topics

presence of flatus or bowel movements or the lack of vomiting, as these findings may develop later. If clinical suspicion is high enough, consider starting with a CT scan

instead of radiographs. If the patient appears acutely ill,

begin with resuscitation and consult a surgeon immediately even if imaging studies have not been completed.

TREATMENT

Establish intravenous (IV) access promptly and begin

administration of fluids. An initial bolus of 1-2 L of

0.9 normal saline is appropriate, but some patients may

require more aggressive fluid resuscitation to replace thirdspaced volume loss. Antiemetics should be given (ondansetron 4 mg IV, prochlorperazine 10 mg IV, promethazine

25 mg IV). Consider narcotic pain medications (morphine

4 mg IV, hydromorphone 0.5 mg IV) and repeat as needed.

An NG tube should be inserted once the diagnosis of

obstruction has been made and should be placed to low

CHAPTER 31

intermittent suction (LIS). This results in decompression

of the bowel lumen, provides symptomatic relief, and may

avoid the need for surgery. Broad-spectrum antibiotics

that cover gram-negative and anaerobic organisms (eg,

piperacillin-tazobactam, ciprofloxacin plus metronida

zole) should be given in the presence of fever, peritonitis,

or evidence of strangulation. Surgical consultation should

be obtained in case the patient requires surgical intervention. For patients with adynamic ileus, treatment involves

cessation of any narcotic medications and initiation of

motility agents (eg, metoclopramide).

DISPOSITION

..... Admission

All patients with intestinal obstruction require admission,

either to a surgical service or a medicine service with a

surgeon on consult. Most patients can be admitted to floor

units.

• Abdominal radiographs can demonstrate

obstruction, but computed tomography is more

sensitive.

INTRODUCTION

Intestinal obstruction refers to failure of intestinal contents

to pass through the bowel lumen. Mechanical obstruction

refers to physical blockage of luminal contents. This occurs

in either small bowel (80% of cases) or large bowel (20%

of cases). The most common cause of mechanical obstruction is adhesions from prior abdominal surgery (SOo/o),

followed by malignancy (20%), hernias ( 10%), inflammatory bowel disease (So/o), and volvulus (3%).

Intestinal obstructions can be either partial or com

plete. Partial obstructions are often managed nonopera

tively. Complete obstructions carry more risk of morbidity

and can result in strangulation. As bowel contents are

prevented from forward flow, increased secretions result in

overdistention, which causes bowel wall edema and

reduced lymphatic and venous outflow. This is referred to

as strangulation and can progress to bowel ischemia,

necrosis, perforation, and peritonitis. Up to 40% of small

bowel obstructions become strangulated, most commonly

from volvulus, adhesions, and hernias. A closed-loop

obstruction occurs when there is mechanical blockage

both proximal and distal to a bowel segment. This results

in very high risk of strangulation because bowel contents

are prevented from both forward and retrograde flow.

Small bowel obstructions represent lSo/o of hospital

admissions for acute abdominal pain. Approximately

1 3 1

• Intesti nal obstruction is treated with intravenous fluids,

nasogastric suctioning, antiemetics, narcotic pain medications, and anti biotics in select cases.

• Strangulation is a compl ication of obstruction that can

lead to bowel ischemia, peritonitis, and sepsis.

300,000 operations are performed every year in the United

States for obstruction. Mortality rate overall is approximately So/o, whereas the mortality rate from strangulated

obstructions approaches 30%.

In contrast to mechanical obstruction, functional

obstruction (eg, adynamic ileus) occurs when intestinal

contents fail to pass because of disturbances in gut motility.

It most commonly occurs immediately after surgery, but

can also be seen in inflammatory conditions, electrolyte

abnormalities, and from certain medications (namely,

narcotics). Unless noted otherwise, the remainder of this

chapter refers to mechanical obstruction.

CLINICAL PRESENTATION

.... History

The most common initial complaint is intermittent colicky

abdominal pain. If the obstruction is proximal, the patient

may also complain of nausea and vomiting. More distal

obstructions can result in delayed onset of vomiting.

Although obstipation (lack of flatus and bowel movements) can suggest an obstruction, the presence of flatus or

bowel movements should not be used as evidence that an

obstruction has not occurred, as these can be seen early in

the course of even complete obstructions. The patient history should include questions about prior surgeries, history

CHAPTER 31

of hernias, and history of obstruction in the past, as prior

intestinal obstructions have up to SOo/o recurrence rate.

� Physical Examination

Vital signs may be normal or abnormal. Fever, tachycardia,

and hypotension are ominous signs and may suggest peritonitis or sepsis. Patients will usually appear uncomfortable regardless of their position. Physical exam is significant

for a distended, diffusely tender abdomen, tympany to

percussion, and hyperactive bowel sounds. If strangulation

has occurred there may be peritonitis on exam. Patients

should be examined for evidence of prior abdominal surgeries (eg, incision scars) and examined for hernias.

DIAGNOSTIC STUDIES

� Laboratory

Electrolyte abnormalities such as hypokalemia and acidbase disturbances can occur due to vomiting. Third spac- A

ing of fluid and dehydration from vomiting may cause

elevated blood urea nitrogen or creatinine. Intestinal ischemia can cause an anion gap metabolic acidosis with an

elevated lactic acid. Leukocytosis may be present on a

complete blood count and also suggests ischemia or peritonitis. Consideration should be given to checking liver

function studies, amylase, lipase, and urinalysis to evaluate

for other etiologies of the patient's symptoms.

� Imaging

Radiographs are 50-66% sensitive in diagnosing an intestinal obstruction. An "obstructive series" classically consists

of 3 radiographs: upright chest film, supine abdominal

film, and upright abdominal film. A lateral decubitus x-ray

may also be included. The upright chest film is used to

evaluate for evidence of perforation (free air under the

diaphragm). The upright abdominal film will show dilated

loops of bowel (>3 em), air-fluid levels (layering of

intestinal contents), and absence of air in the rectum

(Figure 31-1A). The "string of pearls" sign is a series of

small pockets of gas in a row. It represents a predominance

of fluid in the bowel lumen with small amounts of air

trapped between the valvulae conniventes of the bowel. In

adynamic ileus, radiographs will demonstrate dilation of

the bowel without air-fluid levels.

An abdominal CT scan is much more sensitive than

radiographs (92-100% sensitive) (Figure 31- lB). CT also

has the advantage of being able to determine the location

of obstruction, as well as bowel wall edema, and findings

suggestive of bowel ischemia. A CT scan may also show the

cause of the obstruction (eg, hernia, malignancy). If no

cause is identified, adhesions may be the etiology. In

patients with fever, localized abdominal pain, or abnormal

vital signs, a CT scan should be the initial study of choice

owing to its greater sensitivity and the need for timely

diagnosis.

or patients with symptoms concerning for

coronary ischemia. Silent ischemia can occur as a result of

decreased oxygen delivery related to blood loss.

PROCEDURES

Nasogastric aspiration should be performed on patients

suspected of having an upper GI bleed. Aspirate appearing

like gross blood or "coffee grounds" is evidence of an upper

GI source. The stomach may then be lavaged with 200-300 mL

saline to see if the aspirate clears. Note that false negatives

may occur with bleeding distal to the pylorus, and false

positives may occur from nasal trauma. NG aspiration is

an especially uncomfortable and anxiety-provoking procedure for the patient, and the use of topical anesthetic is

advised. Although NG aspiration in GI bleeding is routinely performed, it will only yield a useful diagnostic

result in a minority of cases.

MEDICAL DECISION MAKING

The exact location of GI bleeding is usually not determined

in the initial ED evaluation. Examination of any emesis,

stool, or NG aspirate may help to determine the general

location of the hemorrhage and direct further diagnostic

and treatment strategies (Figure 30-1).

TREATMENT

Patients with active GI bleeding should be placed on a cardiac monitor with supplemental oxygen. Large peripheral

IV catheters should be inserted in unstable patients. If these

Figure 30-1 . Gl bleeding diagnostic algorithm.

Gl, gastrointestinal; NG, nasogastric.

lines cannot be inserted, a large-bore (SF) central line should

be placed to maximize vohune resuscitation. N fluid bolus

of 1-2 L of normal saline should be administered. If the

patient remains unstable after the fluid bolus, administration of packed red blood cells (RBCs) is indicated. Uncrossmatched type 0 blood is ordered for patients with unstable

vital signs and significant blood loss. If a coagulopathy is

suspected, fresh-frozen plasma is also ordered.

For upper GI bleeding, histarnine-2 antagonists are fre

INTRODUCTION

Gastrointestinal (GI) bleeding accounts for 5% of admissions from the emergency department (ED). An intervention is required to stop ongoing hemorrhage in 10% of

patients. Bleeding can occur anywhere along the GI tract

and can be grossly divided into upper and lower sources.

Upper GI bleeding is defined as occurring proximal to the

ligament of Treitz (the suspensory ligament of the duodenum). Lower GI bleeding is defined as occurring distal to

the ligament of Treitz. Upper GI bleeding is 4-8 times

more common than lower GI bleeding.

It is not always possible to clinically distinguish between

upper and lower GI bleeding in the ED, but appearance of

the gastric contents and stool can provide clues to the source

of the hemorrhage. Hematemesis is the vomiting of blood

and indicates an upper GI bleed. "Coffee ground" emesis

suggests that the blood has partially digested and that bleeding is either slow or has stopped. A nasogastric (NG) tube

aspirate positive for blood also indicates an upper GI source

of bleeding. NG lavage can be negative in 25% of patients

with an upper GI source of bleeding because the nasogastric

tube does not reliably pass the pylorus.

Melena is black, tarry stool that reflects the presence

of blood in the GI tract for more than 8 hours. At least

• Octreotide should be administered in patients with

liver disease and significant upper Gl bleeding, even

when the diagnosis of esophageal varices has not been

confirmed.

• Emergent endoscopy should be arranged when active

upper Gl bleeding is present.

300 mL of blood must be present to produce melena.

Melena is 4 times more likely to be from an upper GI

source of bleeding and almost always reflects bleeding

proximal to the right side of the colon. Hematochezia is

bright red or maroon-colored blood per rectum. It is 6

times more likely to be from a lower GI source. An exception is a rapid upper GI source of bleeding. Hematochezia

is present in 1 0% of upper GI bleeds.

The three most common causes of upper GI bleeding

are peptic ulcer disease, gastritis, and varices ( Table 30-1).

Lower GI bleeding may be due to multiple causes, but

Table 30-1. Causes of upper Gl bleeding.

Cause

Peptic ulcer (duodenal 2/3)

Erosive gastritis

varices (esophageal and gastric)

Mallory-Weiss tear

Other (epistaxis, aortoenteric fistula, carcinoma,

GASTROI NTESTINAL BLEEDING

Table 30-2. Causes of lower Gl bleeding.

Cause

Diverticulosis

Inflammatory bowel disease

Hemorrhoids, anal fissure

Neoplasia

Coagulopathy

Arteriovenous malformation

http://sonoguide.com/biliary.htrnl

O'Connor OJ, Maher MM. Imaging of cholecystitis. A]R Am

] Roentgenol 201 1;1 96:W367-W374.

Strasberg SM. Clinical practice. Acute calculous cholecystitis.

N Eng! ] Med 2008;358:2804S-281 1S.

Abdominal Aortic

Aneu rysm

Alex de Ia Fuente, MD

Key Points

• Diagnosis of ruptured abdominal aortic aneurysm (AM)

is frequently missed or delayed. The most common

misdiagnosis is renal colic.

• AM must be considered in any elderly patient with

back, flank, or groin pain.

INTRODUCTION

Abdominal aortic aneurysm (AAA) is an increase in the

diameter of the aorta of more than 50%, or an infrarenal

aortic diameter greater than 3 em. The etiology and patho

genesis of AAA is unclear, although atherosclerosis, c onnective tissue disorders, genetic factors, and smoking have all

been implicated. A family of enzymes known as matrix

metalloproteinases may be largely responsible for the inflammatory destruction of elastin and collagen fibers in the

medial and adventitial layers of the aortic wall that can ulti -

mately lead to AAA formation, enlargement, and rupture.

The rate of expansion and risk of rupture are related to

tension on the wall of the aneurysm, which in turn is

related to the diameter of the aneurysm and to the underlying pressure. Rupture of aneurysms smaller than 4 em is

rare, whereas the annual risk of rupture for aneurysms

larger than 8 em has been estimated at 30-50%.

AAA causes 15,000 deaths in the United States a year. It is

a common cause of sudden death and is responsible for

1-2% of all deaths in men older than 65 years. The overall

mortality rate of a patient with a ruptured AAA is 90%, and

50% of patients with ruptured AAA do not survive to reach

the hospital. In patients who arrive at the hospital, the mortality rate improves to 60%. The mortality rate for elective

open operative repair is 2-7%; recent advances in endovascular technique have mitigated early morbidity and mortality.

• Suspected ruptured AAA requires emergent consu ltation, with the goal of immediate open or endovascular

repair.

• Patients with incidentally discovered AAAs must be

referred for surveillance or elective repair.

The incidence of AAA begins to increase in men older

than 55 years. By age 80 years, 5% of men have an AAA, and

5% of women age 90 years have AAA. There is an increased

incidence in smokers, whites, and those with a family history

of AAA. First-degree relatives of patients with AAA have up

to an 8-fold increase in the chance of developing AAA.

CLINICAL PRESENTATION

..... History

The emergency department (ED) presentation of AAA is varied, with symptoms due to expansion and rupture, distal

thromboembolic complications, local mass eff ects, or erosion

into adjacent structures. Most AAAs are asymptomatic and

discovered incidentally while evaluating patients for unrelated

conditions. These patients require little more than referral. At

the other end of the spectrum, AAA rupture can constitute one

of the most acutely life-threatening emergencies in medicine.

The classic triad of abdominal/back pain, hypotension,

and a pulsatile abdominal mass is present in substantially

less than one half of patients with a r uptured AAA. The vast

majority of patients with ruptured AAA will have pain,

typically in the abdomen, back, flank, or groin, depending

on the extent and direction of rupture. Rarely, patients with

rupture can present with syncope alone or with nonspecific

symptoms such as vomiting, diarrhea, or dizziness.

1 25

CHAPTER 29

..... Physical Examination

Patients with ruptured AAA may present with evidence of

hemorrhagic shock: hypotension, tachycardia, and exam

findings of poor perfusion. However, the patient may be

normotensive or even hypertensive. Transient hypotension

may also occur and can be erroneously attributed to a vasovagal etiology. Abdominal examination may detect a pulsatile mass, but this can be difficult with small aneurysms or

obese patients and is subject to significant interobserver

variability. Absence of a pulsatile mass on exam does not

exclude the diagnosis of AAA. Lower extremity pulses should

be assessed, as lower limb ischemia is present in 5% of cases.

DIAGNOSTIC STUDIES

..... Laboratory

Any patient with a possible ruptured AAA should have

blood sent for type and crossmatch, although often

uncrossmatched blood will be required emergently.

Anemia can be seen in ruptured AAA, with hematocrit less

than 38 in 40% of patients. D-dimer assays have been

investigated as a possible screen for patients deemed to be

at low risk for AAA, but their use for this indication has not

yet been validated.

.... Imaging

Ultrasound has a sensitivity approaching 100% and can be

obtained at the bedside even in unstable patients. In addition to the aneurysm, ultrasound may reveal intraperito

neal free fluid in cases of rupture. However, because many

AAAs rupture into the retroperitoneum, ultrasound is

insensitive in detecting this complication, and a lack of free

fluid should not be reassuring. Ultrasound can also be

limited by obesity and by overlying bowel gas.

.&.Figure 29-1 . CT sca n showing a ruptured AAA. This

AAA is rupturing into the peritoneal cavity (a rrow). The

majority of ruptured AAAs are retroperitoneal (70%).

Abdominal computed tomography (CT) is helpful for

preoperative planning, is better at detecting suprarenal

aneurysms, and shows retroperitoneal bleeding not visible

on ultrasound. CT can also reveal alternative etiologies for

abdominal pain and can be considered a first-line diagnostic modality in stable patients (Figure 29-1) .

PROCEDURES

Bedside ultrasound allows for rapid detection of an aortic

aneurysm. Place the abdominal probe in the epigastric area in

the transverse plane (Figure 29-2). The aorta is located anterior and just to the left of the vertebral bodies. Move the probe

inferiorly until the aorta bifurcates at the umbilicus. Next,

rotate the probe 90 degrees to obtain a longitudinal view.

Figure 29-2. U ltrasound of an AAA. A. Transverse position of probe. 8. Transverse view of AAA.

ABDOMINAL AORTIC ANEURYSM

Elderly patient with:

Abdomina l/back/flank/ groin pain

± hypotension/syncope/pulsati le

abdominal mass

Suspect ruptured AAA

.A. Figure 29-3. AAA diagnostic algorithm.

MEDICAL DECISION MAKING

AAA must be ruled out in any elderly patient who presents

with abdominal, back, flank, or groin pain. Hemodynamically stable patients can be evaluated with CT, whereas

unstable patients are better assessed with a bedside ultrasound (Figure 29-3). Other emergent causes of abdominal,

back, and flank pain should be considered and evaluated

concurrently. Consider ruptured AAA in elderly patients

"found down" or with otherwise unexplained hypotension.

Any patient with abdominal pain and previous repair of

AAA, either open or endovascular, merits consultation

with the patient's surgeon.

TREATMENT

Patients with ruptured AAA require immediate treatment

in the ED with 2 large-bore ( 16-gauge) IV lines in the antecubital veins or a large-bore (SF) central line and subse

quent resuscitation with IV crystalloid and uncrossmatched

blood. The ideal goal blood pressure is not known, and

many practitioners will allow relative hypotension pending

definitive operative repair. A vascular surgeon should be

consulted immediately, and the patient should be taken to

the operating room or angiography suite as soon as possible to repair the AAA.

Unruptured, symptomatic AAAs require evaluation by

a vascular surgeon. These patients may benefit from early

elective repair, depending on the size of the aneurysm.

Patients with incidentally discovered asymptomatic aneu

Ultrasound evaluation of the gallbladder and common bile

duct remains the best test for identifying cholecystitis. The

sensitivity ( 88-94%) and specificity ( 80-90%) vary

depending on what criteria are used to establish the diagnosis. On ultrasound examination, gallstones appear as

hyperechoic intraluminal structures, and larger stones will

cast an ultrasound shadow (Figure 28-1 ). Findings suggestive

of cholecystitis include gallbladder wall thickness greater

than 3-5 mm and pericholecystic fluid. A common bile

duct diameter greater than S-8 mm is abnormal. The

sonographic Murphy sign is positive when maximal pain is

produced with transducer pressure over the gallbladder.

When combined with the presence of gallstones, the sono

graphic Murphy sign has a positive predictive value of

92%. The sonographic Murphy sign can be masked by

Figure 28-1. Short axis view of the gall bladder

demonstrating a gall bladder neck stone (large arrow)

and gallbladder wall thickening (small arrows).

ACUTE CHOLECYSTITIS

Figure 28-2. Abdominal CT sca n showing an enlarged gallbladder with

pericholecystic fluid (black arrows) and a di lated common bile duct

prior pain medication and can be absent in diabetics or

gangrenous cholecystitis.

Abdominal computed tomography (CT) scan is helpful

when other diagnoses are also being considered. CT scanning is less sensitive for acute cholecystitis than ultrasound

( 50-90%), but is as sensitive for choledocholithiasis and can

identify complications such as perforation or abscess formation. CT findings include wall thickening, pericholecystic fluid, and biliary tree dilation (Figure 28-2). Notably,

only 20% of gallstones are radio-opaque, which limits the

utility of CT in early cases of cholecystitis or for patients

with biliary colic.

MEDICAL DECISION MAKING

The patient with classic symptoms of biliary colic or acute

cholecystitis is easy to identify, but many patients present

with atypical symptoms (Figure 28-3). It is important to

consider other conditions that may masquerade as gall

bladder pain. This may include pyelonephritis of the right

kidney or retrocecal appendicitis. Right lower lobe pneumonia can also present with right upper quadrant pain

and vomiting. Patients with choledocholithiasis are often

misdiagnosed as having pancreatitis or gastritis. In elderly

patients or those with coronary disease, it is important to

consider the possibility of an inferior myocardial infarc

tion. Patients who appear septic or with peritoneal signs

may have perforation or ascending cholangitis. Other gastrointestinal (GI) conditions such as pancreatitis, peptic

ulcer disease, or hepatitis should also be considered.

lab tests, IV flu ids, pain

meds

• Reeva luate the patient

• Consider alternate diagnoses

• If suspicion remains high, consider

abdominal CT scan and/or admission.

.A Figure 28-3. Acute cholecystitis diagnostic algorithm.

CT, computed tomography; IV, intravenous; RUQ, right

upper quadrant.

CHAPTER 28