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436 CHAPTER 9: The Abdomen, Perineum, Anus, and Rectosigmoid
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is common after the rst few days. Without warning, the patient devel-
ops excruciating epigastric pain often with radiation to the back or ank.
Irritation of the left hemidiaphragm causes pain radiating to the left shoulder via the phrenic nerve afferents. Occasionally, the pain spreads over
the entire abdomen (generalized peritonitis) or primarily to the RLQ. The
pain is knife-like with a boring quality, going directly through to the back.
Because pain is aggravated when supine, the patient may sit leaning forward or curl up in the fetal position. Retching and vomiting are severe. The
symptoms are more intense and prolonged than with a perforated stomach.
Shock can occur. Since the process is conned to the retroperitoneum, there
is often a disparity between the severity of symptoms and the paucity of
abdominal ndings. Epigastric tenderness is always present, but muscle
rigidity is usually absent; when present, it is conned to the epigastrium.
Occasionally a tender transverse mass is felt deep in the epigastrium. Two
or three days after onset, blue or green ecchymoses can appear in the ank
(Turner sign) or the umbilicus (Cullen sign) from extravasation of hemolyzed
blood. Pseudocysts (an accumulation of blood, necrotic debris, and uid
in the retroperitoneum) are a late complication; they are rarely palpable.
Acute pancreatitis may be an acute exacerbation of chronic, relapsing pancreatitis. Common causes of acute pancreatitis are alcohol and gallstones.
Other causes include hypertriglyceridemia, pancreatic ductal obstruction
and stricture, pancreas divisum, perforated peptic ulcer, ampulla of Vater
dysfunction, mumps, and drugs.
Mesenteric ischemia. The superior mesenteric artery and vein are most
commonly affected, by either embolism or thrombosis. Half of patients
with arterial thrombosis have a history of postprandial abdominal
pain. Arterial occlusion produces the typical clinical picture. There is
sudden onset of severe epigastric pain minimally relieved by narcotics followed by distention, ileus, and vomiting. Blood may pass per
rectum. There are few localizing signs though a tender mass may be
palpated in the epigastrium. Venous thrombosis often presents atypically. There is a severe metabolic acidosis as endotoxemia and shock
supervene. Common causes are atherosclerosis, atheroembolism, bromuscular dysplasia, acute bacterial or fungal endocarditis, embolism
of mural cardiac thrombus, nonbacterial thrombotic (marantic) endocarditis, and thrombophilic states including paroxysmal nocturnal
hemoglobinuria.
Aortic dissection. See Chapter 8, page 354. Dissections extending into
the abdominal aorta may produce abdominal and back pain, pain in
the groins. Occlusion of the abdominal branches of the aorta produces
ischemia in the downstream tissues. Epigastric pain can be associated
with involuntary abdominal muscle splinting. The blood pressure is initially unaffected. Branches of the abdominal aorta can be progressively
occluded. Spinal cord ischemia causes paraplegia. Unequal pulses are
important clues for diagnosis. Dissection may be slow and symptomless. Etiologies to consider include hypertensive vascular disease, giant
cell arteritis, arteriosclerosis, Marfan syndrome, and pseudoxanthoma
elasticum.
Abdominal aortic aneurysm leak and rupture. AAA is often painless
until it leaks blood into the adventitia and retroperitoneal space. Pain is
Renal stone colic
Small intestine colic
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moderate to severe, usually well localized, and often accompanied by
nausea. Pain may radiate to one or both groins. Pain in the back and
ank can dominate the presentation. Gentle palpation and urgent diagnosis are necessary.
Acute RUQ Pain: The liver, gallbladder, duodenum, head of the pancreas,
right kidney, and pleural reections of the right lung are the leading causes
of RUQ pain. Failure to consider pneumonia with pleural involvement and
myocardial infarction in the differential diagnosis can lead to inappropriate
abdominal surgery.
Cholelithiasis with biliary colic.
Gallstones, composed of cholesterol and/
or bile pigments, rarely cause symptoms unless a stone obstructs the cystic
duct, common bile duct, or pancreatic duct, or perforates the gallbladder wall.
Forceful peristaltic contractions against a stone impacted in an obstructed duct
produces colic. An attack of biliary colic may be uncomplicated or associated
with acute cholecystitis, obstructive jaundice, and/or gallstone pancreatitis.
Onset of pain in the epigastrium or RUQ is sudden with radiation to the inferior border of the right scapula (Fig. 9-33). The pain is severe, recurring in cyclic
paroxysms, and associated with nausea and vomiting. During the attack, the
RUQ is rigid. Ultrasonography is diagnostic. Calcied gallstones are seen on
plain X-ray lms. Gallstones are common in patients with hemolytic anemias
and in certain racial groups, e.g., Native Americans. Stones are more prevalent
with obesity, female sex, multiparity, diabetes, and some drugs.
Acute cholecystitis. Cystic duct obstruction, usually by gallstone impac-
tion, results in distention and sterile inammation of the gallbladder wall.
Acalculous cholecystitis complicates surgical or medical illness with progressive gallbladder enlargement, ischemia, and rupture with high mortality. The
Scapula
Gallstone colic
Large bowel colic
FIG. 9-33 Locations of Abdominal Colic. Colic is notable for its paroxysmal occurrence, severity, and crescendo–
decrescendo cycling. It occurs when a hollow viscus is obstructed. Pain results from smooth-muscle contractions trying to
overcome the obstruction. Note the radiation of gallstone colic from the RUQ to the angle of the right scapula posteriorly. The
colic of renal calculus frequently radiates to the testis on the same side.
Testes
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onset is acute or subacute, the pain is poorly localized, and may radiate to
the top of the right shoulder. Episodes of mild postprandial RUQ pain may
precede an acute attack. Nausea and anorexia are usual; vomiting, although
less common, may be severe. The gallbladder, felt at the inferior margin
of the liver, is tender. Pressing under the right costal margin as the patient
inspires produces inspiratory arrest (Murphy sign). Fist percussion over the
liver produces pain with acute cholecystitis and acute hepatitis. The abdomen is not rigid unless peritonitis is present. Sometimes the gallbladder is
palpable as an exquisitely tender globular mass below liver edge. Fever is
usual, but high fever or chills suggests ascending cholangitis or suppurative
cholecystitis. Ultrasonography demonstrates the thickened, edematous gallbladder wall with luminal sludge or stones. Gallstones are the most common
cause, including microlithiasis with sludge. Uncommonly, parasites, bacterial infection, and primary biliary cancer precipitate attacks. The diagnosis
is conrmed with a radionuclide scan conrming cystic duct obstruction.
Hospitalized patients who have been fasting for many days, can have falsepositive radionuclide studies because the uid-lled gallbladder does not
easily contract.
Acalculous cholecystitis—gallbladder hydrops. A dilated gallblad-
der with poor muscular contractions results in a thin tense edematous wall predisposed to rupture. This is an infrequent but serious
complication of other serious medical and surgical illnesses. It is
asymptomatic or accompanied by epigastric pain, nausea, and vomiting. There is fever and RUQ tenderness and a tender RUQ mass may
be appreciated.
Acute RUQ pain—gallbladder rupture, bile peritonitis. Gallbladder per-
foration is a consequence of an eroding stone, infection, ischemic necrosis, or postoperative leak. Bile is extremely irritating to the peritoneum,
producing a chemical peritonitis. The initial picture suggests cholecys-
titis or gallstone colic, but the pain gradually spreads throughout the
abdomen with signs of generalized peritonitis progressing to prostration
and shock.
Leaking duodenal ulcer. Small duodenal perforations leak duodenal con-
tents into the retroperitoneum and right abdominal gutter producing localized inammation. The presentation is RUQ pain, tenderness, and rigidity.
Pain may radiate through to the back. There may be a history of peptic ulcer
disease. The tenderness is midline without peritoneal signs. The spill can
track into the RLQ leading to RLQ pain and mass (Fig. 9-32).
Ureteral colic. Acute ureteral obstruction induces vigorous intensely painful
peristaltic ureteral smooth muscle contractions. The pain localizes poorly
and can radiate to the testicle, vulva, or groin. Proximal obstructions radiate
pain to the ank (see Fig. 9-33). Patients are restless, frequently changing
position seeking comfort. Anorexia is constant, nausea and vomiting can be
severe. Microscopic hematuria is expected and sometimes gross hematuria
occurs. A calcium-containing stone may be seen on plain X-ray lms. DDX:
Patients with peritonitis, pancreatitis and leaking aneurysms prefer to hold
still, not move.
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Acute pyelonephritis. Infection, usually ascending from the bladder, produces
inammation and swelling in the kidney, distending the capsule and producing pain. Upper quadrant and ank pain is poorly localized and exacerbated
by st percussion at the CVA. The pain may be severe and accompanied by
nausea. RUQ tenderness is deeper and less severe than with acute cholecystitis.
Urinalysis and culture are usually diagnostic. In women with recurrent infections or men with a rst infection, suspect congenital or acquired anatomic
abnormalities in the urinary tract (stones, tumor, diverticulum, etc.).
Renal or pararenal abscess.
progressive necrotizing pyelonephritis spreads into the perinephritic space
and can track along tissue planes into the pelvis. The patient has abdominal
pain radiating into the groin with CVA tenderness and fever. If the cortex, but
not the medulla, has been seeded by bacteremia, pyuria may be absent.
Acute hepatitis. Acute hepatic inammation resulting from hepatocyte injury
and secondary inammation is a consequence of infections, alcohol, or drugs.
Acute parenchymal swelling distends Glisson capsule causing pain. Fever,
malaise, and anorexia are usually present. Smokers may lose their taste for
cigarettes. The entire liver edge is tender, blunt, and smooth. Fist percussion
over the liver produces a dull aching pain. Jaundice appears after several days.
Pleurisy. Right lower lobe pneumonia can present with RUQ pain and no
ndings on abdominal exam. When breathing accentuates pain, breaths
become shallow. A pleural rub and signs of pneumonia should be sought.
Chest X-ray is mandatory when evaluating upper abdominal pain.
Acute LUQ Pain: The spleen, stomach, left kidney, splenic exure of the colon,
and pleural reections of the left lung base are the most likely sources of LUQ
pain.
Splenic infarction.
ture creates a low redox environment susceptible to ischemic injury. Severe,
sharp pain develops in the LUQ with splinting of the abdominal muscles.
Pain frequently radiates to the top of the left shoulder. Fever and leukocytosis may be present. A splenic friction rub may be heard. CT identies
splenic infarction resulting from emboli (e.g., endocarditis), vasculitis, or
in situ vascular occlusion (as with sickle cell disease). Splenomegaly from
polycythemia vera, chronic myelocytic leukemia, and myelobrosis can
also lead to infarction.
The spleen is highly vascular, and the sinusoidal struc-
Often complicating urinary tract obstruction,
Ruptured spleen.
infarction can rupture either spontaneously or with minimal trauma. Large,
soft spleens have been ruptured by palpation. Intense pain occurs in the LUQ,
radiating to the top of the left shoulder (Kehr sign). The pain may be accentuated by elevating the foot of the bed, increasing contact between peritoneal
blood and the diaphragm. Abdominal CT scan is diagnostic.
Pyelonephritis, ureteral colic, and pararenal abscess. See RUQ pain above.
Pleurisy. See RUQ pain above.
A spleen enlarged by infectious mononucleosis, sepsis, or
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Acute RLQ Pain: The cecum, appendix, and terminal ilium are usually located
in the RLQ, each with unique inammatory disorders.
Acute appendicitis. Obstruction of the appendix leads sequentially to
inammation, transmural inammation involving the peritoneum, ischemia, perforation, and localized or generalized peritonitis. Appendicitis
usually results from impaction of fecal material or foreign matter in the
appendicular lumen. Less commonly, carcinoid tumors, vasculitis, or
lymphoma are implicated. Initial pain, mediated by vagal afferents, is
poorly localized, accompanied by nausea and vomiting, and referred to
the epigastrium. Local peritonitis, sensed by peritoneal somatic afferent
nerves, is sharper locating to the appendix, commonly the RLQ. Generalized peritonitis pain is diffuse sharp and accompanied by generalized
abdominal and systemic signs. Poorly localized epigastric pain without
epigastric tenderness is usually the rst in a predictable sequence of
symptoms and signs. Nausea or vomiting may occur. As the pain worsens, it shifts to the RLQ accompanied by fever and leukocytosis. Until
localization occurs appendicitis is often not considered. With a different
sequence of events, the diagnosis of appendicitis should be questioned.
Deep tenderness often starts a little more than halfway between the umbilicus and the anterior superior iliac spine. When the appendix is retrocecal there is less RLQ tenderness. With pelvic appendicitis the RLQ is not
tender, but the peritoneal pouches may be tender on rectal examination.
Acute appendicitis with perforation. Cecal edema and inammation,
felt as a tender mass (phlegmon), is indistinguishable from contained
perforation with abscess. Perforation without containment transiently
reduces the pain, only to increase over a couple of hours as generalized peritonitis with intense involuntary abdominal muscle rigidity
supervenes. Variant presentations occur depending on the location of
the appendix.
back muscles are inamed with tenderness below the twelfth rib on the
right. Psoas irritation causes the right hip to be held in exion or rigid
extension. Flexing and extending the thigh against resistance aggravates the pain (iliopsoas test, Fig. 9-13A, page 403). An appendiceal
abscess lying medially behind the ileum can involve the right ureter
causing painful urination and pyuria. Intrapelvic appendix. When the
appendix is in the true pelvis there is diffuse suprapubic pain and the
abdominal muscles are not rigid. Bladder and rectal irritation causes
painful urination and tenesmus. Rectal exam discloses a tender mass in
the peritoneal pouch. If the abscess contacts the obturator muscle, exing the thigh and rotating the femur internally and externally produces
suprapubic pain (obturator test, Fig. 9-13B). Typhlitis, Crohn disease,
pelvic inammatory disease, ovarian disease, and ectopic pregnancy
are frequently in the differential.
Neutropenic enterocolitis (typhlitis, cecitis). Neutropenia, particularly
following chemotherapy for acute leukemia, is associated with acute
inammation of the cecum, progressing rapidly to ischemia with bloody
diarrhea and perforation. Aerobic gram-negative bacteria play a role and
bacteremia is common. Symptoms and signs are like acute appendicitis,
although the patient may be more toxic early on. CT reveals the thick
cecal wall.
Extrapelvic appendix. With retrocecal perforation the
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Terminal ileitis (Crohn disease, regional enteritis). See page 448.
Perforated peptic ulcer. See page 435.
Acute LLQ Pain: The left lower quadrant is lled with colon which is the
source of most LLQ pain.
Diverticulitis. Diverticulosis is common and usually asymptomatic.
Obstruction of a diverticulum can lead to inammation, abscess, and perforation (diverticulitis). LLQ pain and tenderness may be accompanied by
muscular guarding. Pelvic diverticulitis cannot be distinguished clinically
from pelvic appendicitis, though prior diverticulitis and appendectomy favor
diverticulitis. CT is required to distinguish between perforations of a rightsided diverticulum, a colon cancer, or a ruptured appendix.
Acute Suprapubic Pain: Acute suprapubic pain most often results from pel-
vic pathology. Visceral pain from the pelvic organs localizes poorly until the
peritoneum is involved.
Urinary bladder rupture. Blunt abdominal trauma can burst a full blad-
der. Pelvic fractures can directly lacerate the bladder. Perforation is into
the peritoneal cavity or retroperitoneum. Urine leaking into the perito-
neal cavity produces mild peritonitis with suprapubic pain and tenderness. The usual bladder is not felt above the prostate on rectal or vaginal
exam. Urine leaking into the retroperitoneum dissects to the perineum
producing palpable bogginess about the rectum and vagina on rectal
exam. Scrotal swelling can occur, but it is not as pronounced as after a
severed ureter.
Acute salpingitis (pelvic inammatory disease). See Chapter 11, page 498.
Ovarian torsion.
An ovarian cyst or mass increases the likelihood of the
ovary twisting on its mesentery producing strangulation.
is accompanied by vomiting and tenderness over the ovarian mass.
Ectopic pregnancy. See Chapter 11, page 498.
Diabetic radiculopathy (diabetic amyotrophy).
thoracic pain follows ischemic or inammatory radiculopathy of one or more
thoracic and/or lumbar spinal nerves. This is unrelated to the duration or
control of the diabetes. Dermatomal pain and allodynia and weakness of the
muscles supplied by affected nerves are demonstrable by careful physical
exam. This is often mistaken for an acute intraabdominal event because of the
acuity and severity of the pain. The pain persists for 6 to 24 months or longer.
EMG is diagnostic.
Subacute Abdominal Pain Syndromes
Diabetic radiculopathy (diabetic amyotrophy). See above.
Abdominal angina (visceral ischemia, intestinal ischemia). The increased
intestinal oxygen demand required for digestion and absorption of food
Sudden pelvic pain
Acute abdominal and/or
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following a meal exceeds the supply because of mesenteric artery obstruction. Because of limited collaterals, the bowel perfused by the inferior mesenteric artery is most vulnerable. Visceral ischemia is characterized by the
triad of postprandial pain, anorexia from fear of eating, and weight loss.
The pain is usually in the upper abdomen or periumbilical and sometimes
radiates to the back. It is typically intermittent, coming on 30 minutes after
eating and persisting from 20 minutes to 3 hours. Sometimes there is no
relationship between meals and pain. Diarrhea, occasionally bloody, is frequent. Sometimes a short systolic bruit is heard in the epigastrium or umbilical region.
though these patients develop gastric and esophageal varices.
Pancreas carcinoma. Pain results from acute or chronic pancreatitis or invasion of retroperitoneal structures and celiac plexus. Retroperitoneal invasion
causes constant, dull, poorly localized pain in the mid epigastrium, ank,
or back. When the head of the pancreas is involved painless persistent jaundice is the rule. As the tumor enlarges, the triad of pain, weight loss, and
jaundice is nearly universal. The rst sign of pancreatic carcinoma may be
migrating supercial thrombophlebitis (Chapter 8, page 379), recurrent deep
vein thromboses (Trouseau syndrome), or nonbacterial thrombotic endocarditis
(marantic endocarditis, Chapter 8, page 358).
Rectus hematoma. The epigastric artery and vein run vertically within the
rectus sheath. Hemorrhage within the sheath above the arcuate line is conned within the sheath, but hemorrhage below the arcuate line dissects into
the lateral abdominal wall. Inciting events are direct trauma, coughing, para-
centesis, and operative injury. Debilitated and anticoagulated patients are
especially susceptible. The mass may be tender and painful. Though often
mistaken for an intraabdominal mass, the hematoma remains palpable when
the abdominal wall is tensed, while an intraabdominal mass is obscured
(Fig. 9-26, page 425). Ultrasonography or CT is diagnostic.
DDX: Similar symptoms are seen with mesenteric vein occlusion
Chronic and Recurrent Abdominal Pain
Chronic abdominal pain. See page 408. Pain is the presenting symptom
for many chronic abdominal disorders. Chronic disease usually produces
less severe pain in the same location as an acute process (Fig. 9-19, page
408).
Recurrent abdominal pain. Recurrent pain suggests an intermittent mechanical problem, a partially treated inammatory disorder, or an episodic metabolic/toxic syndrome.
CLINICAL OCCURRENCE: Congenital: Porphyria, sickle cell disease, familial
Mediterranean fever, other familial fever syndromes; Degenerative/Idiopathic:
Chronic pancreatitis, sphincter of Oddi dysfunction; endometriosis;
Chronic hepatitis, schistosomiasis, H. pylori ulcers and gastritis; Inammatory/
Immune: SLE, autoimmune gastritis; Mechanical/Traumatic: Biliary colic, ure-
teral colic, adhesions, and partial bowel obstruction; Metabolic/Toxic: Lead
poisoning; cannabinoid hyperemesis; Neoplastic: Partial bowel obstruction from luminal masses; Psychosocial: Domestic, sexual, and child abuse;
Vascular: Mesenteric ischemia.
Infectious:
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Cannabinoid hyperemesis. Long-term use of cannabis leads to cyclic episodes of nausea, epigastric or periumbilical abdominal pain, and hyperemesis. Most commonly patients are under age 50 and use cannabis daily. Hot
showers relieve the symptoms temporarily leading to compulsive showering.
Symptoms resolve with cessation of use.
Abdominal wall pain syndromes. Look for point tenderness (trigger points)
not abolished by contracting the abdominal muscles, sensitivity to light touch
by clothing (hyperesthesia or allodynia), abdominal wall defects (with or without hernia), masses, surgical and varicella-zoster scars, and abdominal wall
weakness or asymmetry. Injecting local anesthetic into trigger points frequently answers the diagnostic question.
disorders referring pain to the abdomen.
DDX: Fully examine the spine for
Abdominal cutaneous nerve entrapment.
es from T7 to L1 become entrapped as they pass through the rectus sheath.
Entrapment can occur from overuse of the rectus muscles or weight gain
increasing traction on the nerve. The pain usually occurs lateral to the entrap-
ment site and is increased by tensing the rectus muscles. Pain is reproduced
by pressure over the small fascia defect marking the exit site and is relieved
by trigger point injection.
Chronic epigastric pain. See the discussion of Acute Epigastric Pain, page
434.
Xiphoid-sternal arthritis. Epigastric or retrosternal pain radiates around to
the back and is reproduced by palpating the xiphoid-sternal joint. Injecting
local anesthetic gives complete relief.
pectoris, peptic ulcer, hiatal hernia, biliary colic, or chronic pancreatitis if the
xiphoid cartilage is not specically palpated.
Peptic ulcer.
gastrin-secreting islet cell tumor (Zollinger–Ellison syndrome). Ulcer pain
is caused by gastric acid irritating exposed nerves.
predictably 1–4 hours after meals and is relieved by food, H2 blockers, and
antacids. The symptoms are similar whether the ulcer is gastric, pyloric,
duodenal, anastomotic, or marginal. Ulcer pain is aggravated by fasting,
drinking alcohol, or coffee. The pain is described as gnawing, aching, burning, or hunger and is felt in the epigastrium near the xiphoid, sometimes
radiating to the back. The pain varies from mild discomfort to severe and
may awaken the patient from sleep. Untreated, ulcer symptoms may recur
with periods of pain lasting from a few days to several months. Frequently
there is moderate tenderness localized to the epigastrium. Endoscopy is
diagnostic.
Peptic ulcer is caused by H. pylori infection, NSAIDs, or
Anterior cutaneous nerve branch-
DDX: This may be mistaken for angina
Epigastric pain occurs
Pyloric obstruction.
rus from peptic ulceration. Pain is not invariable but, if present, it ranges
from vague discomfort to colicky epigastric pain, usually soon after eating. Emesis of undigested food eaten many hours or days before can occur.
Abdominal palpation may elicit a succussion splash. Anatomic outlet
Usually obstruction results from scarring of the pylo-
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obstruction must be distinguished from pylorospasm caused by peptic ulcer
and gastroparesis.
Postgastrectomy syndrome.
sphincter function after subtotal gastrectomy often causes uncontrolled
dumping of hypertonic stomach contents into the small intestine. The large
amount of uid in the small bowel and increased intestinal motility contribute
to the symptoms. Gastric stapling procedures create a defunctionalized pouch
which can develop inammation (pouchitis) and the small remnant stomach
can be a source of postprandial discomfort.
shortly after eating, the patient experiences epigastric discomfort without
pain, weakness, sweating, nausea but not vomiting, tachycardia, palpitation,
and epigastric fullness. Reclining may relieve the symptoms. Foods with high
osmotic loads exacerbate the symptoms. Late Dumping Syndrome occurs
more than 2 hours after eating with symptoms of sweating, trembling, weakness, hunger, nausea, vomiting, and, rarely, syncope.
Chronic pancreatitis. See page 450.
Gastric carcinoma. Pain is usually preceded by anorexia, weight loss, and
weakness. The pain is a steady, unremitting ache in the epigastrium, sometimes radiating to the back, or resembles peptic ulcer pain.
Chronic RUQ pain. See the discussion of RUQ Pain, page 437.
Chronic cholecystitis with or without cholelithiasis. See page 437.
Hepatocellular carcinoma.
er, particularly following chronic hepatitis from hepatitis B and/or C viruses.
Abdominal pain is the most common symptom. A hard, nodular, localized
liver mass with centrifugal extension may be palpable, sometimes with an
overlying peritoneal friction rub. A bruit may be heard.
Losing gastric storage capacity and pyloric
Early Dumping Syndrome occurs
Hepatocellular carcinoma arises in a cirrhotic liv-
Metastatic carcinoma. Pancreatic and colon cancers frequently metastasize
to the liver via the portal vein. Metastases from lung and breast cancer are
also common. Poorly localized upper abdominal pain or discomfort, usually
without abdominal distention or mass, is a common presentation. Most often the liver is diffusely stony hard. When a single discrete liver mass is felt,
also suspect hepatocellular carcinoma or abscess. Peritoneal friction rubs and
bruits are rare.
Bloating and Distention Syndromes: Bloating and distention are common
complaints associated with mechanical or functional bowel obstruction and
abnormal digestion. These symptoms are often unaccompanied by abdominal distention or obstruction on exam. Visceral hyperalgesia may explain this
discrepancy.
Stomach distention. Gastroparesis is a consequence of reex loss of gas-
tric tone following abdominal surgery or upper intestinal inammation,
autonomic neuropathy as in diabetes, vagotomy, or decreased bowel
motility associated with chronic illness and bed rest. In acute distention,
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the patient, often bedridden from another disorder, becomes acutely more
ill with vomiting, upper abdominal distention, and hypotension. The
greatly dilated stomach lls the epigastrium, rarely reaching to the pelvis. There is tympany on LUQ percussion and often a succussion splash.
Visible peristalsis can be present initially. Later, weak or absent peristaltic sounds indicate ileus. Nasogastric suction yielding a large volume
of uid resolves the distention. The major provocative factors are pain,
abdominal trauma, and immobilization. Postoperative cases are common.
Chronic gastroparesis is more frequent, less dramatic, and more difcult to diagnose. Glucose control in diabetics is difcult because of the
irregular
hours after eating suggests gastroparesis. Diabetes mellitus is the most
frequent cause, but other causes of visceral autonomic neuropathy should
be considered.
Ascites. See page 416.
Irritable bowel syndrome. See page 452.
Lactose and fructose intolerance. See page 448.
Diarrhea Syndromes
Diarrhea. Diarrhea is >200 g of stool per day on a Western low-residue
diet. “Diarrhea” is also used to describe watery or loose stools, or increased
stool frequency. Several general pathophysiologic mechanisms underlie
increased fecal volume and stool water loss. Osmotic diarrhea results from
ingestion of nonabsorbable osmotically active solutes that draw water
into the bowel.
(e.g., Zollinger–Ellison syndrome) or secretion of abnormal uid into the
lumen (e.g., cholera). Inammatory/immune diarrhea results from inammation of the bowel wall with exudation of uid, proteins and cells, usually
combined with increased motility and decreased absorption. Increased
bowel motility decreases the time available for absorption of solutes (small
intestine) and water (colon).
the former from loss of effective absorptive surface (e.g., celiac disease),
and the latter from inadequate digestion of food (e.g., pancreatic insufciency). Short bowel syndrome results in loss of absorptive surface (surgical
resection or stulas) and bile acid malabsorption producing colonic irritation.
chronic, or recurrent. Second, obtain a detailed description of the stools,
their frequency, and pattern. Ask specically about nocturnal diarrhea,
which is always pathologic. Third, focus on exposures (travel, drugs, previous surgery, dietary habits, contact with others with a similar illness), and
associated symptoms (anorexia, nausea, vomiting, fever, weight loss, or
abdominal pain). On completion of the history formulate a hypothesis for
the diarrhea’s pathophysiologic mechanism(s). During physical exam look
for signs of weight loss, volume depletion, increased bowel motility (borborygmi), and abdominal distention and/or tenderness. Laboratory evaluation is usually not required for suspected viral diarrhea. If you suspect
a bacterial or protozoal etiology, stool culture and tests for bacterial and
protozoal antigens are necessary. Always inspect atypical stool. Diarrhea in
gastric emptying. Nausea and emesis of undigested food several
Secretory diarrhea results from increased normal secretions
Malabsorption and maldigestion cause diarrhea,
First, determine exactly what is meant by diarrhea, and if it is acute,
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