Emergency medicine block 2017

first problem
A Bloody Situation
Thursday, 28 September 2017
 Group 9
Name of Tutor : dr. Okta
- Kelvin Pangestu 405130095
- Paat Natalia D A 405130128
- Fenny Irawan 405130143
- Chairani 405140025
- Ivanny Lestari G 405140070
- Sheren Maharani 405140078
- Leonardo Bernard 405140089
- Kurnia Halim 405140128
- Marsella Epifania S 405140166
- Indriani 405140178
- Diajeng Fatimah 405140213
- Faza Ghani Y 405140214
 A bloody Situation
A 65-year-old male is brought to an emergency department after he vomited 3 times,
500 cc – 1000 cc each time, 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 beats per minute, respiratory rate is 24 breaths per minute and
temperature is 39°C. 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
Discuss the case, assess the patient’s condition and plan proper treatment while
considering all possibilities!
 DD: Ruptur gaster, DD: Varices
Patient’s History: ulcer peptic esophagus
• CAD
• alkoholic liver
disease gastric mucosal Shock
Vomiting blood fresh
irritation  relief by hypo-
• aspirin daily + coffee colored
antacids volemic
consumption

Physical exam:
• Hypotension
• tachycardi
• CT Scan
• tachypneu
• fever (Temp >39⁰C) ABC • endoscopy
• Resistence culture
• Blood gas analysis

DD:
-appendicitis
- Syok septic
- Acute abdomen
 Learning issues
• MM SHOCK
• MM GI BLEEDING
• MM ACUTE ABDOMEN
 Shock
• Clinical syndrome that results from
inadequate tissue perfusion
• Lack of blood flow means that the cells and
organs do not get enough oxygen and
nutrients to function properly.
• As a response of oxygen decrease, aerobic
metabolism change into anaerobic
metabolism. Our body can tolerate this
condition only for a while.
 Resistensi vaskuler

Vasodilatasi
 SVR ↓

Heart rate

Kontraksi

V preload

Preload Kontraksi ↓
volume ↓  ESV ↑
 EDV ↓
Classification dan etiology
Rosen’s emergency medicine: concept and clinical practice, 8th ed.
 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

Longo D, Fauci AS, Kasper D, Hauser S, Jameson JL, Loscalzo J, editors. Harrison’s Principles of Internal Medicine. 18th
edition.
Hemorrhagic Shock
• Hemorrhage is the most common cause of shock after injury, and virtually all
patients with multiple injuries have an element of hypovolemia.
• Hemorrhage is defined as an acute loss of circulating blood volume.
• Normal adult blood volume is approximately 7% of body weight.
Hemorrhagic Shock

Management
 Cardiogenic shock
• Cardiogenic shock (CS) : characterized by
systemic hypoperfusion due to severe
depression of the cardiac index (<2.2
[L/min]/m2) and sustained systolic arterial
hypotension (<90 mmHg) despite an elevated
filling pressure (pulmonary capillary wedge
pressure [PCWP] >18 mmHg)
• Results when >40% of the myocardium
undergoes necrosis from ischaemia,
inflammation, toxins, or immune destruction
 Etiology
• Circulatory failure based on
cardiac dysfunction may be
caused by primary
myocardial failure, most
commonly secondary to
acute myocardial infarction
(MI), and less frequently by
cardiomyopathy or
myocarditis, cardiac
tamponade, or critical
valvular heart disease

Longo D, Fauci AS, Kasper D, Hauser S, Jameson JL, Loscalzo

J, editors. Harrison’s Principles of Internal Medicine. 18th
edition.
 Clinical findings
• Dyspnea
• Appear pale
• Diaphoretic
• Mental status may be altered
• The pulse is typically weak and rapid, often in the range of 90–110
beats/min, or severe bradycardia due to high-grade heart block may
be present.
• Systolic BP is reduced (<90 mmHg or ≥30 mmHg below baseline)
• Tachypnea
• Cheyne-Stokes respirations
• Jugular venous distention may be present
• Systolic murmurs
 Laboratory Findings
• WBC elevated with left shift
• Blood urea nitrogen and creatinine rise progressively
• Hepatic transaminases markedly elevated.
• Anion-gap acidosis and elevation of the lactic acid level.
• Arterial blood gases: hypoxemia and metabolic acidosis (or
compensated: alkalosis)
• Cardiac markers, creatine phosphokinase and its MB fraction,
and troponins I and T are markedly elevated.
Diagnosis

Rosen Emergency Medicine ed.7th

 Management

Longo D, Fauci AS, Kasper D, Hauser S, Jameson JL, Loscalzo J, editors. Harrison’s Principles of Internal Medicine. 18th
edition.
 Septic shock
• The harmful host response to infection;
systemic response to proven or suspected
infection plus some degree of organ
hypofunction sepsis (or severe sepsis)
• Septic shock: sepsis accompained by
hypotension that cannot be corrected by the
infusion of fluids
Longo D, Fauci AS, Kasper D, Hauser S, Jameson JL, Loscalzo J, editors. Harrison’s Principles of Internal Medicine. 18th
edition.
Longo D, Fauci AS, Kasper D, Hauser S, Jameson JL, Loscalzo J, editors. Harrison’s Principles of Internal Medicine. 18th
edition.
 Etiology
• Most common (64%): respiratory infection

Longo D, Fauci AS, Kasper D, Hauser S, Jameson JL, Loscalzo J, editors. Harrison’s Principles of Internal Medicine. 18th
edition.
Management
Rosen Emergency Medicine ed.7th
 Anaphylactic shock
- acute, potentially fatal,
multi organ systemicrx
caused by released of
chemical mediators
from mast cell and
basophil by IgE.
 Signs and Symptoms

Tintinalis’ Emergency Medicine

Tintinalis’ Emergency Medicine
 Obstructive Shock
• Tension pneumothorax
• Air trapped in pleural space with 1 way valve,
air/pressure builds up
• Mediastinum shifted impeding venous return
• Chest pain, SOB, decreased breath sounds
• No tests needed!
• Rx: Needle decompression, chest tube
 Obstructive Shock
• Cardiac tamponade
• Blood in pericardial sac prevents venous return to
and contraction of heart
• Related to trauma, pericarditis, MI
• Beck’s triad: hypotension, muffled heart sounds,
JVD
• Diagnosis: large heart CXR, echo
• Rx: Pericardiocentisis
 Obstructive Shock
• Pulmonary embolism
• Virscow triad: hypercoaguable, venous injury,
venostasis
• Signs: Tachypnea, tachycardia, hypoxia
• Low risk: D-dimer
• Higher risk: CT chest or VQ scan
• Rx: Heparin, consider thrombolytics
 Obstructive Shock
• Aortic stenosis
• Resistance to systolic ejection causes decreased
cardiac function
• Chest pain with syncope
• Systolic ejection murmur
• Diagnosed with echo
• Vasodilators (NTG) will drop pressure!
• Rx: Valve surgery
 GI bleeding
• Upper and lower • Predictors:
gastrointestinal bleeding – Age older than 70yrs
(GIB)  based on their – Intestinal ischemia
loc relative to the – Comorbid illness
ligament of Treitz in the – Coagulation defects
terminal duodenum. – Transfusion of packed red
• UGIB mortality rates have blood cells
remained constant at abt – Male gender
15% over past 2 decades
• LGIB mortality rate is
approximately 4%
 GI bleeding
Differential Considerations
• UGIB:
– Bloody or coffee-
ground-like vomit
termed hematemesis
or as dark, tarry stools
termed melena.
– Peptic ulcer disease
makes up >50% of all
acute cases of UGIB
seen in the emergency
department (ED).
– In pediatric patients,
gastric and duodenal
ulcers, esophagitis,
gastritis, esophageal
varices, and Mallory-
Weiss tears account for
most cases of UGIB, in
descending order of
frequency.
 GI bleeding
LGIB
• Usually produces bright red
/ maroon blood per rectum,
termed hematochezia.
• May classified according to
pathophysiology cause
inflammatory, vascular,
oncologic, traumatic or
iatrogenic.
• Common causes: anorectal
sources (hemorrhoids)
• In adults, common causes of
hematochezia are colonic
diverticula and
angiodysplasia.
• Major causes in children:
anorectal fissures and
infectious colitis
• Bleeding can also be caused
by intussusception and
Meckel’s diverticulum in
infants & toddlers
• Death from GIB is rare. • Epistaxis, dental
• There are two causes of bleeding, or red food
GIB that may rapidly coloring can mimic
the appearance of
cause death if not hematemesis.
recognized and
• Bismuth-containing
mitigated, esophageal medications and iron
varices & aortoenteric supplements can
fistula. create melanotic-
appearing (but
guaiac-negative)
stools. Vaginal
• bleeding, gross
hematuria, and red
foods (eg, beets) can
all be mistaken for
hematochezia
Relevant comorbid conditions
 GI bleeding
What to do?
• Reviewing the patient’s vital
signs, appearance of the stool,
and basic laboratory studies
will help identify the bleeding
source and guide treatment.
A useful starting point for the
emergency clinician
• Determine the time of onset,
duration of symptoms, and
relevant supporting historical
facts.
• Often, the degree of bleeding
is better gauged by assessing
symptoms associated with
significant intravascular loss,
such as:
- weakness
- shortness of breath
- angina
- orthostatic dizziness
- confusion
- palpitations
- report of cool extremities.
 GI bleeding
• Blood loss >800 mL will usually
result in the onset of these
complaints, with severe
symptoms being described at
a threshold >1500 mL.
• Such symptoms indicate a
decreased oxygen-carrying
capacity that often
accompanies significant blood
loss and should prompt a
thorough and expeditious
evaluation and resuscitation
• Strongly suggests a UGI
source: Vomiting of fresh
blood or blood with the
appearance of coffee
grounds, the passage of
melena, dark digested
stools
• hematochezia, bright red or
maroon stools, usually
signifies LGIB.
 Relevant Medical History
• This is especially • Patients with GIB
important with UGIB and a history of
because most of these
presentations are
coronary artery
caused by rebleeding of disease, congestive
previously identified heart failure, liver
sources. disease, or
diabetes  require
earlier or more
extensive
interventions.
 Relevant Medical History
• Medications such as NSAIDs,
aspirin, warfarin, clopidogrel,
corticosteroids, and certain
chemotherapeutic agents are
known to increase the risk of
GIB by as much as 3x.
• Patient’s social history can
identify activities that increase
risk for GIB.
• Alcohol abuse is associated
with gastritis and peptic ulcer
disease result in cirrhosis,
portal hypertension and,
ultimately, esophageal variceal
bleeding.
• Smoking cigarettes results in
slower healing and greater
recurrence of ulcers.
• These two social habits are
also closely associated with GI
malignancy— another, albeit
rare, risk factor for GIB
 Signs
• Hypotension and • In the unstable patient,
tachycardia can suggest pallor might reinforce the
moderate hypovolemia  impression of malperfusion
the early indicators of caused by massive blood
impending sh loss.
• Mental status is evaluated • Cold clammy skin on the
for signs of poor cerebral extremities signal significant
perfusion. volume loss consistent with
• Generalized pallor in a hemorrhagic shock.
hemodynamically stable • Finally, jaundice, palmar
patient might indicate the erythema, or spider
anemia of a subacute or angiomata suggests the
chronic GIB possibility of UGIB from
esophageal varices.
 Signs
• Hyperactive bowel sounds are a
nonspecific finding, but might
indicate UGIB
• Tenderness to palpation can be
seen in many cases of peptic
ulcer disease.
• Severe diffuse tenderness on
examination warrants the
consideration of bowel ischemia,
mechanical obstruction, ileus, or
bowel perforation.
• Evidence of peritonitis  rapid
surgical consultation for possible
operative management
• The abdominal examination may
also show further signs of portal
hypertension with the presence
of hepatomegaly, ascites, or
caput medusae.
• The rectal examination helps
determine the type of bleeding
and should be performed in most
patients with GIB.
• The examination should include
evaluation of the external anus,
digital rectal examination and,
when local bleeding is thought to
be the cause, anoscopy for
hemorrhoids, polyps, or fissures.
 Laboratory Studies
• Minimum resting: • The serum lactate level ↑
evaluation of the Hb, BUN  circulatory shock is
levels (increase), present
coagulation studies, and
platelets
• Leukocytosis bcs of the
stress response to acure
blood loss and should not
be considered to
re[present underlying infx
unless other indications
of infx are present
 Electrocardiography(ECG)
• Subsequent anemia can • Findings: consistent w/
reduce the oxygen myocardial ischemia
carrying capacity of the likely represent demand
blood, patients should be ischemia rather than
screened for signs of coronary thrombosis are
myocardinal ischemia treated with restoration
• Recomended obtaining of adequate circulatory
ECG  >40yrs, those volume, including blood,
with any symptoms of if needed.
ischemia, with known
coronary artery disease
(higher risk for ischemic
events)
 Imaging
• Abdominal CT scan • When endoscopy is not
bowel perforation is possible or cannot
suspected on the basis locate the hemorrhage
of peritoneal findings source, CT angiography
on examination (CTA) is the principle
• Abdominal plain diagnostic imaging tool
radiographs no value, and has the benefit of
except rare case: bowel allowing for therapeutic
obstruction is strongly options via
suspected embolization.
Diagnostic & management GIB
Disposition
Harrison's Principles of Internal Medicine 19th 2015.pdf
 Appendicitis
• Inflammation & obstruction of the vermiform
appendix

http://www.privatehealth.co.uk/EasysiteWeb/getresource.axd?AssetID=2683&amp;type=full&amp;servicetype=inline&amp;cus
 Insidence & Epidemiology
• Approximately 100/100,000 person-years in
Europe and the Americans or about 11 cases
per 10,000 people annually
• Most commonly in 10 to 19 y.o
• Overall, 70% of patients are less than 30 y.o
and most are men
• ♂ : ♀ ratio is 1.4 : 1
• Approximately 20% of all patients have
evidence of perforation at presentation, but
percentage risk is much higher in patients
Fauci, Braunwald, Kasper, dkk. Harrison’s Principles of Internal Medicine. 19th edition. USA: Mc Graw Hill,
 Appendicitis
• Etiology
– In approximately one third of cases, no direct
cause of obstruction
– In this cases, it is surmised that inflammation is
caused by viral, bacterial or parasitic infection
with subsequent mucosal ulceration or lymphoid
hyperplasia

Marx JA, Hockberger RS, Walls RM, Biros MH, eds. 2014. Rosen’s Emergency Medicine: Concept and Clinical
Practice, 8th edition. Philadelphia: Elsevier
 Pathophysiology
• Afferent fibers that conduct visceral pain from the appendix accompany the
sympathetic nerves and enter the spinal cord at the level of the tenth thoracic
segment  referral of pain to the umbilical area
• In majority of affected patients  due to an acute obstruction of the appendiceal
lumen
• After acute obstruction, intraluminal pressures ↑ & mucosal secretions are unable
to drain
• The resulting distention stimulates visceral afferent pathways  dull, poorly
localized pain
• Next, ulceration & ischemia develop as the intraluminal pressure exceeds the
venous pressure & bacteria & PMN cells begin to invade the appendiceal wall
• With time, appendix  swollen & factors elaborated in the pathologic process
begin to irritate surrounding structures, including peritoneal wall (the pain now
become more localized to RLQ)
• If swelling does not abate, hypoxia leads to gangrene and ultimately, perforation
through the appendiceal serosal layer. (this can lead to abscess formation or
diffuse peritonitis

Marx JA, Hockberger RS, Walls RM, Biros MH, eds. 2014. Rosen’s Emergency Medicine: Concept and Clinical
Practice, 8th edition. Philadelphia: Elsevier
 Appendicitis
• Sign and symptom
– Vague onset of dull periumbilical pain
– Anorexia
– Nausea & vomiting
– Pain migrates to RLQ
– If the appendix is retrocecal or retroiliac  pain
may be blunted
– If the appendix is elongated  pain may be
referred to the flank, pelvis or RUQ
– Marx
Other less typical symptoms  increased urinary
JA, Hockberger RS, Walls RM, Biros MH, eds. 2014. Rosen’s Emergency Medicine: Concept and Clinical
Practice, 8th edition. Philadelphia: Elsevier
 Appendicitis

• Physical examination
– Localized abdominal
tenderness  RLQ
– Abdominal guarding
and rigidity to
palpation
– McBurney’s sign
– Rovsing’s sign
– Psoas sign
–MarxObturator sign
JA, Hockberger RS, Walls RM, Biros MH, eds. 2014. Rosen’s Emergency Medicine: Concept and Clinical
th
Practice, 8 edition. Philadelphia: Elsevier
 Appendicitis
• Physical examination
– Rebound tenderness to palpation is a late finding
in patients with appendicitis and usually is noted
only after the appendix is significantly inflamed or
ruptured
– The presence of peritoneal irritation also can be
elicited by other maneuvers that cause the
visceral and parietal peritonei to rub against each
other  cough

Marx JA, Hockberger RS, Walls RM, Biros MH, eds. 2014. Rosen’s Emergency Medicine: Concept and Clinical
Practice, 8th edition. Philadelphia: Elsevier
 Appendicitis
• Diagnostic
– Leukocyte count
• Approximately 80-90% of patients with acute
appendicitis have an elevated WBC count above
10.000/mm3
– Urinalysis
• Helpful in differentiating urinary tract disease from
acute appendicitis and is suggested in all patients
– Pregnancy test
• Should be performed in all women of child-bearing age
because a positive result broadly expands the scope of
Marx JA, Hockberger RS, Walls RM, Biros MH, eds. 2014. Rosen’s Emergency Medicine: Concept and Clinical
the DD for RLQ pain th
Practice, 8 edition. Philadelphia: Elsevier
 Appendicitis
• Imaging studies
– Plain radiography  not useful (low sensitivity and specificity)
– Barium enema  sensitivity approximately 80 to 90%, but a
normal appendiceal lumen often is not visualized with this
technique
– USG  sensitivity and specificity (75-90% and 85-90%). USG
examination  a non compressible appendix with a diameter >
6 to 7 mm is considered diagnostic for appendicitis
– CT-scan  sensitivity and specificity (87-100% and 89-98%).
Enlarged appendix (diameter > 6 mm), pericecal inflammation,
presence of appendicolith and periappendical phlegmon or
abscess
– MRI  sensitivity similar to that for CT-scan
– Laparoscopy  for diagnosis or definitive treatment

Marx JA, Hockberger RS, Walls RM, Biros MH, eds. 2014. Rosen’s Emergency Medicine: Concept and Clinical
Practice, 8th edition. Philadelphia: Elsevier
 Appendicitis
• Differential diagnosis
All patients Women Children
Nonspesific Ovarian cyst Henoch-Schonlein
abdominal pain purpura

Gastroenteritis Ovarian torsion Testicular torsion

Ascending PID Mesenteric

diverticulitis adenitis/ileocolitis

Gallbladder disease Ectopic pregnancy Meckel’s

diverticulum
IBD

Renal colic
Marx JA, Hockberger RS, Walls RM, Biros MH, eds. 2014. Rosen’s Emergency Medicine: Concept and Clinical
Practice, 8th edition. Philadelphia: Elsevier
 Appendicitis
• Management
– Dehydrated patients  IV crystalloid fluids
– Nausea or vomiting  parenteral antiemetics
– Patients with more than mild discomfort  pain
medication
– Once the decision to operate has been made,
prophylactic antibiotics should be given to provide
coverage for gram-negative and aerobic organisms
 IV 2nd gen. cephalosporin (cefotetan or
cefoxitin
– Marx
In JA,cases with high likelihoodPractice, perforations
th 
8 edition. Philadelphia: 2nd
Hockberger RS, Walls RM, Biros MH, eds. 2014. Rosen’s Emergency Medicine: Concept and Clinical
Elsevier
 Appendicitis
• Complications
– Infection
– Perforation
– Prolonged ileus
– Small bowel obstruction
– Urinary retention and infection

Marx JA, Hockberger RS, Walls RM, Biros MH, eds. 2014. Rosen’s Emergency Medicine: Concept and Clinical
Practice, 8th edition. Philadelphia: Elsevier
 Acute Peritonitis
• Peritonitis is an inflammation of the
peritoneum
• It may be localized or diffuse in location, acute
or chronic in natural history, and infectious or
aseptic in pathogenesis.
• Primary or spontaneous peritonitis : no
intraabdominal source is identified
• Secondary peritonitis : usually related to a
perforated viscus

Harrison's Principles of Internal Medicine, 18th Edition

• 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 (e.g., a
chronic peritoneal dialysis
catheter).
• In the absence of immune
compromise, host defenses
are capable of eradicating
small contaminations.
Etiology
– Ruptured appendix
– Ruptured diverticulum
– Perforated peptic ulcer
– Incarcerated hernia
– Gangrenous gall bladder
– Volvulus
– Bowel infarction
– Cancer
– Inflammatory bowel disease
– Intestinal obstruction.
Harrison's Principles of Internal Medicine, 18th Edition
Clinical Features
• Acute abdominal pain and
tenderness, usually with fever
• Diffuse abdominal tenderness and
rebound.
• Tachycardia, hypotension, and
signs of dehydration
• Leukocytosis and marked acidosis
• Free air under the diaphragm is
associated with a perforated viscus.
• CT and/or ultrasonography  free
fluid or an abscess.
• Ascites  paracentesis with cell
count (>250 neutrophils/L), protein
and lactate dehydrogenase levels,
and culture is essential.
Treatment
• Antibiotic to treat infection
• Removal of indwelling
devices (e.g., a peritoneal
dialysis catheter or a
peritoneovenous shunt)
may be required for
effective therapyof
recurrent infections
• Emergency surgery
if peritonitis has been caused by
conditions such as appendicitis, a
perforated stomach ulcer, or
diverticulitis.
Harrison's Principles of Internal Medicine, 18th Edition
 Intussusception
• Intussusception occurs when a portion of the intestine
folds like a telescope, with one segment slipping inside
another segment. It can occur in the colon, the small
bowel, or between the small bowel and colon.
• Further, a red mucus or jelly-like stool is usually seen
with intussusception. Symptoms of intussusception,
such as fever, lethargy, vomiting bile, diarrhea,
sweating, dehydration, and an abdominal distention or
lump, may resemble other conditions or medical
problems
 Symptoms of Intussusception
• abdominal swelling.
• vomiting.
• vomiting up bile, a
bitter-tasting
yellowish-green
fluid.
• passing stools
(poop) mixed with
blood and mucus,
known as currant
jelly stool.
invagination
• grunting due to
 History in patients with acute abdomen
Question
Where is the pain?
What is the pain like?
Potential responses and indication
Differential diagnosis of abdominal pain by location
•Acute waves of sharp constricting pain that “take the
breath away” (renal or biliary colic)
•Waves of dull pain with vomiting (intestinal obstruction)
•Colicky pain that becomes steady (appendicitis,
strangulating intestinal obstruction, mesenteric ischemia)
•Sharp, constant pain, worsened by movement (peritonitis)
•Tearing pain (dissecting aneurysm)
•Dull ache (appendicitis, diverticulitis, pyelonephritis)

Have you had it before? Yes suggests recurrent problems such as ulcer disease,
gallstone colic, diverticulitis, or mittelschmerz

http://www.merckmanuals.com/professional/gastrointestinal_disorders/acute_abdomen_and_surgical_gastroenterol
ogy/acute_abdominal_pain.html#v890312
 History in patients with acute abdomen
Question
Was the onset sudden?
How severe is the pain?
Does the pain travel to
any other part of the
body?
Potential responses and indication
•Sudden: “Like a light switching on” (perforated ulcer, renal
stone, ruptured ectopic pregnancy, torsion of ovary or
testis, some ruptured aneurysms)
•Less sudden: Most other causes
•Severe pain (perforated viscus, kidney stone, peritonitis,
pancreatitis)
•Pain out of proportion to physical findings (mesenteric
ischemia)
•Right scapula (gallbladder pain)
•Left shoulder region (ruptured spleen, pancreatitis)
•Pubis or vagina (renal pain)
•Back (ruptured aortic aneurysm, pancreatitis, sometimes
perforated ulcer)

http://www.merckmanuals.com/professional/gastrointestinal_disorders/acute_abdomen_and_surgical_gastroenterol
ogy/acute_abdominal_pain.html#v890312
 History in patients with acute abdomen
Question
What relieves the pain?
What other symptoms
occur with the pain?
Potential responses and indication
•Antacids (peptic ulcer disease)
•Lying as quietly as possible (peritonitis)
•Vomiting precedes pain and is followed by diarrhea
(gastroenteritis)
•Delayed vomiting, absent bowel movement and flatus
(acute intestinal obstruction; the delay increases with a
lower site of obstruction)
•Severe vomiting precedes intense epigastric, left chest, or
shoulder pain (emetic perforation of the intra-abdominal
esophagus)

http://www.merckmanuals.com/professional/gastrointestinal_disorders/acute_abdomen_and_surgical_gastroenterol
ogy/acute_abdominal_pain.html#v890312
 65 yo, complained: Physical exam:
Vomited 3 times Tachycardi,
Hypovolemic hipotension,
containing fresh blood
shock tachypnea, febrile,
+ coffee colored blood
abdomen tenderness,
decreased bowel
The last 5 days, he sound, lab :
complained: leukocytosis, << HB
Stomachache and Acute abdomen
nause  better after pain
antacids
Septic shock
History :
Coronary artery • BASED ON THE DISCUSSION WE
disease  aspirin, HAVE LEARNED :
Consumed alcohol  UGI bleeding
- MM SHOCK
alcoholic liver disease
- MM GI BLEEDING
- MM ACUTE ABDOMEN

Given jamu  itchy

and swelled all over Anaphylactic
the face shock
SUGGESTIONS REFERENCES
- patients are advised to 1. Rosen Emergency
reduce until stop drinking Medicine ed.7th
alcohol 2. Fred Ferri’s Clinical Advisor
- Bedrest 2017 Volume 5
3. Harrison's principles of
internal medicine 18th
4. Tintinalis’ Emergency
Medicine
5. CURRENT Medical
Diagnosis & Treatment
2017