1st Problem Emergency Medicine Block

“A Bloody Situation”
Group 1
Faculty of Medicine
Tarumanagara University
Friday, September 29th 2017
 Group Identity
• Tutor
– dr. Mira Amaliah, Sp.THT-KL
• Leader
– Willyanti (405140035)
• Secretary
– Elisa Hadiwijaya (405140057)
• Writer
– Archangela Luisa Keyko (405140173)
• Members
– Daniel Akbar R Patterson (405130106)
– Arliza Prasetyawati (405130200)
– Phoenix Hong (405140015)
– Agustina Cynthia Cesari S (405140066)
– Andreas Natan (405140099)
– Jatinder Pall Singh (405140155)
– Vinny Desyagiarini (405140182)
– Sugiarto Kamarudy Lay (405140208)
– Richard Cristanto T (405140254)
 Problem
“A Bloody Situation”
A 65-year-old male is brought to an emergency department after he vomited 3 times,
500cc – 1000cc each times, containing fresh blood mixed with coffee colored blood
since an hour ago. In the last 5 days, he complained of stomachache and nausea which
got better after he ate and took antacids, but the symptoms still persist after some
time. He has a history of coronary artery disease and took aspirin daily. He also
consumed alcohol daily in his thirties and was once hospitalized because of alcoholic
liver disease. Before he was brought to the ED, he was given a traditional medicine
(jamu) by his son to help him stop vomiting. Soon after he drank the medicine, he felt
itchy and his face is swelled all over.

From initial physical examinations, the patient’s blood pressure is 60/20 mmHg, heart
rate is 120 bpm, respiratory rate is 24 breaths per minute and temperature is 39oC.
Physical thorax examination results are unremarkable. On physical abdomen
examinations results, there are tenderness on the patient’s whole abdomen when
palpated, decreased and weak bowel sounds on auscultation.

Initial laboratory results showed that the patient’s Hemoglobin is 9.4 g/dL, leucocyte is
17.000/mm3 and thrombocyte is 300.000/mm3 .
 Problems
1. Apa yang menyebabkan muntah berwarna coffee dan fresh blood?
2. Mengapa setelah minum antacids, sakit perut dan mual menghilang sedangkan
gejala yang lainnya tidak?
3. Mengapa setelah minum jamu terasa gatal dan muka bengkak?
4. Apa penyebab terasa sakit saat di palpasi & bising usus menurun?
5. Apakah ada hubungan coronary artery disease dan pemakaian aspirin setiap hari
terhadap keluhan?
6. Apakah ada hubungan umur dengan keluhan? Perbedaan tata laksana?
7. Apakah hubungan penggunaan alkohol di awal umur 30 tahun dan alkoholik liver
disease terhadap keluhan muntah?
8. Apa hasil interpretasi lab, PF, dan vital sign pasien?
9. Pemeriksaan penunjang apa yang dibutuhkan?
10. DD dari kasus?
11. Apa tatalaksana untuk kasus?
 Brainstorm
1. Warna muntah seperti coffee  berasal dari GI bleeding yang sudah bercampur dengan
asam lambung. Fresh blood  berasal dari upper GI tract. Hemoptisis  batuk berupa
darah segar, berbusa, berasal dari paru.
2. Peptic ulcer, severe GERD.
3. Reaksi alergi  shock anaphylactic (circulation  vasodilatasi, respiraroty  wheezing &
broncospasm, cutaneus  edem, pruritus, urticaria).
4. Alkoholik liver disease  sirosis hepar, penyebab tergantung quadran abdomen, peptic
ulcer  perforasi  peritonitis.
5. Aspirin; meningkatkan resiko perdarahan, menurunkan proteksi lambung, pengencer
darah, koagulasi terganggu, GI bleeding.
6. Epidemiologi peptic ulcer  usia 60 tahunan. Tata laksana pada orang tua  resusitasi
agresif.
7. Esophageal varises  ruptur. Alkohol + aspirin  meningkatkan resiko GI bleeding.
Muntah. Sirosis hepatis  meningkatkan tekanan V. porta  meningkatkan tekanan
intraabdomen.
8. TTV; Hipotensi, takikardi, takipneu, febris, shock hypovolemik. PF abdomen; nyeri seluruh
abdomen dan penurunan bising usus. Lab; Hb turun, leukositosis, trombosit normal.
9. Endoscopy & surgery, kateterisasi kandung kemih, SOFA score, AGD, USG, CT SCAN
abdomen dan jantung, CVP.
10. Anaphylactic shock, hypovolemic shock, septic shock, GI bleeding, cardiogenic shock, acute
abdomen (peritonitis).
11. ABC, 1-2 L I.V crystaloid, transfusi PRBC, anaphylactic  epinephrine.
 Mind Map
- CAD - Alkohol
- Aspirin daily - Alkoholik liver disease

Laki-laki 65 tahun muntah 3x @500-1000cc, warna fresh blood+coffee, selama 5 hari sakit perut dan mual
muntah (membaik setelah minum antacids), minum jamu  gatal dan muka membengkak

PF abdomen; nyeri Lab; Hb turun,

TTV; hipotensi, takikardi,
seluruh abdomen, bising leukositosis, trombosit
takipneu, febris
usus menurun normal

DD:
• GI bleeding (upper, lower)
• Anaphylactic shock
• Cardiogenic shock
• Hypovolemic shock
• Septic shock
• Acute abdomen
 Group’s Learning Issues
1. Shock
2. GI Bleeding (Upper & Lower)
3. Acute Abdomen
SHOCK
 Shock
• Shock is the clinical syndrome that results from
inadequate tissue perfusion.
• The hypoperfusion-induced imbalance between the
delivery of and requirements for oxygen and substrate
leads to cellular dysfunction.
• This leads to a vicious cycle in which impaired
perfusion is responsible for cellular injury that causes
maldistribution of blood flow, further compromising
cellular perfusion; the latter ultimately causes multiple
organ failure (MOF) and, if the process is not
interrupted, leads to death.
 Shock
• MAP = CO x SVR
• O2 saturation
Classification dan etiology
 Physical findings

Tintinalis’ Emergency Medicine

 Stage of Shock
• Initial Stage : tissue are under perfused, increased
anaerobic metabolism, lactic acid is building
• Compensatory stage : reversible, SNS activated by low
CardiacOutput, attempting to compensate for the
decrease tissue perfusion
• Progression stage : Failing compensatory mechanism
 profound vasoconstriction from the SNS Ischemia 
Lactic acid production is high  metabolic acidosis
• Irreversible or refractory stage : celluler necrosis and
multiple organ dysfunction Syndrome may occur
 Hypovolemic Shock
• This most common form of shock results either
from the loss of red blood cell mass and plasma
from hemorrhage or from the loss of plasma
volume alone due to extravascular fluid
sequestration or GI, urinary, and insensible
losses.
• The normal physiologic response to hypovolemia
is to maintain perfusion of the brain and heart
while attempting to restore an effective
circulating blood volume.
 Infusion Rates
Access Gravity Pressure

18 g peripheral IV 50 mL/min 150 mL/min

16 g peripheral IV 100 mL/min 225 mL/min
14 g peripheral IV 150 mL/min 275 mL/min
8.5 Fr CV cordis 200 mL/min 450 mL/min
• Primary Survey: A B C D E
• Secondary Survey
• Dugaan syok sepsis et causa peritonitis
Septic Shock

Rosen’s Emergency Medicine 8th Ed

Septic Shock

Rosen’s Emergency Medicine 8th Ed

 Risk Factors
• Diabetes
• Diseases of the genitourinary system, biliary system, or intestinal
system
• Diseases that weaken the immune system, such as AIDS
• Indwelling catheters (those that remain in place for extended
periods, especially intravenous lines and urinary catheters, and
plastic and metal stents used for drainage)
• Leukemia
• Long-term use of antibiotics
• Lymphoma
• Recent infection
• Recent surgery or medical procedure
• Recent use of steroid medicines
• Solid organ or bone marrow transplantation
Rosen’s emergency medicine: concept
and clinical practice, 8th ed. p.72
 Anaphylactic Shock
• Allergic reactive that severe enough to cause shock.
• 2 Types of Anaphylactic shock : Immunologic and non-Immunologic
• Etiology :
– antibiotics (penicillins, cephalosporins, amphotericin B,
nitrofurantoin, quinolones)
– pollen extracts (ragweed, grass, trees)
– nonpollen allergen extracts (dust mites, dander of cats,
dogs, horses, and laboratory animals)
– Food (peanuts, milk, eggs, seafood, nuts, grains, beans,
gelatin in capsules)
– occupation-related products (latex rubber products)
• Symptoms: Flushing on the skin, Swelling, Itchiness, Bronchospasm
Harrison's principles of internal medicine, 18th
 Pathophysiology
• Sensitization : When the person first exposed
to an Allergen. Allergen Interact with B-cells (
Create Antibodies IgE ) and then antibodies
docks on other immune cells ( Mast Cell )
• Allergen will dock on Antibodies+MastCell 
Activated ( Cytokines & Histamin )
• Histamin is a potent Vasodilator  Decreased
Blood Pressure  Shock
Anaphylactic Shock
 Diagnosis Anafilaksis

Resuscitation Council (UK). Emergency treatment of anaphylactic reactions – Guidelines for healthcare providers. Jan 2008.
http://www.bsaci.org/guidel
ines/wao_anaphylaxis_guide
http://www.bsaci.org/guidelines/wao_anaphylaxis_
 Treatment
• ABC  established the airway
• Epinephrine ( Vasopressor ) Maintain BP
and treatment for Bronchospasm
• IV Fluids
• Anti-Histamin
 Cardiogenic shock
Etiology

• Results when 40% myocardium undergoes necrosis

from ischemia, toxins, immune destruction

Classification

• Cardiac Failure
• Clinical evidence of impaired forward flows of the
heart including presence of dyspnea, tachycardia,
pulmo edema, peripheral edema, cyanosis.
• Cardiogenic Shock

Specific Treatment

• Treat the increase work of breathing (provide

oxygen & positive end expiratory pressure (PEEP)
for pulmo edema
• Vasopressor / inotropic support (norepinephrine
(0.5 mikrog/min) & dobutamine (5mikrog/kg/min)
• Reverse the insult (initiate trombolysis, arrange
percutaneous transuminal angioplasty)
• Consider intra-aortic balloon pump counter
pulsation for refractory shock
Cardiogenic Shock
Cardiogenic shock
• Defined as: • Signs:
– SBP<90mmHg – Chest pain/pressure
– CI < 2,2 L/m/m2 – Dyspnea
– PCWP > 18mmHG – Orthopnea
– Jugular venous distention
– Cool, clammy, sweaty
extremities
– Rales
– Wheezes
– Dullness at lung bases
– S3 gallop
Cardiogenic shock
• Pathophysiology
– After ischemia happensloss of LV
functionclinical shock ensues
– CO reduction  hypoxia,lactate acidosis
– Stroke volume reduce  tachycardia,ischemia and
infarction worsens
Cardiogenic shock
• Cardiogenic Shock
– ↑ work of beathing (oxygen and positive end-
expiratory pressure for pulmonary edema)
– Vasopressor or inotropic : norepinephrine (0.5
ug/min) and dobutamine (5 ug/kg/min)
– Seek to reverse the insult (initiate thrombolysis,
arrange percutaneous transluminal angioplasty)
– Consider intra-aortic balloon pump
counterpulsation for refractory shock
• Early revascularization
• Thrombolyric therapy
• Intra-aortic ballon pump counterpulsation
Treatment for infark miokard:
• Resusitation (Vasopressor)  NE/ Dopamin 
>> MAP
• MECHANICAL CIRCULATORY SUPPORT  IABP
(intraaortic balloon pump)
• Revascularization  PCI or coronary artery
bypass graft (CABG)
 Neurogenic Shock
• Autonomic dysfunction due to spinal cord
injury (blunt or penetrating trauma) that
causes hypotension and bradycardia

Greenberg
 Phatophysiology
• Injury to the spinal cord disorders  disruption
of the sympathetic autonomic outflow (the signal
comes from the gray cornu lateralis)
• Decrease tone adrenergic  inability to improve
the performance of cardiac inotropic, poor
constriction of peripheral vascularity
• Vagal tone which does not experience resistance
 hypotension and bradycardia
• peripheral vasodilatation  warm skin and
redness
• does not occur if the injury is below T6
 Treatment
• Hypotension  crystalloid IV fluid
• Pressor drugs (dopamine and dobutamine) if
response to IV fluids is suboptimal
• bradycardia  atropine
• traumatic spinal cord injury  corticosteroids
(methylprednisolone  blunt injury)
• Evaluation of neurological and neurosurgical
emergencies
GI BLEEDING
 Peptic Ulcer
• fullness, nausea,early satiety, and bloating.
• Pain usually occurs 2 to 5 hours after a meal or at
night.
• awaken a patient from sleep (3 am  gastric acid
output is highest at about 2 am)
• Relief pain after eating
• pain from duodenal ulcer  worse immediately
before a meal
• complex of pain-eating-relief  duodenal ulcer.
 Bacteria
• Campylobacter pyloridis -> gram (-) microaerophilic rod
• Found commonly in deeper portion of mucous gel coating
gastric mucosa / between mucous layer & gastric
epithelium
• Initially H. pylori resides in antrum -> migrate to more
proximal segment of stomach
• H. pylori antral infection -> increased acid production,
increased duodenal acid & mucosal injury
• Risk factors of H pylori :
– Birth / residence in developing country
– Domestic crowding
– Unsanitary living conditions
– Unclean food / water
• Transmission : person-person, oral-oral, fecal-oral route
 Diagnose
• Upper endoscopy
• Complete blood count : anemia
• Lipaase enzyme : pancreatitis
• Pregnant test : women childbearing age
• Radiology
 Esophageal varices - Symptoms
• Esophageal varices usually don't cause signs and
symptoms unless they bleed. Signs and symptoms
of bleeding esophageal varices include:
• Vomiting and seeing significant amounts of blood in
your vomit
• Black, tarry or bloody stools
• Lightheadedness
• Loss of consciousness (in severe case)
• Your doctor might suspect varices if you have signs
of liver disease, including:
• Yellow coloration of your skin and eyes
(jaundice)
• Easy bleeding or bruising
• Fluid buildup in your abdomen (ascites)
Esophageal varices
 Risk factors

• Although many people with advanced liver disease develop

esophageal varices, most won't have bleeding. Varices are
more likely to bleed if you have:
• High portal vein pressure. The risk of bleeding increases with
the amount of pressure in the portal vein (portal
hypertension).
• Large varices. The larger the varices, the more likely they are
to bleed.
• Red marks on the varices. When viewed through an
endoscope passed down your throat, some varices show
long, red streaks or red spots. These marks indicate a high risk
of bleeding.
• Severe cirrhosis or liver failure. Most often, the more severe
your liver disease, the more likely varices are to bleed.
• Continued alcohol use. Your risk of variceal bleeding is far
greater if you continue to drink than if you stop, especially if
your disease is alcohol related.
 Diagnosis
• Endoscope exam
• Imaging tests  both abdominal CT scans and Doppler
ultrasounds of the splenic and portal veins can suggest the
presence of esophageal varices.
• Capsule endoscopy  swallow a vitamin-sized capsule
containing a tiny camera, which takes pictures of the
esophagus as it goes through your digestive tract.
Endoscope exam
 Treatment to prevent bleeding

• Treatments to lower blood pressure in the portal vein may

reduce the risk of bleeding esophageal varices. Treatments
may include:
• Medications to reduce pressure in the portal vein  beta
blocker  reduce blood pressure in portal vein, decreasing
the likelihood of bleeding  These medications include
propranolol (Inderal, Innopran) and nadolol (Corgard).
• Using elastic bands to tie off bleeding veins  if
esophageal varices appear to have a high risk of bleeding
 recommend a procedure called band ligation.
 Treatment if you're bleeding
• Bleeding varices are life-threatening, and immediate treatment is
essential. Treatments used to stop bleeding and reverse the
effects of blood loss include:
• Using elastic bands to tie off bleeding veins.
• Medications to slow blood flow into the portal vein 
octreotide (Sandostatin) + endoscopic therapy  to slow the
flow of blood from internal organs to the portal vein 
continued for five days after a bleeding episode.
• Diverting blood flow away from the portal vein  transjugular
intrahepatic portosystemic shunt (TIPS) to place a shunt.
• Restoring blood volume  transfusion to replace lost blood and
clotting factor to stop bleeding.
• Preventing infection. There is an increased risk of infection with
bleeding, so you'll likely be given an antibiotic to prevent
infection.
• Replacing the diseased liver with a healthy one  option for
people with severe liver disease or those who experience
recurrent bleeding of esophageal varices.
• Portal hypertension results from
increased intrahepatic vascular
resistance and portal–splanchnic
blood flow.
• In addition, cirrhosis is characterized
by splanchnic and systemic arterial
vasodilation.
• Splanchnic arterial vasodilation 
increased portal blood flow and thus
elevated portal hypertension 
increased hepatic venous pressure
gradient  formation of
portosystemic venous collaterals.
• Esophagogastric varices represent
the most clinically important
collaterals given their associated
high risk of bleeding.
• Treatment consists of pharmacologic
therapy to decrease portal pressure,
endoscopic treatment of varices
(band ligation or sclerotherapy) to
treat variceal bleeding, and creation
of a transjugular intrahepatic
portosystemic shunt (TIPS) to reduce
portal pressure if drug therapy and
endoscopic treatment fail.
 Diverticulitis
• Diagnosis • Treatment
– CT scan (IV and oral – Fluids
contrast) – Correct electrolyte
• Pericolic fat stranding abnormalities
• Diverticula – NPO
• Thickened bowel wall – Abx: gentamicin AND
• Peridiverticular abscess metronidazole OR
– Leukocytosis present in clindamycin OR
only 36% of patients levaquin/flagyl
– For outpatients (non-toxic)
• liquid diet x 48 hours
• cipro and flagyl
(Patient Teaching Guides - Evidence-Based Diagnosis) Fred F. Ferri-Ferri’s Clinical
Advisor 2017. 5 vols.-Expert Consult Com. (2017).pdf
Evaluation and Management of Upper
GI Bleeding
Evaluation and Management of Lower
GI Bleeding
ACUTE ABDOMEN
Acute Appendicitis
Acute appendicitis
• Appendicitis is defined as an inflammation of
the inner lining of the vermiform appendix
that spreads to its other parts.
• The clinical presentation of appendicitis is
notoriously inconsistent. The classic history
of anorexia and periumbilical pain followed
by nausea, right lower quadrant (RLQ) pain,
and vomiting occurs in only 50% of cases.
Etiology
– obstruction of the appendiceal lumen.
– lymphoid hyperplasia secondary to inflammatory
bowel disease (IBD) or infections (more common
during childhood and in young adults),
– fecal stasis and fecaliths (more common in elderly
patients),
– parasites (especially in Eastern countries)
– foreign bodies and neoplasms (rarely)
http://emedicine.medscape.com/article/773
895-overview
 Features include the  Features of the
following: abdominal pain are as
follows:
• Abdominal pain: Most
common symptom • Typically begins as
periumbilical or
• Nausea: 61-92% of epigastric pain, then
patients migrates to the RLQ [3]
• Anorexia: 74-78% of • Patients usually lie
patients down, flex their hips,
• Vomiting: Nearly always and draw their knees up
follows the onset of to reduce movements
pain; vomiting that and to avoid worsening
precedes pain suggests their pain
intestinal obstruction • The duration of
• Diarrhea or symptoms is less than
constipation: As many 48 hours in
as 18% of patients approximately 80% of
adults but tends to be
longer in elderly
persons and in those
with perforation.

http://emedicine.medscape.com/article/773
895-overview
 Physical examination
findings include the
following:
• Rebound tenderness, pain
on percussion, rigidity, and
guarding: Most specific
finding
• RLQ tenderness: Present
in 96% of patients, but
nonspecific
• Male infants and children
occasionally present with
an inflamed hemiscrotum
• In pregnant women :
RLQ pain and tenderness
dominate in the first
trimester, but in the latter
half of pregnancy, right
upper quadrant (RUQ) or
right flank pain may occur
 The following accessory
signs may be present in
a minority of patients:
• Mc. Burney sign
• Blumberg sign
• Rovsing
• Obturator sign
• Psoas sign
• Dunphy sign
• RLQ pain in response to
percussion of a remote
quadrant of the
abdomen or to firm
percussion of the
patient's heel: Suggests
peritoneal inflammation
• Markle sign
http://emedicine.medscape.com/article/773
895-overview
Appendicitis: Psoas Sign
 Diagnose  CBC
• WBC >10,500 cells/µL: 80-
• CBC 85% of adults with
• C-reactive protein (CRP) appendicitis
• Neutrophilia >75-78% of
• Liver and pancreatic patients
function tests • Less than 4% of patients
with appendicitis have a
• Urinalysis (for WBC count less than 10,500
differentiating cells/µL and neutrophilia less
appendicitis from than 75%
 C-reactive protein
urinary tract conditions)
• CRP levels >1 mg/dL are
• Urinary beta-hCG (for common in patients with
differentiating appendicitis
appendicitis from early  Urinary 5-HIAA
• HIAA levels increase
ectopic pregnancy in significantly in acute
women of childbearing appendicitis and decrease
age) when the inflammation
shifts to necrosis of the
• Urinary 5- appendix. Therefore, such
hydroxyindoleacetic decrease could be an early
warning sign of perforation
acid (5-HIAA) of the appendix.
http://emedicine.medscape.com/article/773
895-overview
  Appendectomy remains the
 Management only curative treatment of
• Emergency department appendicitis, but management
care is as follows: of patients with an appendiceal
• Establish IV access and mass can usually be divided
administer aggressive into the following 3 treatment
crystalloid therapy to categories:
patients with clinical 1. Phlegmon or a small abscess:
signs of dehydration or After IV antibiotic therapy, an
septicemia interval appendectomy can
be performed 4-6 weeks later
• Keep patients with
suspected appendicitis 2. Larger well-defined abscess:
NPO After percutaneous drainage
with IV antibiotics is
• Administer parenteral performed, the patient can
analgesic and antiemetic be discharged with the
as needed for patient catheter in place; interval
comfort; no study has appendectomy can be
shown that analgesics performed after the fistula is
adversely affect the closed
accuracy of physical 3. Multicompartmental abscess:
examination These patients require early
surgical drainage
http://emedicine.medscape.com/article/773
• Antibiotic prophylaxis should be administered before
every appendectomy
• Broad-spectrum gram-negative and anaerobic coverage
is indicated
• Cefotetan and cefoxitin seem to be the best choices of
antibiotics
• In penicillin-allergic patients, carbapenems are a good
option
• Pregnant patients should receive pregnancy category A
or B antibiotics
• Antibiotic treatment may be stopped when the patient
becomes afebrile and the WBC count normalizes
http://emedicine.medscape.com/article/773
895-overview
 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 associated with decreased
intestinal motor activity, resulting in distention
of the intestinal lumen with gas and fluid
 Etiology
• Infectious agents gain access to the peritoneal cavity
through a perforated viscus, a penetrating wound of
the abdominal wall, or external introduction of a
foreign object that is or becomes infected (for example,
a chronic peritoneal dialysis catheter). The conditions
that most commonly result in the introduction of
bacteria into the peritoneum are ruptured appendix,
ruptured diverticulum, perforated peptic ulcer,
incarcerated hernia, gangrenous gall bladder, volvulus,
bowel infarction, cancer, inflammatory bowel disease,
or intestinal obstruction.
 Bacteria
• 62% were gram-negative bacteria
(Pseudomonas species and Escherichia coli
were most common), 47% were gram- positive
bacteria (Staphylococcus aureus was most
common), and 19% were fungi (Candida
species )
Harrison’s
 Types of Peritonitis
• Spontaneous peritonitis
– an infection that develops in the peritoneum
– Caused by
• Liver disease with cirrhosis
– Such disease often causes a buildup of abdominal fluid
(ascites) that can become infected.
• Kidney failure getting peritoneal dialysis.
– This technique, which involves the implantation of a catheter
into the peritoneum, is used to remove waste products in the
blood of people with kidney failure.
– It's linked to a higher risk of peritonitis due to accidental
contamination of the peritoneum by way of the catheter.
 Types of Peritonitis
• Secondary peritonitis
– which usually develops when an injury or infection in the
abdominal cavity allows infectious organisms into the
peritoneum
– Caused by
• A ruptured appendix, diverticulum, or stomach ulcer
• Digestive diseases such as Crohn's disease and diverticulitis
• Pancreatitis
• Pelvic inflammatory disease
• Perforations of the stomach, intestine, gallbladder, or appendix
• Surgery
• Trauma to the abdomen, such as an injury from a knife or gunshot
wound
• acute abdominal pain and tenderness, usually with fever
• widespread inflammation and diffuse abdominal tenderness and
rebound.
• Tachycardia, hypotension, and signs of dehydration are common.
• Leukocytosis and marked acidosis are common laboratory findings.
• Free air under the diaphragm is associated with a perforated viscus.
• CT and/or ultrasonography can identify the presence of free fluid or
an abscess.
• When ascites is present, diagnostic paracentesis with cell count
(>250 neutrophils/L is usual in peritonitis), protein and lactate
dehydrogenase levels, and culture is essential. In elderly and
immunosuppressed patients, signs of peritoneal irritation may be
more difficult to detect.
 Clinical features
• Acute abdominal pain and tenderness, usually with fever.
• Localized peritonitis is most common in uncomplicated
appendicitis and diverticulitis, and physical findings are
limited to the area of inflammation.
• Generalized peritonitis is associated with widespread
inflammation and diffuse abdominal tenderness and
rebound.
• Rigidity of the abdominal wall is common in both localized
and generalized peritonitis.
• Bowel sounds are usually absent.
• Tachycardia, hypotension, and signs of dehydration are
common.
 Diagnose
• Leukocytosis and marked acidosis are common
laboratory findings.
• Plain abdominal films may show dilation of large and
small bowel with edema of the bowel wall.
• Free air under the diaphragm is associated with a
perforated viscus.
• CT and/or ultrasonography can identify the presence of
free fluid or an abscess. When ascites is present,
diagnostic paracentesis with cell count (>250
neutrophils/μL is usual in peritonitis), protein and
lactate dehydrogenase levels, and culture is essential.
 Therapy
• Treatment relies on rehydration, correction of
electrolyte abnormalities, antibiotics, and
surgical correction of the underlying defect.
 Prognosis
• Approximately 20–35% of patients with severe sepsis and
40–60% of patients with septic shock die within 30 days.
Others die within the ensuing 6 months. Late deaths often
result from poorly controlled infection,
immunosuppression, complications of intensive care,
failure of multiple organs, or the patient’s underlying
disease.
• Mortality rates are <10% for uncomplicated peritonitis
associated with a perforated ulcer or ruptured appendix or
diverticulum in an otherwise healthy person.
• Mortality rates of 40% have been reported for elderly
people, those with underlying illnesses, and when
peritonitis has been present for >48 hour.
 Kole(doko)lithiasis

• Cholelithiasis  the presence of gallstones

which are concretions that form in the biliary
tract, usually in the gallbladder.
• Choledocholithiasis  the presence of 1 or
more gallstones in the common bile duct
(CBD).
 Pathophysiology
Gallstone formation occurs because
• Bile is concentrated in the gallbladder 
supersaturated with substances such as
cholestrol  precipitate from the solution 
microscopic crystals  trapped in gallbladder
mucus  gallbladder sludge  crystals grow,
aggregate, and fuse  macroscopic stones.
• Occlusion of the ducts by sludge and/or stones
produces the complications of gallstone disease.
Cholesterol as their major component.
• Liver cells secrete:
– Cholesterol into bile along w/ phospholipid
(lecithin)  unilamellar vesicles.
– Bile salts  detergents  the digestion and
absorption of dietary fats.
• Bile salts in bile dissolve the unilamellar
vesicles  mixed micelles. This happens
mainly in the gallbladder, where bile is
concentrated by reabsorption of
electrolytes and water.
Risk factor :
• The metabolic syndrome of truncal obesity,
insulin resistance, type II diabetes mellitus,
hypertension, and hyperlipidemia
• Obesity
• Pregnancy
• Gallbladder stasis
• Drugs
• Heredity
Calcium, bilirubin, and pigment gallstones
• High heme turnover (such as chronic hemolysis or
cirrhosis), unconjugated bilirubin may be present in
bile at higher than normal concentrations.
• Ca + Bilirubin  crystallize  form stones
• Bile  may be colonized with bacteria  bacteria
hydrolyze conjugated bilirubinn  increase in
unconjugated bilirubin  precipitation of calcium
bilirubinate crystals.
• Bacteria also hydrolyze lecithin to release fatty
acids, which also may bind calcium

*Cholesterol  black pigment gallstones  form

almost exclusively in the gallbladder
*Ca, bilirubin  Brown pigment gallstones often
form in the bile ducts.
 Sign and symptoms
Gallstone disease  4 stages:
• Lithogenic state
• Asymptomatic gallstones
• Symptomatic gallstones, characterized by episodes
of biliary colic
– Pain that is poorly localized and visceral; an
essentially benign abdominal examination without
rebound or guarding; absence of fever
• Complicated cholelithiasis
– Well-localized pain in the RUQ
– usually with rebound and guarding
– Murphy sign + (nonspecific)
– Frequent presence of fever
– absence of peritoneal signs
– frequent presence of tachycardia and diaphores
– Severe cases  absent or hypoactive bowel sounds
Effects occurring within the gallbladder or from stones that escape the
gallbladder to lodge in the CBD :
• Sporadic and unpredictable episodes
• Pain localized to the epigastrium or right upper quadrant, sometimes
radiating to the right scapular tip
• Pain that begins postprandially  intense and dull (typically lasts 1-5
hours), >> steadily over 10-20 minutes, and then gradually wanes
• Pain that is constant, not relieved by emesis, antacids, defecation,
flatus, or positional changes; and sometimes accompanied by
diaphoresis, nausea, and vomiting
• Nonspecific symptoms (eg, indigestion, dyspepsia, belching, or
bloating)
• Fever
• Yellowing of skin and whites of the eyes (jaundice)
• Loss of appetite
• Nausea and vomiting
• Clay-colored stools
 Diagnosis
• Uncomplicated cholelithiasis or simple biliary
colic  normal laboratory test
(laboratory studies  if complications are
suspected).
• Blood tests, when indicated, may include the
following:
– Complete blood count (CBC) with differential
– Liver function panel
– Amylase
– Lipase
 Imaging
• Abdominal radiography
• Ultrasonography  suspected gallbladder or biliary disease 
cholelithiasis
• Endoscopic ultrasonography (EUS)  identifying stones in the distal CBD
• Laparoscopic ultrasonography  bile duct imaging during laparoscopic
cholecystectomy
• Computed tomography (CT)  demonstrating stones in the distal CBD
• Magnetic resonance imaging (MRI) with magnetic resonance
cholangiopancreatography (MRCP)  choledocholithiasis is suspected
• Scintigraphy – Highly accurate for the diagnosis of cystic duct obstruction
• Endoscopic retrograde cholangiopancreatography (ERCP) 
choledocolithiasis
• Percutaneous transhepatic cholangiography (PTC)
• Choledocholithiasis with acute common bile duct (CBD)
obstruction initially –
– Acute increase AST & ALT  within hours  >>> serum
bilirubin level. (CBS stone when serum bilirubin levels
greater than 3 mg/dL).
• If obstruction persist :
– <<< level of transaminases
– >>> alkaline phosphatase + bilirubin levels (several days)
– PT may be >>> (if prolonged CBD obstruction, secondary to
depletion of vitamin K)).
– if happened w/ obstruction of the pancreatic duct by a
stone in the ampulla of Vater  serum lipase and amylase
levels may >>>
 Treatment
- Asymptomatic gallstones may be indicated if :
• Gallstone d = >2 cm
• nonfunctional or calcified gallbladder observed on imaging
studies + high risk of gallbladder CA
• spinal cord injuries or sensory neuropathies affecting the
abdomen
• sickle cell anemia in whom the distinction between painful
crisis and cholecystitis may be difficult

Ursodeoxycholic acid (ursodiol)  Medical dissolution of

gallstones
 dose of 8-10 mg/kg/d PO divided bid/tid  gradual
gallstone dissolution

- Symptomatic gallstone / + complication

 Cholecystectomy or Endoscopic sphincterotomy
 Complication
• Cholecystitis
• Cholangitis
• Pancreatitis
• Other systemic causes
 Intussusception

• Invagination of one
portion of the bowel into
an immediately adjacent
portion
• The proximal segment,
or intussusceptum, is
carried by progressive
smooth muscle
contractions into the
distal segment, or
intussuscipiens
Source: Sands DR. Intestinal intussusception [Internet]. Clin Colon Rectal Surg. 2008 May; 21(2): 106–113. Available from:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2780199/
 • Intussusception may occur anywhere in the
small or large intestine
• Nomenclature reflects location in the bowel:
enteroenteric, appendiceal, appendiceal-
ileocolic, ileocolic, colocolic, rectoanal, and
stomal

Source: Sands DR. Intestinal intussusception [Internet]. Clin Colon Rectal Surg. 2008 May; 21(2):
106–113. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2780199/
 Clinical Presentation (pediatric)
• Sudden onset of abdominal pain exhibited by the drawing up
of the knees, screaming, and lethargy between painful bouts
• The onset of pain is shortly followed by obstructive symptoms
such as bilious vomiting and abdominal distension
• Half of cases progress to bloody, mucoid “currant jelly” stools
within 12 hours
• Depending on timing of presentation they may or may not
have fever and leukocytosis

Source: Sands DR. Intestinal intussusception [Internet]. Clin Colon Rectal Surg. 2008 May; 21(2): 106–113. Available from:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2780199/
 Clinical Presentation (adult)
• Abdominal pain
• Nausea/vomiting
• Diarrhea/constipation
• Rectal bleeding
• Common physical findings  distension,
hypoactive bowels, abdominal tenderness,
and guaiac positive stools
• Abdominal mass is identified infrequently
Source: Sands DR. Intestinal intussusception [Internet]. Clin Colon Rectal Surg. 2008 May; 21(2):
106–113. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2780199/
 Patient evaluation (pediatric)
• Abdominal ultrasound  target or donut sign
or bull’s eye on transverse view and the
pseudokidney sign on longitudinal view
• Air or contrast studies  an air crescent sign
on films caused by the filling of the contrast
around the “head” of the intussusception at
the end of the contrast column

Source: Sands DR. Intestinal intussusception [Internet]. Clin Colon Rectal Surg. 2008 May; 21(2):
106–113. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2780199/
 Patient evaluation (Adult)
• CT scan  to evaluate the location and the cause
of the obstruction  reveal the signs of
obstruction including the target sign or sausage-
shaped mass
• When chronic intermittent small bowel
obstruction is the initial presenting sign and adult
enteroenteric intussusception is suspected 
Barium small bowel follow through  a spiral,
“coil spring” or “stacked coin” appearance with
narrowed central canal
Source: Sands DR. Intestinal intussusception [Internet]. Clin Colon Rectal Surg. 2008 May; 21(2):
106–113. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2780199/
 Patient evaluation (Adult)
• Colonic obstruction  barium enema and
colonoscopy
• Laparoscopy  identification of the location,
the nature of the lead point, and the presence
of compromised bowel

Source: Sands DR. Intestinal intussusception [Internet]. Clin Colon Rectal Surg. 2008 May; 21(2):
106–113. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2780199/
 Treatment
• For all patients who present with signs of
perforation, shock, or peritonitis, immediate
laparotomy is necessary
• In the absence of these signs, the therapeutic
approach to pediatric and adult
intussusception is different

Source: Sands DR. Intestinal intussusception [Internet]. Clin Colon Rectal Surg. 2008 May; 21(2):
106–113. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2780199/
 Treatment (pediatric)
• Barium suspension with air under fluoroscopic
guidance, or saline plus/minus soluble
contrast media under sonographic guidance
• Water-soluble contrast agents
• Pneumatic reduction

Source: Sands DR. Intestinal intussusception [Internet]. Clin Colon Rectal Surg. 2008 May; 21(2):
106–113. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2780199/
 Treatment (adult)
• Definitive surgical intervention is mandatory and
preoperative reduction with barium or air is not
recommended as a part of definitive treatment
• Resect the intussusception en bloc and reduce
the intussusception
• En bloc resection of all colonic lesions, due to the
higher rate of malignancy, but a more limited
resection of small bowel, where malignancy is
less common
Source: Sands DR. Intestinal intussusception [Internet]. Clin Colon Rectal Surg. 2008 May; 21(2):
106–113. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2780199/
 INTESTINAL PERFORATION
Clinical Nausea
Presentation Vomiting
Pain
Fever
Diffuse peritonitis
The small bowel – most common
Pathophysiology Nontraumatic: Traumatic:
Increased intraluminal pressure Blunt trauma
Local erosion of bowel wall Penetrating trauma
Ingested object -increasing use of firearms,
seatbelts & speed travel-
Diagnosis Chest/abdominal radiography : free air
Ct scan + oral contrast : specific & sensitive for perforation
For peritoneal lavage : RBC > 100.000/ WBC 500 – but not spesific
Complication Hemorrhage & spillage of the intestinal contents -> sepsis & multiple organ
failure
Surgical : short-gut syndrome
Management Broad-spectrum antibiotic: third-gen cephalosporin & metronidazole
Treatment for the perforation: surgical, resection the damage bowel->
diversion->reanastomosis
 Botulism
• Botulism is an acute neurologic disorder that
causes potentially life-threatening
neuroparalysis due to a neurotoxin produced
by Clostridium botulinum.
 Sign and Symptomps
• More than 90% of patients with botulism have 3-
5 of the following signs or symptoms:
• Nausea
• Vomiting
• Dysphagia
• Diplopia
• Dilated/fixed pupils
• Extremely dry mouth unrelieved by drinking
fluids
• The autonomic nervous system is also involved in
botulism, with manifestations that include the
following:
• Paralytic ileus advancing to severe constipation
• Gastric dilatation
• Bladder distention advancing to urinary retention
• Orthostatic hypotension
• Reduced salivation
• Reduced lacrimation
 Diagnosis
• A mouse neutralization bioassay confirms
botulism by isolating the botulinum toxin.
Toxin may be identified in the following:
• Serum
• Stool
• Vomitus
• Gastric aspirate
• Suspected foods
• Meticulous airway management - Of paramount
importance, since respiratory failure is the most important
threat to survival in patients with botulism
• Nasogastric tube feeding can be used for nutritional
supplementation
• Foley catheter - Often used to treat bladder incontinence;
the catheter must be monitored conscientiously and
changed regularly
• Antibiotic therapy - Useful in wound botulism, but has no
role in foodborne botulism
• Magnesium salts, citrate, and sulfate should not be
administered, because magnesium can potentiate the
toxin-induced neuromuscular blockade.
 Conclusions and Suggestions
• The different diagnosis of this patient are GI
bleeding, acute abdomen, or shock.
• We suggest the patient to do more supporting
examination.
• Do general treatment of shock; monitor the
arterial pressure, pulse, respiratory, mental
status, transfussion for shock with blood loss,
fluid shifts, cardiac disfunction, and optimize
oxygen delivery.
 References
• Rosen’s Emergency Medicine 8th Ed
• Harrison's principles of internal medicine,
18th
• Medscape