Abdomen Agudo Clinics

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Canc er Em ergenc ies :Th e Acut e Abdom en

Jonathan S. Ilgen, MD*, Amy L. Marr, MD

The most common complaints among patients with cancer who present to the emer-gency department (ED) are related to the gastrointestinal system, and 40% of these

patients complain of abdominal pain.1 These presentations can stem from the under-

lying malignancy itself, the treatment directed toward the disease, or the full range of

pathologies present in a healthy population. Moreover, immunosuppression may blunt

many of the findings one expects in a healthy population of patients, thus rendering the

clinical examination less reliable in patients with cancer. This article focuses specifi-

cally on patients with cancer who present with an acute abdomen, and discusses

how a concurrent malignancy can shape the differential diagnosis in these cases.

To facilitate an organized approach to this article, the authors have considered

these processes within three broad categories for the acute abdomen in patientswith cancer: intestinal obstruction, intestinal perforation, or pathology unique to immu-

nosuppression and malignancy.

THE IMPACT OF IMMUNOSUPPRESSION

Clinical findings and the spectrum of infectious processes are affected by the patients

degree of immunosuppression. For simplicity, these can be classified as mild-to-

moderate or severe forms of immunosuppression (Table 1).2 Patients in group I

(mild-to-moderate) are not undergoing chemotherapy, though they have blunted

symptoms due to their lack of an appropriate inflammatory response. Because ofthis, they often seek medical attention later in the course of their disease. Other

than the direct impact of the malignancy itself, however, these patients have patholo-

gies similar to those of a healthy population.2 Patients with profound immunosuppres-

sion associated with chemotherapy (group II) are more challenging. It is in this group of

patients that classic examination findings of fever and abdominal tenderness may be

replaced by vague signs or symptoms such as tachycardia, hypotension, and confu-

sion.2 Concurrently, the differential diagnosis must be expanded to include a wide

variety of atypical opportunistic infections.2

Department of Emergency Medicine, Oregon Health & Science University, 3181 SW Sam JacksonPark Road, CDW-EM, Portland, OR 97239, USA* Corresponding author.E-mail address: [email protected] (J.S. Ilgen).

KEYWORDS

Malignancy Abdominal pain Immunosuppression Management Malignant bowel obstruction

Emerg Med Clin N Am 27 (2009) 381399doi:10.1016/j.emc.2009.04.006 emed.theclinics.com0733-8627/09/$ see front matter 2009 Elsevier Inc. All rights reserved.
mailto:[email protected]://emed.theclinics.com/http://emed.theclinics.com/mailto:[email protected]


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MALIGNANT BOWEL OBSTRUCTION

In the United States, intestinal obstruction is a common cause of hospitalization, rep-

resenting roughly 15% of all emergency admissions for abdominal pain, or 300,000

hospitalizations per year.3 This risk increases in patients with cancerapproximately

3% per year as a groupand is substantially higher in those affected by colorectal and

ovarian cancer (10%28% and 20%50% per year, respectively).4,5 Breast cancer

and melanoma are the most common nonintra-abdominal cancers to cause bowel

obstruction, and this typically presents as diffuse peritoneal carcinomatosis.6,7

Obstruction can occur anywhere along the gastrointestinal tract. In some cases, this

represents the initial symptom of the underlying malignancy, whereas in others itdevelops during the course of disease. A recent consensus conference defined

a malignant bowel obstruction (MBO) as one of the following: clinical evidence of

bowel obstruction (by history, physical, and/or radiologic examination); bowel

obstruction beyond the ligament of Treitz, in the setting of a diagnosis of intra-abdom-

inal cancer with incurable disease; or a diagnosis of nonintra-abdominal primary

cancer with clear intraperitoneal disease.8 Many treatment options exist for these

patients, and because MBOs rarely need to be managed emergently,9 the treatment

team, patient, and family have time to discuss these decisions in the context of the

patients goals of care and underlying burden of disease.10

Obstruction is categorized as either partial or complete. In partial obstruction, gas orliquid stool can pass through the point of intestinal narrowing. With complete obstruc-

tion, no substance can pass. Such obstructions can be secondary to mechanical or

functional pathology. Mechanical obstructions are characterized as intraluminal

(enlarging primary or secondary tumor), intramural (infiltration of the bowel wall), or

extramural (extrinsic compression from masses, nodes, or adhesions) (Fig. 1). Func-

tional obstruction is characterized by an adynamic ileus. This can result from tumor

infiltration of the mesentery that affects the bowel wall muscle and nerves, or it can

be induced by the many pain medications used by this population. Ileus may also

result from a paraneoplastic neuropathy, particularly in patients with lung cancer.6

In the setting of a mechanical obstruction, distinction should be made betweensimple and closed-loop obstructions. Simple obstructions result when the intestinal

lumen is partially or completely occluded at one or more points, with resultant prox-

imal distention and distal decompression of the intestine. In contrast, closed-loop

obstructions result from two sequential occlusions. In a healthy population, this is typi-

cally a result of an incarcerated hernia or volvulus. These obstructions can rapidly

dilate and progress to strangulation and compromise the mesenteric vascular supply,

Table1

Clinical categories of immunocompromised patients

Group IMild-to-Moderate Group IISevere

Elderly

MalnourishedMalignancy

No chemotherapy

Transplant (high-dose steroids)

AIDS (CD41


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which results in ischemia. Strangulated closed-loop obstructions are surgical emer-

gencies. If left untreated, these types of obstructions can have mortality rates of

20% to 30%.1113

The following sections address etiologies that can precipitate malignant small- and

large-bowel obstructions. In each section, the authors have highlighted the underlying

pathophysiology, differences in patient presentations, and management options.

Small Bowel Obstruction

In Western countries, the most common causes of small-bowel obstruction (SBO) are

postsurgical adhesions (74%), Crohns disease (7%), and neoplasm (5%).14 Deter-

mining the etiology of postsurgical SBO in patients with cancer can be particularly

challenging. SBOs can be caused by intrinsic narrowing from the malignancy or

extrinsic compression of the bowel by tumor or adhesions. Once an obstruction is

present, intestinal secretions and swallowed air accumulate, resulting in dilation of

the proximal small bowel.15 This stretch stimulates additional secretory activity and

microvascular changes in the bowel wall, with resultant translocation of bacteria to

the mesenteric lymph nodes.

The most common presenting symptoms of SBO are abdominal cramps, nausea,vomiting, and abdominal distention. A source of continuous pain may point to the

location of the tumor, but patients may also have diffuse, nonlocalized signs.6 The

time course of symptoms, character of the emesis, and degree of distention also

provide helpful historical clues. For example, a rapid course, bilious emesis, and

minimal distention point toward a high-grade obstruction, whereas a more insidious

course, nonbilious emesis, and marked abdominal distension suggest a more distal

SBO or large-bowel obstruction (LBO).6,9 Passage of flatus or loose stools may

confound a history of obstruction as these can result from peristalsis above and below

the obstruction early on in the course of disease.

Although the history, clinical examination, and screening laboratory tests may behelpful in the management of SBO, imaging is the cornerstone of establishing the

definitive diagnosis. Imaging helps determine the level of obstruction, potential for

concurrent strangulation, and the need for immediate operative intervention.16,17

Plain radiographs using two views (flat and upright) have a sensitivity of 66% for

detecting an SBO,18 with low specificities affected by the inability of this modality

to distinguish between SBO and etiologies causing functional or mechanical

Obstruction

Mechanical Functional

-Intra-luminal

-Intra-mural

-Extra-mural

- Paraneoplastic neuropathy

Simple Closed-loop

-luminal occlusion -sequential occlusion

-incarcerated hernia

-volvulus

Fig.1.Categorizing a malignant bowel obstruction.

Cancer Emergencies: Acute Abdomen 383


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LBOs.16,18 Moreover, abdominal plain films, in conjunction with clinical and laboratory

findings, cannot reliably distinguish between a simple and strangulated obstruc-

tion.13,14,1922 Despite these limitations, these images can be rapidly obtained, per-

formed at the bedside, and can guide the early management and subsequent

imaging. Images that show dilated gas or fluid-filled loops of small bowel with a gasless

colon are pathognomonic of SBO (Fig. 2).23 Additionally, the presence of air-fluid

differential height in the same small-bowel loop and a mean level width greater than

2.5 cm suggest a high-grade or complete SBO.14,24

Early studies of CT performed to assess for SBO found 90% to 96% sensitivity and

96% to 100% specificity.6,2527 Subsequent work questioned these results, with

substantially lower sensitivity (63%) and specificity (78%) when the study population

had a higher percentage of low-grade SBO.28 Further complicating this data, most of

these earlier studies were performed with mono-slice CT, in contrast to the multidetec-

tor machines currently in use. Despite these conflicting results, CT offers distinct advan-

tages over conventional radiography, especially in patients with underlying malignancy.

First, CT can determine the presence of a closed-loop obstruction and strangula-

tion.16,2937A negative predictive value of 89% 30,38 makes this a useful test for patients

in whom a conservative management strategy is planned.23,39 Second, multiplanar CT

can more accurately visualize adjacent anatomy, define the point of obstruction (the so-

called transition point), and identify intestinal pneumatosis. Lastly, recent evidence

suggests that a CT augmented with enteroclysisa process in which water-soluble

contrast is infused by way of a catheter into the duodenum or proximal small bowel

offers a greater sensitivity and specificity for partial obstructions (89% and 100%,

Fig. 2. Small bowel obstruction radiograph. (From MedicalFinals.co.uk. Available at: www.medicalfinals.co.uk. Accessed December 12, 2008; with permission.)

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respectively) and allows for greater differentiation between malignant and benign

causes of SBO.23

In past decades, amid concern for strangulation and the limited diagnostic yield of

abdominal radiographs, SBO was routinely managed operatively, following the adage

of never let the sun set or rise on an SBO.40 Management has evolved in the setting

of improved imaging modalities, and it is increasingly recognized that a conservative

approach employing fluid resuscitation and nasointestinal suction may obviate

surgery.39,41 This is encouraging for patients with MBOs, because surgical interven-

tions carry a high operative mortality (5%32%, often due to progression of disease),

involve high morbidity (42%), and are often unsuccessful, with reobstruction rates of

10% to 50%.19,4248 Conversely, among patients who develop a malignant SBO,

26% are because of underlying adhesions. In one series, this subgroup of patients

lived longer and had more effective relief when they were managed surgically.49

A conservative approach begins with nasointestinal decompression as a means to

relieve the small bowel of fluid accumulation. Typically, this is achieved by way of

a nasogastric tube. Some investigators believe that more effective decompression

can be achieved if the tube is advanced beyond the pylorus, which may result in better

outcomes.15,50 Placement of these long intestinal tubes is more challenging than the

typically used Salem sump nasogastric tube (Sherwood Medical, St Louis, MO, USA)

and requires fluoroscopy, which may limit their widespread application in the ED.51

In the context of a nonsurgical management plan, pharmacotherapy may be a useful

adjunct to bowel rest. Somatostatin analogs (octreotide) and anticholinergic agents

(scopolamine) have been employed to reduce gastrointestinal secretions and lengthen

small bowel transit time, with marked symptomatic relief and resolution of symp-

toms.5256

Because octreotide has been shown to dramatically reduce the rate ofnausea and vomiting with few side effects, and because complete relief of these

symptoms is rare with typical antiemetics, some authors advocate the early use of

this agent.10 The dose of octreotide used to manage MBO in small case series has

ranged from 0.1 to 1.2 mg/d, administered by either a continuous or bolus subcuta-

neous infusion.6 Corticosteroids have not been shown to definitely affect the relief

of MBOs, although they can act to treat obstruction-related pain.44 Corticosteroids

should thus be reserved for patients in the terminal stages of their disease and be

administered after consultation with the oncologist.10

Because of high mortality rates associated with nonsurgical care, the diagnosis of

a closed-loop obstruction or strangulation should prompt the consideration of imme-diate surgical intervention. Additionally, if conservative management of a simple SBO

fails, surgery may become a necessary next step. Laparoscopic adhesion lysis has

grown in popularity as a minimally invasive technique to relieve SBO, with success rates

of 40% to 70% in the general population.16 In patients with malignant SBO, CT imaging

may be helpful to define the etiology of obstruction (tumor vs adhesions) and to map

the location and type of adhesions.16 This may ultimately dictate whether a surgical

approach is at all possible, and if so, whether the lesions are amenable to laparoscopic

reduction. Palliative procedures such as ostomies, stenting, debulking, and intraperito-

neal chemotherapy may also be considered.10

Large Bowel Obstruction

LBOs are much less common than SBO. However, when they are encountered, their

most common cause is an underlying malignancy.57 Other etiologies include divertic-

ulitis and volvulus of the sigmoid colon or cecum. In the setting of a malignant LBO, the

cause is typically an intraluminal tumor growth, but it can also be the result of intussus-

ception (discussed in a later section). Up to 20% of patients with colorectal cancer



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develop an LBO, which can have a substantial morbidity and mortality. Postopera-

tively, up to 25% of patients with a colorectal cancer resection develop an LBO.5861

Similar to SBO, mechanical obstruction of the large bowel causes bowel dilatation

above the site of obstruction. This precipitates mucosal edema, impaired vascular

flow to the bowel wall, increased mucosal permeability, and subsequent bacterial

translocation. A nonpatent ileocecal valve can create a second anatomic barrier,

thus setting the stage for a closed-loop obstruction. It is essential for the practitioner

to distinguish between LBO and non-obstructive causes of large bowel dilation, such

as a toxic megacolon. The latter refers to dilation of the colon associated with acute

colitis, either segmental or diffuse, without associated obstruction. A wide range of

etiologies can result in acute colitis: inflammation, ischemia, infection, or radiation.

Symptoms of LBO typically follow an indolent course, with progression over several

days. Initially, lower abdominal or diffuse colicky pain is accompanied by abdominal

distention and changes in bowel habits (stool caliber changes or obstipation). De-

pending on the patency of the ileocecal valve, these symptoms can eventually prog-

ress to nausea and vomiting.62 Rarely, this emesis is feculent, a result of bacterial

overgrowth in the stagnant fluid proximal to the obstruction.62 Evidence of systemic

symptoms, such as fever or tachycardia, and laboratory abnormalities, such as a white

blood cell count over 20,000/mm3, may suggest the presence of a gangrenous bowel

or perforation.57 However, immunocompromised patients may continue to have unim-

pressive abdominal examinations, even in the presence of these abdominal

catastrophes.

Abdominal radiographs, when performed for evaluation of LBO, have a sensitivity

and specificity of 84% and 72%, respectively (Fig. 3).63 In patients who are mobile,

the addition of a contrast enema plain radiograph improves the sensitivity (96%)and specificity (98%) of this study to detect a mechanical obstruction.63 These studies

do not, however, evaluate the viability of the proximal bowel, determine the extent of

the primary malignancy or distant metastases, or significantly affect subsequent

procedural planning.58

Fig. 3. Large bowel obstruction radiograph. (From Ho V, Lee YC. Acute colonic pseudo-obstruction in an elderly alcoholic man. Internet J Gastroenterol 2007;5(2); with permission.)

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Early studies using CT to detect LBO found that it was able to confirm the diagnosis

in over 90% of cases, with one study citing a sensitivity of 96% and specificity of

93%.64,65 This same study found an improved diagnostic accuracy, sensitivity, and

negative predictive value of CT when compared to the contrast enema outlined

earlier.64 The use of multidetector CT, with improved spatial resolution and multiplanar

images, likely improves its diagnostic accuracy for LBO, although evidence to support

this is scarce.58,66 CT also enables the clinician to accurately exclude closed-loop

obstructions or strangulation, evaluate for the nonobstructive causes of colonic dila-

tion outlined earlier, and assess for nonmalignant causes of LBO such as volvulus

and diverticulitis.

Once identified, malignant LBOs necessitate prompt intervention. Historically, this

has involved operative management, with approximately 85% of emergency large

bowel surgery performed to relieve malignant LBO.67 These obstructions can be

addressed by either a palliative stoma or a rectosigmoid resection with accompanying

colostomy, although these operations portend frequent complications and high

mortality rates (8.8%27%).59,61,6871 Recent advances in endoscopy have estab-

lished a role for colonic stenting in the management of malignant LBO, either as a palli-

ative measure or as a bridge toward definitive operative management in patients with

resectable disease.68,72 Stenting carries the risk of perforation (3%4%), migration

(10%11%), and reobstruction (7%10%).58,73 A meta-analysis that compared oper-

ative versus endoscopic management of malignant LBO found that colonic stents

were associated with significant reductions in length of hospital stay, mortality rate,

eventual need for a palliative stoma, and medical complications.68 Moreover, mortality

rates were similar between patients who underwent emergency surgery and those

who were stented in anticipation of an elective bowel resection, although there wassubstantial heterogeneity among the two groups.68 A prospective trial that compares

these two interventions is ongoing (http://www.crstrial.com).

Gastric Outlet Obstruction

Gastric outlet obstruction (GOO) results from an underlying malignancy in 63% of

cases.4,74 Typically, cancer involving organs of the lesser sac results in intrinsic or

extrinsic obstruction of the adjacent pyloric channel or duodenum. This obstruction

may result from a combination of local infiltration, edema, and adhesions. The symp-

toms of GOO may be intermittent until occlusion is complete. Pancreatic cancer is the

most common malignancy to cause GOO (10%20%). Other etiologies that causeGOO include ampullary cancer, duodenal cancer, cholangiocarcinoma, gastric

cancer, and metastases to the gastric outlet from lung and breast cancer.6,75

Early symptoms of GOO may include gastroesophageal reflux, early satiety, and

weight loss. Eventually, patients progress to nausea and vomiting, usually nonbilious

with undigested food particles, along with abdominal pain and distention. Although

nausea and vomiting are frequent complaints in patients with any underlying malig-

nancy, especially in the context of ongoing chemotherapy, this sequence of symp-

toms should also prompt consideration of GOO.

Although it is difficult to definitively establish the diagnosis of GOO in the ED,

patients can be managed symptomatically with fluid resuscitation and gastric decom-pression. Gastrojejunostomy remains the definitive surgical treatment of choice,

although self-expandable metallic stents have become a viable nonsurgical alterna-

tive, with relief of obstruction in more than 90% of cases.7679 Studies that compare

these two interventions have shown equivalent survival rates, although patients who

received endoscopic stents had shorter hospital stays, lower costs, and an improved

ability to consume food orally.6,80 Patients managed surgically, however, had

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a reduced need for reintervention, a result attributed to delayed stent occlusion.81,82

As an additional option, gastric venting can be achieved by way of a percutaneously

placed gastrostomy tube.6

Malignant IntussusceptionIntussusception occurs in all age groups, but is primarily a disease of infancy and early

childhood. Overall, only 5% of intussusceptions occur in adults, and intussusceptions

account for approximately1% to 5% of adult SBOs.83,84 Childhood causes tend to be

idiopathic, whereas a mechanical cause is present in more than 90% of adult cases.

Solid tumors, benign and malignant, act as the lead point in over 65% of adult

cases.83,85 Intussusception results when a segment of bowel lumen that either

contains a mass lesion or has altered peristaltic activity telescopes into an adjacent

segment. This results in obstruction and ischemic injury to the intussuscepting

segment.84 A neoplastic mass must be strongly considered in children older than

4 years and adults who present with intussusception.

Patients with intussusception have acute, subacute, or chronic nonspecific symp-

toms. In small studies, the most common complaint reported is intermittent abdominal

cramping (79%), followed by obstructive signs, such as nausea, vomiting, and

abdominal distention.83,84 Plain radiographic evaluation of the abdomen is similarly

nonspecific. The abdominal radiograph may suggest partial or complete bowel

obstruction, although occasionally a soft-tissue density outlined by two strips of air

may be seen.83,84,86 The use of CT in adults has been recently advocated to better

differentiate an associated mass and rule out other etiologies. Characteristic imaging

findings include the target sign or sausage-shaped appearance.83,85 Manage-

ment of adult intussusceptions is dictated by their location. Pure colonic intussuscep-

tions are typically resected because of their high malignant potential, whereas ileocolic

lesions may be approached with intraoperative colonoscopy to identify the lesion

before intervention and potentially avoid resection.84,86

PERFORATION

MBOs, transmural erosion of primary gastrointestinal cancers, metastatic lesions to

the gut, and atypical infections have the potential to cause bowel perforation and peri-

tonitis. The clinical severity of these perforations and therapeutic options for treatmentare affected by the location, involvement of adjacent structures, and the time to

patient presentation. Intra-abdominal perforations are categorized as either free,

when bowel contents are spilled into the abdominal cavity, or contained, if contiguous

organs wall off the area. In an immunocompromised population, over 90% of colonic

perforations result in pneumoperitoneum because of these patients inability to

localize infection and the late onset of presentation.2

The differential for peritonitis in this population is shaped by the patients underlying

malignancy and degree of immunosuppression. Common causes of colonic perfora-

tions in immunocompromised patients include diverticular disease, ischemic colitis,

fecal impaction, neutropenic enterocolitis, and opportunistic infections such as cyto-megalovirus (CMV) andCandida.2,87,88 Perforations secondary to CMV have also been

found in the ileum and jejunum among patients undergoing chemotherapy.8992

CT has the ability to demonstrate small amounts of free air, pneumatosis intestinalis,

portal venous air, and the site of intestinal obstruction.2,93 Once perforation is estab-

lished, broad-spectrum antibiotics along with rapid surgical consultation should be

initiated with likely operative management.

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PATHOLOGY UNIQUE TO PROFOUND IMMUNOSUPPRESSION

All patients with an underlying malignancy who present to the ED should be consid-

ered immunosuppressed. The degree to which this immunosuppression affects their

clinical presentation is dependent upon whether they recently received chemo-

therapy, their current absolute neutrophil count, and associated medical problems.Patients that are categorized as severely immunosuppressed (see group II in Table 1)

require a special consideration of unique diagnoses. The most common cause of an

acute abdomen in neutropenic patients, neutropenic enterocolitis, is discussed in

detail elsewhere in this issue. Additional pathologies are outlined in Table 2.

Neutropenic Enterocolitis

Neutropenic enterocolitis, or typhlitis, is a necrotizing inflammation of the cecum that

is found almost exclusively in patients who are immunocompromised. This entity hasreceived a multitude of names: neutropenic colitis, necrotizing enterocolitis, ileocecal

syndrome, and cecitis.9496 The incidence of this disease among adults varies widely

in the literature (0.8%26%), likely due to the heterogeneity of the diagnostic criteria.97

When identified, this diagnosis carries a mortality rate of 50% and higher.97103Among

patients with solid or hematologic malignancies, typhlitis typically manifests in the

setting of chemotherapy-induced neutropenia or bone-marrow transplantation, and

it has emerged as the most common cause of the acute abdomen in the neutropenic

cancer patient.2 Case reports also cite neutropenic enterocolitis as a presenting

symptom in patients with acute myelogenous and acute lymphoblastic leukemia,

before the onset of chemotherapy.104109 Moreover, it has also been described inpatients with AIDS, as well as patients who require immunosuppression after organ

transplantation.110,111 Despite its name, patients can develop neutropenic enteroco-

litis in the absence of neutropenia.112114

The etiology and pathogenesis of this syndrome remain poorly understood. It has

been postulated that the disease is caused by the inability to maintain an intact intes-

tinal mucosa. This lack of mucosal integrity likely results from a combination of neutro-

penia, impaired host defenses, and direct injury from chemotherapeutic agents.111

Table 2

Additional presentations unique to underlying malignancy or immunocompromise

Disease State Manifestations

CMV GI tract mucosal ulcers (mouth to rectum),commonly with secondary bleeding thatcan progress to perforation.

Varicella (diffuse & primary) Acute abdomen can occur withoutcutaneous findings. Typically in stem-celltransplant patient, associated withhyponatremia secondary to SIADH. Treated

with acyclovir and IVIG.GVHD Skin (rash/dermatitis), liver (hepatitis/

jaundice), GI tract (abdominal pain/diarrhea). Findings can occur together orin isolation.

Abbreviations: GI, gastrointestinal; GVHD, graft-versus-host disease; IVIG, intravenous immuneglobulin; SIADH, syndrome of inappropriate antidiuretic hormone.



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Transmucosal migration of bacteria causes systemic bacteremia, endotoxin

production, mucosal or transmural necrosis, and focal hemorrhage.94,110

There is considerable variation in presentation among patients with neutropenic

enterocolitis. The most common symptoms are fever, right lower quadrant abdominal

pain, nausea, and vomiting. Computed tomography is the imaging modality of choice

because this constellation of complaints poses a fairly wide differential. Ultrasound

and abdominal plain films may provide clues to this diagnosis, but have higher false

negative rates.115 Typical CT findings (Fig. 4) include circumferential cecal wall thick-

ening; dilated, fluid-filled cecum; and adjacent mesenteric fat stranding.94 The degree

of bowel-wall thickening may correlate with prognosis, with one retrospective study

showing a mortality of 60% if the bowel wall was 10 mm or more by ultrasound,

and only 4.2% if 10 mm or less.116 Focal findings of high attenuation in the cecal

wall may represent hemorrhage.

Neutropenic enterocolitis is an uncommon diagnosis, and there are no randomized

prospective trials to guide management. Most authors advocate broad-spectrum

antibiotics, bowel rest, aggressive nutritional supplementation, and correction of

underlying cytopenias and coagulopathies.94,104 If the patient is neutropenic, admin-

istration of granulocyte colony-stimulating factor may provide benefit. A more detailed

review of neutropenic enterocolitis is presented elsewhere in this issue.

ETIOLOGIES UNIQUE TO PATIENTS WITH CANCER

Malignant Ascites

Malignant ascites is defined as the collection of fluid containing cancerous cells in the

abdomen. Malignant ascites can occur from direct invasion of the peritoneum (perito-

neal carcinomatosis), or as a result of venous or lymphatic obstruction.117 Ovariancancer is the most common malignancy to cause ascites, occurring in 37% of all re-

ported cases. Because of this, malignant ascites is twice as likely in females as males

(67% vs 33%).118,119 Additional malignancies complicated by ascites include, but are

not limited to, pancreaticobiliary, gastric, esophageal, and colorectal cancers. The

pathophysiology of ascitic fluid accumulation is multifactorial and may result from

venous and lymphatic obstruction, oncotic shifts, or enhanced vascular permeability

as a result of diffuse cytokine release.120

Patients with malignant ascites can present with abdominal distention, pain, dysp-

nea, nausea, anorexia, and vomiting. In more than 50% of patients ultimately

Fig. 4. Computed tomography image of neutropenic enterocolitis. (From Lodhawala T,Shaikh A, Carmosino L. Gastroenterology photo quiz. Resid Staff Physician 2007;53(1),with permission.)

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diagnosed with malignant ascites, this fluid accumulation caused the first presenting

signs and symptoms of their underlying malignancy.118 Because of the many potential

etiologies that can cause ascites, paracentesis is necessary to establish a malignant

source. In these cases, cytology is diagnostic in 50% to 60% of cases, with sensitiv-

ities of 58% to 75%.117,118

Management strategies for malignant ascites are directed toward symptomatic

relief, similar to the treatment of patients with nonmalignant ascites. Initial interven-

tions include diuretics and therapeutic paracentesis.118 When these measures are

unsuccessful, a peritoneal drain can be placed, with relief in 83% to 100% of

cases.120,121 A peritoneovenous shunt (PVS) incorporates 1-way valves allowing

flow from the peritoneum to the vena cava and is a more invasive alternative to the ex-

traperitoneal drain. Although there is little data to compare these two interventions,

PVS has been shown to have a higher rate of patency at 72 days.118 There is a theo-

retical risk of disseminated intravascular coagulation in patients with PVS, because of

shunting of cancerous cells into the vena cava.118

Patients with malignant ascites are at risk for spontaneous bacterial peritonitis,

although this risk is believed to be lower than in patients with nephrotic or cirrhotic

ascites.122 That said, because of the concurrent immunosuppression, physicians

should have a low threshold to perform diagnostic paracenteses as part of their infec-

tious work-up. To address the malignant ascites itself, palliative intraperitoneal

chemotherapy can be considered.121,123

Radiation Enteritis

Radiation enteritis occurs in patients receiving irradiation of the abdomen or pelvis

during the course of their cancer treatment. The disease is characterized by diffusecollagen deposition and progressive occlusive vasculitis that results in local narrowing

of the intestinal lumen.124 These microvascular changes result in bowel dilation prox-

imal to affected segments and mucosal damage, with secondary effects of bowel

ulceration, perforation, and massive gastrointestinal bleeding.125,126 Pelvic irradiation,

where the greatest volume of bowel is affected, is predominantly used in the treatment

of gynecologic and urologic cancers. A recent United Kingdom study cited a 50% inci-

dence of radiation-induced bowel damage among their cohort of 12,000 patients with

pelvic cancer. Although only 4% to 8% of these patients had life-threatening compli-

cations, as many as 80% were chronically affected by malnutrition, fistula formation,

and strictures.126,127

The small bowel is particularly susceptible to radiation enteritis, especially at doses

greater than 45 Gy.124 The most important factors to prevent both acute and chronic

radiation-induced injury are the reduction of dose and field size.125,128 Once radiation

enteritis is diagnosed, medical therapy can include 5-aminosalicylate, octreotide, and

the administration of probiotics. These measures have been shown to be most effec-

tive in the acute phase. Unfortunately, few pharmacologic choices for chronic radia-

tion enteritis have shown an established benefit.126,128 Ongoing research is

evaluating cytokine levels as a means to predict which patients are most susceptible

to radiation enteritis, manipulation of growth factors in formation of fibrotic tissue, and

dietary supplementation.124,126,128

Budd-Chiari Syndrome

The Budd-Chiari syndrome (BCS) describes the clinical manifestations of hepatic

venous outflow obstruction at the level of the hepatic venules, large hepatic veins,

inferior vena cava, or right atrium.129131 These obstructive thromboses occur most

frequently in the setting of an underlying hypercoagulable state and in rare cases



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can result from tumor invasion. The malignancies that most frequently precipitate BCS

are hepatocellular, renal-cell, and adrenal carcinoma.130 The resultant venous stasis

and hepatic congestion cause hypoxic parenchymal cell injury, centrilobular necrosis,

and eventual cirrhosis.130 Unless hepatic congestion is relieved, obstruction prog-

resses to liver failure and death.132

Typical symptoms of the Budd-Chiari syndrome include ascites, hepatomegaly, and

abdominal pain, with some cases progressing to jaundice, portal hypertension, and

variceal bleeding.131 Coagulopathy, encephalopathy, and development of the hepa-

torenal syndrome all indicate a poor prognosis.130 The diagnosis can be established

using ultrasound, CT, or MRI. If advanced imaging is inconclusive, a liver biopsy

may be necessary.133,134 The sensitivity of Doppler ultrasonography for diagnosing

BCS is 85% to 90%, and this should be the initial imaging technique performed

when this diagnosis is entertained.135,136 Ultrasonography findings in BCS include

nonvisualization of hepatic veins, absence of flow in the hepatic vein, stenosis of

or thrombosis within the hepatic veins, intrahepatic collaterals, and obstruction of

the infrahepatic inferior vena cava.135 CT and MRI offer the advantages of better

identification of necrotic areas of the liver and improved detail of liver perfusion.135

For relatively asymptomatic patients with BCS who have normal liver function tests,

medical therapy with sodium restriction, diuretics, anticoagulation, and intermittent

paracenteses can constitute the initial management strategy. In the setting of hepato-

cellular necrosis, however, patients need either surgical or percutaneous portosyste-

mic shunting (mesoatrial, mesocaval, transjugular intrahepatic portosystemic shunting

or hepatic vein angioplasty).132,137 Both treatments are typically followed by lifelong

systemic anticoagulation.132 Fulminant or refractory cases of Budd-Chiari syndrome

may require liver transplantation.

SUMMARY

Gastrointestinal complaints among patients with cancer can pose a diagnostic

dilemma with significant rates of morbidity and mortality. Mass lesions or adhesions

related to intra-abdominal malignancies place these patients at higher risk for bowel

obstruction or perforation, while ongoing chemotherapy or functional immunosup-

pression can mask many of the findings among healthy patients. This affects the

timing of patients presentation and their clinical examination in the ED. Moreover,

in the setting of profound immunosuppression, a wide range of atypical infections

and pathologies must be considered. Clinical vigilance by the practitioner is thus

essential, with a low threshold to use advanced imaging modalities and careful

consideration of this expanded differential.

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