventriculo-pelvis
o
Lumbo-peritoneal shunt - is used for communicating
Requirements for Shunting
i.
I t must be one-way diversion
ii.
The system must recognize excessive shunting of CSF. This is mediated by a
valve, (which regulates uni-directional flow & pressure) Note, most shunts are
pressure-regulators, though there are some volume-regulators but expensive.
1
Complications of Shunt
a. Common
Obstruction - due to clogging with choroids plexus or tissue
debris
i.
Mechanical failure of shunt
ii.
Over-drainage or 'siphoning' - Shunt ventricle syndrome
v.
Infection : meningitis, peritonitis & sepsis
v.
Recurrence
vi.
Subdural haematoma
vii.
Subdural hygroma
viii.
Hemiparesis
,
,,
b. Uncommon
Shunt migration
279
i.
ii.
v.
v. .
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
Perforation of gut, abdominal wall

Hernia
Endocarditis
Nephritis
s.
ENCEPHALOCOELE
Definition
I s abnormal protrusion of brain or meninges through bony defects in the skull
I t is common in
a. Vault - which can be synciput or occiput. Occipital is most common.
b. Base - through the nose
I t is often covered by skin.
Complication ( of Occiptal encephalocoele)
i.
Hydrocephalus - occurs in 40% cases
Treatment
i.
ii.
Excision & Closure

Cranioplasty - if defect is very large
CRANIOSYNOSTOSIS
Introduction
Sutures are the growing points of the skull.
I t is defined as premature fusion of cranial sutures
Types
a. Simple
b. Complex
Examples
Types
Suture involved
Saggital
1. Scaphocephaly
Coronal
2. Brachycephaly
3. Plagycephaly
Lam bo id
The head elongates in the direction of prematurely fused suture.
n
280
Scaphocephaly
Treatment
i.
ii.
Brachycephaly
Plagycephaly
Treat underlying problem

Surgery - craniectomy & Suture removal & Anterior segment advancement
Complex Syndromal Synostosis
'
I s autosomal dominant
Coronal Craniosynostosis
Introduction
Is very common
May be isolated or part of syndromes e.g
a.
Crouzon's syndrome
i.Coronal craniosynostosis
ii.
Exorbitus - shallow orbit A protruded eye
iii.
Hypertelorism
iv.
High arched palate
v.
Hypoplastic sinuses
b. Alpert's syndrome
i.
As above +
ii.
Syndactyly - which can be bony or soft tissue
Treatment
Crouzon's syndrome
Requires an emergency treatment to prevent raised intracranial pressure which constrict the
optic nerve resulting into blindness.
Release the suture - when the rate of growth of brain is at maximum speed. ( 6months - 1 year)
CONGENITAL DERMOID CYST

Introduction
This lesion made Ibadan famous. I t was described by Prof. Adeloye & Odeku
The dermoid cyst grows over the anterior fontanelle
I t is present at birth and enlarges with age
I t is covered by skin
Treatment
':..,.
Excision & Drainage
281
Complications
i.
Enteringinto superior saggital sinus.
HEAD INJURY
Definition
I s injury to the brain with or without the coverings.
Mechanism
Causes
1. Road t r a f f i c accident
2. Warfare
3. Occupational
4. Sports
5. Domestic
Types
i.
ii.
iii.
iv.
Closed head injury

Penetrating
Torsion - causes rotation of brain stem. I t occurs in boxing. Blood supply is
compromised.
Concussion - is microscopic haemorrhage within the brain

Contusion - I s parenchymal damage with intact surface
Penetrating - damage involving surface & parenchyma. I t is usually ragged.
Types of Contusion
a. Pure
b. Haemorrhagic contusion
SCALP
;#y
a.
Bruise - is subepithelial haemorrhage
b.
Incision
c.
Scalp loss
d.
Associated skull fractures

i.
Depressed open /closed fracture
ii.
Pond fracture
e.
Skull fracture
f.
Skull loss
g.
Dura
h.
Haemorrhage
i.
Arachnoid mater can go in between the linear space and continue to cause erosion.
NEUROLOGICAL TRAUMA
i.
ii.
v.
Brain
Spinal cord
Peripheral nerves
Coverings
Associated Injuries
Injuries
Pulmonary
Musculoskeletal
Abdominal
Cardiovsacular
Endocrine
Spinal
Head
Head injuries (%)

78
43
53
3
23
6
6
Spinal injury (%)

10.5
18
2.5
1.5
Management Protocol of Head Injury

Primary Survey & Resuscitation
i.
Airway maintenance and C-spine protection
ii.
Breathing
iii.
Circulation and control of haemorrhage
iv.
Rapid neurologic survey
v.
Level of consciouness
vi.
Exposure - remove all clothes
vii.
Ventilation 6\ oxygenation
viii.
Reverse shock
ix.
Urinary catheter
x.
ICU care
xi.
Theatre
16
Secondary Survey
i.
Detailed systemic
ii.
X-rays - chest, spine
iii.
Peritoneal lavage
iv.
CT scan
v.
Other x-rays
vi.
Laboratory tests
vii.
Tetanus toxoid A ATS
Tertiary Survey
i.
Definitive care - depends on the results obtained from above
Hypoxia <5 Hypotension
20% of head injury patients
Aggravates spinal cord injury
I t is inversely correlated to outcome
Mechanism of Injury
i.
ii.
Hypotension
Microvascular changes
Conflicts <& Priorities

For all, those in f i r s t column should be considered f i r s t
a. Airway maintenance vs C-spine injury
b. Airway maintenance vs basal skull fracture
c. Fluid resuscitation vs Brain swelling
d. Head & spine injury vs Abdominal injury
HEAD INJURY
Definition
Is trauma to the brain and/or its covering. I t must arise from mechani
First Classification
This is based on mechanism
a.
Closed - the brain is not exposed e.g

o Blunt force
o RTA, Assaults
o High or low velocity
b. Penetrating - the brain is exposed e.g
o
Gunshot wounds
o
Stab wound
o
High or low velocity
Second Classification
This is based on severity : using Glassgow coma score
Mild
Moderate
Severe
GC5
13-15
9-12
3-8
Fully awake
Drowsy but obeys
Does not obey
I t consists of 3 parts
a. Eye opening
b. Motor response
c. Verbal response
Eye opening - 4
Spontaneous
To call
To pain
None
4
3
2
1
Obeys commands
Localises to pain
Withdrawals to pain
Decorticate to pain
Extends to pain
None
6
5
4
3
2
1
Oriented
Confused
Inappropiate
Incomprehensible
None
5
4
3
2
1
Motor response - 6
Verbal response -5
Third Classification
This is based on morphology
1. Scalp injuries
2. Skull fractures
a.
Linear / Stellate
b.
Depressed or non-depressed. "Depressed" means fragments are re

positions deeper than the inner table.
c.
Basal with or without CSF leakage / Cranial nerve palsy
3. Intracranial lesion
a. Coverings' haematoma
Extradural haematoma - is biconcave
i.
Subdural haematoma - is concavo-convex
ii.
b.
1
]
Brain lesion - contusion
Management
a. Mild head injury - the patient is fully awake, though may be disoriented
History
i. Physical examination
ii. Plain radiographs - skull, spine, chest
v. Laboratory tests
v. Observe in Accident & Emergency dept.
vi. CT brain - if persistent for 24 hours and there is worsening deficit or there is
history of drug or alcohol ingestion
vii. Discahrge with warning list
1
]
]
b. Moderate head injury - the patient is drowsy, but obeys commands

I n addition to above steps
i.
ii.
v.
v.
vi.
CT scan
Admit
Serial observations
Discharge - if improves (90)
Appropiate otherwise
1
1
Severe head injury - the patient does not follow simple commands
I n addition to above steps, do the following
II.
CTscan
ICU care
Appropiate therapy
]
]
]
Medical Therapy f o r Head Injury

1. Anticonvulsants
For 5 -15% of patients that develop post-traumatic seizure
The seizure is divided into
a.
Immediate -
b.
c.
Early - in 1 st week. Here, prophylaxis is beneficial

Late seizure - The risk factors for it are
Early seizures
i.
Depressed skull fracture
ii.
Intracranial haematoma
1
]
]
2. Intracranial pressure monitoring

3. Mannitol
4. Frusemide (Lasix)
5. Barbiturates
]
286
Note
Steroids
is NOT used at all!!!. I t causes

Infections
(51 ulcerations
More problems
Surgical Therapy
1. Wound debridement - to evacuate intracranial haematoma
2. Drainage of haematomas
Glassqow Outcome Scale

I : Good recovery - return to pre-injury level of function
II:
Moderate disability - there is dimished level of function but cares f o r self
III:
Severe disability-Unable to care for self
IV : Vegetative state - No awareness of self and environment
V : Death
TRAUMA OF THE SPINAL CORD

Anatomy
Dura
Epidural space
Extends from foramen magnum to S2 vertebra.
I t ending point in
I n f a n t s - L2/L3
Adults - L1/L2
Spinal cord ends as conus medullar is
Filum terminale ends at dorsum of the coccyx
Cauda equina
I t consists of
Loose connective tissue
i. Fat
ii. Intervertebral plexus of veins haemorrhage
v. Dentate ligament - piamater
There are 33 vertebrae.
Cervical - 7
i.
Thoracic - 12
ii.
Lumbar - 5
v.
Sacral - 5
v.
Coccyx - 4
]
]
Structure of a vertebra
o
Trasnsverse processes have 2 facets - Superior & Inferior
1
]
]
Stability of the Spine
I s by ligaments
i.Anterior longitudinal ligament
ii.
Posterior longitudinal ligament
iii.
Supraspinous ligament
iv.
Interspinous ligament
v.
Ligamentum f lavum
1
1
]
]
3
1
]
]
]
Columns of the Spine

a. Anterior column- consists of
Anterior longitudinal ligament
Anterior \ of centrum
Anterior \ of Annulus fibrosis
b. Middle column
Posterior longitudinal ligament
Posterior \ of centrum
Posterior \ of Annulus fibrosis
II.
c.
Posterior column
Facet joints
Interspinous ligament
Supraspinous ligament
Ligamentum f lavum
Note,
Disruption of more than 1 column makes the spine unstable.
Abnormalities
i.
ii.
1
1
Kyphosis - posterior convexity

Lordosis - Anterior convexity
Tracts
- I s defined as collection of fibers of the same origin, course and destination.
a. Ascending tracts
i.
Dorsal column - is responsible for touch, pressure, joint position 2-point
discrimination and vibration
]
288
1
!
ii.
Spinothalamic
Anterior spinothalamic - is for light & touch
Lateral spinothalamic - is for pain <& temperature
iii.
Spinocerebellar
b.
Descending tracts
i. Corticospinal
- F. cuneatus - is found only in cervical region.
Pathophysiology
Note, thoracic vertebrae are relatively immobile.
Forces
Hinging - hyperflexion or hyperextension /lateral flexion

Compression forces /Axial loading - the force is on the long axis of the cord.
Shearing - is due twisting forces. I t affects the axons.
Types
a.
Ligamentous / Disc injury

i.
Rupture
ii.
Avulsion
Burst fracture - the intervertebral disc becomes smaller or disappeared. The vertebral
bodies widen.
b.
c.
'
Bones
i.
ii.
iii.
iv.
v.
vi.
Angulation
Subluxation
Dislocation
Wedging
Fracture
Stable /Unstable - depending on the column involved.
Cord
i.
ii.
iii.
iv.
v.
Incomplete/complete
Anterior cord syndrome
Posterior cord syndrome
Lateral cord syndrome
Central cord syndrome
Hyperflexion
the posterior ligament is stretched and becomes ruptured
i
There is posterior subluxation or posterior wedging
i
Hyper-extension
The anterior ligament ruptures
There is anterior subluxation or anterior wedging
BONE INJURY
Subluxation - incomplete disarticulation
Dislocation - complete loss
Angulation
Fracture - discontinuity in bony tissue

Common Types of fractures
1.
Fracture of Odontoid peg
Types
I - Shoulder
I I - Base
I I I - Base + Anterior arch
-ZL
Cf
2.
Hangman's fracture - is a bipedicular fracture of C2 + Anterior subluxation

neurological deficit because of the space.
Complications
i. Paralysis of diaphragm
Treatment - Laminectomy ( I t is laso done for cauda equine
syndrome)
3.
Jefferson's fracture - through the axis
SPINAL CORD COMPRESSION

Aetiology
1.
2.
3.
4.
5.
6.
7.
Road t r a f f i c accident - accounts for 63%

c. Passenger
d. Pedestrian
Fall from heights - accounts for 25%
Violence
Sports
Industrial
Domestic
Assault
8. Penetrating /Stab wound
Mechanism
a.
Hyper-extension - is called Whip lash injury
b.
Hyperf lexion - occurs in a diver hits his head on the floor of the swimming pool
c.
Direct force
d.
Penetrating spinal cord injury e.g bullets, secondary missies by bone
e.
Rotation
Forms i.
ii.
iii.
Transection
Contussion
Concussion
Types
a. Complete spinal core injury - there is loss of all functions i.e
o
Sensory
o
Motor
o
Autonomic
o
Visceral
o
Endocrine
o
Metabolic
o
Thermoregulation
b. Incomplete spinal cord injury
T
Central
Anterior
UJ
Posterior
Brown-sequard
The sub-types are

i.
Central cord syndrome
The transaction is more at central than periphery
I t is seen in hyper-extension
Occurs in the elderly
Affects corticospinal tracts, but the effect on upper limb is more than
lower limb becauses lower limb fibres are located more laterally.
50 -75% of patients recover.
ii.
Anterior cord syndrome

Affects all corticospinal ttracts i.e motor
]
Posterior column tracts are spared
Has worst prognosis : 20 - 25% recover
III.
Posterior cord syndrome

- Loss of dorsal column
IV.
Brown Sequard syndrome

i. Ipsilateral loss of motor function
ii. Ipsilateral loss of dorsal column ( dorsal column tracts do not cross the
midline in spinal cord)
iii. Contralateral loss of pain A temperature - because spinothalamic tracts cross
the midline.
a. Motor
i.
ii.
b. Sensory
i.
ii.
iii.
c.
Anaesthesia
Hyposthesia
Dysaethesia
1
]
Autonomic - causing incontinence
Associated Injuries
o Head injury
o Blunt chest injury
o Abdominal visceral injuries
o Skeletal - fractures of long bones
]
]
]
]
Management of Spinal Cord Injury

I t is grouped into
a. Pre-hospital care
Carrying patient as a single unit or using hardboard or log rolling
Use sand bag to support
Plaster
Transport the patient lying flat
b. Peripheral care - involving Private & General hospital
Transport
Resuscitation
Analgeisa
Antibiotics
Tetanus toxoid & Anti-tetanus serum.
c.
1
]
]
Plegia
Paresis
d. Neck pain
e. Back pain
f.
]
3
]
Specialised care
i.
ABC of resuscitation
Breathing using
292
3
1
]
]
1
i
o
o
o
o
Oropharyngeal airway
Endotracheal
Tracheostomy
Intermittent positive pressure ventilation
Care of the spine

Investigation
i. X-ray
Anteroposterior
Lateral
Open mouth view (OM.V) - to see the odontoid peg. I t is at CZ
level
Special view eg Foraminal to see the brachial plexus
ii. CTscan
iii. MRI
Treatment
- Immobilisation of spine using :
a. Cervical collar - in patient with subluxation or neurological deficit
b. Traction devices e.g
Gardener's Well Tongs - the weight used is 2.2kg X level of
injury.
Halobrace
Crushfield calipers
.,
Icetong
c. Plaster of Paris ( Mineaval j a c k e t )
,;
Indications for Surgery

i.
Non-healing when under conservative means
ii.
Clots
iii.
Fragments
Long term treatment- to avoid complications
a.
b.
Respiratory
i. Acute respiratory f a i l u r e - i f the injury is > C3
ii. Atelectasis
iii. Bronchopneumonia
iv. Septicaemia
Treatment
Chest physiotherapy
Chest percussion
Cardiovascular
i.
Hypotension - I t is orthostatic and is due to autonomic loss
Gastrointestinal
-
i.
Paralytic ileus - is due autonomic loss
Treatment - Pass Nasogastric tube
Faecal incontinence
ii.
iii.
Faecal impaction
Treatment
o Apply liquid paraffin
o Give adequate fluid
o Give liquelax
o Do manual manipulation
o Give enema
iv.
Genitourinary
i.
ii.
iii.
iv.
v.
Aspiration pneumonitis - due to reduction in the lower oesophageal

sphincteric tone.
Erectile impotence
Urinary tract infection
Bladder stones - resulting from the stasis of urine
Strictures
Atrophy of the bladder
Treatment - Re-intermittent catheterisation
Oermatolooical
i.
Bed sores - may cause septic shock
]
]
1
1
]
1
1
1
]
Prevention of Bed sores

i.
2-hourly turning in bed
ii.
Prevent soilage of beddings
iii.
Massage the skin - to improve blood flow
iv.
Put powder
v.
Use Foam trough
vi.
Strieker
vii.
High-tech devices
viii.
Use of water bed
->
Treatment
]
]
i.
ii.
v.
Wound m/c/s
Antibiotics
Daily dressing with honey
Debridement - can be chemical or surgical ( excision & flap)
Consult to Plastic surgeons
Musculoskeletal
i.
Contracture
ii.
Myositis ossificans
Prevention - Physiotherapy
j
~
~
I
g.
HaematoloQical
i. Deep vein thrombosis (DVT) - leading to pulmonary
thromboembolism
Treatment
o
Prophylactic anticoagulant e.g clexane, heparin or
warfarin
h.
Psychological
i.
ii.
Occupational
o
o
o
Psychosis
Neurosis
Rehabilitation
Wheel chair
Home adaptation
Adaptation of the working places
BRAIN TUMOURS <& TUMOUR-LIKE MASSES

Introduction
A brain tumour do not have to be histologically malignant before it behaves so
Brain tumours are also known to hardly metastasize except if there is VP shunt in the patient.
The gravity and tempo or presentation does not show malignancy
Incidence
I t is rare in newborns
I t increases with age
is 1 - 2/100 post-mortem bodies
Glioblastoma multiforme is the most common anaplastic brain tumour
H
3
\a
fd
Aetiology
i i
M
!!
a.
Hereditary
i.
von-Reclinghausen disease - is associated with
Acoustic neuroma
Astrocytoma
Meningioma
Neuroblastoma
295
* !
ii.
von-Hippel Lindau syndrome
Haemangioblastoma
iii.
Tuberous sclerosis
Astrocytoma
Causes of genetic damaqe

i.
Random errors
ii.
Radiation
iii.
Chemicals
iv.
- v .
b.
Viral
Host
o
o
o
factors
Proliferative state of cells
Trauma
Immune status
Embryonic
Craniopharyngioma
Chordomas
Classification
The type are
'-.
a. Gross morphology
b. By Kuslon & Bailey - this based on cells of origin. I t is valuable for understabding & therapy.
c. Based on histologic differentiation
d. Combination of 'b' and 'c' ( WHO'S recommendation)
e. Biochemical classification (Immunochemistry) e.g
Glial tumours - Glial fibrillary acidic protein (GFAP)
f. Chromosomal & genetic classification
g. Degree of anaplasia
WHO 's Classification
a. Neuro-epithelial cells
i.
Astrocytoma - most common non-neural cell
ii.
Oligodendrocytoma
iii.
Ependymoma
iv.
Neuronal tumours - are very rare because neuronal cells are permanent cells
v.
Pineal gland tumour
Posterior fossa tumour
i.
Cerebellar astrocytoma
ii.
Medulloblastoma - there are no focal signs. The incidence is fairly high in
childhood, (commonest)
iii.
Ependymoma - is also common in childhood
'
Poorly differentiated
Neuro-epithelial
tumours
i.
Glioblastoma mulitif orme - is the most common anaplastic brain tumour
ii.
Medulloblastoma - *
- Know it well
b. Tumours of nerve sheath
i.
Schwannoma
ii.
Neufibroma
c.
Tumours of Meninges
i.
Meningioma - The subtypes are
ii.
Others
d. Primary cerebral lymphoma - involves cells of reticuloendothelial system

e. Tumours of germ cell origin
i.
Primitive yolk sac tumour
ii.
Teratomas
iii.
Choriocarcinoma
iv.
Seminoma
'
f.
Vascular origin
i.
Angiomas
g.
Malformation tumour
i.
Craniopharyngioma - from cells in Rathke's pouch
ii.
Rathke's cyst
iii.
Colloid cyst
iv.
Dermoid cyst
v.
Harmatomas of hypothalamus
h. Vascular malformation
i.
Arterio-venous malformation
ii.
Carvernous angioma
iii.
Capillary end haemangioma
i.
Tumours of anterior pituitary
j.
Local extension of regional tumour

i.
Chordoma - from nucleus pulposus
ii.
Sarcoma from maxillary sinus
iii.
Carcinoma of
sinus
k.
Metastatic tumours - is common and the history is usually short. Genrally, they
and produce significant brain oedema,
i.
Carcinoma of breast
ii.
Carcinoma of prostate
iii.
Carcinoma of cervix
iv.
Choriocarcinoma (gestational) - is frequent
v.
Melanoma
vi.
Renal carcinoma
Note, the last 2 cause intracerebral haemorrhage

I.
Unclassified tumours
|j 5 Common Brain Tumours
|!
Glioblastoma multiforme - 25% (glioma)

Anaplastic astrocytoma - 20% (glioma)
Meningiomas - 20%
4.
5.
Astrocytomas (benign) - 5% (glioma)

Pituitary tumors - 5%
Note
I
!
1.
2.
3.
Gliomas account for 50% CNS tumour in adults, and they are usually supratentorial
I n children, they are usually infra-tentorial i.e posterior fossa tumour.
Meningioma &. Pituitary tumours are rare in children
i Pathogenesis
I
(
I
'
The tumour cells are likely to arise from the dividing cells in the cell cycle
Most tumours arise from DNA abnormality which may be inherited or acquired.
The mechanisms involved are
i.
Failure of tumour suprressor gene
ii.
Increased activityof oncogene - This is f i r s t identified in oncogenic
viruses e.g Ebstein barr virus, Burkitt's lymphoma, Hepatitis B virus
Tumourigenesis - The f i r s t step is the formation of clone of cells with abnormal

DNA. This leads to tumour growth and extension beyond the surrounding tissue.
Note, spontaneous mutation cells can be removed by reticulo-endothelial system.
Or it can be dominant and transferred to offspring e.g neurofibromatosis
j
f
l|
Common Clinical Features

1. Features of raised ICP
Headache
Frontal- f or supratentorial
Occipital - suggests inf ratentorial
I t is usually worse on awakening
I t is due to impaired venous return in supine position
'o
o
o
Effotless vomiting - usually without nauses, but if the tumour is the floor e.g
ependymoma, it may be associated with nausea.
Drowsiness /alteration in level of consciouness
PapiIloedema - I t is NOT seen in
Children with open sutures
Adults with optic atrophy
Bilateral paralysis of 6 t h cranial nerve - is due to its stretching as it passes across the
petrous bone.
>
2. Seizures - Occurs in tumour closed to the cortex e.g in thalamus. I t is said that a tumour
occurring for the f i r s t time in adult is caused by tumour until proven otherwise.
298
3. Focal neurologic deficits - the focal signs help to localize the lesion e.g
o
Bitemporal hemianopia
o
Loss of speech - Broca's area
o
Visual field defects
o
Truncal ataxia - Vermis tumour of cerebellum
o
Numbness in right ankle + incontinence + tonic-clonic seizure + frontal headache =
Superior Paracentral lobule
4. Neighbourhood syndrome - i.e a brain tumour employs neighbouring neurons to behave in abnormal
way e.g seizures
Note
- these are extended focalizing features e.g cranial nerve palsy ( I I , IV, V I ) , paraplegia
5.
Hydrocephalus
6.
Endocrine features - suggests tumour from pituitary gland e.g prolactinoma
7. Meningeal irritation - it is very rare, but may follow a bleeding episode. I t may be due a pituitary
tumour or metastatic cancer or malignant melanoma.
8. Tumours can be located in the silent areas in the brain ( Silent tumours ) e.g anterior temporal
lobe, non-dominant frontal lobe.
- Involves the tumour-1 ike masses
1.
Vascular lesions - Aneurysm
2. Inflammatory
i.
ii.
Cerebral abscess
Subdural empyema
3. Trauma
4. Toxic disorder
Management
Aim
i.
ii.
Locate the site of the lesion

Find out the cause
Investigation
j
1. Plain skull
I
o
|
o
o
o
o
o
x - r a y - m a y show
Copper-beating appearance
Enlarged skull
Dilated sutures ( i n children)
Sella turcica expansion - suggests pituitary tumour
Hyperostosis - suggest meningioma
Calcification in tumours e.g
299
i.
ii.
o
Craniopharyngioma
Oligodendroma
Meningioma
Collapse of spine or erosion of pedicles e.g neurofibroma
2. Ventriculography - to check for distortion

3. Angiography - as large meningioma are highly vascular. I t is supplied by Middle meningeal artery
4. CT scan - for direct visualization. I t shows
o
Location
o
Size
o
Configuration
j o
Relatioship to structures in the head
o
Histology
o
Vascularity
Note
Hyperdense lesion suggests melanoma & GIT adenocarcinoma
5. MRI - for direct visualization as well
1
1
1
1
1
1
1
]
CT scan vs MRI
i.
ii.
CT scan shows histology but MRI does not

MRI gives ultimate anatomical separation
Treatment
_
J
Depends on the type of tumour

Principles of Treatment
1. Reduction of raised ICP
i.
Give dexamethasone - if the oedema is due to vasogenic cause
ii.
Head raise from the bed - to reduce venous, thus increasing the perfusion pressure.
Hi.
Improved ventilation - Increased oxygen leads to reduction in PC02 and consequent
reduction in vasoconstriction
j
|
.
J
2. Treatment of underlying cause e.g

a. Seizures - Anticonvulsant : Phenobarbitone
b. Endocrine symptoms - give Bromocriptine for prolactinoma. I t is a dopamine
receptor blocker, and it must be used for life
|
c. Hydrocephalus - shunt
3. Treatment
i.
ii.
j
I
Modalities
Do nothing
Surgery
is required for VP shunt
To take sample for biopsy
To ascertain the nature of tumour
I t is therapeutic - for both benign & malignant ( i t helps to reduce the mass e.g
glioblastoma.
Embolisation may be done pre-operatively for vascular tumours.
1
1
1
1
300
Types
a.
b.
Simple biopsy
Excision biopsy (Partial or total) e.g for meningioma, pituitary tumour and
craniopharnygioma which are benign and well defined. Note, astrocytome is
benign, but NOT well defined, thus making it difficult to cure. For other
tumours, the modalities listed below are used.
Radiotherapy
I s used for the following because they are rapidly growing tumours
o Anaplastic astrocytoma
o Glioblastoma multiforme
I t is also good for multiple metastasis
I t is given in fractions for 2 weeks.
Types
a. Conventional teletherapy
From linear acceleration
I t targets the site of tumor, thus small surrouding field
receives the radiation.
Side effects
Dermatitis
Alopecia
b.
Brachytherapy
This is short-distant radiation
I t is very good for carcinoma of the cervix ,
c. Gamma knife
- I t is called Stereostatic radio-surgery
- 90% of the radiation gets to the tumour
Advantage
To increase the intensity of radiation
Chemotherapy
Success rate is poor for primary tumours, but secondary tumours are
sensitive to it
histology & grading of the tumour

Meningioma can be cured. I t hardly transforms to malignant lesion
The prognosis of benign astrocytoma is also good if discovered early because it
naturally transforms into malignant lesion.
DEGENERATIVE DISEASES OF THE SPINE

Pathophysiology
Nucleus pulposus contains a lot of water which decreases with age
The leads to loss of shock absorption and resulting into fracture
The decrease in disc height causes increased friction and eventually formation of osteophytes
Complications
1. Myelopathy - due to vascular compromise
Investigation
- 1. MRI - to see the soft tissue involvement
Treatment
Laminectomy
Cervical discectomy
Fenestration
Microdiscectomy
Fibreoptic discectomy
i.
ii.
v.
i.
OPEN DEPRESSED SKULL FRACTURE (ODSR

Anatomy
o
o
o
o
Scalp
Bones
Suture
Sinuses
Definition
Is simple depressed facture ( closed injury)
No underlying laceration
No risk of infection
Compound
Scalp laceration
Communited
May co-exist with linear fracture
May associate with intracranial haemorrhage
i.
Extradural
ii.
Subdural
iii.
Intracerebral
!
May involve frontal sinus, dural venous and other vascular structures e.g middle meningeal vessel
Aetiology
Mechanism
I
i.
II
Blunt
302
ii.
iii.
iv.
v.
vi.
vii.
viii.
ix.
Direct crushing force

Penetrating
Scalp
Skull fracture/Diploic vein
Dural tear
Parenchymal damage
Laceration cotussion
Dural venous sinuses/ventricular
a.
Deformity
b.
Underlying brain injury
i.
Head injury
ii.
Loss of consciouness
iii. Vomiting
iv. LS
v.
Seizures
c.
Polytrauma
d.
Infection - of scalp, skull, meninges, intracranial abscess
Investigations
1. Plain skull x-rays
a. Anteroposterior
b. Lateral
c. Towne's view d. Tangetial views
2. CTscan
3. Cervical spine x-rayy
4. MRI
5. Ful blood count
6. Serum electrolytes <& urea
7. PT, PTTK
8. Blood sugar
9. ECG
10. Chest x-ray
Treatment
Objective
Remove fracture fragments
Debride devatilised soft tissue
Dural closure within 24 hours. Replace large bone fragments. I f it is > 24 hours,
discard.
Surgery
Positioning depends on site of fracture
Liberal irrigation
Examination under anaesthesia
Retractions + haemostasis
303
1.
V.
vi.
vii.
viii
Inspect the bed

Debride
Nylon
Drain
Immediate Post-operative
X-rays
CT scan
ii.
Antibiotics
iii.
iv.
Head injury protocol
Complications
1. Cosmetic deformity
2. Infection
3. Epilepsy
4. CSF fistula
5. Focal neurological deficit
6. Hemiparesis
7. Tinnitus
CARDIOTHORACIC SURGERY
CHEST TRAUMA
Introduction:
Associated injuries are present in about 30% of cases, commonly in extremity or cranium.
Less than 15% of chest trauma patients will require any procedure more invasive than the insertion of a
chest tube
Mode
Q
> D
D
D
of Injury:
Penetrating, Blunt or Blast.
Gunshot or stab wound.
Low-velocity or high velocity injury.
Multiple injuries or thoracic only.
! Initial Assessment:
History
Examination - AIRWAY, BREATHING AND CIRCULATION

'Location of injury
Lower 6 ribs: consider abdominal penetration and blunt organ injury
Upper 6 ribs: lung, heart, and great vessel injury
304
]
1
-
ft-
Immediately Treatable cause of death

1. Open pneumothorax
2. Airway Obstruction
3. Flail Chest
4. Tension Pneumothorax
5. Massive Haemothorax
6. Cardiac Tamponade
1. Open Pneumothorax
Cyanosis, respiratory embarrassment, sucking wound of the chest and shock.
Ineffective respiration
Immediate therapy -
Occlusive dressing to the wound

Definitive therapy chest intubation, usually 5 th intercostal space, midaxillary line.
r;
r
2. Airway Obstruction:
o Obstruction usually at level of larynx (e.g. clothesline injury) or trachea
o Presents with stridor change in quality of voice, indrawing of suprasternal notch and epigastrium.
o therapy is establishment of patent airway with endotracheal intubation.
3. Flail Chest
comminuted fracture of two or more ribs usually anterior or lateral in location
^paradoxical respiration -> abnormal airflow in the lung

major cause of hypoxia = pulmonary contusion
Initial Chest Xray may be negative

Flail Chest: A
Flail Chest: B
. r
Management
oxygen therapy, judicious intravenous fluid hydration, intercostal or epidural nerve block and chest
physiotherapy.
mechanical ventilation
careful monitoring in Intensive Care Unit
4. Tension Pneumothorax:
blunt injury with failure of complete collapse of the damaged lung
creates a one-way-valve = airflow into the pleural space without means of exit
mediastinal displacement, compromise of the ipsilateral lung and decrease in venous return
'severe respiratory distress,
hypotension,
305
absent breath sounds in ipsilateral chest

chest pain
tachycardia
tracheal deviation
neck vein distension.
TREATMENT:
-IMMEDIATE
insertion of "large-bore" needle (size 14FS or larger) 2nd intercostal space MCL
insertion of No. 11 scalpel blade (supracostal) 5 th intercostal space MAL
-DEFINITIVE
closed thoracostomy drainage
'5. Haemothorax
Considered massive with rapid loss of >1500mls of blood from the pleural cavity.
I Commonest source of bleeding from trauma is chest wall vessels
Treatment:
;
Fluid replacement through large caliber intravenous lines

oxygen supplementation
closed thoracostomy drainage
Close monitoring of drainage, and blood replacement
6. Cardiac Tamponade
Most commonly results from penetrating injuries
Diagnosis ->
location of the injury
hypotension with neck vein distension
muffled heart sounds
weak extremity pulses
Investigation:
urgent ultrasound examination
subxiphoid pericardiocentesis
Therapy
Immediate percutaneous drainage
Thoracotomy f o r definitive
Fracture Ribs
Commonest Chest Injury
Localised pain
Tenderness on palpation
Crepitus
Deformity; palpable or visible
Treatment: analgesics -> systemic, intercostal or epidural
CONGENITAL HEART DISEASE

1. ATRIAL SEPTAL DEFECT
Incidence:
5 t h most common CHD when single
Seen in 33-50% of other CHD
Secundum ASD commoner in females
Pathology: Types
Secundum -defect in the foramen ovale
Sinoseptal-sinus venosus defect
Primum - involve A-V valve apparatus
Common atrium - total absence of septum
Pathophysiology:
L e f t -> right shunting -> t PBF
S h u n t flow depends on RV compliance and PVR
E a r l y presentation due additional shunts - PDA, VSD
F
f
r
r
\ ;
Clinical features:
M a j o r i t y asymptomatic
W h e n large ->easy fatigability and dyspnoea
Hyperactive precordium with TRV impulse
Second heart sound is split
A systolic (crescendo-decrescendo) murmur at the left upper sternal border
Congestive heart failure
Treatment:
For CHD - medical therapy.
Surgery - closure , early for large defects >8mm or failed medical control.
Surgery - closure for all defects with Qp:Qs >1.5:1 after age 3yrs.
Surgery - closure for all adults.
Complications: of unrepaired defects
Pulmonary vascular obstructive disease
R -> L shunt -> cyanosis
Subacute bacterial Endocarditis
307
1
"1
Paradoxical emboli- stroke

Arrhythmias- AF and atrial flutter
2. PATENTDUCTUS ARTERIOSUS
Incidence:
6 t h most common CHD
Related to rubella infection
Frequent in premature
t Frequency at high altitudes
... J
'I
I
]
3
Clinical features:
M a j o r i t y asymptomatic
Symptomatic cases -> CHF , from excessive pulmonary flow
Continuous syst. And diast. (Machinery) murmur It. Subclavicular/lt. Upper sternum
Easy fatigability, SOB, pallor sweating and cool extremities with exertion.
Bounding pulses, increase LV apical impulse, thrill, continuous murmur
Sounds consistent with pulmonary edema -> rales and wheezing.
1
]
1
1
Medical therapy:
Supplemental oxygen -> closure in full term.
Indomethacin -> closure in pre-term and premature; 80% success.
Operative therapy:
Coil occlusion when feasible.
Surgical closure - ligation or division and suture.
J
]
COARCTATION OF AORTA
"]
Incidence
Unknown but < among Caucasians
Present in 9% of all congenital heart diseases
Commoner in females than males
Clinical features:
Usually asymptomatic
Incidental findings of t Bp. Of upper extremities, I femoral pulses, systolic murmur over
precordium and back
]
]
Management:
coarctectomy with end-to-end anastomosis with or without use of subclavian artery flap
Re-coarctation recurs earlier with early repair
Balloon angioplasty for recurrence
J
|
308
1
1
TETRALOGY Of FALLOT
incidence:
Occurs in 0.19-0.26/1,000 live births.
Constitutes 8% of CHD.
M o s t common cyanotic CHD beyond 1 week of age.
'atholoqy:
V S D located in the membranous septum
Large VSD= equalization of LVP/RVP
RVOT is hypoplastic(small PA valve)
RV hypertrophy
Foramen ovale patent in A0%
linical features:
25% cyanotic at birth; 75% at 1 year
Cyanotic spells in infants/toddlers
Squatting attacks T SVR I venous return -> I cyanosis
Systolic murmur due RVOT obstruction and pulmonary stenosis
Management:
Medical; Cyanotic spells
Knee chest position ->TSVR
Morphine -> 4RVOTO
Propanolol -> i RVOTO
Epinephrine -> tSVR -> Tl_VOTO-> i R->L shunting
Management:
Surgical
Palliative; Rarely required f o r critical infants with complex anatomy
->Aorto-pulmonary shunt
Complete repair 6mth to 1 year
5. TRANSPOSITION (T6A)
Incidence:
0.2-0.4/1,000 live births.
Second most common congenital heart disease encountered in early infancy.
'atholoqy
A o r t a anterior to right of MPA
A V anterior/right to RV
L V f low-> MPA; RV f low-> Aorta
V S D present in 50%
PDA and patent foramen ovale af birth
309
linical features:
Usually full term; 64% males
V S D present->cyanosis + CHF
VSD absent->cyanosis -ve to Oz therapy
Systolic murmur of vsd or LVOTO
]
1
ianaqement:
Palliative; Now rarely required:-.
Rashkin procedure (atrial septostomy) to improve atrial mixing for small PFO.
MPA banding with multiple VSDs or preparatory in older children for arterial switch operation.
Definitive
A t r i a l switch - mustard or Senning
Arterial switch- f o r infants minus VSD< 2wks' or plus VSD at 2-3 mths
Rastelli f o r LVOTO with VSD
0
H
ACQUIRED) HEART DISEASE
^natomy - Pericardium
Consist of visceral (epicardium) and parietal layers lined with mesothelial cells.
Parietal layer non-compliant, but distensible over time
Pericardial fluid volume not linearly relatedto
pericardial pressure
|athophysioloqy - Pericardium
{Definitions:
[pericardial effusion = accumulation of fluid with no haemodynamic alteration
[-Pericardia/ tamponade - accumulation with haemodynamic derangement
rPulsusparadoxus = I in arterial systolic pressure of 10 mmHg or more with inspiration
Pericardial Disease
1.
2.
Purulent Pericarditis
Constrictive Pericarditis
1
1
310
PURULENT (INFECTIVE) PERICARDITIS

ji
!
j|
I.
IT.
III.
IV.
V.
VI.
g.
/êtiological factors (Developed countries)
pneumococcal pneumonia
infective endocarditis
cardiac surgical procedures
septicaemia
immunological compromise patients
commoner in children than adults
b. /êtiological factors (Developing countries')

i. disease of children >75% of cases
ii. bronchopneumonia
j!
iii. Pyomyositis
!!
iv. Osteomyelitis
v. Septicaemia
vi. Liver abscess
Clinical features:
Fever, chills, dyspnoea
pericardial friction rub, when fluid minimal
muffled heart sounds common
elevated neck veins frequent
!
low volume pulse
paradoxical pulse uncommon
Investigation
1. Electrocardiogram- diffuse ST segment elevation; low QRS voltage common
2. Chest Xray:
globular shaped cardiomegaly
pleural effusion usually bilaterally
presence of pneumonic changes
l
3. Echocardiogram:
most sensitive test
confirms, localizes, and quantifies pericardial effusion.
4.
Pericardiocentesis
establishes the diagnosis
provides material for culture
[Treatment:
J
| pericardiostomy tube drainage with irrigation and breakdown of fibrinous adhesions

appropriate antibacterial drugs
pericardiectomy, rarely required
CONSTRICTIVE PERICARDITIS
Aetiological factors:
,
-Ûnknown in majority
Specific infections -> Bacterial, TB, Fungal, Viral, Parasitic (Amoebic)
Connective Tissue disease
Neoplastic disease / Radiotherapy
Trauma
!
Metabolic (uraemic; common in US)

......
Pathophysiology:
constricting envelope surrounds the entire heart and interferes with diastolic filling.
Symptoms:
j
Dyspnoea; Abdominal swelling
|!
Oedema; Palpitations
Cough; Orthopnoea
Signs:
|
"Distended neck veins
;!
Hepatomegaly
;|
|
!j
Massive ascites common ->diagnostic pitfalls in DDx.

'Paradoxical pulse uncommon
*Pericardial knock common
Investigation:
|| 1. Chest Xray
I
2. Echocardiography
3. Cardiac Catheterization
i; 4. CT scan and MRI
1!
i
'
'
'
"
Treatment:
Pericardiectomy only effective therapy
excision of parietal/visceral pericardium from phrenic to phrenic nerve anteriorly
Result:
perioperative, may require inotropic support and intensive care
Hnaemodynamic response may be delayed

resolution of ascites gradual
operative mortality 10-20%
I ; I
jt
VALVULAR HEART DISEASE
fr
MITRAL STENOSIS
Aetiology
majority due rheumatic heart disease
1 post group A beta-haemolytic Strep. Infection in childhood
early presentation of valve pathology in Africans; within 5-10yrs
late presentation in Caucasians; within 10-30yrs
Clinical Features:
Dyspnoea on exertion; Orthopnoea
, Paroxysmal Nocturnal Dyspnoea
i Fatigue; Haemoptysis rare
Clinical Signs:
Hepatomegaly, Ascites and oedema
Systemic thromboembolism (20% of cases)
Auscultatory signs-presystolic murmur
- t f i r s t heart sound
-opening snap
I
-apical diastolic rumble
r
r
Investigations:
1. Chest Xray
2. Electrocardiogram
3. Echocardiogram
4. Cardiac catheterization and angiography
rarely required for assessment of associated cardiac pathology
Treatment:
Medical
Control of Right heart failure
Control of arrhythmia
Prevention of thromboembolism
Percutaneous balloon valvuloplasty
Surgical
For all symptomatic patients
indicated for >NYHA Class I I
Classification.
I - Activity without symptoms
I I - Symptoms with ordinary activity
I I I - Symptoms with < ordinary activity
IV - Symptoms at rest
313
MTRAL INCOMPETENCE
Aetiology
Majority still due rheumatic in developing countries
Myxomatous degeneration in 30 -70% in developed countries
Other causes -> EMF, Papillary muscle dysfunction, endocarditis
finical Features:
Late onset of onset of symptoms
Weakness, fatigue, dyspnoea on exertion
Hyperdynamic & displaced apex beat
apical systolic murmur, blowing, & moderately harsh, radiating to axilla
[investigations:
i. EK-> AF, LVH, RVH (15%)
ii. Chest Xray -> t LA TLV
iii. Echo -> abnormalities documented
iv. boppler colour flow mapping -> assess degree of regurgitation
v. Cardiac catheterization and angiography
vi. MRI ->assess cardiac structure and function
30
fherapy:
1
]
]
]
1
3
1
Medical -> mainstay afterload reduction; include digoxin and diuretics

Surgery ->for symptomatic patients with chronic mitral regurgitation (NYHA c\ass I I or greater)
MV repair or replacement
Results:
Prognosis determined by degree of LV systolic dysfunction present
Mortality less with repair (1-4 vs. 4-12%) but reoperation greater (5-30% at 5yrs.)
Age and anticoagulant usage determinant of type of replacement valve
fypes of Valves:
Preservation of "native" valve
Tissue valves: Homograft, Porcine or pericardial (bovine)
Mechanical Valve: Ball or disc
|Complications of Valves:
Technical -> periprosthetic leaks
Mechanical -> Strut fracture, rupture leaflet, calcification
HaematologicaI -> Haemolysis, thrombosis
Bacteriological -> Endocarditis
j
[[Anticoagulation Control
-Types*
Aspirin and Dipyridamole
Warfarin and Coumadin drugs
314
T
1
"
Heparin
-Indications
LUNG CANCER ANO MEDIASTINAL TUMOUR

LUNG1 CANCER
Incidence'(Leading cause of smoking &. cancer related mortality in US
Commonest malignancy worldwide
5 8 % new cases occur in developing world
Mortality/morbidity:
Highly lethal-> 5yr survival 14% in US, 8% in Europe and 3 rd world
\o\ecu ar biology:
Mutation of rasoncogenes;Also c-mycand c-raf
Abnormality of p53 suppressor gene
i
Symptoms due to primary tumor

W Central-> cough, dyspnoea, atelectasis, pneumonia, haemoptysis
Peripheral'-> effusion, chest pain
Symptoms due to regional spread
+SVC obstruction, phrenic or recurrent laryngeal palsy.
Horner's syndrome.
Brachial plexus compression.
Pericardial effusion.
Symptoms due paraneoplastic syndrome:
Hypercalcemia (PTH).
[Finger clubbing, & osteoarthropathy.
Trousseau syndrome (hypercoagulopathy).
' [ I
Histological/Clinical characteristics
AdenoCa (30-40%) -> peripheral, scar Ca, non-smokers
Subtype-> Brochoalveolar-> interstitial or pneumonic or multifocal
Squamous (25-30%) -> cavitary, proximal t calcium
Large cell (10-15%) -> large & peripheral, + gynaecomastia
Aetiological factors:
Cigarette smoking: in US 90% patients
Asbestos; silicate type
Radon; product of uranium
H I V infection (?)
Aromatic polycyclic hydrocarbons (beryllium, nickel, copper, chromium, diesel exhaust)
linical features:
N o n specific
cough, chest pain, haemoptysis, dyspnoea etc
signs of chronic parenchymal lung disease +/- paraneoplastic syndrome
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
<
c Evaluation
putum Cytology
lain chest X-ray
CT scan
Bone scintigraphy
Positron emission tomography
MRI
Flexible fiberoptic bronchoscopy.
iAediatinoscopy/Mediastinotomy.
"T guided needle biopsy.
Thoracoscopy.
0
i.i
herap( utic Determinants:

T N M Staging system ( 4 stages).
Evaluation f o r resectability.
Evaluation f o r operability.
.1
freatm :nt
Surgery f o r Stages I , I I and I l i a .
Chemotherapy/Radiotherapy f o r others.
j
Results of treatment:
S t a g e I -> 55-75%
S t a g e I I -> 40-50%
VStage I I I -> 5-35%
S t a g e I V -> less than 5%
1
MEDIASTINAL TUMOUR
Anatomy
From thoracic inlet to diaphragm - sternal notch to xiphoid process anteriorly; T 1 to T 11
posteriorly; parietal pleural reflections laterally.
3
1
Surgically divided into anterior, middle and posterior.

A n t e r i o r : bordered by sternum and anterior pericardial reflection.
Middle: between anterior and posterior pericardial reflection.
Posterior: between posterior pericardial reflection and vertebral column.
Anatom / - Contents:
A n t e r i o r -> thymus gland, aortic arch and its branches, great veins, lymphatics, and f a t t y areolar
tissue.
Middle -> heart, pericardium, phrenic nerves, tracheal bifurcation and main bronchi, hila of each
lung, and lymph nodes.
316
r
Posterior -> esophagus, vagus nerves, sympathetic nervous chain, thoracic duct, descending aorta,
azygous and hemiazygous systems, paravertebral lymphatics, and f a t t y areolar tissue
Anatomical - Location
A n t e r i o r - 54%
Posterior - 26%
Middle - 20%
li
r
*' "
-*
Anterior.
Thymoma - 31% (*local 28%).

Lymphoma - 23% (*local 28%).
Germ Cell - 17% ("local 16%).
Endocrine - 5% ("local 19*).
*
*-*
"*^
I*!
r
__
Adegboye et al. 2002 Nig. J . Surg. Vol 8. No. 2.
Middle.
Pericardial Cysts - 35%.
Lymphoma - 21%.
Bronchogenic Cysts - 22%..
*Local: Cysts - 57%; Lymphoma 28%.
* Adegboye et al. 2002 Nig. J . Surg. Vol 8. No. 2.
Posterior.
Neurogenic - 52% *(62%).
Bronchogenic Cysts - 22%.
Enteric Cysts - 7% *(8%).
*Local - Endocrine-12%.
*Adegboye et al. 2002 Nig. J . Surg. Vol 8. No. 2.
Clinical Features:
Asymptomatic-> 5 6 - 6 5 % (76% Benign)
Symptomatic -> 62% Malignant
Anterior -> 75%
Posterior -> 50%
Middle-> 45%
Associated Systemic Syndromes:
Thymoma -> MS., RBC aplasia, SLE.
Lymphoma -> Anaemia, MG.
Neurofibroma -> von Recklinghhausen's.
Enteric Cyst-> Vertebra! anomalies, DU.
Hodgkin's Ds.-> Pel-Ebstein fever.
Evaluation
History
Radiology
Standard chest films
Tomography
Fluoroscopy
Arteriography
Venography
Computed tomography
Magnetic resonance imaging
f'*
Barium swallow
Myelography
Ultrasonography
Operative procedures: Radioisotope scanning, Mediastinoscopy Serology

Endoscopy, Thoracotomy, Bronchoscopy
Needle aspiration and biopsy
, Mediastinotomy
Treatment
Thymoma -> Curative resection possible in majority.
Lymphoma -> Chemotherapy.
Hodgkin's Lymphoma -> megavoltage external-beam radiation.
Endocrine tumours -> surgical excision via sternotomy.
Primary Cysts -> Surgical excision.
Mesenchymal tumours (sarcomas) -> surgical resection offers best prognosis.
Germ Cell tumour - Resection when possible.

Surgery Lecture Notebook

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Surgery Lecture Notebook

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University

Upper gastrointestinal tract bleeding

Lower gastrointestinal tract bleeding

Diseases of the large bowel

Diseases of the ano-rectum

Peptic ulcer and complications (DrLadipo)

Varicose veins, peripheral arterial disease (Prof. Ajao)

Section H- Hepatobiliary & Endocrine Surgery

Non-malignant Thyroid Diseases ( M r Akute)

Non-malignant Thyroid Diseases (DrAfolabi)

Thyroid Crisis (Seminar)

Thyroid Storm (Tutorial)

Neck Swelling : Non-goitrous (h^Akute)

Surgical Jaundice (DrAfolabi)

Benign Breast Diseases (Dr Ogundiran)

Malignant Breast Disease (Dr Ogundiran)

Portal Hypertension (Dr Afolabi)

Liver, Gall Bladder, & Pancreatic Diseases

Section ill- Oncology ( Part I )

Congenital Anomalies of the GIT (Dr Ogundoyin)

Surgical Jaundice in Children

Undescended Testis & Hernia

Intantile Hypertrophic Pylroric senosis

Congenital Anomalies of Anterior Abdominal Wall

Congenital Neck Masses

Section VI- Plastic & Reconstructive Surgery

Wound closure, skin grafts, flaps, pedicles

Wound healing & Complications

Chronic Ulcers, Pressure Ulcer & Lymphoedema

Burns & Scalds

Surgical skin lesions

Plastic surgery of the head and neck

Plastic surgery of the hand

Definition, Classification and PrilclplJjof Management of Fracture

Complications of fractures and dislocation

Fractures and dislocations of tha lowfllimbs

Fractures and dislocations of the]upf

Infections of the bones and joints

Back pain, Tuberculosis of the spine

Club Foot (Congenital talipes equinovarus)

Evaluation of the patient with neurological diseases

Cranial congenital malformations

Trauma of the spinal cord

Brain tumours & Tumour like Masses-1

Spinal cord tumours

Cervical and lumbar disc disease

Bleeding duodenal ulcer

PCM <24% or HB ddlWgj f

In Chronic liver disease

Epigastric tenderness - Duodenal/Gastric ulcer / Gastritis

Double contrast barium studies

Depends on the cause

a. Bleeding duodenal ulcer

c. Stress Ulcers/Acute gastritis

Vasopressin, Lysopressin - to vasoconstrict splanchnic veins. I t is given

Flexible Endoscopy - for

Note, all the above procedures are PALLIATIVE !

Gastric tumour - Resection

Blood Dyscrasias - Exclude other conditions

Rectal and Anal

Carcinoma of rectum/ anus - Carcinoma of rectum is the commonest of bleeding per

b. Secondary -as a result of

Full blood count

b. Specific - I s aimed at localizing the bleeding sites