PROBLEM 3B

Felix Halim
405110204
ACUTE ABDOMEN
 Definition
Acute abdomen sign and
symptoms of abdominal pain and
tenderness, a clinical presentation
that often requires emergency
surgical therapy.
Nonsurgical Causes of
Acute Abdomen
Endocrine and Metabolic Causes
Uremia
Diabetic crisis
Addisonian crisis
Acute intermittent porphyria
Hereditary Mediterranean fever
Hematologic Causes
Sickle cell crisis
Acute leukemia
Other blood dyscrasias
Toxins and Drugs
Lead poisoning
Other heavy metal poisoning
Narcotic withdrawal
Black widow spider poisoning
 Surgical Acute Abdominal
Conditions
Hemorrhage
Solid organ trauma
Leaking or ruptured arterial aneurysm
Ruptured ectopic pregnancy
Bleeding gastrointestinal deiverticulum
Arteriovenous malformation of gastrointestinal tract
Intestinal ulceration
Aortoduodenal fistula after aortic vascular graft
Hemorrhagic pancreatitis
Mallory Weiss syndrome
Spontaneous rupture of spleen
Infection
Appendicitis
Cholecystitis
Meckels diverticulitis
Hepatic abscess
Diverticular abscess
Psoas abscess
Perforation
Perforated gastrointestinal ulcer
Perforated gastrointestinal cancer
Boerhaaves syndrome
Perforated diverticulum
Obstruction
Adhesion related small or large bowel obstruction
Sigmoid volvulus
Cecal volvulus
Incarcerated hernias
Inflammatory bowel disease
Gastrointestinal malignancy
Intussusception
Ischemia
Buergers disease
Mesenteric thrombosis or embolism
Ovarian torsion
Ischemic colitis
Testicular torsion
Strangulated hernias
 Classification

Visceral
pain
Abdomin Parietal
al Pain pain
Reffered
pain
 Classification
Visceral pain
Tends to be vague, poorly localized to the epigastrium,
periumbilical region, or hypogastrium
Depending on its origin from the primitive foregut,
midgut, or hindgut
Mediated by autonomic nerves (sympathetic and
parasympathetic)

Parietal pain
Coorresponds to the segmental nerve roots innervating
the peritoneum
Tends to be sharper and better localized
 Referred pain
Perceived at a site that is distant from the
sourced of stimulus
For example irritation of the diaphragm
may produce pain in the shoulder
Locations of Reffered Pain and
Its Causes
Right Shoulder
Liver
Gallbladder
Right hemidiaphragm
Left Shoulder
Heart
Tail of pancreas
Spleen
Left hemidiaphragm
Scrotum and Testicles
Ureter
 Some mechanisms of pain
originating in abdomen
Inflammation of the parietal peritoneum
Pain of parietal peritoneal inflammation is steady and aching
in character and is located directly over the inflamed area
transmitted by somatic nerves supplying the parietal
peritoneum
Pain intensity type and amount of material to which the
peritoneal surfaces are exposed in a given time period
The pain of peritoneal inflammation is invariably accentuated
by pressure or changes in tension of the peritoneum
Produced by palpation or by movement, as in coughing or sneezing
Lies quietly in bed, preferring to avoid motion,
In contrast to the patient with colic, who may writhe incessantly
Tonic reflex spasm of the abdominal musculature, localized to
the involved body segment
 Obstruction of hollow viscera
Intermittent, or colicky
Distention of a hollow viscus steady pain + very occasional
exacerbations
The colicky pain of obstruction of the small intestine
periumbilical or supraumbilical, poorly localized
Acute distention of the gallbladder pain in the right upper
quadrant with radiation to right posterior region of the thorax / to
the tip of the right scapula
Distention of the common bile duct pain in the epigastrium
radiating to the upper part of the lumbar region
Obstruction of the urinary bladder dull suprapubic pain, usually
low in intensity
In contrast, acute obstruction of the intravesicular portion of the ureter
severe suprapubic and flank pain radiates to penis, scrotum, or inner aspect
of the upper thigh
 Vascular Disturbances
Pain associated with intraabdominal vascular
disturbances is sudden and catastrophic in nature
Embolism or thrombosis of the superior mesenteric artery
Severe & diffuse; only mild continuous diffuse pain for 2 or 3 days before
vascular collapse or findings of peritoneal inflammation appear
Impending rupture of an abdominal aortic aneurysm
Abdominal pain with radiation to the sacral region, flank, or genitalia;
persist over a period of several days before rupture and collapse occur

Abdominal wall
Pain from the abdominal wall constant & aching
e/ Movement, prolonged standing, and pressure
accentuate the discomfort and muscle spasm
Ex: hematoma of the rectus sheath
 Approach to the patient
Only those patients with exsanguinating
intraabdominal hemorrhage (e.g., ruptured
aneurysm) operate
But in such instances only a few minutes are
required to assess the critical nature of the
problem

Orderly, pains takingly detailed history

Even though a reasonably accurate diagnosis
can be made on the basis of the history alone in
the majority of cases
Differential diagnose
 Examination
Simple critical inspection of the patient
facies, position in bed, and respiratory activity

Gentle percussion of the abdomen (rebound tenderness on a

miniature scale), a maneuver that can be far more precise and
localizing
Abdominal signs may be virtually or totally absent in cases of pelvic
peritonitis

Auscultation of the abdomen

strangulating small intestinal obstruction or perforated appendicitis normal
peristaltic sounds
proximal part of the intestine above an obstruction becomes markedly
distended and edematous weak or absent even when peritonitis is not
present
Severe chemical peritonitis truly silent abdomen
 Laboratory examination
White blood cell count
>20,000/L may be observed perforation of a viscus, but
pancreatitis, acute cholecystitis, pelvic inflammatory disease, and
intestinal infarction
Normal count is not rare in cases of perforation of abdominal viscera
Urinalysis
state of hydration or rule out severe renal disease, diabetes, or
urinary infection
Serum amylase levels may be increased by many diseases other than
pancreatitis, e.g., perforated ulcer, strangulating intestinal
obstruction, and acute cholecystitis
Plain & upright or lateral decubitus radiographs of the
abdomen
Intestinal obstruction, perforated ulcer, and a variety of other
conditions
ILEUS
 Ileus
Ileus is the failure of intestinal peristalsis without
evidence of mechanical obstruction.
Lack of normal gut motility interferes with abnormal
movement of intestinal contents and in children is most
often associated with abdominal surgery or infection
(pneumonia, gastroenteritis, peritonitis).
Ileus also accompanies metabolic abnormalities, such
as uremia, hypokalemia, or acidosis, and occurs with
administration of certain drugs, such as opiates and
vincristine.
Ileus may also occur when antimotility drugs such as
loperamide are used during episodes of gastroenteritis.
 Clinical features
Increasing abdominal distention and initially minimal pain
Pain increases with increasing distention
Examination
Bowel sounds are minimal or absent, in contrast to early
mechanical obstruction, when they are hyperactive.
Radiographs
Plain abdominal many air-fluid levels throughout the
abdomen.
Serial do not show progressive distention as they do in
mechanical obstruction.
Contrast slow movement of the barium through a patent
lumen.
 Treatment
Correction of underlying abnormality.
Nasogastric decompression is used if abdominal distention
is associated with pain or to relieve recurrent vomiting.
Ileus after abdominal surgical procedures usually results in
return of normal intestinal motility within 24-72 hr.
Prokinetic agents such as metoclopramide or erythromycin
may stimulate the return of normal bowel motility and be
of assistance to children with prolonged ileus.
Oral administration of drugs that block gastrointestinal
opiate receptors but do not block central nervous system
opiate action may reduce the ileus in postoperative
patients receiving narcotics.
ACUTE APPENDICITIS
 Acute Appendicitis
Acute appendicitis is the most common condition
requiring emergency abdominal operation in
childhood.
Diagnosis is difficult in young children, a factor
contributing to perforation rates of 30-60%.
50% of children with perforated appendicitis have
been seen by a physician before the diagnosis.
The risk of perforation is greatest in 1- to 4-yr-old
children (70-75%) and is lowest in the adolescent
age group (30-40%), which has the highest age-
specific incidence of appendicitis in childhood.
 Epidemiology
Approximately 80,000 children experience appendicitis in
the United States annually
A rate of 4/1,000 children younger than age 14 yr.
Rare in developing countries, where diets are high in fiber.
However, no causal relationship has been established between
lack of dietary fiber and appendicitis.
The incidence of appendicitis increases with age,
peaking in adolescence and rarely occurring in children
younger than 1 yr old.
A familial predilection to appendicitis has been reported.
Cases occur more often in males.
Cases occur more often in the autumn and spring.
 Pathogenesis
occur as a result of appendiceal luminal obstruction
Obstruction is most commonly caused by a fecalith
Enlarged lymphoid follicles associated with viral infections (e.g.,
measles)
inspissated barium
worms (e.g., pinworms, Ascaris, and Taenia)
tumors (e.g., carcinoid or carcinoma)
appendiceal ulceration
Infection with Yersinia organisms may cause the disease
Luminal bacteria multiply and invade the appendiceal wall
venous engorgement and subsequent arterial compromise
gangrene and perforation occur
slow: terminal ileum, cecum, and omentum (localized abscess); rapid:
perforation with free access to the peritoneal cavity
 Clinical manifestations
abdominal discomfort and anorexia
The pain is described as being located in the periumbilical
region initially and then migrating to the right lower
quadrant
resulting from distention of the appendiceal lumen; pain is carried
on slow-conducting C fibers and is usually poorly localized in the
periumbilical or epigastric region
In general, this visceral pain is mild, often cramping and
usually lasting 46 h
As inflammation spreads to the parietal peritoneal surfaces
pain becomes somatic, steady, and more severe and
aggravated by motion or cough
Nausea and vomiting occur in 5060% of cases
Differential diagnosis
 Physical findings
tenderness to palpation will often occur at McBurney's point
Abdominal tenderness may be completely absent if a retrocecal
or pelvic appendix is present tenderness in the flank or on
rectal or pelvic examination
Referred rebound tenderness is often present and is most likely to be
absent early in the illness
Flexion of the right hip and guarded movement by the patient are
due to parietal peritoneal involvement
The temperature is usually normal or slightly elevated [37.2
38C (99100.5F)], >38.3C (101F) perforation
Rigidity and tenderness more marked as the disease
progresses to perforation and localized or diffuse peritonitis
Perforation is rare before 24 h after onset of symptoms, but the
rate may be as high as 80% after 48 h
 Any infant or child with diarrhea, vomiting, and
abdominal pain is highly suspect
Fever is much more common in this age group
abdominal distention is often the only physical finding

In the elderly, pain and tenderness are often blunted

the diagnosis is also frequently delayed and leads to
a 30% incidence of perforation in patients over 70
often present initially with a slightly painful mass (a
primary appendiceal abscess) or with adhesive
intestinal obstruction 5 or 6 days after a previously
undetected perforated appendix
 Laboratorium findings
moderate leukocytosis of 10,00018,000
cells/microL is frequent
Leukocytosis of >20,000 cells/microL perforation
Anemia and blood in the stool suggest a primary
diagnosis of carcinoma of the cecum, especially in
elderly individuals
urine may contain a few white or red blood cells
without bacteria if the appendix lies close to the
right ureter or bladder
Urinalysis is most useful in excluding genitourinary
conditions that may mimic acute appendicitis
 Radiographs
opaque fecalith (5% of patients) is observed in
the right lower quadrant (especially in
children)
intestinal obstruction or ureteral calculus may
be present
Ultrasound an enlarged and thick-walled
appendix
CT will include a thickened appendix with
periappendiceal stranding and often the
presence of a fecalith
 Treatment
early operation and appendectomy as soon as the patient
can be prepared
A different approach is indicated if a palpable mass is
found 35 days after the onset of symptoms
phlegmon / abscess
broad-spectrum antibiotics, drainage of abscesses >3 cm,
parenteral fluids, and bowel rest usually show resolution of
symptoms within 1 week
Interval appendectomy can be performed safely 612 weeks
later
antibiotics alone can effectively treat acute,
nonperforated appendicitis in 86% of male patients
(higher recurrence rate)
PERITONITIS
 Peritonitis
Peritonitis is an inflammation of the
peritoneum; it may be localized or diffuse in
location, acute or chronic in natural history,
infectious or aseptic in pathogenesis.
Acute peritonitis is most often infectious
and is usually related to a perforated viscus
(and called secondary peritonitis).
When no intraabdominal source is
identified, infectious peritonitis is called
primary or spontaneous.
 Acute peritonitis is associated with decreased
intestinal motor activity, resulting in distention
of the intestinal lumen with gas and fluid. The
accumulation of fluid in the bowel together with
the lack of oral intake leads to rapid
intravascular volume depletion with effects on
cardiac, renal, and other systems.

The cardinal manifestations of peritonitis are

acute abdominal pain and tenderness,
usually with fever.
 Primary (spontaneous) bacterial
peritonitis
Usually caused by single organism
Etiology
Occurs most commonly in conjunction with
cirrhosis of the liver (frequently the result of
alcoholism)
Metastatic malignant disease
postnecrotic cirrhosis
chronic active hepatitis & acute viral hepatitis
congestive heart failure
systemic lupus erythematosus
lymphedema
 Clinical manifestation
Fever (80%)
Acites predates infection
Abdominal pain, an acute onset of symptoms, and peritoneal irritation
(physical examination)
Nonlocalizing symptoms malaise, fatigue, or encephalopathy

Other examination
>250 PMNs/L is diagnostic for PBP
Blood culture
enteric gram-negative bacilli (Escherichia coli) most commonly encountered
gram-positive organisms (streptococci, enterococci, or even pneumococci)
sometimes found
Aerobic bacteria
Contrast-enhanced CT intraabdominal source for infection
Chest & abdominal radiography to exclude free air
 Treatment
Third-generation cephalosporins (cefotaxime 2 g q8h,
administered IV) initial coverage in moderately ill patients
Broad-spectrum antibiotics, such as penicillin/-lactamase
inhibitor combinations (piperacillin/tazobactam 3.375 g q6h IV
for adults with normal renal function); ceftriaxone (2 g q24h IV)
Prevention
Up to 70% of patients experience a recurrence within 1 year
Antibiotic prophylaxis reduces this rate to <20%
Prophylaxis agents
fluoroquinolones (ciprofloxacin, 750 mg weekly; norfloxacin, 400 mg/d)
trimethoprim-sulfamethoxazole (one double-strength tablet daily)
 Secondary peritonitis
Develops when bacteria contaminate the peritoneum
as a result of spillage from an intraabdominal viscus
chemical irritation and/or bacterial contamination
Found almost always constitute a mixed flora in which
facultative gram-negative bacilli
anaerobes predominate, especially when the contaminating
source is colonic
Early death in this gram-negative bacillary sepsis
and to potent endotoxins circulating in the
bloodstream
E. coli, are common bloodstream isolates, but Bacteroides
fragilis bacteremia also occurs
 Clinical manifestation
local symptoms may occur in secondary peritonitis, ex:
Epigastric pain from a ruptured gastric ulcer
Appendicitis vague, with periumbilical discomfort and nausea;
number of hours pain localized right lower quadrant
lie motionless
knees drawn up to avoid stretching the nerve fibers of the
peritoneal cavity
Coughing and sneezing increase pressure within the
peritoneal cavity sharp pain
Physical examination
voluntary and involuntary guarding of the anterior abdominal
musculature
tenderness, especially rebound tenderness
 Treatment
antibiotics aimed particularly at aerobic gram-negative
bacilli and anaerobes
penicillin/-lactamase inhibitor combinations
(ticarcillin/clavulanate, 3.1 g q46h IV); cefoxitin (2 g
q46h IV)
Patients in the intensive care unit imipenem (500
mg q6h IV), meropenem (1 g q8h IV), or combinations
of drugs, such as ampicillin plus metronidazole plus
ciprofloxacin
Surgical intervention + antibiotics (bacteremia)
decrease incidence of abscess formation & wound
infection; prevent distant spread of infection
 Peritonitis in Patients Undergoing
CAPD
CAPD (continuous ambulatory
peritoneal dialysis)
CAPD-associated peritonitis usually
involves skin organisms
Pathogenesis
skin organisms migrate along the
catheter serves as an entry point and
exerts the effects of a foreign body
usually caused by a single organism
 Clinical presentation
diffuse pain and peritoneal signs are common

dialysate is usually cloudy and contains >100

WBCs/L, >50% of which are neutrophils
Organisms:
most common organisms are Staphylococcus spp
Gram-negative bacilli and fungi such as Candida
spp. are also found
Vancomycin-resistant enterococci and vancomycin-
intermediate S. Aureus
 Treatment
should be directed at S. aureus, coagulase-negative
Staphylococcus, and gram-negative bacilli until the results of
cultures are available
first-generation cephalosporin such as cefazolin (for gram-
positive bacteria)
fluoroquinolone or a third-generation cephalosporin such as
ceftazidime (for gram-negative bacteria)
MRSA vancomysin
If the patient is severely ill, IV antibiotics should be added at
doses appropriate for the patient's degree of renal failure
if the patient has not responded after 48 h of treatment,
catheter removal should be considered
PERFORATION
 Perforation
Perforated Ulcer
Perforated gastric/duodenal ulcer
requires immediate operative therapy
Anterior gastric perforations cause
peritonitis
Posterior gastric and duodenal
perforations may not cause peritonitis,
and after the acute episode of pain, the
leak may wall off, giving the impression
that the patient is improving
Free air (80% of perforated ulcers)
 Etiology
Helicobacter Pylori
Smoking
NSAIDs
Patophysiology
 Treatment
Immediate surgery
For a perforated duodenal ulcer,may include:
a highly selective vagotomy, a truncal vagotomy and
pyloroplasty, or vagotomy and antrectomy.
For a perforated gastric ulcerdepends on the
patient's condition:
If the patient is moribund, the ulcer is best excised
by grasping it with multiple Allis clamps and using a
GIA-60 linear stapler. Or,can be excised with
electrocautery
In a stable patient, the ulcer is excised and sent for
frozen section analysis to exclude malignancy
INTUSSUSCEPTION
 Intussusception
Intussusception occurs when a portion of the
alimentary tract is telescoped into an adjacent
segment.
It is the most common cause of intestinal obstruction
between 3 mo and 6 yr of age.
60% younger than 1 yr, and 80% before 24 mo; it is
rare in neonates.
The incidence varies from 1-4 in 1,000 live births;
The male : female ratio is 4:1
A few intussusceptions reduce spontaneously, but if
left untreated, most will lead to peritonitis,
perforation, and death.
 Etiology & Risk factors
The etiology is unknown correlation with
adenovirus & rotavirus
Risk factors Meckel diverticulum, intestinal
polyp, neurofibroma, intestinal duplication,
hemangioma, or malignant conditions such as
lymphoma, cystic fibrosis
Postoperative intussusception is ileoileal
occurs within 5 days of an abdominal operation
Lead points are more common in children older than 2
yr of age
 Pathology
Most often ileocolic and ileoileocolic, less
commonly cecocolic
Engorgement of the intussusceptum follows,
with edema & bleeding from the mucosa
bloody stool, sometimes containing mucus
The apex of the intussusception may extend into
the transverse, descending, or sigmoid colon
Most intussusceptions do not strangulate the
bowel within the first 24 hr, but may later
eventuate in intestinal gangrene and shock
 Clinical manifestations
Sudden onset, in a previously well child severe paroxysmal
colicky pain that recurs at frequent intervals and is accompanied
by straining efforts with legs and knees flexed and loud cries
The infant may initially be comfortable and play normally between the
paroxysms of pain; but if the intussusception is not reduced, the infant
becomes progressively weaker and lethargic.
Eventually a shocklike state may develop with fever
The pulse becomes weak and thready
The respirations become shallow and grunting
The pain may be manifested only by moaning sounds
Vomiting occurs in most cases and is usually more frequent
early
In the later phase, the vomitus becomes bile stained
 After the first few hours fecal
excretions are small or more often do
not occur and little or no flatus is passed
Blood generally is passed in the first 12
hr but at times not for 1-2 days and
infrequently not at all; 60% of infants
pass a stool containing red blood and
mucus, the currant jelly stool
Some patients have only irritability and
alternating or progressive lethargy
 Examination
Palpation a slightly tender sausage-shaped
mass, sometimes ill defined, increase in size
and firmness during a paroxysm of pain and is
most often in the right upper abdomen
30% of patients do not have a palpable mass
Presence of bloody mucus on the finger as it is
withdrawn after rectal examination supports
the diagnosis
Abdominal distention and tenderness develop
as intestinal obstruction becomes more acute
 Diagnosis
The clinical history and physical findings
Plain abdominal radiographs may
show a density in the area of the
intussusception
Barium enema filling defect or
cupping in the head of barium where its
advance is obstructed by the
intussusceptum
USG sensitive diagnostic tool in the
diagnosis of intussusception
 Treatment
Reduction of an acute intussusception is an
emergency procedure and performed immediately
after diagnosis in preparation for possible surgery
If the patient have signs of shock, peritoneal irritation,
intestinal perforation, or pneumatosis intestinalis,
reduction should not be attempted
Radiologic reduction under fluoroscopic or ultrasonic
guidance
50% if symptoms are present longer than 48 hr; 70-90% if
reduction is done within the first 48 hr
Barium and hydrostatic (saline) reductions
Bowel perforations occur in 0.5-2.5%
 Prognosis
Untreated intussusception in infants is almost always
fatal
Most infants recover if the intussusception is reduced
within the first 24 hr, but the mortality rate rises
rapidly after this time, especially after the 2nd day
The recurrence rate after barium enema reduction of
intussusceptions is about 10%, and after surgical
reduction it is 2-5%
Administration of dexamethasone has been reported
to reduce the frequency of recurrent intussusception
MALROTATION
 Malrotation
Malrotation is incomplete rotation of the intestine during
fetal development.
The gut starts as a straight tube from stomach to rectum.
The midbowel (distal duodenum to midtransverse colon)
begins to elongate and progressively protrudes into the
umbilical cord until it lies totally outside the confines of the
abdominal cavity.
As the developing bowel rotates in and out of the
abdominal cavity, the superior mesenteric artery, which
supplies blood to this section of gut, acts as an axis.
The duodenum, on re-entering the abdominal cavity,
moves to the region of the ligament of Treitz, and the colon
that follows is directed to the left upper quadrant.
 The cecum subsequently rotates counterclockwise within
the abdominal cavity and comes to lie in the right lower
quadrant.
The duodenum becomes fixed to the posterior abdominal
wall before the colon is completely rotated.
After rotation, the right and left colon and the mesenteric
root become fixed to the posterior abdomen.
These attachments provide a broad base of support to the
mesentery and the superior mesenteric artery, thus
preventing twisting of the mesenteric root and kinking of
the vascular supply.
Abdominal rotation and attachment are completed by 3
mo gestation.
 Nonrotation occurs when the bowel fails to
rotate after it returns to the abdominal cavity.
The first and second portions of the duodenum
are in their normal position, but the remainder
of the duodenum, jejunum, and ileum
occupy the right side of the abdomen while
the colon is located on the left.
Malrotation and nonrotation are associated with
abdominal heterotaxia and the asplenia-
polysplenia congenital heart malformation
syndrome anomalad.
Normal fixation ofthe
bowel: Malrotation of the bowel:
 The most common type of malrotation
failure of the cecum to move into the right
lower quadrant.
The mesentery including the superior
mesenteric artery is tethered by a narrow stalk,
which may twist around itself, producing a
midgut volvulus.
Bands of tissue (Ladd bands) may extend from
the cecum to the right upper quadrant,
crossing and possibly obstructing the
duodenum.
The mechanism
of intestinal
obstruction with
incomplete
rotation of the
midgut
(malrotation).
The dotted lines
show the course
the cecum should
have taken.
Failure to rotate
has left
obstructing bands
across the
duodenum and a
narrow pedicle for
the midgut loop,
making it
susceptible to
volvulus.
 Clinical manifestation
The majority, within the 1st yr of life symptoms of
acute or chronic obstruction.
Infants often present within the 1st wk of life
bilious emesis and acute bowel obstruction.
Older infants episodes of recurrent abdominal
pain that may mimic colic.
Older children recurrent episodes of vomiting,
abdominal pain, or both.
Patients occasionally present with malabsorption or
protein-losing enteropathy associated with bacterial
overgrowth.
 Symptoms are caused by intermittent volvulus or
duodenal compression by Ladd bands or other
adhesive bands affecting the small and large
bowel.
25-50% of adolescents with malrotation
asymptomatic.
Adolescents, symptomatic acute intestinal
obstruction or history of recurrent episodes of
abdominal pain with less frequent vomiting and
diarrhea.
Patients of any age with a rotational anomaly can
develop volvulus without pre-existing symptoms.
 Complication
Volvulus associated with malrotation life threatening
Diagnosis
Ultrasound inversion of the superior mesenteric artery and vein
Contrast radiographic studies (Barium enema) malposition of
the cecum (may be normal in 10% of patients)
The abdominal plain film is usually nonspecific duodenal
obstruction double-bubble sign
Upper gastrointestinal series malposition of the ligament of
Treitz
Treatment
Surgical intervention, regardless of age
Persistent symptoms after repair of malrotation should suggest a
pseudo-obstruction-like motility disorder
 How volvulus occurs in a case
ofmalrotation

Malrotation Early volvulus Late volvulus

The first diagram shows the non-fixed terminal ileum and cecum.
The second diagram showsearly volvulusas this area begins to
twist on itself. The twisting continues until, as shown in the third
diagram (late volvulus), the intestines are obstructed and the
blood supply to this area is constricted (shut-off).
HERNIA
 Hernia
Hernia is the protrusion of an organ or
part of an organ through a defect in the
wall of the cavity containing it, into an
abnormal position.
Abdominal wall hernia
Inguinal (direct or indirect)
Femoral
Umbilical & para-umbilical
Incisional
Ventral & epigastric
 Etiology
Weakness in the abdominal wall
Occur at the site of penetration of structures through the
abdominal wall
The layers of the abdominal wall may be weakened following a
surgical incision
Poor healing as a result of infection, hematoma formation
Damage to the nerve paralysis of abdominal muscles
Increase of intra-abdominal pressure
Chronic cough
Constipation
Urinary obstruction
Pregnancy
Abdominal distention with ascites
Weak abdominal muscles
 Varieties
Reducible hernia
Can be replaced completely into the peritoneal cavity
Presents as a lump that may disappear on lying down, not painful
Examination: reveals a reducible lump with cough impulse
Irreducible hernia
Adhesions of its contents to the inner wall of the sac
Painless, absence of cough impulse
Strangulated hernia
The hernia constricted on the neck of the sac circulation is cut off
perforation & gangrene
Severe pain of sudden onset, colicky pain, vomitting, distention, absolute
constipation
Examination: tender, tense hernia, overlying skin become inflamed, noisy
bowel sound
(femoral, indirect inguinal, umbilical)
 Inguinal hernia
Indirect inguinal hernia
Passes through the internal ring, along the canal in front of the
spermatic cord ; if large enough emerges through the external
ring into scrotum
Features
Hernia doesnt reach its full size until patient has been up & around a
little time; doesnt reduce immediately when lies down
Distinct tendency to strangulate
Examination
Can be felt in the mid-inguinal point
Direct inguinal hernia
Pushes its way directly forward through the posterior wall of the
inguinal canal
Features
Appears immediately on standing; disappearing at once when lies down
 Treatment
Herniotomy
Patent processus vaginalis is ligated & hernial
sac excised at the age of about 1 year and adult
Shouldice repair
Excision of the sac & repair of the weakened
inguinal canal by plicating the transversalis
fascia in the posterior wall by nylon suture
Lichtenstein repair
Reinforcing the posterior wall with a nylon or
polypropylene mesh
 Femoral hernia
Hernia passes through the femoral
canal
Clinical features
Commonly in women (wider female
pelvis)
A non strangulated globular swelling
below & lateral to the pubic tubercle; it
enlarged on standing, coughing,
disappear when lies down
Hernia enlargement passes through
the saphenous opening in the deep
 Richters hernia
Occur in femoral sac, only part of the
wall of small intestine herniates
through the defect strangulated
Knuckle of bowel can become
necrotic perforate acute
peritonitis
Treatment
Repaired with excision of the sac &
closure of the femoral canal because the
danger of strangulation
 Umbilical hernia
Exomphalos
Failure of all part of the midgut to return to the abdominal cavity
in fetal life
Bowel is contained within a translucent sac through a defective
anterior wall
Untreated rupture fatal peritonitis (rupture may occur
during delivery)
Treatment
Surgical repair immediately
Congenital umbilical hernia
Result from failure of complete clossure of the umbilical cicatrix
Common in black children
Treatment
Not surgical repair (unless the hernia persist when the child is 2 yo
 Para-umbilical hernia
Acquired hernia that occurs just above or
below umbilicus
Occurs in obese, multiparous, middle-aged
women
Neck is narrow, prone to become
irreducible or strangulated
Treatment
Sac is excised and the edges of the rectus
sheath are overlapped above and below the
hernia (Mayos operation)
 Ventral, epigastric,
incisional hernia
Ventral hernia
Exist as an elongated gap between the recti
No treatment is required
Epigastric hernia
Consists of one or more small protursions through the defects in the
linea alba above umbilicus
Contain only extraperitoneal fat, often surprisingly painful
Treatment
Suturing the defect
Incisional hernia
Occurs through a defect in the scar of a previous abdominal operation
Wide neck, strangulation is rare
Treatment
Dissecting out and suturing the individual layers of abdominal wall
If operation is inadviseable abdominal belt
ADHESIONS
 Adhesions
Adhesions are fibrous bands of tissue that
are a common cause of postoperative small
bowel obstruction after abdominal surgery.
The risk of forming an adhesion that causes
obstructive symptoms in childhood has not
been well studied but seems to occur in 2-
3% of patients after abdominal surgery.
The majority of obstructions are associated
with single adhesions and can occur at any
time after the 2nd postoperative week.
 Diagnostic
Abdominal pain, constipation, emesis, and a history of intraperitoneal
surgery
Nausea and vomiting quickly follow the development of pain
Bowel sounds initially are hyperactive, and the abdomen is flat
The bowel subsequently dilates abdominal distention bowel
sounds disappear
Fever and leukocytosis are suggestive of necrotic bowel and peritonitis
Plain radiographs obstructive features; contrast studies may be
needed to define the cause
Treatment
Nasogastric decompression, intravenous fluid resuscitation, and broad-
spectrum antibiotics in anticipation of surgery
Nonoperative intervention is contraindicated unless a patient is stable
with clear evidence of clinical improvement.
IBD
Irritable Bowel Syndrome
Definition
A disorder characterized most commonly by cramping,
abdominal pain, bloating, constipation, and diarrhea.

Symptoms
Some people have constipation
Abdominal pain
Bloating
Discomfort ( the main symptoms of IBS )
Some people with IBS experience diarrhea, which is
frequent, loose, watery, stools
Inflammatory Bowel Disease
Symptoms
Abdominal cramps and pain
Diarrhea
Fever
Loss of appetite
Weight loss
Anemia
Bleeding ( intestines )
Inflammatory Bowel Disease
Ulcerative Colitis
Clinical manifestation:
Bloody diarrhea
Mucus
Fever
Abdominal pain
Tenesmus
Weight loss
Inflammatory Bowel Disease
Ulcerative Colitis
Complication:
Toxic megacolon
Colonic perforation

Diagnostic:
sigmoidoscopy / colonoscopy mucosal
erythema, granularity, friability, exudate,
hemorrhage, ulcers, inflammatory polyps
Inflammatory Bowel Disease

Crohns Disease
Clinical manisfestation:
Fever
Abdominal pain
Diarrhea (often without blood)
Fatigue
Weight loss
Growth retardation in children
Inflammatory Bowel Disease

Crohns Disease
Diagnosis
Sigmoidoscopy/colonoscopy:
nodularity, rigidity, ulcers that may
deep or longitudinal, strictures,
fistulas
CT-scan
Inflammatory Bowel Disease
Treatments
Aminosalicylates
These drugs can be given either orally or rectally (enema,
suppository formulations). They are useful both for treating flare-
ups of the IBD and the maintenance of remission.

Corticosteroids
Corticosteroids are rapid-acting anti-inflammatory agents. The
indication for use inIBD is for acute flare-ups of the disease only.
There is no role for corticosteroids in the maintenance of
remission.

Immune modifiers
They are useful in reducing or eliminating some persons'
dependence on corticosteroids.
Inflammatory Bowel Disease
Treatments
Anti-TNF agent
Infliximab (Remicade) is an anti-TNF agent.
TNF is produced by white blood cells and is believed to be
responsible for promoting the tissue damage noted in persons with
Crohn's disease.
Infliximab acts by binding to TNF, thereby inhibiting its effects on
the tissues.

Antibiotics
Metronidazole and ciprofloxacin are the most commonly used.
In persons withulcerative colitis, they have an increased risk of
developing antibiotic-associated pseudomembranous colitis (a
type of infectious diarrhea).
In persons with Crohn's disease, antibiotics are used for
thetreatment of complications (perianal disease, fistulae,
inflammatory mass).