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406 CHAPTER 9: The Abdomen, Perineum, Anus, and Rectosigmoid
1.
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2. 3.
FIG. 9-17
the orifice (1), until the external sphincter relaxes. Rotate the tip of the finger (2) into the axis of the canal and (3) insert
gently. The entire procedure should be slow and gentle.
Insertion of the Gloved Finger into the Anus. The pad of the gloved index finger is placed gently over
FIG. 9-18 Comparison of Lengths of Rectosigmoid Segments with Rigid Examining Instruments. All
lengths are drawn to scale. A. The rectosigmoid and anal canal. B. An average index finger (10 cm long and
22 mm in diameter). C. A typical anoscope. D. A proctoscope of 15 cm.
(Fig. 9-16) and digital exam is done to exclude obstruction. Lubricate the anoscope with the obturator in place, then gently insert the tip and tube aiming
toward the umbilicus. Once fully inserted, remove the obturator to inspect
the rectal mucosa and anal canal during slow withdrawal.
Examining the Rectum: The three parts to the rectal examination are palpa-
tion of the lower peritoneal cavity (see above), palpation of adjacent internal
urogenital organs (see Chapters 11 and 12), and exam of the rectum itself.
Rectal palpation. This is a continuation of anal canal palpation, the nger
pushing beyond the anal canal to feel the walls of the ampulla. In the male,
on the anterior wall, the nger sequentially palpates the anterior wall, prostate, seminal vesicles, and rectovesical pouch. Next, palpate the lateral walls,
Abdominal, Perineal, and Anorectal Symptoms 407
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the hollow of the sacrum, and the coccyx. On the anterior wall of the female,
the uterine cervix, uterine fundus (if retroverted), and rectouterine pouch are
sequentially palpated. Palpate the rectal walls for masses and narrowing of
the lumen.
Examining the Sigmoid Colon: The rectosigmoid and descending colon are
inspected through a exible sigmoidoscope (Fig. 9-18) which provides a wide
eld of view and can often be advanced to the splenic exure without anesthesia. Indications for sigmoidoscopy are beyond the scope of this text.
ABDOMINAL, PERINEAL, AND ANORECTAL SYMPTOMS
Nonspecific Symptoms
Six-dermatome pain—esophageal discomfort. See Six Dermatome Pain,
Chapter 8, page 350, and Chapter 9, page 432.
Acute abdominal pain. See also page 431.
organ (somatic versus visceral, vagus, and/or sympathetic) helps interpretation of the patient’s pain. Depending on the organ, some stimuli are painful, others are not, e.g., bowel distention is painful, laceration is not. Visceral
pain is transmitted by vagal visceral afferent nerves and sympathetic afferent
nerves. It is deep, boring, poorly localized pain frequently accompanied by
autonomic features such as nausea, vomiting, and diaphoresis. Body wall and
peritoneal pain, transmitted via the spinal somatic afferent nerves, is sharp
and well localized.
ald benign or immanently life-threatening disorders. The specic diagnosis
must be pursued with a sense of urgency since early surgical intervention
will be lifesaving in some conditions (abdominal aortic aneurysm, bowel perforation) but is contraindicated in others (acute intermittent porphyria, sickle
cell crisis). Accurate diagnosis relies on history, physical exam and imaging; laboratory tests are less helpful. Repeated exams by a single observer,
be it day or night, are mandatory. Particularly important are the locations of
pain and tenderness (Fig. 9-19), and change in location and variations in the
quality of pain. Relatively few ndings distinguish several conditions. For
example, with intraabdominal visceral pain the patient may walk about, but
if peritonitis supervenes, the patient holds very still to guard the abdomen.
With acute pain patients usually seek care within a few hours of onset. Pain
increased with walking, jumping, sneezing, or coughing is equivalent to the
jar test (page 423) suggesting peritoneal inammation. A pregnancy test must
be obtained in all women of childbearing age with acute abdominal pain.
CLINICAL OCCURRENCE: Congenital: Meckel diverticulum, sickle cell
crisis, pancreas divisum, angioedema; familial Mediterranean fever, AIP
and variegate porphyria;
Degenerative/Idiopathic: Diverticulitis, endometriosis, diabetic radiculopathy,
transverse myelitis, mononeuritis multiplex; Infectious: Typhoid fever and
enteritis; Clostridium difcile enterocolitis; viral gastroenteritis; visceral lar-
val migrans; varicella-zoster virus; cytomegalovirus; viral hepatitis; tuberculous peritonitis and lymphadenitis; purulent peritonitis (spontaneous or
secondary to perforation or penetration); Inammatory/Immune: Pancreatitis,
gastritis, esophagitis, autoimmune hepatitis, peritonitis, serositis, mesenteric
Acute severe abdominal pain, the acute abdomen, can her-
Endocrine: Gastrinoma, adrenal insufciency;
Knowing the innervation of each
408 CHAPTER 9: The Abdomen, Perineum, Anus, and Rectosigmoid
Obstruction of transverse colon
Diverticulitis of colon
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Acute cholecystitis
Acute pyelonephritis
Well-established
appendicitis
Leaking duodenal
ulcer
Pyelonephritis
Regional ileitis
Mecke’s
diverticulitis
Early appendicitis
Acute pancreatitis
Acute intestinal
obstruction
Acute gastritis
Acute mesenteric
lymphadenitis
Coronary occulsion
Splenic rupture
Cancer of colon
FIG. 9-19 Common Locations of Acute Abdominal Pain. In general, the p ainful spot is al so tender, but not always.
Note especially that the pain of acute appendicitis is in the epigastrium early and later in the RLQ. Pain in the spleen commonly radiates to the top of the left shoulder. These pains are ordinarily constant, in contrast to the intermittent pain of colic.
lymphadenitis, systemic lupus erythematosus (SLE), vasculitis, inammatory bowel disease (Crohn disease, ulcerative colitis);
Metabolic/Toxic: Familial
Mediterranean fever, AIP and variegate porphyria, ingestions, heavy metal
poisoning (lead, cadmium, arsenic, mercury), nonsteroidal anti-inammatory
drug (NSAID) gastroduodenitis, macrolide antibiotics; Mechanical/Traumatic:
Deceleration injuries especially with improperly worn lap seat belts, may
cause injury to the urinary bladder, bowel, mesentery, and intraabdominal
vessels; fracture of a solid organ, perforation of bowel, bladder, or gallbladder, obstruction of the cystic, common bile, pancreatic ducts, ureter, ureteropelvic junction, or bowel by stones, masses, parasites, or bezoars; volvulus or
strangulation of bowel in internal or abdominal wall hernias; penetrating and
blunt trauma, abdominal cutaneous nerve entrapment;
Neoplastic: Mass effect
of tumors pressing on other structures or causing traction on bowel or mesentery, hemorrhage into tumor, ischemia and necrosis of tumor, erosion into
or metastasis to blood vessels, nerves or adjacent organs;
Psychosocial: History
of physical, emotional or sexual abuse in childhood or as an adult; poisoning,
substance abuse with drug seeking, drug withdrawal; Vascular: Abdominal
aortic aneurysm or dissection, ischemic bowel, infarction of bowel or solid
organs, vasculitis, mesenteric venous thrombosis or emboli (bland, septic, or
atheroembolic), Henoch Schölein purpura, strangulation of hernias, rectus
sheath hemorrhage, retroperitoneal hemorrhage.
Chronic and recurrent abdominal pain. Chronic pain is physiologically
distinct from acute pain. The role of conditioning in the spinal cord and
thalamus with chronic pain is under study, as is the decreased threshold
to pain perception with visceral stimulation in some individuals with
chronic abdominal pain. The pain pattern and associated symptoms help
make inferences about pathophysiology, whereas location suggests the
organs involved. Pain that is vague in onset but steadily worsens suggests
progressive anatomic obstruction or mass effect. Intermittent symptoms
suggest painful smooth-muscle contraction from visceral obstruction,
relapsing infection, and recurring inammation or ulceration. A careful
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history identies precipitating factors (e.g., meals and type of food), timing
(e.g., relation to menstrual cycle or starting new medications), and previous
surgeries, symptoms, or illnesses that could help explain the current problem (e.g., adhesions from surgery or irradiation, trauma, infections, and
travel). Nonspecic abdominal and pelvic pain is a common presentation
of persons with a history of abuse. An empathetic, nonjudgmental history
with specic questions relating to current safety, sexual practices, sexual
abuse, and physical or emotional abuse is essential. Up to 30% of women
presenting to a physician in the ambulatory setting have a history of abuse,
and one-third of these have been abused within the last 12 months. The link
between abuse and abdominal pain is not understood. Many thousands of
dollars are wasted on fruitless laboratory and imaging investigations when
a few minutes of directed history might have produced the diagnosis. If the
history and physical exam do not suggest specic leads for further investigation, a barrage of laboratory and imaging tests are unlikely to be helpful.
There is a tendency to project pain arising in the abdominal wall inward
to intraabdominal structures. Identifying abdominal wall disorders avoids
many unnecessary studies.
CLINICAL OCCURRENCE: Congenital: Malrotation, familial pancreatitis,
polycystic kidney disease, porphyrias, familial Mediterranean fever, sickle
cell anemia, Meckel diverticulum, cystic brosis, hereditary angioedema;
Endocrine: Adrenal insufciency, hypothyroidism; Degenerative/Idiopathic:
Diverticulosis, diverticulitis, gastroesophageal reux disease, gastritis, pancreatitis, ovarian cysts, arthritis of axial skeleton, AAA, gastric ulcer, endometriosis; Infectious: Whipple disease, viral hepatitis (B, C), tuberculosis, Giardia,
duodenal and gastric ulcers, diverticulitis, chronic malaria, schistosomiasis,
visceral larval migrans, leishmaniasis, hookworm, roundworms, bartonellosis
(peliosis hepatitis), HIV, syphilis with tabes; Inammatory/Immune: Ulcerative
colitis, Crohn disease, gastritis, chronic pancreatitis, autoimmune hepatitis,
chronic cholecystitis, sclerosing cholangitis, pancreatic pseudocyst, celiac
disease, adhesions, peritonitis, SLE, sarcoidosis, retroperitoneal and mesenteric brosis;
cholelithiasis, nephrolithiasis, pancreatic duct stricture, sphincter of Oddi
spasm and stricture, biliary stricture, dumping syndromes; adhesions; ureteral obstruction, ureteropelvic junction obstruction, chronic hydrosalpinx;
Metabolic/Toxic: Heavy metal poisoning, porphyrias, ketoacidosis, uremia,
NSAID gastropathy and gastric ulcer; Neoplastic: Splenic and retroperitoneal
lymphoma, primary carcinomas of the esophagus, stomach, colon, pancreas,
liver, bile ducts, gallbladder, ovary; metastatic cancer to the liver (especially
from pancreas, colon, lung, breast, pancreatic islets, carcinoid), spleen (lymphoma), retroperitoneal lymph nodes (cervix, testis, lymphoma, melanoma,
bladder), and peritoneal surface (especially ovary); Neurologic: Postspinal
cord injury, postherpetic neuralgia, diabetic radiculopathy, diabetic autonomic neuropathy, abdominal cutaneous nerve entrapment; Psychosocial:
History of domestic, sexual, or child abuse, substance abuse, opiate withdrawal; Vascular: Intestinal ischemia, vasculitis, atheroemboli, abdominal
aortic or iliac aneurysm.
Mechanical/Traumatic: Partial bowel obstruction and strictures,
Nausea and vomiting. Nausea is an unpleasant sensation referred to the
stomach often suggesting that vomiting is imminent. Vomiting is an involuntary integrated movement of pharyngeal and thoracoabdominal smooth and
410 CHAPTER 9: The Abdomen, Perineum, Anus, and Rectosigmoid
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voluntary muscles to expel stomach contents. Nausea and vomiting are triggered by cortical (emotional), gastrointestinal (GI), vestibular, and chemical
(via the central nervous system chemoreceptor trigger zone) stimuli; vomiting
is coordinated by the brainstem.
vomiting often make them a presenting complaint. Vomiting is usually preceded by nausea. The history should include inciting events and exposures,
the nature of the vomitus and its relationship to meals.
Projectile Vomiting is a particularly forceful type associated with increased
intracranial pressure and lacking antecedent nausea. Retching involves all
movements of vomiting except that gastric contents are not expelled.
CLINICAL OCCURRENCE: Congenital: Pyloric stenosis; Endocrine: Adrenal
insufciency, pregnancy; Degenerative/Idiopathic: Pyloric stricture, gastroparesis, other GI motility disorders (e.g., scleroderma, pseudo-obstruction),
Ménière disease, glaucoma; Infectious: Viral gastroenteritis, CNS infections,
peptic ulcer (Helicobacter pylori); Inammatory/Immune: Numerous disorders
of the alimentary canal, biliary system, and pancreas, for example, hepatitis, pancreatitis, peritonitis; Mechanical/Traumatic: Upper GI obstruction;
Metabolic/Toxic: Bacterial food poisoning; drugs—opiates, ipecac, chemo-
therapy agents, macrolide antibiotics, chemical toxins, many more; uremia,
hepatic failure, ketoacidosis; cannabinoid hyperemesis; Neoplastic: Brain
tumors, primary or metastatic; Neurologic: Autonomic reexes associated
with visceral stimulation, for example, myocardial infarction, ureteral stone,
biliary colic, post-vagotomy, head injury with concussion, intracranial mass;
Psychosocial: Offensive tastes, odors, and sights; severe pain; psychogenic;
Vascular: Myocardial infarction, superior mesenteric ischemia (arterial or
venous), migraine.
The violence and discomfort of nausea and
Variants of Vomiting:
Abdominal bloating. See Distended Abdomen, page 416.
tion is caused by gaseous bowel distention, increased sensitivity to normal
bowel gas, enlargement of abdominal or pelvic organs, ascites, and masses.
Patients often try to induce burping, during which they swallow more gas.
Smoking, carbonated beverages, and chewing gum also lead to swallowing
gas. Patients with the irritable bowel syndrome have pain and complaints of
distention at intestinal gas volumes not sensed by others.
Belching, atus, and sensible peristalsis. See Tympanites, page 422, and
Bloating Syndromes, page 444.
Site-Attributable Symptoms
Abdominal wall pain. Injury to the muscles, nerves, skin, and soft tissues
of the abdominal wall, and pain referred from bones, nerve roots, and soft
tissues of the spine may present as abdominal pain. Well-localized (nger-
tip precise) pain suggests somatic body wall pain. Band-like pain described
as wrapping around the body suggests neuropathic pain, sclerotomal pain
from bone lesions, or myotomal pain originating in the muscles, tendons, or
ligaments at that segmental level. Pain exacerbated by specic motions and
tenderness to palpation support this diagnosis.
CLINICAL OCCURRENCE: Congenital: Urachus abnormalities; Degenerative/
Idiopathic: Xiphodynia; Infectious: Abscess, herpes zoster, pyomyo-
sitis; Inammatory/Immune: Suture abscess, mononeuritis, polyneuritis,
A bloating sensa-
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diabetic polyradiculopathy and amyotrophy, myositis; Mechanical/Traumatic:
Abdominal cutaneous nerve entrapment (rectus abdominis nerve entrapment
syndrome), abdominal wall hernia, abdominal wall muscle tear, rib cartilage
injury, rib tip syndrome, spinal disc herniation, burns, retention sutures,
foreign bodies; Metabolic/Toxic: Diabetic neuropathy; Neoplastic: Desmoid
tumors, lipoma, sarcoma, metastases;
drome, postherpetic neuralgia, mononeuritis multiplex, diabetic amyotrophy; Psychosocial: Abuse, somatization, malingering; Vascular: Vasculitis with
mononeuropathy or polyneuropathy.
Esophagus, Stomach, and Duodenum Symptoms
Regurgitation. See Heartburn below. Regurgitation is reux of esophageal
and stomach contents into the mouth or upper airway without active vomiting. It is passive, occurring under the inuence of normal body positions and
activities, suggesting poor esophageal sphincter function or increased intraabdominal pressure.
complaint. Ask about regurgitation while lying down, at night, or after meals.
Regurgitation while fasting produces a sour bitter taste (water brash or pyrosis), whereas postprandial regurgitation returns food. Regurgitation of food
more than 2 hours after eating suggests achalasia or delayed gastric emptying.
CLINICAL OCCURRENCE: Congenital: Abnormal lower esophageal sphinc-
ter (LES) and upper esophageal sphincter tone; Degenerative/Idiopathic:
Decreased LES tone with or without hiatal hernia, achalasia; Infectious:
Chagas disease; Inammatory/Immune: Esophagitis, scleroderma, CREST syndrome; Mechanical/Traumatic: Achalasia, gastric outlet and upper intestinal
obstruction, gastroparesis; Metabolic/Toxic: Alcohol, tobacco, caffeine, pepper-
mint, uremia; Neoplastic: Esophageal or gastric cardia cancer.
Unlike vomiting, regurgitation may not be volunteered as a
Neurologic: Complex regional pain syn-
Heartburn.
in the esophagus with or without esophagitis. Patients complain of burning
retrosternal pain aggravated by alcohol, tobacco, caffeine, large fatty or acidic
meals and obesity, frequently occurring after meals. Symptoms increase with
recumbency and are decreased by antacids. Gastroesophageal reux caused
by decreased LES tone is the most common cause.
Difculty swallowing—dysphagia. See also Chapter 7, pages 190 and 251.
Swallowing is a complex neuromuscular activity involving both consciously
controlled striated muscles and smooth muscle innervated by the autonomic
system and the intestinal myenteric plexus. Abnormalities in voluntary
motor function of the pharynx, smooth-muscle function, salivary function, or
mechanical obstructions in the pharynx or esophagus lead to dysphagia. Have
the patient indicate where the difculty is felt. Ask if the problem is greater
with liquids or solids.
ing indicating a pharyngeal or laryngeal problem. Regurgitating food after
meals may indicate esophageal obstruction by mass or achalasia. If swallowing is painful (odynophagia), infection, neoplasm, or erosions are likely.
Dysphagia lusoria (aberrant right subclavian artery). See Chapter 7, page
252. Pain is rarely present. The esophagram shows a transverse indentation
produced by an anomalous right subclavian artery arising from the descending aorta.
Regurgitation of gastric acid or bile produces chemical irritation
DDX: Ask whether they cough or choke with swallow-
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Pain with swallowing—odynophagia. See Six-Dermatome Pain with
Dysphagia in Syndromes, page 432.
Hematemesis.
mouth, pharynx, esophagus, stomach, duodenum, or, less frequently, the tracheobronchial tree. Bright red blood is arterial whereas dark blood is either
venous or has been in the stomach for some time. Exposure to gastric acid and
pepsin give blood a brown coffee grounds appearance.
mate the volume of blood lost. Patients frequently overestimate the amount,
especially if mixed with water, as in a sink or toilet bowl. Occasionally, the
patient has difculty distinguishing between hematemesis and hemoptysis,
especially when coughing induces vomiting. Hematemesis following prolonged and violent retching or vomiting is characteristic of a mucosal tear at
the gastroesophageal junction (Mallory–Weiss tear). If a bleeding site is not evident in the nose, mouth, or pharynx, upper endoscopy should be performed
for diagnosis and possible therapy.
CLINICAL OCCURRENCE: Congenital: Hereditary hemorrhagic tel-
angiectasia (HHT) (Osler–Weber–Rendu), Dieulafoy lesion; Endocrine:
Gastrinoma (Zollinger–Ellison syndrome), hyperparathyroidism; peptic
ulcer, Degenerative/Idiopathic: Duodenal diverticulum, gastritis; Infectious:
H. pylori ulcers; Inammatory/Immune: Gastritis, esophagitis; Mechanical/
Traumatic: Mallory–Weiss tear, portal hypertension (esophageal and gastric
varices), foreign bodies, gallstone erosion; Metabolic/Toxic: NSAID gastropa-
thy; Neoplastic: Cancer of the esophagus, stomach, and pancreas; Psychosocial:
Factitious; Vascular: Arteriovenous malformations, gastric antral vascular
ectasia, esophageal and gastric varices, portal gastropathy, thrombocytosis,
coagulation defects.
Small Intestine and Colon Symptoms
Diarrhea. See Syndromes page 445.
Constipation. See Syndromes page 451.
Bloody emesis indicates recent or active bleeding in the nose,
Ask the patient to esti-
Fecal incontinence. Loss of bowel control results from severe diarrhea of any
cause, rectal inammation, damage to the anal sphincters, or loss of normal
sensory, autonomic, or voluntary muscle function. Vaginal delivery commonly injures the anal sphincter and pelvic nerves accounting for the large
female predominance of fecal incontinence.
are most common in women, especially those in institutions. Evaluation of
mental status, and vaginal, neurologic, and rectal exams, including anal sensation and sphincter tone and strength, are necessary. Look for dementia, a
accid anal sphincter, rectocele, rectal prolapse, impacted feces, mass, and
sacral nerve decit. Further evaluation requires specialty consultation.
CLINICAL OCCURRENCE: Congenital: Cerebral palsy, mental retardation,
meningomyelocele; Endocrine: Hyperthyroidism; Infectious: Herpes simplex,
gonorrhea or cytomegalovirus proctitis, dysentery syndrome caused by bacterial infection, infectious diarrhea, perirectal abscess;
Ulcerative colitis, Crohn disease, ulcerative proctitis, microscopic colitis,
amyloidosis; Metabolic/Toxic: Drugs, especially cathartics, laxative abuse;
Mechanical/Traumatic: Fissure, stula, fecal impaction, pelvic oor relaxation,
Fecal and urinary incontinence
Inammatory/Immune:
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rectal prolapse, rectocele; Neoplastic: Anal or rectal carcinoma, metastatic invasion of the sacral plexus or spinal cord;
syndrome, transverse myelitis, sacral plexopathy, weakness or immobility,
Parkinson’s, peripheral neuropathy including diabetes, postherpetic neuralgia;
Psychosocial: Malingering, psychosis; Vascular: Ischemic colon, stroke.
Pruritus ani. Pruritus is the symptom, and excoriation and perianal skin
thickening (lichenication) are the signs. Patients may have a maddening,
uncontrollable desire to scratch, but relief is very short-lived. Pinworms are
common in children and in adults with young children. When the involved
skin is moist, the etiology may be bacterial or fungal infection (Candida). Poor
hygiene, contact allergies, irritation from bathroom tissue, and perianal dermatitis of unknown cause are also common.
Pain with bowel movements. See Anal Fissure, page 426.
Pelvic Symptoms
Pain in the perineum. Perineal pain accompanies many pelvic disorders and
can involve somatic or sacral sympathetic afferents. Take a history and per-
form a physical exam looking for pathology involving the rectum, anus, scrotum and its contents, vagina, pelvic oor muscles, pelvic bones, and perineal
skin.
CLINICAL OCCURRENCE: Infectious: Intertrigo, candidiasis, condyloma,
vaginitis, cervicitis, urethritis, cystitis, prostatitis, epididymitis; Inammatory/
Immune: Eczema, nonbacterial prostatitis, Bartholin gland inammation;
Mechanical/Traumatic: Thrombosed hemorrhoids, ssure in ano, stula in ano,
anal ulcer, cystocele, rectocele, testicular torsion or trauma, proctalgia fugax;
Neoplastic: Anal, rectal, bladder, prostate, vaginal, cervical, and uterine can-
cer; intramedullary tumors.
Neurologic: Dementia, cauda equina
Pelvic pain. See Abdominal Pain, pages 407 and 410 and Pelvic Pain,
Chapter 11, page 489.
Blood in the feces. Blood in the bowel eventually passes in the feces, its
appearance depending on the volume of blood, the bleeding site, and the transit time. Partially digested blood appears as bright blood, black loose stools
or frank melena. Small volumes of blood, insufcient to change stool color or
character, is occult bleeding. Immunochemical tests specic for human globin
chains quanties occult blood loss.
Black tarry stools—Melena. Fifty to sixty milliliters of blood in the stomach exposed to gastric acid and digestive enzymes produces a black, sticky
(tarry) stool. Black, but not tarry, stools occur with ingestion of iron, bismuth
and some fruits (e.g., black cherries and blueberries) or leafy green vegetables
(e.g., spinach and collard greens). Difculty cleaning the sticky stool from
around the anus characterizes melena but not other causes of black stools.
Melena can have a reddish hue and an acrid-sweet odor similar to creosote.
Bloody red stools—Hematochezia. Blood unchanged by passage through
the gut usually has entered the bowel in the colon, or passed very quickly
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through the gut. Blood is cathartic so large bleeds stimulate rapid transit.
Blood mixed with stool suggests bleeding onto partially formed stool in the
colon. The source of blood on the surface of an otherwise normal stool is near
the anus.
CLINICAL OCCURRENCE: Congenital: Congenital polyps and hamarto-
mas; HHT; pseudoxanthoma elasticum; von Willebrand disease; hemophilia;
Meckel diverticulum, Dieulafoy lesion; Degenerative/Idiopathic: Arteriovenous
malformations, colonic diverticulosis, duodenal diverticulum;
Acute Bloody Diarrhea, page 447, C. difcile colitis, typhoid enteritis, leptospirosis, herpes simplex esophagitis and proctitis, parasites; Inammatory/
Immune: Immune thrombocytopenia, ulcerative colitis, Crohn disease, gas-
tritis; Mechanical/Traumatic: Mallory–Weiss tear, ulcers, intussusception, anal
ssure, anal stula, fecal impaction, epistaxis, swallowed blood; Metabolic/
Toxic: Vitamin K deciency, scurvy, heavy metal poisoning, NSAIDs;
Neoplastic: Polyps or cancer anywhere in the GI tract, cancer invading the
bowel wall, for example, pancreatic cancer, gastrinoma (Zollinger–Ellison
syndrome);
nous malformations, ischemic bowel, erosion of AAA into the gut, gastric
antral vascular ectasia, esophageal varices, gastric varices, portal gastropathy, hemorrhoids.
Psychosocial: Factitious; Vascular: Thrombocytopenia, arteriove-
Infectious: See
ABDOMINAL SIGNS
Inspection
Jaundice. Technically, jaundice means yellow. Medically, jaundice means bili-
rubin staining of tissues and uids. Bilirubin stains all tissues, but jaundice is
most intense in the face, trunk, and sclerae. Jaundice is usually visible when
the serum concentration of conjugated bilirubin exceeds 3 mg/dL. Jaundice
is less visible in articial light than daylight. Long standing jaundice may
acquire a green hue. Yellow skin is also caused by carotene and rare chemical
toxins, conditions that must be distinguished from jaundice.
Normal Bile Pigment Cycle. When senescent erythrocytes are destroyed in
the spleen and other reticuloendothelial tissues, hemoglobin is metabolized
to unconjugated bilirubin, iron, and globin. Unconjugated bilirubin is insoluble in water and circulates bound to albumin, so it is not ltered by the
kidneys. The liver takes up unconjugated bilirubin, combining it with glucuronic acid to form water-soluble conjugated bilirubin. Conjugated bilirubin
is excreted into the bile and gut where bacterial enzymes convert it to urobilinogen. Most urobilinogen is lost in the feces, but some is reabsorbed and reexcreted in the bile (enterohepatic circulation) and urine. Excess water-soluble conjugated bilirubin in the blood is ltered by the kidneys and excreted in
the urine. Jaundice occurs with markedly increased production or impaired
hepatocellular uptake or conjugation of unconjugated bilirubin, excretion of
conjugated bilirubin, or obstruction of the intra- or extrahepatic bile ducts.
Scleral Color. Bilirubin is distributed uniformly throughout the sclera,
in contrast to the yellow subscleral fat that collects in the periphery, farthest
from the limbus. Carotene does not stain the sclerae.
Pruritus. Itching often accompanies obstructive jaundice and biliary cirrhosis. The intensity of the itching is usually proportional to the bilirubin concentration and the duration of jaundice.
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Urine Color. Conjugated, but not unconjugated, bilirubin is excreted in
the urine. High urine concentrations impart a dark-yellow to brown color and
a shaken specimen produces yellow foam, the bile salts lowering the surface
tension of water. Jaundice without urine darkening suggests unconjugated bilirubinemia. Acholic Feces: In complete biliary obstruction or with severe hepatocellular loss, the stools are malodorous and appear white or gray like clay.
Unconjugated hyperbilirubinemia. Hemolysis produces unconjugated biliru-
bin faster than maximal liver uptake, conjugation and excretion. Impaired
hepatic uptake or conjugation are less common causes. Stool color is normal.
Increased bilirubin in the gut leads to elevated urinary urobilinogen. The
urine contains no bilirubin because only water-soluble conjugated bilirubin is
excreted in the urine. Tests for intrinsic liver disorders are negative.
CLINICAL OCCURRENCE: Increased Production—Hemolysis of Normal
Red Cells. Autoimmune hemolytic anemia, transfusion hemolysis, hemoly-
sis from chemicals, drugs, or infections. Red Cell Defects. Sickle cell disease,
thalassemia, glucose-6-phosphate dehydrogenase (G-6-PD) deciency, pyruvate kinase deciency, paroxysmal nocturnal hemoglobinuria. Ineffective
Erythropoiesis. Thalassemia major, folate, and vitamin B12 deciency.
Miscellaneous. Absorption of hematoma, pulmonary infarction. Decient
Hepatic Uptake. Sepsis, fasting, hypotension, and drugs. Decient Hepatic
Conjugation—Congenital: Gilbert syndrome, Crigler–Najjar syndromes;
Acquired: Advanced hepatocellular disease, sepsis, competitive inhibition by
drugs metabolized to glucuronides.
Conjugated hyperbilirubinemia.
conjugated bilirubin into the bile canaliculi or obstruction of biliary ow
through the canaliculi, intrahepatic, and extrahepatic bile ducts to the duodenum. The feces may be acholic in which case the urine lacks urobilinogen
but contains bilirubin. The serum alkaline phosphatase is elevated out of
proportion to the transaminases.
mechanical extrahepatic obstruction from intrahepatic obstruction resulting
from mechanical obstruction or altered hepatocyte and canalicular function
(cholestasis). In extrahepatic obstructive jaundice dilated bile ducts are seen
by ultrasonography.
CLINICAL OCCURRENCE: Intrahepatic Cholestasis—Congenital: Dubin–
Johnson syndrome, Rotor syndrome; Acquired: Hepatocellular disease, drugs
(especially sex steroids), sepsis, hypotension, primary biliary cirrhosis.
Extrahepatic Obstruction—Intrinsic: Gallstones, biliary sludge, biliary car-
cinoma, sclerosing cholangitis, stricture, parasites; Extrinsic: Pancreatic carcinoma, porta hepatis lymphadenopathy, pancreatitis, pancreatic pseudocyst.
Mixed hyperbilirubinemia. This results from combined hepatocellular and
biliary tract injury which is common in advanced hepatobiliary disease of
almost any etiology.
The plasma contains both conjugated and unconjugated
bilirubin. The serum transaminase level depend upon the amount of active
hepatocellular injury and the remaining hepatocyte mass. The alkaline phosphatase is variably elevated. The primary etiology of hepatobiliary injury
needs to be distinguished from the secondary consequences (e.g., cirrhosis
or pigment stones). More than one process may be present. The stools may
This results from impaired excretion of
Clinically, it is important to distinguish
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