Markovchick Vincent J., Pons Peter T., Bakes Katherine M.(ed.) Emergency medicine secrets. 5th ed
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Chapter 31 HYPERTENSION, HYPERTENSIVE CRISIS, AORTIC DISSECTION, AND AORTIC ANEURYSMS228
BIBLIOGRAPHY
1. Adams HP Jr, del Zoppo G, Alberts MJ, et al: Guidelines for the early management of adults with ischemic
stroke. Stroke 38(5):1655–1711, 2007.
2. Bessen HA: Abdominal aortic aneurysm. In Marx J, Hockberger R, Walls R, et al: Rosen’s emergency
medicine: concepts and clinical practice, ed 6, Philadelphia, 2006, Mosby, pp 1330–1341.
3. Broderick J, Connolly S, Feldmann E, et al.: Guidelines for the management of spontaneous intracerebral
hemorrhage in adults. Stroke 38(6):2001–2023, 2007.
4. Chaikof EL, Brewster DC, Dalman RL, et al: The care of patients with an abdominal aortic aneurysm: The
Society for Vascular Surgery practice guidelines. J Vasc Surg 50:S2–S49, 2009.
5. Chobanian AV, Bakris GL, Black HR, et al: The seventh report of the Joint National Committee on prevention,
detection, evaluation, and treatment of high blood pressure: The JNC 7 report. JAMA 289(19):2560–2572,
2003.
6. Corey MS, Alluru SR: Increased blood pressure without evidence of acute end organ damage. Ann Emerg Med
51(3):S7–S9, 2008.
7. Decker WW, Godwin SA, Hess EP, et al: Clinical policy: critical issues in the evaluation and management of
adult patients with asymptomatic hypertension in the emergency department. Ann Emerg Med 47(3):237–249,
2006.
8. Gray RO: Hypertension. In Marx J, Hockberger R, Walls R, et al: Rosen’s emergency medicine: concepts and
clinical practice, ed 7, St. Louis, 2010, Mosby, 13076–1087.
9. Pancioli AM: Hypertension management in neurologic emergencies. Ann Emerg Med 51(3 Suppl):S24–S27,
2008.
10. Shayne PH, Pitts SR: Severely increased blood pressure in the emergency department. Ann Emerg Med
41:513–529, 2003.
229
John L. Kendall, MD, and Christopher B. Colwell, MD
PERICARDITIS AND MYOCARDITIS
CHAPTER 32
PERICARDITIS
1. Describe a normal pericardium.
The pericardium is 1 to 2 mm thick and envelops the heart. It has two layers. Between
the two layers is the pericardial space, which normally contains 25 to 50 mL of fluid.
2. What is pericarditis?
Inflammation of the pericardium.
3. What causes pericarditis?
Infectious agents, such as viruses and bacteria, can cause pericarditis as a result of
direct spread of infection to the pericardium. Pericarditis also may be caused by the
antibody-mediated autoimmune reaction that occurs 2 to 4 weeks after a viral illness
(see Table 32-1). This postviral pericarditis, termed idiopathic because a viral source has
Infectious
Immunologic
Mediated
Diseases Trauma Drugs Other
Viral:
Coxsackie B
Echovirus
HIV
Autoimmune
disorders
Blunt Procainamide Sarcoidosis
Bacterial: Acute rheumatic
fever
Penetrating Cromolyn
sodium
Amyloidosis
Staphylococcus
Tuberculosis
Fungal Rheumatoid
arthritis
Postcardiac injury
syndrome
Hydralazine Uremia
Parasitic Connective
tissue diseases
Postpericardiotomy Radiation
Rickettsia Lupus
erythematosus
Neoplasm
Postinfarction Aortic
dissection
TABLE 32–1. CAUSES OF PERICARDITIS
Chapter 32 PERICARDITIS AND MYOCARDITIS230
not been isolated, is probably the most common form of pericarditis. An autoimmune reaction
to cardiac antigens may occur after cardiac instrumentation or acute myocardial infarction
(MI). The likelihood of postinfarction pericarditis is reduced by half (from approximately 12%
to 6%) when a thrombolytic agent is used.
4. Who is most susceptible to infectious pericarditis?
Viral and idiopathic pericarditis occur most commonly in healthy persons between 20 and 40
years old. Bacterial pericarditis occurs in patients with a bacterial infection of the lungs,
endocardium, or blood. Patients with HIV are susceptible to pericarditis caused by
opportunistic infections.
5. Describe the clinical presentation of pericarditis.
The most common symptom is chest pain, often described as midline and sharp. The pain is
generally worse with movement and breathing, and relief is obtained from sitting up and
leaning forward. It may radiate to the neck, back, or left shoulder. Dyspnea, malaise, and fever
may occur. The pathognomonic clinical finding is a friction rub, which is a scratchy noise,
similar to creaking leather. The optimal patient position for a rub to be auscultated is sitting
up, leaning forward, and in full expiration. The diaphragm of the stethoscope should be
pressed firmly to the chest at the lower left sternal border. A little luck may be needed to
detect a rub because it occurs intermittently.
6. How does the electrocardiogram (ECG) appear in pericarditis?
The ECG typically evolves through four stages:
n
In stage 1, The first hours to days of illness may show ST segment elevation and PR
segment depression in all leads except aVR and V
1
, in which reciprocal changes occur.
n
In stage 2, the ST and PR segments normalize, and the T waves flatten.
n
In stage 3, deep T-wave inversion occurs.
n
In stage 4, the ECG reverts to normal. Occasionally, stage 4 does not occur, which
results in permanent generalized or focal T-wave inversions and flattenings. The ST
segment displacement seen in stage 1 is attributed to the associated subepicardial
myocarditis, whereas the PR segment depression is attributed to subepicardial atrial
injury.
7. How can acute pericarditis be distinguished from acute MI?
ST segment elevations in stage 1 of acute pericarditis tend to be upwardly concave rather
than convex, and simultaneous T-wave inversions are not typically seen. The progression to
T-wave inversions in stage 2 tends to occur after the ST segments have returned to baseline,
whereas in acute MI, the T-wave inversion is more likely to accompany ST segment elevation.
The ST segment elevations in acute pericarditis typically are diffuse as opposed to an
anatomic distribution, which is more likely to be seen in the setting of an acute MI.
Patients with acute pericarditis are more likely to be younger, to be otherwise healthy, and
to have a history of a preceding viral illness and pleuritic-type chest pain. Patients with acute
MI are more likely to be older with risk factors for coronary artery disease. Ventricular
arrhythmias are not associated with isolated pericardial disease and suggest the presence of
underlying cardiac disease.
8. How can acute pericarditis be distinguished from musculoskeletal chest pain?
Musculoskeletal chest pain generally is not relieved by sitting up, and the characteristic
friction rub and ECG abnormalities of pericarditis are not present.
9. Is pericardial effusion a concern in patients with pericarditis?
Yes. Pericardial effusion occurs most commonly in patients with acute viral or idiopathic,
neoplastic, postradiation, or posttraumatic pericarditis. Its effects range from insignificant to
life-threatening if tamponade occurs.
Chapter 32 PERICARDITIS AND MYOCARDITIS 231
10. How much pericardial effusion is significant?
The answer depends entirely on the clinical situation. A patient with a stab wound to the heart
may be able to accommodate only 80 to 200 mL of pericardial fluid before tamponade
develops. Patients with long-standing pericardial fluid collections may tolerate 2,000 mL or
more without hemodynamic compromise.
11. How can a pericardial effusion be diagnosed?
The physical examination is unreliable in detecting or excluding a pericardial effusion.
Similarly, the cardiac silhouette is not enlarged on chest radiograph until at least 250 mL of
fluid has accumulated. Echocardiography has excellent sensitivity and specificity; it can detect
as little as 15 mL of pericardial fluid.
12. What is cardiac tamponade?
Cardiac tamponade exists when accumulating pericardial fluid leads to increased pericardial
pressure to the point that it prevents the atria and ventricles from filling adequately during
diastole, decreasing the volume of blood available to be pumped during systole and causing
hemodynamic compromise. Although any form of pericarditis may lead to cardiac tamponade,
acute tamponade usually is caused by trauma. Subacute tamponade occurs most commonly
in neoplastic pericarditis.
13. How is cardiac tamponade diagnosed?
The first step is to confirm the presence of a pericardial effusion by echocardiography.
Absence of a pericardial effusion rules out cardiac tamponade. If an effusion is present, a
combination of physical examination and echocardiographic findings can confirm the
diagnosis of tamponade. Physical examination findings suggestive of tamponade include
tachycardia, hypotension, cyanosis, dyspnea, jugular venous distention, pulsus
paradoxus, and elevated central venous pressure (.15 mm Hg). Echocardiographic
findings are more specific and develop sequentially as pericardial pressure increases:
right atrial collapse, right ventricular collapse, and bowing of the interventricular septum.
Another helpful finding is to perform the sniff test. Instruct the patient to inhale quickly
through the nose while the ultrasonographer visualizes the inferior vena cava. Incomplete
collapse of the inferior vena cava correlates well with elevated central venous pressure
measurements.
14. What is pulsus paradoxus?
An abnormally large (.10 mm Hg) drop in the systolic blood pressure with inspiration.
Kussmaul termed this phenomenon paradoxical because of the disappearance of the pulse
during inspiration when the heart was obviously beating. Pulsus paradoxus is a pulse, not a
pressure, change and is an exaggeration of the normal inspiratory fall in arterial flow and
systolic pressure. Inspiration favors right-sided heart filling by decreasing pericardial
pressure, whereas expiration favors left-sided heart filling. Pulsus paradoxus usually signals
large reductions in ventricular volumes and equilibration of mean pericardial and all cardiac
diastolic pressures. The detection of pulsus paradoxus on physical examination suggests (and
may be one of the earliest clues to) the existence of cardiac tamponade.
15. What is the appropriate ED management of pericarditis?
Anti-inflammatory agents, such as indomethacin (Indocin), 25 to 75 mg four times a day;
aspirin, 650 mg every 3 to 4 hours; or ibuprofen, 600 mg four times a day, should be
administered. The use of corticosteroids is controversial. Although corticosteroids are
effective anti-inflammatory agents, 10% to 20% of patients develop recurrent pericarditis as
tapering occurs. Echocardiography is indicated to rule out pericardial effusion. If cardiac
tamponade is present, percutaneous pericardiocentesis should be performed to relieve
intracardiac pressure. Intravenous fluids should be infused rapidly to increase arterial pressure
and cardiac output.
Chapter 32 PERICARDITIS AND MYOCARDITIS232
16. What is the prognosis for patients with pericarditis?
Most patients recover fully, although 15% to 20% have a recurrence, probably because of an
autoimmune mechanism. Nonsteroidal anti-inflammatory drugs are used for recurrences. If
these agents are ineffective, corticosteroid therapy is initiated. Colchicine holds promise as an
adjunctive therapy in recurrent pericarditis. If medical interventions fail, pericardiectomy
usually is performed.
MYOCARDITIS
17. What is myocarditis?
An inflammation of the myocardium in the absence of ischemia.
18. What causes myocarditis?
In the United States, myocarditis is caused most commonly by viruses. Enteroviruses,
especially the Coxsackie B virus, predominate as causative agents. Infectious agents cause
myocardial damage by three basic mechanisms:
a. Direct invasion of the myocardium
b. Production of a myocardial toxin (e.g., diphtheria)
c. Immunologically mediated myocardial damage. The immunologically mediated destruction
of cardiac tissue from infiltration of host cellular immune components is probably the more
common mechanism in adults, whereas in neonates, damage from direct viral invasion is
more likely.
Worldwide, Chagas disease is the leading cause of myocarditis. Other organisms that are known
to infiltrate the myocardium include influenza A and B, adenovirus, hepatitis A and B, tuberculosis,
Chlamydia pneumoniae, Borrelia burgdorferi (Lyme disease), Legionella pneumophila,
cytomegalovirus, Toxoplasma gondii, Trichinella spiralis, and Corynebacterium diphtheriae.
19. When should a diagnosis of myocarditis be considered in the ED?
Diagnosing myocarditis in the ED can be a challenge, and because the presenting symptoms
and signs are typically nonspecific, this is often a diagnosis of exclusion. Nonspecific
symptoms include fatigue, myalgias, nausea, vomiting, fever, dyspnea, palpitations, and
precordial discomfort. Chest pain may reflect associated pericarditis. Patients may present
with a dilated cardiomyopathy without evidence of ischemia or valvular disease. Myocarditis
probably should be considered in any previously healthy person who develops dyspnea,
orthopnea, decreased exercise tolerance, palpitations, or syncope when no other obvious
cause is found. Patients should be asked about concomitant or recent upper respiratory or
gastrointestinal illness.
20. What clinical findings may be present?
Tachycardia is common and can be disproportionate to the temperature or apparent toxicity.
This may be the only clue that something more serious than a simple viral illness exists.
Clinical evidence of congestive heart failure occurs only in more severe cases. A pericardial
friction rub may be auscultated if myopericarditis is present. Complications of myocarditis
include ventricular arrhythmias and left ventricular aneurysms.
21. Are there any chest radiograph or ECG abnormalities?
n
The chest radiograph may be normal or abnormal, depending on the extent of disease. The
cardiac silhouette may be enlarged, which can be due to a dilated cardiomyopathy or a
pericardial effusion.
n
The ECG commonly shows a sinus tachycardia and may show low electrical activity.
Nonspecific ST segment and T-wave abnormalities, a prolonged corrected QT interval,
atrioventricular block, or acute MI pattern also may occur. Atrial arrhythmias have been
described.
Chapter 32 PERICARDITIS AND MYOCARDITIS 233
22. How is myocarditis diagnosed?
Making the diagnosis clinically can be difficult. Endocardial biopsy is considered the gold
standard, although it has highly variable sensitivity and specificity. In contrast to patients with
pericarditis, cardiac enzymes frequently are elevated in patients with myocarditis. White blood
cell count and erythrocyte sedimentation rate may be elevated but are nonspecific. Indium-111
antimyosin antibodies show myocardial necrosis by binding to exposed myosin in damaged
myocardial cells. When myocarditis is suspected clinically, indium-111 antimyosin imaging
may be helpful. Viral titers have been suggested but have a low yield. Echocardiography often
shows global dysfunction that does not correspond to a specific coronary artery distribution.
23. How can acute myocarditis be distinguished from acute MI?
Myocarditis occurs primarily in young healthy patients without significant cardiac history or
risk factors for coronary artery disease. Chest pain, dyspnea, ECG abnormalities, and cardiac
enzyme elevation may occur in both conditions. In the ED, it may be impossible to distinguish
between these two entities, in which case treatment for acute MI should be initiated.
24. Is myocarditis a concern in AIDS?
Yes. The incidence of myocarditis found at autopsy of AIDS patients has been reported as
high as 52%, compared with less than 10% in the population as a whole. The increased risk
of myocarditis in patients with AIDS may be due to an abnormal autoimmune reaction,
opportunistic infections, or HIV itself.
25. In what other clinical situations should myocarditis be considered?
Myocarditis and dilated cardiomyopathy have been associated with cocaine use. Myocarditis is
a common autopsy finding in patients who have died from cocaine abuse.
26. Describe the appropriate ED management of a patient with myocarditis.
The current recommended treatment consists of supportive therapy. The only uniformly
accepted beneficial therapy is bed rest. All patients with suspected myocarditis should be
admitted to a monitored bed in the hospital. Antibiotics are appropriate when a bacterial cause
is suspected. Dilated cardiomyopathy is treated with diuresis, afterload reduction, and digoxin.
In severe cases, temporary pacing and external circulatory support may be needed. Patients
with a fulminant clinical course may require cardiac transplantation. Immunosuppressive
therapy has been studied, but controlled studies have not established efficacy. High-dose
gamma globulin has been studied and may be associated with improved left ventricular
function and better survival during the first year after initial presentation.
27. What is the prognosis for patients with acute myocarditis?
Mortality for patients with myocarditis has been reported to be 20% at 1 year and 56% at
4 years, although many patients do recover completely.
KEY POINTS: PERICARDITIS AND MYOCARDITIS
1. The physical examination or chest radiography is neither sensitive nor specific for
pericardial effusion; echocardiography is the gold standard.
2. Myocarditis should be considered in patients with significant tachycardia that cannot
otherwise be explained or in any patient with the combination of viral symptoms and
evidence of cardiac disease.
3. Viruses are the most common causes of pericarditis and myocarditis, and a history of
preceding or concurrent viral illness is quite common.
4. Myocarditis is very common in AIDS patients, with rates at autopsy as high as 52%.
Chapter 32 PERICARDITIS AND MYOCARDITIS234
BIBLIOGRAPHY
1. Brady WJ, Ferguson JD, Ullman EA, et al: Myocarditis: emergency department recognition and management.
Emerg Med Clin North Am 22:4865–4885, 2004.
2. Chan TC, Brady WJ, Pollack M: Electrocardiographic manifestations: acute myopericarditis. J Emerg Med
17:865, 1999.
3. Jouriles NJ: Pericardial and myocardial disease. In Marx JA, Hockberger R, Walls R, et al, editors: Rosen’s
emergency medicine: concepts and clinical practice, ed 6, Philadelphia, 2006, Mosby, pp 1280–1300.
4. McCarthy RE III, Bochmer JP, Hruban RH, et al: Long-term outcome of fulminant myocarditis as compared
with acute (non-fulminant) myocarditis. N Engl J Med 342:690–695, 2000.
5. Spodick DH: Pathophysiology of cardiac tamponade. Chest 113:1372–1378, 1998.
6. Wheeler D, Kooy N: A formidable challenge: the diagnosis and treatment of myocarditis in children. Crit Care
Clin 19:365, 2003.
235
ESOPHAGUS AND STOMACH DISORDERS
CHAPTER 33
Rakesh Talati, MD, and Philip L. Henneman, MD
VII. GASTROINTESTINAL TRACT
1. How are gastrointestinal (GI) problems differentiated from acute
myocardial infarction?
Esophageal or gastric pain can present with visceral-type chest pain (e.g., ache,
pressure) or upper abdominal pain and nausea that are difficult to differentiate from pain
and nausea related to myocardial ischemia or infarction. Description of the pain,
determination of cardiac risk factors, and appropriate use of an electrocardiogram (ECG)
in adult patients with visceral-type pain or cardiac risk factors will minimize clinical
errors. Nitroglycerin, antacids, and GI cocktails are therapeutic interventions, not
diagnostic tests. Patients with esophageal spasm may respond to nitroglycerin and
antacids, or GI cocktails may provide a placebo-like benefit to patients with cardiac
ischemia. The response to these interventions can mislead the unwary physician.
2. What is a GI cocktail?
The two most commonly used GI cocktails contain antacids (30 mL), viscous lidocaine
(10 mL), and either Donnatal (10 mL) or dicyclomine (Bentyl; 20 mg). These cocktails
may provide temporary symptomatic relief of minor esophageal and gastric irritation. Of
note, it has been concluded that these cocktails are no more effective than antacids
alone.
3. What is heartburn?
Retrosternal burning discomfort that may radiate to the sides of the chest, neck, or jaw.
The description of the pain may be similar to the pain of cardiac ischemia. Heartburn is
characteristic of reflux esophagitis and often is made worse by bending forward or lying
recumbent after meals. It may be relieved by upright posture, liquids (including saliva or
water), or more reliably, antacids. Heartburn is probably due to heightened mucosal
sensitivity to acid and can be reproduced by infusion of dilute hydrochloric acid into the
esophagus (Bernstein test).
4. How is reflux esophagitis treated?
In addition to antacids, general measures include elevation of the head of the bed
(e.g., 4 inches), weight reduction, and elimination of factors that increase abdominal
pressure. Patients should avoid alcohol, chocolate, coffee, fatty foods, mint, orange
juice, smoking, ingestion of large quantities of food and drink, and certain medications
(e.g., anticholinergics or calcium channel blockers). Antacids after meals, H
2
-blockers
(e.g., cimetidine) before bedtime or daily proton pump inhibitors (e.g., omeprazole) are
often helpful. Treatment is usually for 1 to 2 months, and the disease may recur.
5. What are the esophageal causes of odynophagia?
Odynophagia, or painful swallowing, is a characteristic of nonreflux esophagitis.
Infectious esophagitis is a common cause and usually occurs in immunocompromised
patients, and it can be due to fungal (e.g., monilial), viral (e.g., herpes, cytomegalovirus),
bacterial (e.g., Lactobacillus, b-hemolytic streptococci), or parasitic organisms. Other
types of nonreflux esophagitis include radiation, corrosive, pill-induced, and certain
systemic diseases (e.g., Behçet’s, Crohn’s, pemphigus vulgaris, Stevens-Johnson
Chapter 33 ESOPHAGUS AND STOMACH DISORDERS236
syndrome). Odynophagia is unusual in reflux esophagitis but may occur with a peptic ulcer of
the esophagus (Barrett’s ulcer).
6. How does esophageal obstruction present?
Except in infants, there is usually a history of eating or swallowing something that is followed
by the onset of chest pain, odynophagia, or inability to swallow. Foreign bodies usually lodge
at one of four locations: cervical esophagus, upper esophageal sphincter, aortic arch, and
lower esophageal sphincter. Obstruction by food may occur wherever there is narrowing of
the lumen because of stricture, carcinoma, or a lower esophageal ring. Foreign bodies,
especially those that are sharp, or impacted food are best removed endoscopically. Round,
blunt objects may be removed using a Foley catheter, a procedure most often done under
fluoroscopy. Meat tenderizer should not be used to facilitate passage of obstructed meat.
Glucagon, 0.5 to 2 mg intravenously, may relieve distal esophageal food obstruction in a
minority of patients.
7. What is Mallory-Weiss syndrome?
Mallory-Weiss syndrome is a mucosal tear that usually involves the gastric mucosa near the
squamocolumnar mucosal junction; it also may involve the esophageal mucosa. It usually is
caused by vomiting and retching. Patients with a Mallory-Weiss tear may present with upper
GI bleeding.
8. What causes esophageal perforation, and how is it diagnosed and treated?
Esophageal perforation, a true emergency, can be caused by iatrogenic damage during
instrumentation, trauma (most often penetrating), increased intraesophageal pressure
associated with forceful vomiting (Boerhaave’s syndrome), or diseases of the esophagus (e.g.,
corrosive esophagitis, ulceration, neoplasm). Esophageal perforation causes chest pain that is
often severe and may be worsened by swallowing and breathing. Chest radiograph may reveal
air within the mediastinum, pericardium, pleural space (pneumothorax), or subcutaneous
tissue, pleural effusion, or may appear normal. Esophageal perforation may lead to leakage of
gastric contents into the mediastinum and secondary infection (i.e., mediastinitis). The
diagnosis is confirmed radiographically by swallow and leakage of radiopaque contrast
material. Treatment includes broad-spectrum antibiotics, gastric suction, and surgical repair
and drainage as soon as possible.
9. What are causes of abdominal pain that are gastric or duodenal in origin?
An estimated 10% of cases of abdominal pain seen in the ED are due to gastric or duodenal
disease. Gastritis and peptic ulcer disease (PUD; ulcer of the stomach or duodenum resulting
from gastric acid) account for most patients with abdominal pain secondary to gastric or
duodenal disease. Perforated PUD and gastric volvulus are the two most serious conditions
requiring immediate diagnosis and treatment.
10. What are the common causes of gastritis and PUD?
Gastritis is associated with alcohol, salicylates, nonsteroidal anti-inflammatory drugs (NSAIDs),
and hiatal hernia. PUD is related to family history, associated diseases (e.g., chronic obstructive
pulmonary disease [COPD], cirrhosis, or chronic renal failure), male gender, advanced age, and
smoking. The use of certain drugs, such as aspirin or NSAIDs, may be related to PUD, but diet
(e.g., caffeine and spicy foods) and alcohol are not. Helicobacter pylori has been shown to be a
frequent cause of duodenal ulcers. First-line treatment for patients with H. pylori is the
combination of a proton pump inhibitor (PPI), clarithromycin, and amoxicillin.
11. How does perforated PUD present?
Perforated PUD (and gastric volvulus) presents with sudden onset of abdominal pain that may
or may not be related to eating. It often radiates to the back but also may radiate to the chest
or upper abdomen. The pain is usually steady and refractory to antacids. Vomiting is present
in approximately 50%.
Chapter 33 ESOPHAGUS AND STOMACH DISORDERS 237
On physical examination, patients appear in acute distress and often have tachycardia.
Blood pressure may be elevated secondary to pain or decreased secondary to extensive fluid
loss from generalized peritonitis. Patients usually lie still and avoid movement. Involuntary
guarding, rebound tenderness, and abdominal rigidity are common. Bowel sounds are usually
absent or significantly decreased.
Laboratory work may reveal nonspecific leukocytosis; 40% have a white blood cell count
.14,000 white blood cells/mm
3
. If vomiting has been protracted, hypochloremic, hypokalemic,
or metabolic alkalosis may be seen. A small percentage of patients have mild elevation in
amylase or lipase. Free air is present on upright chest radiograph or abdominal left lateral
decubitus view in more than 70% of patients.
12. How should a patient suspected of having a perforated ulcer be managed?
Patients with severe abdominal pain should be undressed, placed on cardiac and SaO
2
monitors, and have a large-bore intravenous catheter placed for fluid resuscitation with
crystalloid (e.g., normal saline). Patients with oxygen saturation ,93% should be given
supplemental oxygen. A prompt but thorough physical examination should be done, including
pelvic and rectal examinations. Blood should be drawn for complete blood count, electrolytes,
blood urea nitrogen (BUN), creatinine, lipase, and type and screen. An ECG should be obtained
on patients older than 40 years. Urine should be obtained for urinalysis and a pregnancy test
should be performed for all menstruating females. Patients should have nothing by mouth
(NPO). A portable upright chest radiograph or abdominal left lateral decubitus view often
helps to show free intraperitoneal air. A nasogastric (NG) tube should be placed after
anesthetizing the nasopharynx and prompt surgical consultation obtained. Broad-spectrum
antibiotics should be given and the patient prepared for emergency laparotomy. Intravenous
analgesics (opiates) should be given for patient comfort.
13. What differentiates upper from lower GI hemorrhage?
Upper GI hemorrhage is bleeding that is proximal to the ligament of Treitz, and lower GI
bleeding is distal. In the ED, this is evaluated by placement of a nasogastric (NG) or orogastric
tube and aspiration of gastric and proximal duodenal contents. Physical appearance of the
aspirate (coffee grounds, red-tinged fluid, or fresh blood) is the best way of determining the
presence of significant upper GI bleeding. While generally reliable, false-negative and false-
positive results may occur when using Gastroccult cards.
14. Do all patients presenting with only lower GI bleeding require NG tube
placement?
The routine use of NG aspiration (NGA) has been advocated to rule out occult upper GI
bleeding. However, recent studies have added some controversy to this practice. NG tube
placement is a painful procedure that is not without possible complications. Reports state that
10% of patients presenting with only hematochezia will have positive NGA and occult upper GI
bleeding. Some conclude that in low-risk patients, NGA has a low yield and is almost as likely
to yield false-positive as true-positive results.
15. How is a patient classified as low risk for having occult upper GI bleeding?
It has been demonstrated that male sex, history of GI tract bleeding, black stool, hematocrit
,30%, BUN/creatinine ratio 5 30, and age ,50 years were all independently associated with
upper GI bleeding. Three factors, BUN/creatinine ratio, black stool, and age, were shown to be
strong predictors and correlated well with NG aspiration. Patients with no risk factors are
considered low risk. Nasogastric aspiration is mandatory in all patients presenting with any
two of these three factors and those who are hemodynamically unstable.
16. List the causes of upper GI bleeding.
n
PUD (45%)
n
Gastric erosions (23%)
n
Varices (10%)
n
Mallory-Weiss tear (7%)
n
Esophagitis (6%)
n
Duodenitis (6%)