PROBLEM 1

EMERGENCY
MEDICINE BLOCK
Agustina Cynthia Cesari S
405140066
Group 1
SHOCK
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.
 General Pathophysiology of Shock
◦ Hipoperfusion  supply of oxygen to mitochondria
disturbed  ATP decrease
◦ Hipoperfusion  activation sympathetic reflex system
 increase of heart rate contractility and frequency 
cardiac output
◦ Activation sympathetic reflex system  catecolamine,
angiotensin, vasopresin, endothelin output 
increase blood vessel tonus that can maintain
perfusion pressure to make enough perfussion.
◦ Untolerated hypoxia  mitochondria disturbed , ATP
decrease  tissue failure ( heart failure, brain failure,
etc)
Classification dan etiology
Rosen Emergency Medicine ed.7th
Rosen Emergency Medicine ed.7th
 Physical findings

Tintinalis’ Emergency Medicine

Diagnosis

Rosen Emergency Medicine ed.7th

Management

Fred Ferri’s Clinical Advisor 2017 Volume 5 page 1524

Fred Ferri’s Clinical Advisor 2017 Volume 5 page 1524
HYPOVOLEMIC SHOCK
 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.
Pathophysiology
Diagnosis

Rosen Emergency Medicine ed.7th

Management
◦ Initial resuscitation: rapid reexpansion of the circulating intravascular
bood volume along with interventions to control ongoing losses 
rapid infusion of either isotonic saline or a balanced salt solution such
as Ringer’s lactate through large-bore intravenous lines (the infusion
of 2-3L of salt solution over 20-30 min should restore normal
hemodynamic parameters
◦ Continuing acute blood loss with Hb ≤ 10g/dL  blood transfusion
(PRBC)
◦ Severe and/or prolonged hypovolemia  inotropic support with
norepinephrine, vasopressin, or dopamine  mantain adequate
ventricular performance but only after blood volume has been
restored
◦ Supplemental oxygen should always be provided, and endotracheal
intubationmay be necessary to maintain arterial oxygenation
Rosen Emergency Medicine ed.7th
CARDIOGENIC SHOCK
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.
Pathophysiology

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
◦ mMental 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
◦ There is typically a weak apical pulse and soft S1, and an S3 gallop may be
audible
◦ 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.
Electrocardiogram
◦ Due to acute MI with LV failure: Q waves and/or >2-mm ST
elevation in multiple leads or left bundle branch block
◦ >½ infarcts associated with shock are anterior.
◦ Global ischemia due to severe left main stenosis  severe (e.g.,
>3 mm) ST depressions in multiple leads.
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
Septic shock
◦ When an infectious etioogy is proven or strongly suspected and
the response results in hypofunction of uninfected organs  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.
Rosen Emergency Medicine ed.7th
ANAPHYLACTIC SHOCK
Anaphylactic shock
◦ An antigen stimulates the allergic reaction.
◦ Mast cells degranulate.
◦ Histamine releases along with autocoids stimulate an anaphylaxis
cascade.
◦ Vascular smooth muscle relaxes.
◦ Capillary endothelium leaks.
◦ Drop SVR leads to inadequate tissue perfusion.
 Etiology

Tintinalis’ Emergency Medicine

 Signs and Symptoms

Tintinalis’ Emergency Medicine

Tintinalis’ Emergency Medicine
Treatment
◦ Anaphylactic shock:
◦ Intubation for airway compromise
◦ Epinephrine
◦ Subcutaneous in noncritical settings
◦ Intravenous drip for immediate life threats or refractory hypotension
◦ H-1 blockers (diphenhydramine)
◦ H-2 blockers (cimetidine)
◦ Corticosteroids (hydrocortisone or methylprednisolone)
◦ Nebulized H2-antagonists for bronchospasm
◦ Patients taking beta-blockers may be more likely to experience severe
symptoms of anaphylaxis that may manifest as paradoxical
bradycardia, profound hypotension, and severe bronchospasm.
Tintinalis’ Emergency Medicine
Tintinalis’ Emergency Medicine
GI BLEEDING
Upper GI Bleeding
- Definition : Upper GI (UGI) bleeding is any GI bleeding originating
proximal to the ligament of Treitz
- Etiology : Helicobacter pylori rates, socioeconomic conditions,
and prescription patterns of ulcer- healing and ulcer-promoting
medications.2 Increasing age, coexistent organ system disease
Pathophysiology
PEPTICULCERDISEASE
-peptic ulcer disease, which includes gastric, duodenal,
esophageal, and stomal ulcers, is still considered the most
common cause of UGI bleeding
-E/ : Awareness that aspirin, NSAIDs, and smoking cause
bleeding and increased recognition and treatment of H.
pylori infection may be responsible for decreased incidence.
EROSIVEGASTRITISANDESOPHAGITIS
-Common predisposing factors include alcohol, salicylates,
and NSAIDs. Infection, toxic ingestion, radiation, and stress
from severe illness may also cause erosive gastritis. Stress-
related mucosal disease occurs in patients with
overwhelming sepsis, trauma,
ESOPHAGEALANDGASTRICVARICES
- Esophageal and gastric varices result from portal hypertension
and, in the United States, are most often a result of alcoholic
liver disease.

MALLORY-WEISSSYNDROME
- Mallory-Weiss syndrome is bleeding secondary to a longitudinal
muco- sal tear at the gastroesophageal junction
- The classic history is repeated vomiting followed by bright red
hematemesis.
DIAGNOSIS
HISTORY
-Ask about hematemesis, coffee-ground emesis, or melena. Classically,
hematemesis and coffee-ground emesis suggest a UGI source.
-The presence of melena and age <50 years old more likely indicate an
upper GI bleed versus a lower GI bleed, even in patients without
hematemesis
-Vomiting and retching, followed by hematemesis, suggest a Mallory-Weiss
tear.
-Review the patient’s medication list carefully. Salicylates, glucocorticoids,
NSAIDs, and anticoagulants all place the patient at high risk for GI bleed.
-Alcohol abuse is strongly associated with a number of causes of bleeding,
including peptic ulcer disease, erosive gastritis, and esophageal varices.
-Ingestion of iron or bismuth can simulate melena. Liquid medications with
red dye, as well as certain foods, such as beets, can simulate
hematochezia.
PHYSICAL EXAMINATION
-Visual inspection of the vomitus for a bloody, maroon,
or coffee- ground appearance is the most reliable
way to diagnose UGI bleeding in the ED  Consider
keeping a sample of the vomitus or nasogastric (NG)
aspirate at bedside for the gastroenterologist to view.
-Vital signs may reveal obvious hypotension and
tachycardia or more subtle findings such as
decreased pulse pressure or tachypnea.
-Cool, clammy skin is an obvious sign of shock. Spider
angiomas, palmar erythema, jaundice, and
gynecomastia suggest liver disease. Pete- chiae and
purpura suggest an underlying coagulopathy. Facial
lesions, cutaneous macules, or telangiectasias may be
suggestive of the Peutz- Jeghers, Rendu-Osler-Weber,
or Gardner’s syndromes.
LABORATORY TESTING
-In patients with significant bleeding, the single most important
laboratory test is to obtain blood for type and cross-match in case
transfusion is needed.
-UGI hemorrhage will elevate BUN levels through digestion and
absorption of hemoglobin. A BUN:creatinine ratio ≥30 suggests a
UGI source of bleeding.
NASOGASTRICLAVAGE
- NG intubation and aspiration are diagnostic and therapeutic. In
patients without a history of hematemesis, a positive aspirate
provides strong evidence for a UGI source of bleeding.
- Visual inspection of the aspirate for a bloody, maroon, or coffee-
ground appear- ance is the most reliable way to diagnose UGI
bleeding in the ED
Tintinalli's Emergency Medicine - A Comprehensive Study Guide 8th 2016.pdf
 TREATMENT

Tintinalli's Emergency Medicine - A Comprehensive Study Guide 8th 2016.pdf

(Patient Teaching Guides - Evidence-Based Diagnosis) Fred F. Ferri-Ferri’s Clinical
Advisor 2017. 5 vols.-Expert Consult Com. (2017).pdf
Harrison's Principles of Internal Medicine 19th 2015.pdf
Lower GI Bleeding
- Lower GI (LGI) bleeding is the loss of blood from the GI tract distal
to the ligament of Treitz.
- Among patients with an established LGI source of bleeding (i.e.,
bleeding past the ligament of Treitz), the most common cause is
diverticular disease, followed by colitis, adenomatous polyps, and
malignancies.
PATHOPHYSIOLOGY
- Hematochezia is either bright red or maroon-colored rectal
bleeding. If hematochezia originates from a UGI source, it
indicates brisk UGI bleed- ing, which may be accompanied by
hematemesis and hemodynamic instability.
- Melena is dark or black-colored stools and usually represents
bleeding from a UGI source
DIVERTICULOSIS
- Diverticular bleeding is usually painless and results from erosion into
the penetrating artery of the diverticulum.
VASCULARECTASIA
- Vascular ectasia, which includes arteriovenous malformations and
angiodysplasias of the colon, is a common cause of LGI bleeding.
ISCHEMIC COLITIS AND MESENTERIC ISCHEMIA
- Ischemic colitis is the most common cause of intestinal ischemia
and is usually transient.
- The colon is predisposed to ischemia because of its poor vascular
circulation and high bacterial content.
- Aneurysmal rupture, vasculitis, hypercoagulable states, prolonged
strenuous exercise, cardiovascular insult, irritable bowel syndrome,
and certain medications that cause vasoconstriction or slow bowel
motility are known risk factors.
- Mesenteric ischemia can lead to bowel necrosis. Causes include
thrombosis or embolism of the superior mesenteric artery,
mesenteric venous thrombosis, and nonocclusive mesenteric
ischemia associated with low arterial flow with vasoconstriction.
MECKEL’SDIVERTICULUM
-Meckel’s diverticulum
consists of embryonic
tissue, most commonly
found in the terminal
ileum.
-More than half of
lesions contain ectopic
gastric tissue, which can
secrete gastric enzymes,
eroding the mucosal
wall and causing
bleeding.
DIAGNOSIS
- Factors associated with a high morbidity rate are hemodynamic
instability, repeated hematochezia, gross blood on initial rectal
examination, initial hematocrit <35%, syncope, nontender
abdomen (predictive of severe bleeding), aspirin or non- steroidal
anti-inflammatory drug use (predictive of diverticular
hemorrhage),
HISTORY
- Although most patients will volunteer complaints of
hematochezia or melena, signs and symptoms of hypotension,
tachycardia, angina, syncope, weakness, or altered mental
status can all occur as a result of LGI bleeding.
- Ask about previous GI bleeding as well as a history of pain,
trauma, ingestion or insertion of foreign bodies, and recent
colonoscopies.
- Weight loss and changes in bowel habits may suggest
malignancy.
- A history of an aortic graft may suggest the possibility of an
aortoenteric fistula
- Medications, such as salicylates, nonsteroidal anti-inflammatory
drugs, and warfarin, increase the risk of LGI bleeding.14-16
Ingestion of iron or bismuth can simulate melena, and certain
foods, such as beets, can simulate hematochezia.
PHYSICALEXAMINATION
-Hypotension and tachycardia, or decreased pulse
pressure or tachypnea, develop with significant bleeding
-However, changes in vital signs may be masked by
concurrent medications, such as β-blockers, or medical
conditions such as poorly controlled hypertension.
-Cool, pale skin and an increase in capillary refill can be
signs of shock.
-The abdominal examination : disclose tenderness, masses,
ascites, or organomegaly
-In patients with LGI bleeding, a lack of abdominal
tenderness suggests bleeding from disorders involving the
vasculature, such as diverticulosis or angiodysplasia.
Inflammatory bowel disorders with LGI bleeding are
associated with abdominal tenderness on examination.
- Rectal examination : may reveal an obvious source of bleeding,
such as a laceration, masses, trauma, anal fissures, or external
hemorrhoids
- digital rectal examination to detect gross blood (either bright red
or maroon) and for guaiac testing. Rectal examination can also
detect the presence of masses.
LABORATORYTESTING
- The most important laboratory tests are the CBC,
coagulation studies, and typed and cross-matched
blood
- Coagulation studies, including prothrombin time,
partial thromboplastin time, and platelet count, are
of obvious benefit in patients taking anticoagulants
or those with underlying hepatic disease.
• Bleeding from a source higher in the GI tract may
elevate blood urea nitrogen levels through digestion
and absorption of hemoglobin.
• Obtain an ECG in patients with coronary artery
disease. Silent ischemia can occur secondary to the
decreased oxygen delivery accompanying
significant GI bleeding.
IMAGING
- Angiography can sometimes detect the site of bleeding and
help guide surgical management. Moreover, angiography
permits therapeutic options such as transcatheter arterial
embolization or the infusion of vasoconstrictive agents.
- angiographic diagnosis and therapy require a relatively brisk
bleeding rate (at least 0.5 mL/ min). Serious complications can
also occur with angiography in up to 10% of cases.
- Scintigraphy appears more sensitive than angiography and
can localize the site of bleeding at as low a rate as 0.1 mL/min.
It also has potential value over angiography if bleeding occurs
intermittently but requires a minimum of 3 mL of blood to pool.
- Multidetector CT angiography has a sensitivity and specificity of
up to 100% and 99%, respectively, for detecting active or
recent GI bleeding and is about 93% accurate in determining
the site of bleeding.23,24 It can be a useful tool prior to
treatment with conventional angiography.
TREATMENT
-Resuscitate unstable or actively bleeding patients. Administer
oxygen and institute cardiac monitoring. Place two large-bore IV
lines and replace volume with crystalloids.
-Blood transfusion should be based on the clinical findings of
volume depletion or continued bleeding rather than on initial
hematocrit values. In acute bleeding, hematocrit values may not
represent true blood volume status, because it takes several
hours for the hematocrit to decrease.
-General guidelines for initiation of blood transfusion are
continued active bleeding and failure to improve perfusion and
vital signs after the infusion of 2 L of crystalloid.
-Consider the placement of a nasogastric tube if LGI bleeding is
significant. Hematochezia unexpectedly originates from UGI
sources approximately 10% to 14% of the time.
ACUTE ABDOMEN
Tintinallis’ Emergency Medicine page 483
Harrison’s Principles of Internal Medicine 19th page 1877
Fred Ferri’s Clinical Advisor 2017 Volume 5 page 1524
Fred Ferri’s Clinical Advisor 2017 Volume 5 page 1631
Intussusception
Definition
◦ A process in which a
segment of intestine
invaginates into the adjoining
intestinal lumen, causing
bowel obstruction.
◦ Early diagnosis, appropriate
fluid resuscitation, and
therapy  MR in children <
1%.
◦ Untreated  uniformly fatal
in 2-5 days.
Symptoms
◦ The patient is usually in pediatric,
often one who has had an upper
respiratory infection.
◦ Symptoms:
◦ Vomiting (initial: nonbilious and
reflexive, intestinal obs: bilious)
◦ Abdominal pain (colicky, severe,
intermittent)
◦ Passage of blood and mucus
(currant jelly); diarrhea can also
be an early sign of instussusception
◦ Lethargy
◦ Palpable abdominal mass
Intussusception
Classification
◦ Idiopathic intussusception
◦ Usually starts at the ileocolic
junction
◦ Affects infants and toddlers
◦ Enteroenteral intussusception
◦ Jejunojejunal, jejunoileal, ileoileal
◦ Occurs in oldren children
◦ Associated w/ special medical
situations, ex: Henoch-Schonlein
purpura (HSP), cystic fibrosis,
hematologic dyscrasias
◦ Or may be secondary to a lead
point and occasionally occur in
the postoperative period
Etiology
◦ Unclear, but one theory to explain
the possible etiology of idiopathic
instussusception is that occurs
because of an enlarged Peyer
patch, this hypothesis is derived
from 3 observations :
◦ The illness is preceded by an upper
respiratory infection
◦ The ileocolic region has the highest
concentration of lymph nodes in the
mesentery
◦ Enlarged lymph nodes are often observed in
patients who require surgery.
◦ Whether the enlarged Peyer patch is a
reaction to the instussusception or a
cause of it is unclear.
Intussusception
Physical Examination

◦ Right hypochondrium
sausage-shaped mass and
emptiness in the RLQ.
◦ This mass is hard to detect
and is best palpated
between spasm of colic,
when the infant is quiet.
◦ Abdominal distention
frequently is found if the
obstruction is complete.
Spontaneous Bacterial
Peritonitis
Definition
◦ SBP is an inflammatory reaction
of the peritoneum secondary
to the presence of bacteria or
other microorganisms.
◦ Specifically, SBP is defined as
an ascitic fluid infection
without an evident
intraabdominal surgically
treatable source occurring
primarily in patients with
advanced cirrhosis of the liver.
◦ Synonyms : primary peritonitis
Etiology
◦ Escherichia coli.
◦ Klebsiella pneumoniae.
◦ Streptococcus pneumoniae.
◦ Streptococcus and
Enterococcus spp.
◦ Staphylococcus aureus.
◦ Anaerobic pathogens:
Bacteroides, Clostridium
organisms.
◦ Other: fungal, mycobacterial,
viral.
Spontaneous Bacterial
Peritonitis
Physical Findings & Clinical
Presentation Laboratory Tests
◦ Acute fever with accompanying ◦ Cell count with an absolute
abdominal pain/ascites, nausea, polymorphonuclear cell count
vomiting, diarrhea. >250/mm3.
◦ In cirrhotic patients, presentation ◦ Presence of bacteria on Gram stain.
may be subtle with a low grade ◦ pH <7.31.
temperature (100° F) with or
without abdominal abnormalities. ◦ Lactic acid >32 mg/dl.
◦ In patients with ascites, a ◦ Protein <1 g/dl.
heightened degree of awareness is ◦ Glucose >50 mg/dl.
necessary for detection
◦ Lactate dehydrogenase <225 mU/mL.
◦ Jaundice and encephalopathy.
◦ Positive culture of peritoneal fluid.
◦ Deterioration of mental status
and/or renal function.
Treatment
Acute General Reaction Prophylaxis
◦ Cefotaxime (2 g IV q8h) or ◦ Ciprofloxacin 500 mg PO qd
ceftriaxone (2 g IV q24h) or
ticarcillin-clavulanate or or levofloxacin 250 mg PO
piperacillin-tazobactam. Continue qd.
therapy for 7 days.
◦ If ascites PMN count decreases by
at least 25% at day 2, IV therapy
can be switched to PO
(levofloxacin 250 mg PO bid) to
complete 7 days of therapy.
◦ IV albumin (1.5 g/kg of body
weight upon initial diagnosis and 1
g/kg of albumin on day 3) if BUN
>30 mg/dL, serum creatinine >1
mg/dl, bilirubin >4 mg/dL.
Secondary Peritonitis

Definition

◦ To the acute onset of severe

abdominal pain caused by
peritoneal inflammation.
◦ Secondary peritonitis is a
localized (abscess) or diffuse
peritonitis originating from a
defect in abdominal viscus.
◦ Synonyms : acute abdomen
Peritonitis
Physical Findings & Clinical
Presentation Etiology
◦ Acute abdominal pain ◦ Microbiology
◦ Abdominal distention and ascites
◦ Acute perforation peritonitis
◦ Abdominal rigidity, rebound, and
guarding ◦ Postoperative peritonitis
◦ Fever, chills
◦ Posttraumatic peritonitis
◦ Exacerbation with movement
◦ Anorexia, nausea, and vomiting
◦ Constipation
◦ Decreased bowel sounds
◦ Hypotension and tachycardia
◦ Tachypnea, dyspnea
Peritonitis
Laboratory Tests
◦ Complete blood count:
leukocytosis, left shift, anemia
◦ Liver function tests: ascites
from liver disease,
cholelithiasis
Imaging Studies
◦ Abdominal series: free air from
perforation, small or large bowel
dilation from obstruction,
identification of fecalith
◦ Chest x-ray examination: elevated
diaphragm, pneumonia
◦ Pelvic/abdominal ultrasound:
abscess formation, abdominal
mass, intrauterine versus ectopic
pregnancy, identify free fluid
suggestive of hemorrhage or
ascites
◦ CT: mass, ascites
Treatment
Nonpharmacologic Therapy
◦ V hydration to correct
dehydration, hypovolemia
◦ Blood transfusion to correct
anemia from hemorrhage
◦ Nasogastric decompression,
especially if obstruction is
present
◦ Oxygen: intubation if
necessary
◦ Bed rest
Acute General Reaction
◦ Surgery to correct underlying pathology,
such as controlling hemorrhage,
correcting perforation, draining abscess
◦ Broad-spectrum antibiotics to cover both
gram-negative aerobic and gram-
negative anaerobic bacteria:
◦ Mildmoderate disease: piperacillin
tazobactam 3.375 g IV q6h or 4.5 g IV q8h or
ticarcillin clavulanate 3.1 g IV q6h.
◦ Alternative agents are ciprofloxacin 400 mg
IV q12h or levofloxacin 750 mg IV q24h plus
metronidazole 1 g IV q12h.
◦ Severe life threatening disease: imipenem
500 mg IV q6h or meropenem 1 g IV q8h.
◦ Alternative agents are ampicillin plus
metronidazole plus ciprofloxacin.
◦ Pain control: morphine or meperidine as
needed (hold until diagnosis confirmed)
 Hernia
Incarcerated hernia:
• Painful enlargement of a previous hernia or defect
• Cannot be manipulated (either spontaneously or manually) through the fascial
defect
• Nausea, vomiting, and symptoms of bowel obstruction (possible)

Strangulated hernia:
• Occluded blood supply by pressure at the
neck of hernia
• Patients have symptoms of an
incarcerated hernia

prezi.com 84

http://emedicine.medscape.com.
 Hernia
Sign & symptoms:
• A bulge in the inguinal region or scrotum
• Infants  increased irritability, especially when the hernia is large.
• Older children and adults  dull ache or burning pain that often worsens with
exercise or straining

Management:
• Hernia reduction
• Surgical repair

85

http://emedicine.medscape.com.
Tintinalis’ Emergency Medicine
Appendicitis
Physical Findings & Clinical
Definition Presentation
◦ Abdominal pain : Initially the pain
◦ is the acute inflammation of may be epigastric or periumbilical 
the vermiform appendix. subsequently localizes to the right
lower quadrant within 12 to 18 hr
◦ Psoas sign
◦ Low grade fever  temperature may
be >38° C if there is appendiceal
perforation.
◦ Obturator sign
◦ Rovsing’s sign  physical examination
may reveal right sided tenderness in
patients with pelvic appendix.
◦ McBurney’s point
Appendicitis
Etiology
◦ Fecaliths: 30% to 35% of cases
(most common in adults)
◦ Foreign body: 4% (fruit seeds,
pinworms, tapeworms,
roundworms, calculi)
◦ Inflammation: 50% to 60% of
cases (submucosal lymphoid
hyperplasia [most common
etiology in children, teens])
◦ Neoplasms: 1% (carcinoids,
metastatic disease,
carcinoma)
Laboratory Tests
◦ Complete blood count with
differential reveals
leukocytosis with a left shift
◦ Total white blood cell (WBC)
count is generally lower than
20,000/mm3
◦ Microscopic hematuria and
pyuria may occur in <20% of
patients.
Imaging Studies
Management