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446 CHAPTER 9: The Abdomen, Perineum, Anus, and Rectosigmoid
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HIV infected patients is a complex clinical problem with multiple infectious
and noninfectious causes. Consultation with a specialist in HIV-related
diseases is recommended. Patterns: Recognizing several relatively distinct
diarrheal syndromes helps form a concise differential diagnosis: acute diarrhea, dysentery syndrome, diarrhea with maldigestion/malabsorption, steatorrhea, diarrhea with weight loss, or diarrhea with bloody stools.
Acute nonbloody diarrhea. Diarrhea lasting <2 weeks, and not preceded by
recurrent or relapsing episodes, is acute diarrhea. Infectious and toxic causes
are most common.
CLINICAL OCCURRENCE: Infectious: Enteroviruses, Rotavirus, norovi-
ruses (e.g., Norwalk agent), enterotoxigenic Escherichia coli, Salmonella,
Shigella, Campylobacter spp., Giardia, Cryptosporidium, cyclospora, amebiasis,
C. difcile, Vibrio cholerae; Metabolic/Toxic: Food poisoning (Bacillus cereus,
staphylococcal, Clostridium perfringens), antibiotic-associated diarrhea,
alcohol, osmotic laxatives, sugar-free candy and foods, drug withdrawal;
Vascular: Ischemic colitis.
Traveler's diarrhea.
Travelers ingest contaminated food and water containing
the colonic ora of their host country. Often within a week of arrival travel-
ers experience 1–5 days of self-limited watery diarrhea, abdominal cramping,
and anorexia. The most common organism is enterotoxigenic E. coli. Shigella,
Salmonella, Campylobacter, V. cholerae, Giardia, Cryptosporidium, and viruses can
have the same presentation.
Viral gastroenteritis. Infection of the bowel epithelium causes loss of
absorptive function. Systemic signs may be absent, mild (Norwalk), or severe
(rotavirus, norovirus). Commonly epidemic, there is sudden onset of nausea,
vomiting, and explosive diarrhea, with or without abdominal cramps. Myalgia, malaise, and anorexia, usually without fever, are common. Diarrhea and
vomiting subside within 48 hours though lassitude may persist for several
days. The stools consist of water and fecal remnants; blood, pus, and mucus
are absent. Common causes are rotavirus, noroviruses, adenovirus, caliciviruses, enterovirus, and coronavirus. Specic diagnosis is not required.
Cholera. Cholera toxin inhibits gut Na+ absorption and activates
Cl− excretion, producing severe secretory diarrhea. Waterborne V. chol-
erae infection is locally endemic in some countries, sometimes triggering
epidemic and pandemic disease. There is sudden abdominal cramping,
vomiting, and voluminous watery stools containing ecks of mucus
(rice-water stools) progressing to dehydration, electrolyte imbalances,
prostration, shock, and death.
Food intolerance. Ingestion of specic foods causes local and systemic allergic
reactions.
Symptoms are nausea, vomiting, abdominal cramping, and diarrhea. Angioedema can occur. Identication of the allergen can be difcult.
Shellsh, peanuts, cow’s milk, and cereals are common culprits.
Food poisoning. Usually, preformed bacterial exotoxins are ingested in
contaminated food. B. cereus also causes a longer incubation diarrhea probably from exotoxin production in the gut. Severe cramping abdominal pain,
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nausea, vomiting, diarrhea, and prostration begin 1–6 hours after a meal,
resolving within hours. Large groups of diners are frequently affected. Specic foods are clues to the etiology: potato salad, mayonnaise, and cream
pastries—Staphylococcus aureus; meat, poultry, legumes—C. perfringens; fried
rice—B. cereus.
Chinese restaurant syndrome. This is attributed to monosodium gluta-
mate, a seasoning used in Asian cooking.
headache, burning sensations, and feelings of pressure about the face
starting 10–20 minutes after eating. Occasionally, chest pain, prostration,
gastric distress, and pain in the axillae, neck, and shoulders develop.
Acute bloody diarrhea.
of the bowel mucosa, usually in the colon. Infections that either invade
the mucosa or produce toxic epithelial necrosis are most likely. Chronic
inammatory bowel diseases can present with diarrhea both initially and
with relapse.
tenesmus (dysentery syndrome). Fever and leukocytosis suggest an enteroinvasive organism with risks of local complications and systemic spread.
Painless bleeding in otherwise healthy individuals suggests bleeding from
a structural abnormality (Meckel diverticulum, diverticulosis, polyp, or
cancer).
CLINICAL OCCURRENCE: Congenital: Meckel diverticulum; Inammatory/
Immune: Ulcerative colitis, Crohn disease; Infectious: Bacteria (Campylobacter
jejuni, Salmonella spp., Shigella spp., enterohemorrhagic E. coli 0157:H7), protozoa (Entamoeba histolytica, Balantidium coli), cytomegalovirus; Mechanical/
Traumatic: Rectal foreign body; Metabolic/Toxic: Heavy-metal poisoning
(arsenic, mercury, cadmium, copper, iron); Neoplastic: Villous adenoma with
malignant change; Vascular: Ischemic colitis.
Dysentery.
ecation with stools containing pus and blood, indicative of colon and rectal
inammation. Dysentery is an infectious diarrhea often with mucosal invasion and ulceration. Dysentery is distinct from simple gastroenteritis. Stool
culture and testing for ova and parasites are required; sigmoidoscopy may
be useful. Common etiologies are bacterial (C. jejuni, Salmonella spp., Shigella
spp., enterohemorrhagic E. coli including 0157:H7) and protozoa (E. histolyti-
ca, B. coli, strongyloidiasis).
Patients present without pain or with abdominal pain and
Dysentery is a syndrome of abdominal cramping and painful def-
Acute bloody diarrhea indicates compromise
It is characterized by severe
Amebiasis. Ingestion of water contaminated with E. histolytica leads to ulcer-
ations in the colon and terminal ilium, and liver abscess. Acute infection may
be fulminant with cramping abdominal pain, bloody diarrhea, and tenesmus.
Exam reveals fever, diffuse abdominal tenderness, dehydration, and weight
loss. Subacute infection has milder abdominal cramps, diarrheal stools containing mucus or blood, often alternating with intervals of normal function
and exam may nd fever and RLQ tenderness. Liver abscess is suggested by
spiking fevers, prostration, and RUQ pain with mildly abnormal liver tests.
Ulcerative colitis. See Chronic Constant Diarrhea—Ulcerative Colitis, page
449. Although a chronic disease, its onset may be sudden, resembling acute
dysentery.
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Poisoning with heavy metals or drugs. The heavy metals (such as arsenic,
cadmium, copper, or mercury) may be ingested accidentally or with suicidal or homicidal intent. Nausea, vomiting, cramping abdominal pains, and
bloody diarrhea begin soon after ingestion.
Chronic intermittent diarrhea. Diarrhea lasting more than 2 weeks is chronic
and less likely to be infectious. Intermittent diarrhea implies a disease with a
relapsing-remittent course (e.g., Crohn disease) or an interaction of the host
and the environment, particularly the diet (e.g., lactase deciency). Most
causes of chronic persistent diarrhea can also present as chronic intermittent
diarrhea.
Irritable bowel syndrome. See page 452.
Lactase deciency (lactose intolerance).
lactase leads to incomplete digestion of lactose, the disaccharide in cow’s
milk. The lactose is fermented by colonic bacteria producing gas and diarrhea. This is more common in Blacks and Asians than in Caucasians. Eat-
ing milk products produces watery diarrhea and gas, often with abdominal
cramps. Patients often do not make the association because of the ubiquitous presence of milk products in the diet. Milk product avoidance leads to
prompt resolution and is the treatment of choice. Malabsorption of sorbitol in
sugarless candies causes a similar picture.
Fructose intolerance. Some individuals are unable to absorb fructose in the
quantities ingested, especially those who consume substantial amounts
of soft drinks sweetened with high fructose corn syrup. The unabsorbed
fructose creates an osmotic diarrhea and increased intestinal gas when fermented by colonic bacteria. Symptoms and signs are identical to lactose intolerance.
Regional enteritis (Crohn disease, terminal ileitis). Transmural granulo-
matous inammation of the small and large intestine results in blood loss
and interferes with gut motility and absorption.
attacks of RLQ colic commonly accompanied by diarrhea. Weight loss may
be severe. Perforations, strictures, and stulas are common complications
including perianal stulas and anal stricture. Colon involvement is segmental with skip areas. Extraintestinal manifestations (oligoarthritis, spondylitis, pyoderma gangrenosum) may be the presenting complaint. Barium in
the small bowel may show strictures, stulas, loss of mucosal detail, and
tubular thickening of the submucosa. Diagnosis is by endoscopic biopsy
with gross and microscopic examination of resected tissue. DDX: The rst
attack of ileitis may be clinically indistinguishable from acute appendicitis, although diarrhea usually precedes the attack and a RLQ mass may be
appreciated early in the course. If similar prior episodes have occurred,
the probability is strong for chronic ileitis with an exacerbation. Consider
infection with Yersinia, Salmonella, Shigella, tuberculosis, amebiasis, and
cytomegalovirus.
Deciency of small bowel mucosal
Presenting symptoms are
Ulcerative colitis. See page 449.
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Chronic constant diarrhea. Chronic constant diarrhea suggests an unremit-
ting underlying structural or functional process involving digestion, absorption, bowel motility, or metabolism. The history (age of onset, exacerbating or
palliative maneuvers), comorbid conditions, and characteristics of the stools
are critical to a parsimonious differential diagnosis.
CLINICAL OCCURRENCE: Congenital: Cystic brosis, lactase deciency,
celiac disease;
syndrome, pheochromocytoma; Degenerative/Idiopathic: Irritable bowel syndrome, chronic pancreatitis, diverticulitis; Infectious: Giardia, HIV/AIDS
and opportunistic infections, microsporidiosis, cyclosporiasis, Whipple disease, small bowel bacterial overgrowth, intestinal parasites; Inammatory/
Immune: Ulcerative colitis, Crohn disease, microscopic colitis, mastocyto-
sis, chronic pancreatitis, celiac disease, amyloidosis; Mechanical/Traumatic:
Short-bowel syndrome, enterocolic stulas, radiation enteritis; Metabolic/
Toxic: hyperthyroidism, lactase deciency, drugs (metformin, proton pump
inhibitors, misoprostol, colchicine, digitalis, antacids), bile salt-induced,
laxative abuse, nonsteroidal anti-inammatory drugs, alcohol; Neoplastic:
Mastocytosis, villous adenoma, pancreatic islet cell tumors (producing
vasoactive intestinal peptide, gastrin, glucagon, etc.), small-bowel lymphoma;
Vascular: Vasculitis.
Endocrine: Hyperthyroidism, adrenal insufciency, carcinoid
Neurologic: Autonomic neuropathies; Psychosocial: Laxative abuse;
Ulcerative colitis.
and ulceration with crypt abscesses beginning at the rectum and extending
proximally. The mucosa is red, edematous, and friable, the slightest touch
causing bleeding. Often the entire rectosigmoid is covered by purulent exudate obscuring the multiple ulcers.
entery with fever, abdominal pain, tenesmus, bloody diarrhea, and weight
loss to mild abdominal discomfort with mostly formed stools and little blood.
The rectum is always involved, and inammation extends proximally in continuity. The extent of the disease varies from only rectal involvement to pancolitis. In long-standing disease, the lumen is contracted and irregular with
pseudopolyps. The terminal ileum may be inamed and dilated, in contrast
to the constriction found in regional enteritis. Diagnosis is made by endoscopic inspection and biopsy. Disease duration greater than 10 years and pancolitis, but not the severity of symptoms, are associated with an increased risk
for colon cancer. Ulcerative colitis must be distinguished from Crohn colitis,
ischemic colitis, amebiasis, and bacillary infections.
Amyloidosis. See Chapter 5, page 87. Amyloidosis gives rise to chronic diarrhea, hypomotility, obstructive symptoms, ulceration, hemorrhage, and
protein-losing enteropathy.
Zollinger–Ellison syndrome. A gastrinoma, usually in the pancreas or duo-
denum, produces large amounts of gastrin stimulating excessive gastric HCl
secretion leading to diarrhea and producing ulcers in esophagus, duodenum,
and jejunum. Recurrent attacks of epigastric pain, nausea, vomiting, and diar-
rhea can be accompanied by malabsorption and weight loss. Suspect excess
gastric secretion when severe ulcer disease and diarrhea occur in the absence
of H. pylori infection.
There is intense conuent chronic mucosal inammation
The clinical picture varies from acute dys-
450 CHAPTER 9: The Abdomen, Perineum, Anus, and Rectosigmoid
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Carcinoid syndrome. Liver metastases from a carcinoid tumor in the GI tract
produce large amounts of serotonin.
page 147. Symptoms include recurrent diarrhea, nausea, vomiting, and abdominal pain. Intermittent migratory ushing of face and neck occur with
rapid color changes between red, white, and violet. Right-sided heart failure
may develop from endomyocardial brosis with tricuspid insufciency.
Chronic diarrhea and malabsorption (maldigestion–malabsorption syndrome). Maldigestion results from failure to deliver sufcient pancreatic
enzymes and bile salts into the duodenum, inadequate mixing of luminal contents, or insufcient time in the small bowel for digestion to occur.
Malabsorption results from damage to the small-bowel epithelium or bypass
or loss of absorptive surface area. Steatorrhea occurs when triglycerides are not
digested or absorbed because of poor micelle formation or insufcient pancreatic lipase secretion. Fat appears in the stool as triglycerides. Frothy, greasy,
and foul-smelling stools suggest steatorrhea. Weight loss is common despite
a good appetite. Fat-soluble vitamins (A, D, E, and K) are malabsorbed and
deciency syndromes may be the presenting complaint. Microscopic exam of
stool stained with Sudan III shows fat globules.
Small bowel bacterial overgrowth (Blind Loop syndrome). Decreased small
intestinal motility leading to stasis, loss of protective gastric acid, and decreased ileocecal valve function increase the risk for bacterial overgrowth
and the blind- or stagnant-loop syndrome. Bacteria consume nutrients,
including vitamins, leading to malnutrition and vitamin deciency, particularly vitamin B12. The patient presents with diarrhea, abdominal bloat-
ing, atus, steatorrhea, weight loss, macrocytic anemia, and sometimes
feculent belching. Because the bacterial overgrowth is responsible for the
malabsorption, a short course of antibiotics should lead to demonstrable
improvement. Common antecedent conditions include surgically created
blind pouches, enteroenterostomies, long afferent loops, strictures, stulous
communications, and small bowel diverticula. Tapeworms can produce a
similar picture.
See Carcinoid Syndrome, Chapter 6,
Chronic pancreatitis and pancreatic insufciency.
from alcohol, drugs, or ductal strictures. Extensive loss of pancreatic tissue
leads to inadequate endocrine and exocrine function producing diabetes and
steatorrhea.
pain and stools that are soft, loose, frothy, and malodorous, frequently oating on water. The repeated attacks of pain are identical to acute pancreatitis.
Alcohol abuse and mild forms of cystic brosis are common causes. A palpable pancreatic pseudocyst may develop. Pancreatic calcication is diagnostic.
Celiac disease (gluten-sensitive enteropathy, nontropical sprue).
with specic HLA-DQ2 alleles, ingestion of gluten (gliadin) from wheat our
induces chronic mucosal and submucosal inammation producing characteristic attening of the villi and chronic malabsorption.
fatigue, cramping, diarrhea, steatorrhea, and weight loss without anorexia.
A family history may be present, and patients frequently have made dietary
modications. The stools are soft, frothy, and malodorous from unabsorbed
fat. Unexplained iron deciency, hypocalcemia, neuropathy, dermatitis
Chronic pancreatitis is characterized by episodes of abdominal
Chronic pancreatitis results
Patients present with
In persons
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herpetiformis, and weight loss without complaints of diarrhea are common
presentations.
Whipple disease.
Tropheryma whippelii produces foamy macrophages lled with glycoprotein
leading to lymphatic obstruction and malabsorption. Dissemination produces arthritis, lymphadenopathy, and anindolent meningitis. Presentation
can be at any age, most commonly in white men in their fourth and fth
decades. Migratory polyarthralgias and polyarthritis may precede intestinal
symptoms and weight loss. Abdominal symptoms are cramping and episodic diarrhea with fatty, foul-smelling stools. There is generalized malaise and
weakness; cough and dyspnea can occur. Fever is intermittent and may be accompanied by hypotension, edema, lymphadenopathy, and emaciation. CNS
infection causes slowly progressive chronic meningitis.
Giardiasis.
the duodenum and upper small bowel impairing absorption of nutrients
leading to diarrhea and weight loss. A travel history and exposure to surface
water potentially contaminated by livestock and wildlife is useful. Stool antigen testing is available.
Cystic brosis. An autosomal recessive disease usually diagnosed in childhood. Patients with mild disease may present in adult life with pancreatic
insufciency, rhinosinusitis, and recurrent pulmonary symptoms.
Enteroenteric stula.
duces diarrhea with undigested food in the feces and/or fecal emesis. The
diarrhea may be intermittent and results, in part, from bacteria overgrowth in
the proximal gut. Malabsorption of nutrients, uids, and electrolytes causes
weight loss, hypoproteinemia, and dehydration. Fecal belching and vomiting
suggests gastrocolic stula.
Constipation Syndromes
Constipation. Bowel motility is under autonomic control and requires an
intact myenteric plexus. Multiple factors, including luminal contents, drugs,
emotional state, physical activity, and acquired habits (bowel training) affect
stool frequency and character. Defecation requires a coordinated sequence
of involuntary and voluntary muscular contractions and relaxations. Failure
to properly sequence these events prevents effective defecation. Patients and
physician use “constipation” to mean any combination of infrequent stools,
hard desiccated stools, or stools that are difcult to pass. In the evaluating
constipation, each factor must be investigated as several may be operative at
one time. First, determine the patient’s baseline bowel movement pattern, the
onset of the current difculty, and any therapeutic interventions undertaken.
Many people do very well with two or three evacuations a week. Patients
often describe the gradual development of abdominal fullness. Acute or subacute constipation developing on a lifelong history of normal bowel movements requires investigation. Chronic constipation of years’ duration may
indicate an underlying disorder of the bowel wall, a gut motility problem,
or poorly coordinated defecation. Dyssynergy results from failure to relax the
voluntary sphincter during rectal contraction.
Invasion of the intestinal mucosa and lamina propria with
Giardia organisms adhere to the brush-border of enterocytes in
A stula between the proximal and distal bowel pro-
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CLINICAL OCCURRENCE: Congenital: Hirschsprung disease; Endocrine:
Hypothyroidism, hyperparathyroidism, pregnancy;
Intestinal pseudoobstruction; diverticulosis, diverticulitis;
disease, toxic megacolon;
sive systemic sclerosis), amyloidosis;
intake, mechanical obstruction by stricture or mass, irradiation, anal ssure;
Metabolic/Toxic: Drugs, including opiates, anticholinergics, tricyclic antide-
pressants, and many others; hypokalemia, hypomagnesemia, hypercalcemia;
Neoplastic: Colon polyps, colon and anal cancers; Neurologic: Spinal cord
injury, sacral plexus lesions, multiple sclerosis, Parkinson disease, irritable
bowel syndrome; Psychosocial: Eating disorders, substance abuse (opiates),
depression, dyssynergistic defecation; Vascular: Stroke.
Intestinal obstruction. See Obstructive Syndromes below.
Fecal impaction. There may be no discomfort, or the patient may complain
of constipation, tenesmus, or inability to defecate. Diarrhea is a frequent complaint because liquid stool passes around the impaction. Digital rectal exam
reveals hard fecal masses that must be removed manually. Common inciting
factors are immobilization, bed rest, dehydration, anticholinergic medications, dementia, and barium for GI contrast X-rays.
Irritable bowel syndrome. This common cause of constipation is characterized by periods of constipation alternating with bouts of diarrhea. Either
symptom may be the main complaint. The triad of symptoms is long-standing
intermittent constipation, scybalous stools, and abdominal pain relieved by
defecation. The cause is uncertain, although many patients have increased
sensitivity to visceral discomfort (visceral hyperalgesia).
Laxative abuse, atonic colon.
colonic sensation and reexes producing an adynamic, dilated colon dependent upon laxatives for defecation. The patient has a long history of constipa-
tion, fancied or real. The stools may be alternately voluminous and scanty.
Abdominal palpation often reveals large fecal masses.
Inammatory/Immune: Scleroderma (progres-
Mechanical/Traumatic: Excessive ber
Chronic stimulant laxative use leads to loss of
Degenerative/Idiopathic:
Infectious: Chagas
Dyssynergistic defecation. Normal defecation requires contraction of colonic
and rectal smooth muscle and simultaneous relaxation of the internal (involuntary) and external (voluntary) sphincters. Failure of this coordinated process leads to attempts to defecate against a closed anal sphincter producing
constipation. Patients complain of difculty defecating and having to strain
excessively even with soft stools. On examination, they may be unable to voluntarily relax the external sphincter.
Megacolon. Lifelong constipation with occasional passage of an enormous
formed stool suggests megacolon. Causes are congenital (Hirschsprung disease) or acquired defects in the intrinsic myenteric innervation of the colon
such as idiopathic intestinal pseudoobstruction and Chagas disease.
Drug effects. Many drugs slow bowel motility, including opiates, anticho-
linergic drugs, antihistamines, chronic laxative use, and overuse of bulk
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laxatives. Pill bezoars have been described. Medication history is key with
attention to laxative and enema use. Ophthalmologic medications are systemically absorbed and can affect gut function.
Bowel Obstruction Syndromes.
Noisy tympanites with colic and vomiting—mechanical obstruction.
These ndings suggest localized bowel obstruction with the increased force
of peristaltic contraction proximal to the obstruction producing colic and
proximal bowel distension. Decompression occurs by vomiting retained
luminal contents. Mechanical obstruction is probable. Tympanites is present when the obstruction is distal to the mid jejunum. Increased peristalsis proximal to an obstruction produces frequent, loud peristaltic sounds
(borborygmi) accompanied by cramping and colic. With partial obstructions
high-pitched high-pressure-to-low-pressure sounds (“rushes”) may accompany the pain. Vomiting appears earlier and is more intense the more proximal the obstruction. Distal obstruction may result in feculent emesis which
classically indicates colonic obstruction in a person with an incompetent
ileocecal valve or a cologastric or coloenteric stula. Colic is almost invari-
ably present from the onset. In general, the more proximal the obstruction,
the more severe the symptoms.
is intense, and vomiting is early and severe. If the vomitus contains bile,
the obstruction is beyond the second portion of the duodenum. Abdominal distention limited to the epigastrium appears late. Distal Small Intes-
tine: Symptoms are less severe, vomiting is delayed, but the vomitus may
have become feculent. Diffuse abdominal distention gradually develops.
Colon: The colon narrows beyond the splenic exure making the descend-
ing and sigmoid regions most susceptible to obstruction. Pain is less than in
small bowel obstruction. Vomiting is late and may be fecal. Constipation is
invariable but only after empting stool below the obstruction which delays
recognition. An empty rectal ampulla devoid of gas is strong presumptive
evidence of colon obstruction.
CLINICAL OCCURRENCE: Infectious: Parasites, diverticular abscess;
Inammatory/Immune: Crohn disease, diverticulitis with stricture; Mechanical/
Traumatic: Adhesions (most common), gallstone impaction, bezoars, foreign
body, pyloric stenosis, volvulus, hernias (internal and abdominal wall), intussusception, external compression from intraabdominal cysts and neoplasms;
Neoplastic: Benign and malignant tumors.
Proximal Small Intestine: Epigastric pain
Bezoars. Bezoars are concretions of hair (trichobezoar), plant bers (phy-
tobezoar), or medicines (aluminum hydroxide gel or polystyrene sodium
sulfonate) formed in the GI tract.
when they lodge at the pylorus (gastric outlet obstruction) or ileocecal valve
(small-bowel obstruction). They can cause mechanical erosion of the bowel
wall leading to ulceration, bleeding, and pain.
Strangulated hernias. See page 460.
Intussusception. Intussusception is the invagination of bowel into the lumen
of adjacent bowel. The enfolded portion always points down the fecal stream.
There are four types: ileum into ileum, ileum into ileocecal valve, ileocecal
They present with obstructive symptoms
454 CHAPTER 9: The Abdomen, Perineum, Anus, and Rectosigmoid
B. Location of intussusceptionA. Types of intussusception
Ileocecal-colic
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valve into colon, and colon into colon (Fig. 9-34). This is the most common
cause of intestinal obstruction in infants. In children it is frequently preceded
by a viral infection; in adults, neoplasm in the intestinal wall is usually the
cause. In addition to obstructive symptoms, mucus, and sometimes blood,
is passed. The pathognomonic sign is an oblong mass in the right or upper
mid-abdomen and absence of bowel in the RLQ (Dance sign) [Berger DL,
Mohammadkhani M. Case 26-2002 — An 87-year-old woman with abdominal pain, vomiting, bloody diarrhea, and an abdominal mass. N Engl J Med.
2002;347:601–606].
Colon cancer. After adhesions this is the most common cause of intestinal
obstruction in persons over age 50. Gradually increasing constipation culminates in low intestinal obstruction. Obstruction near the hepatic exure distends the cecum forming a painful, rounded RLQ mass. Distal cancers cause
gradual distention of the sigmoid and/or descending colon which is readily
palpated in the LLQ.
Volvulus. See page 434.
Silent tympanites without colic or vomiting—ileus. A silent abdomen
and distended bowel suggests diffuse ileus without mechanical obstruction
resulting from decreased bowel motility and muscular tone.
pany is always present and peristaltic sounds are diminished or absent. When
Abdominal tym-
Ileo-ileal
Ileo-ileocecal
Colo-colic
FIG. 9-34 Intussusception. This is the prolapse of one segment of intestine into an adjoining segment. A. The four
types of intussusception. The lumen enfolds in the direction of fecal flow, as shown by the arrows. In the colocolic type
the stippling indicates a neoplasm which usually causes the telescoping. B. Locations. The usual sites of palpable masses
are shown as sausage-shaped outlines; these are usually in the colon.
Abdominal, Perineal, and Anorectal Syndromes 455
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present, abdominal pain is mild, and colic is absent. Vomiting is uncommon,
but anorexia and nausea are expected.
CLINICAL OCCURRENCE: Infectious: Peritonitis (spontaneous bacterial
peritonitis in cirrhosis, perforated bowel, perforating neoplasm, ruptured
colonic diverticulum or diverticular abscess, tuberculosis, penetrating
abdominal trauma, surgical wound dehiscence), C. difcile colitis, amebic colitis, typhoid fever, Giardia, Whipple disease;
Inammatory/Immune:
Sterile peritonitis from perforated stomach or duodenum, bile, ruptured
bladder, enzymes released by acute pancreatitis, ruptured ovarian cyst,
blood (e.g., bleeding from follicular cyst), recurrent serositis syndromes
(e.g., SLE, familial Mediterranean fever, familial Hibernian fever), inammatory bowel disease (ulcerative colitis, Crohn disease), toxic megacolon;
Mechanical/Traumatic: Manipulation of the gut (abdominal surgical proce-
dures, abdominal trauma), adhesions, tumors, volvulus, intussusception,
parasites;
Metabolic/Toxic: Hypokalemia, hypothyroidism, acidemia or alka-
lemia, diabetic ketoacidosis, uremia, heavy metal poisoning, porphyria,
toxic megacolon or any major metabolic disorder, drugs (opiates, anticholinergics, vinca alkaloids, ganglionic blocking agents);
Neurologic: Trauma
to the axial skeleton, spinal cord injury, compression fracture, herpes zoster,
urinary retention, fecal impaction, aerophagia;
Vascular: Mesenteric arte-
rial embolism or thrombosis, mesenteric venous thrombosis, hypotension,
ischemic bowel.
Abdominal Masses
Rectus sheath hematoma. See page 442.
Parenchymal organ enlargement.
neys enlarge in several ways: an expanded cell mass (normal or abnormal,
e.g.,
neoplastic inltration, inammatory cells, infection), intra or extracellu-
lar deposition of material (fat, amyloid, mucopolysaccharides, etc.), vascular
congestion, or cystic change.
History and physical exam suggest a mechanism
directing a judicious selection of laboratory and imaging studies to determine
the mechanism.
CLINICAL OCCURRENCE: Congenital: Horseshoe kidney, inltration
by cells of the reticuloendothelial system (e.g., lipopolysaccharidases);
Degenerative/Idiopathic: Single or multiple cysts; Infectious: Granulomatous
diseases (fungal infections, tuberculosis), chronic infection and parasitosis
(amebiasis, hydatid disease); Inammatory/Immune: Inltration by cells of
the reticuloendothelial system (e.g., histiocytosis syndromes), granulomatous diseases (sarcoid), extracellular protein deposition (amyloidosis);
Mechanical/Traumatic: Obstruction of normal efuent systems (hydrone-
phrosis, hepatic vein obstruction), enlargement of uid-containing hollow
organs as a consequence of outow obstruction (e.g., urinary retention
and gallbladder hydrops); Metabolic/Toxic: hypertrophy of normal tissue
as a consequence of increased functional demands (e.g., splenomegaly in
hemolytic anemias), accumulation of intracellular inclusions (steatosis,
glycogen storage diseases and lipopolysaccharidases); Neoplastic: Primary
neoplasms, inltration by metastatic neoplasm either diffusely or
focally, extramedullary hematopoiesis; Vascular: Renal and hepatic vein
obstruction.
The liver, spleen, adrenals, and kid-
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