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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2853_Библиотеки_им_академика_М_И_Перельмана
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426 CHAPTER 9: The Abdomen, Perineum, Anus, and Rectosigmoid
B. ShallowA. Normal
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Lymp
nodes
Aort
Kidne
FIG. 9-27 Shallow Abdominal Cavity. A. Normal small paraaortic lymph nodes are not palpable. B.
Massive enlargement of prevertebral and preaortic lymph nodes. These cannot be distinguished from other
retroperitoneal masses by palpation; they give the impression that the abdomen is shallower than normal.
Lymphadenopath
PERINEAL, ANAL, AND RECTAL SIGNS
Inspection
Pruritus ani. See symptoms page 413.
Prolapsed rectal polyp. When pedunculated, polyps in the lower rectum may
prolapse from the anus as spherical masses.
Hemorrhoids.
They may dilate in normal people forming hemorrhoids. Hemorrhoids are
more common and severe with portal hypertension or IVC obstruction.
Internal hemorrhoids (Fig. 9-3) are irregular globular masses covered with
rectal mucosa arising above the pectinate line. They may prolapse into the
anal canal (Fig. 9-28C). External hemorrhoids arising below the pectinate line
are covered with skin. When thrombosed, they are purple-red, rm, and very
painful (Figs. 9-28B and 9-29). They can appear white when the overlying
skin is edematous.
Fistula in ano. Most stulae in ano arise from anal crypt (crypts of Morgagni)
abscesses and track to the perianal skin. Look for a small sinus track opening
in the perianal skin (Fig. 9-28D). The internal orices of the tracks are just
above the pectinate line (Fig. 9-3 page, 396). Do not probe stulas from the
skin. Gentle palpation around the external orice may reveal the track as a
subcutaneous cord. The origin is inferred from the location of the stula on
the perineum (Fig. 9-30A). DDX: Chronic lesions stimulate a hypertrophied
anal papilla (sentinel pile). Multiple stulas suggest Crohn disease or tuberculous proctitis.
Submucosal hemorrhoidal veins are normal anal cushions.
Fissure in ano. Anal sphincter spasm causes the extreme pain associated with
ssures. If the patient presents with pain, do not attempt a digital rectal exam
before inspecting the mucosa by retracting the skin on both sides looking for
the ssure posteriorly (Fig. 9-30B). It is an extreme unkindness to the patient
to attempt further examination without giving either local anesthetics or
Perineal, Anal, and Rectal Signs 427
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FIG. 9-28 Some External Anal Findings. A. Rectal prolapse appears as a red doughnut of most rectal mucosa
protruding through the anus. B. Thrombosed external hemorrhoids are semispheric masses of erythematous skin at
the mucocutaneous junction with the anus. C. Internal hemorrhoids are mucosal masses sometimes seen through the
retracted anus. D. Fistul as opening on t he skin are acco mpanied by a pap ule of hyper trophied sk in on the margi n of the orifice.
FIG. 9-29 Hemorrhoid. External Hemorrhoid with a small skin break that resulted in bleeding.
analgesics. The ssure is a slit-like separation of the supercial anal mucosa,
suggesting a longitudinal tear. It rarely becomes an ulcerating crater.
Sentinel pile. This term is applied to two structures. More commonly, it refers
to a hyperplastic skin tag found external to a ssure in ano. Resembling an
external hemorrhoidal tag, it is also called a brous anal polyp. The name also
is applied to a hypertrophied anal papilla internal to a ssure in ano (Fig. 9-3).
428 CHAPTER 9: The Abdomen, Perineum, Anus, and Rectosigmoid
B. Retraction of the anusA. Fistulae in the
Area of fistula
draining fr
posterior anal cana
perineum
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l
Area of fistulae
draining from
anterior anal canal
(semicircle with
radius 2.5 cm.)
Usual site of
coccygeal fistula
om
e
FIG. 9-30 Examination of the Perineum. A. Fistulae in the perineum. The dark blue semicircular area anterior
to the anus, with a radius of 2.5 cm, indicates the location of fistulae draining from the anterior surface of the anal canal
(Salmon l aw). Anal fi stulae drai ning to the skin in the light blue area ar ise in abscess es from the pos terior sur face of the cana l.
A coccygeal (pilonidal) fistula is usually in the midline, near coccyx or sacrum. B. Retracting the anus. This is a method
of stretching the anal orifice to inspect for fissure in ano, external hemorrhoids, or prolapsing internal hemorrhoids or polyps.
This lesion arises from the pectinate line, whereas an internal hemorrhoid
arises above it.
Rectal prolapse. When the patient strains as if to defecate, the rectal mucosa
everts below the sphincter (Fig. 9-28). When symptoms suggest prolapse
but the procedure fails to demonstrate it, have the patient squat and strain
in the position for defecation. The prolapse can be mucosal or complete.
Palpation
Anal stricture. Congenital strictures present as narrow crescentic folds at
the rectal end of the anal canal. Fibrous strictures in the same region usually
result from surgery for internal hemorrhoids. Radiation therapy can produce
a sharply delimited stricture.
Carcinoma of the anus. Squamous cell carcinoma of the anal skin is caused
by human papillomavirus infection. It is most common in homosexual men
practicing anal-receptive intercourse. Its incidence is greatly increased in
HIV-infected men. The tumor presents as an exophytic or ulcerating mass
narrowing the anal canal.
Rectal carcinoma. Cancer may cause plateau-like, nodular, annular, or cauliower rectal mass. Endoscopic visualization and biopsy are essential.
Fibrosis of anal sphincter muscles. The entire canal is narrowed so the nger
feels encased in a rigid tube. This frequently produces fecal impaction.
Tight sphincter—apprehension. The most common cause of a tight anal
sphincter is apprehension. Preliminary reassurance should be combined with
a gentle and slow examination. When the sphincter tightens, stop advancing
until the sphincter relaxes. Though the procedure may be uncomfortable, it
should not be painful. When the sphincter is in spasm that cannot be relaxed
by gentleness, suspect a ssure.
Perineal, Anal, and Rectal Signs 429
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Relaxed sphincter—lacerated anal muscles. Childbirth, injury during
surgery, and sexual abuse each damage the anal sphincter.
ter lacerations are more common than lacerations completely disrupting
the sphincter. If the laceration extends through the anal canal the edges of
the anus are either separated or form an irregular line. When the anus is
retracted by pulling the skin from each side, a dimple may be visible in
the posterior anal ring. The sphincter feels weak when the nger is
inserted. Ultrasonography conrms the defect. See Fecal Incontinence,
page 412.
Atonic muscles. Damage anywhere in the peripheral or central sensory and
motor systems controlling the sphincters produces decreased tone. The nd-
ing should prompt a careful neurologic examination.
Rectal Blumer shelf. Debris accumulating in the pelvis from neoplasms or
inammation elsewhere in the abdomen or pelvis is felt through the anterior
rectal wall as a hard shelf in the rectovesical or rectouterine pouch. Peritoneal
metastases from a primary carcinoma higher in the abdomen are most common. It also occurs from pelvic inammatory disease in women and prostatic
abscess in men.
Mistaken normal structures. The cervix, a vaginal tampon, and a pessary
felt through the anterior rectal wall can be misinterpreted as a neoplasm.
When the uterus is retroverted, the normal fundus may similarly mislead.
Occasionally, a loop of normal colon in the pelvic pouches is felt as a soft and
freely movable mass not easily confused with cancer.
Rectal polyps. Some polyps are difcult to palpate , especially if sessile. They
are easily missed since they are soft and may be mobile.
Partial sphinc-
Coccygeal tenderness. When pain in the region of the coccyx is exacerbated
by sitting or defecation test for tenderness in the sacrococcygeal joint during
digital rectal exam. With the index nger in the rectum on the anterior surface
of the coccyx press the posterior surface of the bone with the thumb on the
skin outside. Moving the bone anteriorly and posteriorly elicits pain in the
joint. The coccyx may be displaced from previous injury.
Fecal impaction. Symptoms may be vague. The patient may complain
of constipation or obstipation, but sometimes there is diarrhea, the
fecal stream passing around the impaction producing incontinence. The
debilitated or postoperative patient may only be restless or have fever or
anorexia. Barium suspensions administered for X-ray examination commonly cause impaction. The rectum is filled with hard, dry masses of
feces. These are removed by breaking up and extracting the pieces with
the examining finger.
Coccygeal sinus (pilonidal sinus). A congenital track extending from the
coccyx or sacrum to the perineum drains to the exterior, usually in the midline posterior to the anus (Fig. 9-30). The sinus is lined with epithelium and
hairs, hence the alternate name pilonidal. When blocked, it can form a tender
dimple or bulge just below the coccyx or on one side, usually the left.
430 CHAPTER 9: The Abdomen, Perineum, Anus, and Rectosigmoid
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Ischiorectal abscess. An abscess forms within the pelvic oor muscles and
tissue spaces between the rectum and the ischium. This is often associated
with neutropenia.
tion. Tenderness on deep palpation between the anus and ischial tuberosity
identies the site.
Anal intermuscular abscess. Abscesses between the muscles of the anus
cause agonizing pain during defecation and discomfort during sitting. In
high abscesses, a tender mass is felt just above the anorectal junction. Low
abscesses are most frequently found by palpating the distal end of the anal
canal between two ngers.
Because it is deep-seated there may be no signs on inspec-
ABDOMINAL, PERINEAL, AND ANORECTAL SYNDROMES
Hepatobiliary and Pancreatic Syndromes
Portal vein thrombosis. When occlusion occurs rapidly, symptoms of hepatic
and/or mesenteric vascular congestion (anorexia, pain and tenderness, ileus,
distention, diarrhea, and vomiting) occur before signs of portal hypertension. Ascites and splenomegaly follow rapidly. Infarctions of the upper GI
tract may occur. Slowly developing obstruction presents as ascites or signs
from vessels forming the portosystemic shunts. Occlusion occurs after surgical manipulation of the portal vein, septic thrombophlebitis of the portal
vein (pylephlebitis), trauma, polycythemia vera, neoplastic invasion of the
vein lumen, or prolonged debilitating illness. Clinical suspicion should lead
to imaging.
Portal hypertension. Any obstruction to the blood ow in the portal vein,
liver (presinusoidal, sinusoidal, post-sinusoidal), or hepatic veins produces
portal hypertension. Increased portal pressure causes splenic congestion
with splenomegaly, development of venous collaterals about the esophagus, the rectum, and the abdominal wall, and production of ascites because
of increased hydrostatic pressure in the liver capsule and mesenteric veins
(Fig. 9-31). Search for splenomegaly, visible collateral veins, and ascites.
Collaterals veins can be seen in the anus, abdominal wall, esophagus, and
proximal stomach. Hemorrhoids may be portal collaterals, but their occurrence from local causes is so common that their presence is rarely diagnostic.
Dilatation of the periumbilical veins can produce a venous rosette around the
navel, a caput medusae, but it is rare. The common demonstrable collaterals are
dilated supercial veins in the abdominal wall between the umbilicus and the
lower thorax containing blood owing upward, in the normal direction. When
the veins are greatly dilated, a venous hum with systolic accentuation may
be heard below the xiphoid process, over the epigastric surface of the liver,
or around the navel. The hum comes from varices in the falciform ligament.
Dilated veins in the lower esophagus and gastric cardia produce esophageal
varices and portal gastropathy visible during endoscopy. Ascites is painless
and may be mild, moderate, or severe. DDX: Portal obstruction with ascites
and ankle edema may be mistaken for right heart failure. Both conditions can
produce pleural effusions, hepatomegaly, ascites, and ankle edema. Engorged
neck veins and orthopnea are frequent with heart failure but absent with portal hypertension. Causes of portal hypertension are hepatic vein thrombosis,
Abdominal, Perineal, and Anorectal Syndromes 431
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FIG. 9-31 The Portal Venous System.
liver cirrhosis, intrahepatic tumors and cysts, granulomatous liver diseases,
portal vein thrombosis, and septic thrombosis of the portal vein.
Hepatic vein thrombosis—Budd-Chiari syndrome.
causes hepatic sinusoidal congestion obstructing portal ow through the liver
producing portal hypertension. The acutely distended liver capsule is painful. The onset may be abrupt, with abdominal pain and vomiting. The liver
is tender and enlarges rapidly. Mild jaundice can be present. Ascites rapidly
accumulates. Shock may ensue, with death in a few days. IVC obstruction at
or above the hepatic vein produces similar symptoms and additional signs
related to the legs. If the initial stage is survived, the chronic ndings appear
[Chung RT, Iafrate AJ, Amrein PC, et al. Case 15–2006: A 46-year-old woman
with sudden onset of abdominal distention. N Engl J Med. 2006;354:21662175]. Budd-Chiari syndrome is associated with cirrhosis, acute or subacute
liver disease caused by abscess, malignancy or trauma, polycythemia vera,
paroxysmal nocturnal hemoglobinuria, myeloproliferative disorders, and
thrombophilic states including oral contraceptive use.
Chronic hepatic vein occlusion. This late phase of the Budd–Chiari syndrome
is marked by portal hypertension, ascites, hepatomegaly, and secondary hepatocellular failure. Sudden onset and lack of alcohol intake or hepatitis suggests the correct diagnosis.
Acute Abdominal Pain Syndromes. The abdomen contains the following
paired organs: kidneys, ureters, adrenals, renal and iliac arteries and veins,
and ovaries. A disease or syndrome associated with abdominal pain arising
Hepatic vein thrombosis
432 CHAPTER 9: The Abdomen, Perineum, Anus, and Rectosigmoid
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in one of these organs can present with either right or left lateralization. We
only discuss presentation on one side.
Acute abdominal pain. See General Symptoms, page 407.
Six-dermatome pain. For a discussion of the six-dermatome pain patho-
physiology and differential diagnosis, see Chapter 8, page 292 and Fig. 8-27,
page 293.
Six-dermatome pain—esophageal discomfort.
dinated esophageal contractions often associated with a retrosternal sensation
of food sticking. Hypertensive or nutcracker esophagus is coordinated but
prolonged high-pressure contractions (probably with decreased esophageal
muscle compliance). In achalasia, the LES fails to relax, causing dysphagia and
retrosternal discomfort.
comfort identical in character and location to angina or myocardial infarction.
Gastroesophageal reux causes heartburn, a burning or constricting lower
retrosternal discomfort. The key to distinguishing angina from esophageal
spasm is a careful history. Association with dysphagia, meals, ingestion of cold
liquids, precipitation by reclining or bending over, or relief with antacids all
favor esophageal origin. Because nitroglycerin relaxes smooth muscle, whether
in arteries, veins, or esophagus, it may relieve discomfort from both disorders.
An ECG recorded during intense pain is useful; a normal tracing favors esophageal pain, although it does not exclude cardiac ischemia. The presence of a hiatal
hernia has no diagnostic signicance in the differential diagnosis of chest pain.
Esophageal pain and dysphagia.
ing and activation of esophageal nociceptors produces these ndings.
of the more frequent causes are discussed below.
Esophageal laceration—Mallory–Weiss tear. Esophageal laceration near the
esophagogastric junction follows severe retching and vomiting. Hematemesis
follows the retching and vomiting. Bleeding is usually self-limited.
Acute esophagitis. Retrosternal pain intensied by swallowing is caused by
prolonged vomiting, nasogastric tubes, pill esophagitis, corrosive esophageal
burns, acute infections (herpes simplex, Candida spp., cytomegalovirus), and
reux of gastric acid or bile.
Esophageal motility disorders often cause chest dis-
Mechanical disruption of normal swallow-
Esophageal spasm is uncoor-
Some
Chronic esophagitis. Inammation causing pain and dysphagia persists for
weeks or months and may be complicated by ulceration and/or intestinal
metaplasia (Barrett esophagus), a premalignant lesion. Progressive brosis
produces esophageal stricture. Acid reux is the most common cause. Irradiation, infections (HIV, Candida, herpes, and cytomegalovirus) are less common.
Esophageal achalasia.
al obstruction at the gastroesophageal junction dilating the proximal esophagus. Symptoms include weight loss, dysphagia and regurgitation of food, sa-
liva, and esophageal secretions. Chest pain may be present. Cough, especially
after meals or with recumbency, suggests aspiration.
Unremitting forceful LES contraction causes function-
Abdominal, Perineal, and Anorectal Syndromes 433
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Zenker diverticulum. This is a pulsion diverticulum in the posterior hypopharynx protruding downward between spine and esophagus. It lls with
food, causing dysphagia and regurgitation of putreed food. Occasionally,
there is retrosternal pain. An esophagram visualizes the pouch.
Plummer–Vinson syndrome. Severe iron deciency is associated with a postcricoid esophageal web demonstrated by esophagram that explains the dysphagia in some, but no anatomic basis for the dysphagia is found in many patients.
Esophageal cancer.
Adenocarcinomas at or just above the gastroesophageal
junction are increasing in frequency; squamous cell carcinomas predominate
more proximally. Dysphagia usually precedes pain by weeks or months. The
pain sometimes radiates to the neck or back. Chronic esophagitis with metaplasia (Barrett esophagus) substantially increases the risk for developing adenocarcinoma.
Foreign body. Swallowed rigid objects lodge at the level of the aortic arch or
diaphragm, causing pain and dysphagia.
Acute abdominal pain
Acute peritonitis. Acute infection and/or sterile chemical irritation of
the peritoneum produce an intense inammatory response with transudation of intravascular uid into the peritoneal space. This can be
complicated by bleeding and/or bacterial infection (sepsis) related to
the inciting event. Common causes are penetrating trauma, rupture
of the bowel, and bowel infarction. There are three symptom stages.
(1) Stage of Prostration (Primary Shock). The patient experiences a sud-
den, excruciating epigastric pain, frequently collapsing. The pain soon
spreads over the entire abdomen. The patient is anxious, pale, and diaphoretic. Respirations are shallow because moving the diaphragm is
painful. Retching or vomiting occurs. Hypothermia and hypotension
are common. The initial stage may last from a few minutes to several
hours. (2) Stage of Reaction (Masked Peritonitis). This brief respite for the
patient may deceive the inexperienced physician. The blood pressure
rises, the skin becomes warmer, and the generalized abdominal pain
and tenderness become less intense. The thighs are exed for comfort
and the patient moves cautiously because of pain. Involuntary boardlike rigidity results from abdominal muscle contraction and shallow
respiration. The pelvic peritoneum is tender on rectal exam. Intraperitoneal free uid is rarely demonstrated. Gas under the diaphragm
is suggested by a diminished area of RUQ liver dullness. (3) Stage of
Frank Peritonitis. The classic signs of advanced peritonitis appear. Ileus
distends the abdomen, vomiting resumes and persists with increasing
violence, and the temperature declines to subnormal levels. The entire
abdomen is tender, but rigidity may lessen in the late stage. Dehydration and pain produce the classic facies hippocratica, with hollow
features and anxious expression. An expedited team approach to the
evaluation and management of suspected peritonitis minimizes morbidity and mortality through rapid diagnosis and combined medical
and surgical treatments.
434 CHAPTER 9: The Abdomen, Perineum, Anus, and Rectosigmoid
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Spontaneous bacterial peritonitis. Portal hypertension produces transu-
dative ascites with a low
low in immunoglobulins. Bacteria seeded from the gut lead to infection
with minimal localizing symptoms. Patients have advanced liver dis-
ease. They may present with fever or confusion without abdominal pain
or tenderness. If the serum albumin ascites gradient is <2.1 and there
are >250 PMNs/mm
pending culture results.
Solid organ rupture. Blunt trauma to the lower thorax, back, and/or
abdomen can fracture kidneys, liver, or spleen. The fracture and hemorrhage may be contained by the surrounding capsule, but rupture of the
capsule acutely or delayed by hours or days results in severe hemorrhage.
Upper quadrant and ank pain are present, and tenderness may
be present anteriorly or posteriorly. Renal fracture results in gross hematuria unless the ureter is obstructed. Fracture of solid organs must be
sought emergently by CT.
Volvulus. Volvulus most commonly occurs in the sigmoid colon
(90%) or the cecum (10%) where the gut is suspended on a long mesentery. Twisting compromises blood flow, forms a closed loop of distended bowel, and leads to ischemic perforation. A vague, tender
mass may be felt. Frequently the only findings are distended bowel,
tympany, pain, violent peristalsis, and vomiting. Early diagnosis
and treatment are imperative. A bird beak cutoff of colonic gas may
be seen on noncontrast X-rays. Colonoscopy can be both diagnostic
and therapeutic.
Abdominal pain and pallor. Abdominal pain accompanied by pallor is
an ominous presentation requiring expeditious evaluation. Of greatest
concern is hemorrhage from rupture of a major vessel or organ. Intense
sympathetic activation, even without hemorrhage, may cause pallor and
diaphoresis.
Ruptured ectopic pregnancy. See Chapter 11, page 501.
Corpus luteum hemorrhage. See Chapter 11, page 502.
Ruptured aortic or iliac aneurysm. See page 436.
Bleeding peptic ulcer. An ulcer eroding into a major vessel leads to
life-threatening hemorrhage. Although bleeding may be preceeded
by ulcer disease symptoms, it is not uncommon, especially for
NSAID-induced ulcers, to present with painless hemorrhage and/or
perforation. Blood should be sought in the stools and a nasogastric
aspirate.
Hemorrhagic pancreatitis. Pancreatic inammation erodes blood vessels
in the retroperitoneum, leading to hemorrhage into the necrotic pancreas
and dissection of hemorrhage into the retroperitoneal spaces.
435 for complete discussion.
serum-albumin-ascites-gradient (SAAG) and
3
in the ascites uid, treatment should be started
See page
Acute Epigastric Pain: Visceral pain arising in the intestine from the stomach
to the transverse colon is carried by the vagus nerve and projects to the epigastrium. In addition, somatic pain from the upper abdominal peritoneum
and retroperitoneal structures is localized to the epigastrium.
Early acute appendicitis. See Acute RLQ Pain—Appendicitis, page 440.
Abdominal, Perineal, and Anorectal Syndromes 435
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Perforated peptic ulcer. Perforation causes leakage of acid, digestive
enzymes, blood, bacteria, and bowel contents into the peritoneal cavity,
lesser sac, or retroperitoneum. With free perforation, sterile peritonitis
is followed by purulent peritonitis, septicemia, shock, and death.
There
may be a history of epigastric pain occurring 3 or 4 hours after meals
and relieved by food or antacids. Occasionally, there are no antecedent
symptoms, particularly in elderly patients taking NSAIDs. The patient
describes sudden, excruciating pain in the epigastrium that spreads over
the entire abdomen. Sometimes it intensies in the suprapubic region
because of the downward ow of gastric contents (Fig. 9-32). RLQ pain,
tenderness, and rigidity may be pronounced, suggesting acute appendicitis. Without prompt diagnosis and treatment, generalized peritonitis
will supervene.
Limited perforation of peptic ulcer.
When the perforation is into a closed
space, the released gastric contents are walled off producing a local abscess.
The stage of prostration is mild, with the pain limited to the epigastrium or
ank. The abscess forms in the subphrenic space or lesser peritoneal sac.
Acute gastritis. Inammation of the gastric mucosa is caused by infection,
chemical irritation, autoimmune injury, or drug-induced injury. Frequently,
the cause is unknown. Symptoms are anorexia, nausea, and vomiting, some-
times with hematemesis, and epigastric pain with or without tenderness.
Upper endoscopy is diagnostic revealing mucosal inammation, erosions,
and submucosal hemorrhage. Common causes are ingestion of aspirin,
NSAIDs, alcohol, or contaminated food, uremia, infection with H. pylori, cytomegalovirus, herpes simplex, or enteroviruses, and autoimmune gastritis.
Acute pancreatitis. Auto-digestion of the pancreas, initiated by release
of pancreatic enzymes into the parenchyma as a consequence of ductal
obstruction, inammation, ischemia or trauma, incites an intense sterile inammatory response. The expanding inammatory mass dissects
within the retroperitoneum and occasionally ruptures into the peritoneum
producing hypotension and shock. Secondary infection of necrotic tissue
FIG. 9-32 Iliac Abscess from a Leaking Duodenal Ulcer. A perforated duodenal ulcer drains down the right
paracolic gutter into the right iliac fossa, as indicated by stippling.
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