VISCERAL PAIN

Visceral pain is transmitted by C fibers that are found in muscle, periosteum, mesentery, peritoneum, and viscera. Most painful stimuli from abdominal viscera are conveyed by this type of fiber and tend to be dull, cramping, burning, poorly localized, and more gradual in onset and longer in duration than somatic pain. Because abdominal organs transmit sensory afferents to both sides of the spinal cord, visceral pain is usually perceived to be in the midline, in the epigastrium, periumbilical region, or hypogastrium (Fig. 10-1). Visceral pain is not well localized because the number of nerve endings in viscera is lower than that in highly sensitive organs such as the skin and because the innervation of most viscera is multisegmental. The pain is generally described as cramping, burning, or gnawing. Secondary autonomic effects such as sweating, restlessness, nausea, vomiting, perspiration, and pallor often accompany visceral pain. The patient may move about in an effort to relieve the discomfort.

Figure 10-1. Localization of visceral pain. Pain arising from organ areas depicted in 1, 2, and 3 is felt in the epigastrium, midabdomen, and hypogastrium, respectively, as shown in A. The arrow in A indicates biliary pain that is referred to the right scapular area.

The afferent fibers that mediate painful stimuli from the abdominal viscera follow the distribution of the autonomic nervous system (Fig. 10-2). The cell bodies for these fibers are located in the dorsal root ganglia of spinal afferent nerves. On entering the spinal cord, these fibers branch into the dorsal horn and tract of Lissauer, where afferent nerves from adjacent spinal segments travel in a cephalad direction and caudally over one or two spinal segments before terminating on dorsal horn cells in laminae I and V. The dorsal horn cells within laminae I and V are the primary projection neurons for ascending pain pathways. From the dorsal horn, second-order neurons transmit nociceptive impulses via fibers that pass across the anterior commissure and ascend the spinal cord in the contralateral spinothalamic tract. These fibers project to the thalamic nuclei and the reticular formation nuclei of the pons and medulla. The thalamic nucleus sends third-order neurons to the somatosensory cortex, where the discriminative aspects of pain are perceived. The reticular formation nucleus sends neurons to the limbic system and frontal cortex, where the emotional aspects of pain are interpreted.^8,9

Figure 10-2. Pathways of visceral sensory innervation. The visceral afferent fibers that mediate pain travel with autonomic nerves to communicate with the central nervous system. In the abdomen, these fibers include vagal and pelvic parasympathetic nerves and thoracolumbar sympathetic nerves. Sympathetic fibers (red lines); parasympathetics (blue lines).

Abdominal visceral nociceptors respond to mechanical and chemical stimuli. The principal mechanical signal to which visceral nociceptors are sensitive is stretch; cutting, tearing, or crushing of viscera does not result in pain. Visceral stretch receptors are located in the muscular layers of the hollow viscera, between the muscularis mucosa and submucosa, in the serosa of solid organs, and in the mesentery (especially adjacent to large vessels).^5,10 Mechanoreceptor stimulation can result from rapid distention of a hollow viscus (e.g., intestinal obstruction), forceful muscular contractions (e.g., biliary pain or renal colic), and rapid stretching of solid organ serosa or capsule (e.g., hepatic congestion). Similarly, torsion of the mesentery (e.g., cecal volvulus) or tension from traction on the mesentery or mesenteric vessels (e.g., retroperitoneal or pancreatic tumor) results in stimulation of mesenteric stretch receptors.

Abdominal visceral nociceptors also respond to various chemical stimuli. Chemical nociceptors are contained mainly in the mucosa and submucosa of the hollow viscera. These receptors are activated directly by substances released in response to local mechanical injury, inflammation, tissue ischemia and necrosis, and noxious thermal or radiation injury. Such substances include H⁺ and K⁺ ions, histamine, serotonin, bradykinin and other vasoactive amines, substance P, calcitonin gene-related peptide, prostaglandins, and leukotrienes.^11,12 Accumulation of nociceptor-reactive substances may change the microenvironment of the injured tissue and thereby reduce the pain threshold. The sensation of pain to a given stimulus is thus increased, and otherwise innocuous stimuli become painful. For example, the application of chemical irritants or pressure to normal gastric mucosa is not painful, whereas the application of the same stimuli to inflamed or injured gastric mucosa causes pain.

SOMATIC-PARIETAL PAIN

Somatic-parietal pain is mediated by A-δ fibers that are distributed principally to skin and muscle. Signals from this neural pathway are perceived as sharp, sudden, well-localized pain, such as that which follows an acute injury. These fibers convey pain sensations through spinal nerves. Stimulation of these fibers activates local regulatory reflexes mediated by the enteric nervous system and long spinal reflexes mediated by the autonomic nervous system, in addition to transmitting pain sensation to the central nervous system.¹³

Somatic-parietal pain arising from noxious stimulation of the parietal peritoneum is more intense and more precisely localized than visceral pain. An example of this difference occurs in acute appendicitis, in which the early vague periumbilical visceral pain is followed by the localized somatic-parietal pain at McBurney’s point that is produced by inflammatory involvement of the parietal peritoneum. Somatic-parietal pain is usually aggravated by movement or vibration. The nerve impulses that mediate such pain travel in somatic sensory spinal nerves. The fibers reach the spinal cord in the peripheral nerves that correspond to the cutaneous dermatomes of the skin, the sixth thoracic (T6) to first lumbar (L1) vertebra. Lateralization of the discomfort of parietal pain is possible because only one side of the nervous system innervates a given part of the parietal peritoneum.

Reflexive responses, such as involuntary guarding and abdominal rigidity, are mediated by spinal reflex arcs involving somatic-parietal pain pathways. Afferent pain impulses are modified by inhibitory mechanisms at the level of the spinal cord. Somatic A-δ fibers mediate touch, vibration, and proprioception in a dermatomal distribution that matches the visceral innervation of the injured viscera and synapse with inhibitory interneurons of the substantia gelatinosa in the spinal cord. In addition, inhibitory neurons that originate in the mesencephalon, periventricular gray matter, and caudate nucleus descend within the spinal cord to modulate afferent pain pathways. These inhibitory mechanisms allow cerebral influences to modify afferent pain impulses.^9,14

REFERRED PAIN

Referred pain is felt in areas remote from the diseased organ and results when visceral afferent neurons and somatic afferent neurons from a different anatomic region converge on second-order neurons in the spinal cord at the same spinal segment. This convergence may result from the innervation, early in embryologic development, of adjacent structures that subsequently migrate away from each other. As such, referred pain can be understood to refer to an earlier developmental state. For example, the central tendon of the diaphragm begins its development in the neck and moves craniocaudad, bringing its innervation, the phrenic nerve, with it.¹⁵ Figure 10-3 shows how diaphragmatic irritation from a subphrenic hematoma or splenic rupture may be perceived as shoulder pain (Kehr’s sign).⁹

Figure 10-3. Demonstration of the neuroanatomic basis of referred pain. Visceral afferent fibers that innervate the diaphragm can be stimulated by local irritation (e.g., subdiaphragmatic abscess [circle]). These visceral afferent fibers (A) synapse with second-order neurons in the spinal cord (B) as well as somatic afferent fibers (C) arising from the left shoulder area (cervical roots 3 to 5). The brain interprets the pain to be somatic in origin and localizes it to the shoulder.

APPROACH TO ACUTE CARE

When approaching a patient with acute abdominal pain, the physician should begin with a rapid assessment of the patient’s overall physiologic state. Quickly assessing the three domains according to the mnemonic “ABC” will help identify patients who are unstable and therefore require expedited treatment:

If hemodynamic instability is apparent, including clinical evidence of shock, surgical consultation should be sought immediately, and consideration should be given to endotracheal intubation and resuscitation early in the encounter. The adage in acute care surgery that “death begins in radiology” should be a reminder that hemodynamic resuscitation should precede diagnostic imaging. Patients who are in shock demand urgent care and should not be sent for imaging studies without aggressive resuscitation and monitoring.

HISTORY

Despite the advances made in clinical imaging, history taking remains the most important component of the initial evaluation of the patient with acute abdominal pain.¹⁶ Characteristic features of the pain associated with various common causes of acute abdominal pain are shown in Table 10-1. Attention to these features can lead to a rapid clinical diagnosis or exclusion of important diseases in the differential diagnosis, thus enhancing the reliability and effectiveness of subsequent diagnostic testing.²

Chronology

The time courses of several common causes of acute abdominal pain are diagrammed in Figure 10-4. The rapidity of onset of pain is often a measure of the severity of the underlying disorder. Pain that is sudden in onset, severe, and well localized is likely to be the result of an intra-abdominal catastrophe such as a perforated viscus, mesenteric infarction, or ruptured aneurysm. Affected patients usually recall the exact moment of onset of their pain. Progression is an important temporal factor in abdominal pain. In some disorders, such as gastroenteritis, pain is self-limited, whereas in others, such as appendicitis, pain is progressive. Colicky pain has a crescendo-decrescendo pattern that may be diagnostic, as in renal colic. The duration of abdominal pain is also important. Patients who seek evaluation of abdominal pain that has been present for an extended period (e.g., weeks) are less likely to have an acute life-threatening illness than patients who present within hours to days of the onset of their symptoms.

Figure 10-4. Patterns of acute abdominal pain. A, Many causes of abdominal pain subside spontaneously with time (e.g., gastroenteritis). B, Some pain is colicky (i.e., the pain progresses and remits over time); examples include intestinal, renal, and biliary pain (colic). The time course may vary widely from minutes in intestinal and renal pain to days, weeks, or even months in biliary pain. C, Commonly, acute abdominal pain is progressive, as in acute appendicitis or diverticulitis. D, Certain conditions have a catastrophic onset, such as ruptured abdominal aortic aneurysm.

PHYSICAL EXAMINATION

The physical examination of the patient with acute abdominal pain begins with an assessment of the patient’s appearance and airway, breathing, and circulation (ABC), as described earlier. The patient’s ability to converse, breathing pattern, position in bed, posture, degree of discomfort, and facial expression should be noted. A patient lying still in bed, in the fetal position and reluctant to move or speak, with a distressed facial expression, is likely to have peritonitis. On the other hand, a patient who writhes and changes position frequently likely has purely visceral pain, as in intestinal obstruction or gastroenteritis. Tachypnea may be a sign of metabolic acidosis caused by shock. Atrial fibrillation noted on physical examination or electrocardiogram may suggest mesenteric arterial embolus. All patients should undergo a careful, systematic examination, regardless of the differential diagnosis suggested by the history.

LABORATORY DATA

The history and physical examination findings generally are not sufficient to establish a firm diagnosis in a patient with acute abdominal pain. All patients with acute abdominal pain should have a complete blood count, with a differential count, and urinalysis. The determination of serum electrolyte, blood urea nitrogen, creatinine, and glucose levels is useful for assessing the patient’s fluid and acid-base status, renal function, and metabolic state and should be done for every patient with acute abdominal pain who presents to an emergency department. Urine or serum pregnancy testing must be performed in all women of reproductive age with abdominal pain. Liver biochemical tests and serum amylase levels should be ordered for patients with upper abdominal pain or with jaundice.

Leukocytosis, particularly when associated with immature band forms, is an important finding. Metabolic acidosis, an elevated serum lactate level, or a depressed bicarbonate level are all associated with tissue hypoperfusion and shock. Patients who manifest these findings are likely to require urgent surgical intervention or intensive care.

IMAGING STUDIES

OTHER DIAGNOSTIC TESTS

Other diagnostic imaging modalities such as MRI and radionuclide scanning (e.g., ^99mTc-labeled hydroxyl iminodiacetic acid [HIDA] scan) and endoscopy usually take a secondary role in the evaluation of the patient with acute abdominal pain. Use of these tests is generally guided by the results of CT or ultrasound. Angiography may be useful not only for establishing a diagnosis of visceral ischemia, but also for delivering therapy aimed at improving or reestablishing blood flow. Diagnostic peritoneal lavage, although seldom used now, is useful when a patient is too unstable from a cardiopulmonary standpoint to tolerate radiographic imaging. The finding of leukocytes in the lavage effluent in an unstable patient may, in extreme circumstances, constitute sufficient grounds for laparotomy.

In a patient who is unstable and deteriorating and has signs of an acute abdomen, laparotomy as a diagnostic maneuver should be considered if imaging is considered prohibitively risky. An overall approach to the patient with acute abdominal pain is illustrated in Figure 10-5.

Figure 10-5. An approach to the urgent evaluation of abdominal pain. Specific complaints and physical examination findings are coupled with appropriate radiologic imaging. AAA, abdominal aortic aneurysm; ABC, airway, breathing, circulation; CT, computed tomography; FAST, focused abdominal sonogram for trauma; RLQ, right lower quadrant; RUQ, right upper quadrant; US, ultrasound. *For left lower quadrant pain, the most likely diagnosis is diverticulitis.

ACUTE APPENDICITIS

Acute appendicitis is a ubiquitous problem. In adult patients younger than 60 years, acute appendicitis accounts for 25% of admissions to the hospital from the emergency department for abdominal pain.²⁰ The overall incidence of appendicitis is approximately 11/10,000 population, with a lifetime risk of 8.6% for men and 6.7% for women.²¹ Typically, acute appendicitis begins with prodromal symptoms of anorexia, nausea, and vague periumbilical pain. Within 6 to 8 hours, the pain migrates to the right lower quadrant and peritoneal signs develop. In uncomplicated appendicitis, a low-grade fever to 38°C and mild leukocytosis are usually present. A higher temperature and white blood cell count are associated with perforation and abscess formation. The mnemonic PANT can help the novice remember the classic progression of symptoms in appendicitis—pain followed by anorexia followed by nausea followed by temperature elevation. Uncommon presentations of acute appendicitis, however, are common, and the wary physician will not reject a diagnosis of acute appendicitis simply on the basis of the patient’s history and physical examination alone. Whereas plain abdominal radiographs are not diagnostic and have little role in the diagnosis of acute appendicitis, CT has dramatically improved the accuracy of diagnosis in patients with acute appendicitis. The finding of an appendiceal diameter larger than 6 mm has positive and negative predictive values of 98%.²² Other CT signs of acute appendicitis include periappendiceal fat inflammation, presence of fluid in the right lower quadrant, and failure of contrast dye to fill the appendix²³; these findings have lower degrees of specificity. Traditionally, an erroneous diagnosis of appendicitis, reflected by the finding of normal pathology at surgical exploration, was as high as 33%.²⁴ The addition of CT has reduced the false-negative rate to approximately 6% for men and 10% for women.²⁵ As noted earlier, CT does entail radiation exposure,¹⁸ and some authorities advocate avoiding CT in children and adolescents,²⁶ in whom a higher degree of diagnostic uncertainty is tolerated in favor of lower radiation exposure (see Chapter 116).

ACUTE BILIARY DISEASE

Biliary disease accounts for approximately 5% to 7% of emergency department visits for abdominal pain.^2,20 Most patients in this group present at some point on the spectrum between biliary pain and acute cholecystitis. Biliary pain is a syndrome of right upper quadrant or epigastric pain, usually postprandial, caused by transient obstruction of the cystic duct by a gallstone. Biliary pain is self-limited, generally lasting less than 6 hours. Acute cholecystitis is, in most cases, caused by persistent obstruction of the cystic duct by a gallstone. The pain of acute cholecystitis is almost indistinguishable from that of biliary pain, except that it is persistent. The pain usually is a dull ache and is localized to the right upper quadrant or epigastrium and may radiate around the back to the right scapula. Nausea, vomiting, and low-grade fever are common. On examination, right upper quadrant tenderness, guarding, and Murphy’s sign (inspiratory arrest on palpation of the right upper quadrant) are diagnostic of acute cholecystitis. The white blood cell count is usually mildly elevated but may be normal. Mild elevations in serum total bilirubin and alkaline phosphatase levels are typical. The role of gallstones in the etiology of biliary pain and acute cholecystitis makes ultrasound evaluation of the right upper quadrant the key diagnostic test. Demonstration of gallstones may suggest biliary pain, whereas the finding of stones with gallbladder wall thickening, pericholecystic fluid, and pain on compression of the gallbladder with the ultrasound probe (sonographic Murphy’s sign) is essentially diagnostic of acute cholecystitis, as is positive hepatobiliary scintigraphy (e.g., HIDA scan).²⁷ Patients with acute cholecystitis are best managed with cholecystectomy within 48 hours.^28–30 Patients who are diabetic, particularly those with a leukocyte count over 15,000/mm³, are at particular risk for gangrenous cholecystitis and should have immediate surgical consultation.³¹ These patients are likely to require an emergent open cholecystectomy.

Patients who present with right upper quadrant pain with jaundice and signs of sepsis should be suspected of having obstruction of the bile duct by a gallstone. Right upper quadrant pain, fever and chills, and jaundice (Charcot’s triad) are suggestive of ascending cholangitis.³² These patients require intravenous fluids, antibiotics, and bile duct drainage, usually by endoscopy (see also Chapters 65, 66, and 67).

SMALL BOWEL OBSTRUCTION

Intestinal obstruction may occur in patients of all ages. In pediatric patients, intussusception, intestinal atresia, and meconium ileus are the most common causes. In adults, about 70% of cases are caused by postoperative adhesions; incarcerated hernias make up most of the remainder. Small bowel obstruction is characterized by sudden, sharp, periumbilical abdominal pain. Nausea and vomiting occur soon after the onset of pain and provide temporary relief of discomfort. Frequent bilious emesis with epigastric pain is suggestive of high (proximal) intestinal obstruction, whereas cramping periumbilical pain with infrequent feculent emesis is more typical of distal intestinal obstruction. Examination reveals an acutely ill, restless patient. Fever, tachycardia, and orthostatic hypotension are common. Abdominal distention is usual. Auscultation characteristically demonstrates hyperactive bowel sounds and audible rushes. The patient’s abdomen is diffusely tender to percussion and palpation, but peritoneal signs are absent, unless a complication such as ischemia or perforation has occurred. Leukocytosis and lactic acidosis suggest intestinal ischemia or infarction. Plain radiographs of the abdomen are diagnostic when they reveal dilated loops of small intestine with air-fluid levels and decompressed distal small bowel and colon. Plain abdominal films can be misleading in a patient with proximal jejunal obstruction, because dilated bowel loops and air-fluid levels may be absent. CT is superior for establishing the diagnosis and location of intestinal obstruction.³³ In patients with partial small intestinal obstruction, initial treatment is with bowel rest, intravenous fluids, nasogastric decompression, and close observation. Surgery is required for patients who fail conservative management or have evidence of complete obstruction, especially if ischemia is suspected (see also Chapter 119).

ACUTE DIVERTICULITIS

Acute diverticulitis is a common disease. Approximately 80% of affected patients are older than 50 years,³⁴ but the incidence may be increasing in younger persons.³⁵ Patients with diverticulitis usually present with constant, dull, left lower quadrant pain and fever. They may complain of constipation or obstipation and usually are found to have a leukocytosis. Physical examination demonstrates left lower quadrant tenderness and, in some cases, a left lower quadrant mass. Localized peritoneal signs are frequent. In severe cases, generalized peritonitis may be present, making differentiation from other causes of a perforated viscus difficult. CT is reliable in confirming the diagnosis, with a sensitivity of 97%,³⁶ and should be performed routinely in the emergency evaluation of patients with diverticulitis.

Acute diverticulitis presents as a spectrum of disease from mild abdominal discomfort to gross fecal peritonitis, which is an acute surgical emergency. The severity of diverticulitis, as determined by CT, is best described using the Hinchey grading system (see Table 117-2).³⁷ Patients with mild disease and no CT findings of perforation, in the absence of limiting comorbid disease, can generally be treated as an outpatient. Those with Hinchey grade I diverticulitis (localized pericolic abscess or inflammation) frequently require hospitalization for intravenous antibiotics. Patients with Hinchey grade II diverticulitis (pelvic, intra-abdominal, or retroperitoneal abscess) should undergo CT-guided drainage of the abscess and receive a course of broad-spectrum intravenous antibiotics. Patients with Hinchey III (generalized purulent peritonitis) and IV (generalized fecal peritonitis) diverticulitis frequently require emergency surgery. Optimal surgical management of patients with Hinchey I or II diverticulitis is a matter of debate (see Chapter 117).

ACUTE PANCREATITIS

Hospital admissions for acute pancreatitis in the United States seem to be increasing. The incidence of acute pancreatitis in California rose from 33 to 43 cases/100,000 between 1994 and 2001.³⁸ Acute pancreatitis typically begins as acute pain in the epigastrium that is constant, unrelenting, and frequently described as boring through to the back or left scapular region. Fever, anorexia, nausea, and vomiting are typical. Patients with pancreatitis usually are more comfortable sitting upright, leaning forward slightly, and are commonly found in this position in the emergency department. Physical examination reveals an acutely ill patient in considerable distress. Patients are usually tachycardic and tachypneic. Abdominal examination reveals hypoactive bowel sounds and marked tenderness to percussion and palpation in the epigastrium. Abdominal rigidity is a variable finding. In rare patients, flank or periumbilical ecchymoses (Grey-Turner’s or Cullen’s sign, respectively) develop in the setting of pancreatic necrosis with hemorrhage. Extremities are often cool and cyanotic, reflecting underperfusion. White blood cell counts of 12,000 to 20,000/mm³ are common. Elevated serum and urine amylase levels are usually present within the first few hours of pain. Depending on the cause and severity of pancreatitis, serum electrolyte, calcium, and blood glucose levels and liver biochemical test and arterial blood gas results may be abnormal. Abdominal ultrasonography is useful for identifying gallstones as a potential cause of pancreatitis. CT is reserved for patients with severe or complicated pancreatitis.

Although most cases of acute pancreatitis are self-limited, as many as 20% of patients have severe disease with local or systemic complications,³⁹ including hypovolemia and shock, renal failure, liver failure, and hypocalcemia. Although a number of prognostic physiologic scales, such as the Sequential Organ Failure Assessment (SOFA) and Acute Physiologic Assessment and Chronic Health Evaluation (APACHE) II scores, have been advocated as measures of the severity of acute pancreatitis, the Ranson score, first published in 1974, remains a useful and widely used checklist for the early assessment of patients with acute pancreatitis.⁴⁰ The Ranson score consists of five early and six late factors that indicate severe pancreatitis (see Table 58-2). A minority of patients with severe acute pancreatitis present with a profound intra-abdominal catastrophe, usually caused by thrombosis of the middle colic artery or right colic artery, which travels in proximity to the head of the pancreas, with resulting colonic infarction. This process may not be seen clearly on CT scans obtained early in the course of disease and should be suspected in any case marked by rapid hemodynamic collapse. Such patients require immediate laparotomy (see Chapter 58).

PERFORATED PEPTIC ULCER

The epidemiology of peptic ulcer disease continues to change. The overall incidence of peptic ulcer disease has declined significantly since the late 1970s,^41,42 and the number of patients requiring hospital admission for severe and complicated peptic ulcer disease has also decreased.⁴² Better therapeutic modalities, including proton pump inhibitors, eradication of Helicobacter pylori, and endoscopic methods for control of hemorrhage, have reduced the number of patients with peptic ulcer disease who require surgical intervention,⁴³ although the incidence of complicated disease has increased in older adults, in whom morbidity and mortality related to surgery are also increased.⁴²

Patients with a perforated peptic ulcer typically present with the sudden onset of severe diffuse abdominal pain. These patients may be able to specify the precise moment of the onset of symptoms. In the usual case, the afflicted patient presents acutely with excruciating abdominal pain. Abdominal examination reveals peritonitis, with rebound tenderness, guarding, or abdominal muscular rigidity. In such cases, distinguishing perforated ulcer from other causes of a perforated viscus, such as a perforated colonic diverticulum or perforated appendicitis, may not be possible. Older or debilitated patients may present with less dramatic symptoms, with perforation detected by the presence of free intraperitoneal air on an upright abdominal film or CT scan.

A perforated peptic ulcer should be suspected in any patient with the sudden onset of severe abdominal pain who presents with abdominal rigidity and free intraperitoneal air. Pneumoperitoneum is identified on an abdominal radiograph in 75% of patients (Fig. 10-6). In equivocal cases, CT of the abdomen usually suggests the diagnosis by demonstrating edema in the region of the gastric antrum and duodenum, associated with extraluminal air. CT may not be diagnostic, however, and patients with diffuse peritonitis or hemodynamic collapse should be explored surgically. Laparotomy is acceptable as the primary diagnostic maneuver in such patients. Endoscopy is not advisable when the diagnosis of a perforated peptic ulcer is suspected. Insufflation of the stomach can convert a sealed perforation into a free perforation. Survival following emergency surgery for complications of peptic ulcer disease is surprisingly poor. Patients who require surgery for a complication of peptic ulcer disease are generally older and more medically ill than those seen in the past. Sarosi and colleagues have reported a 23% in-hospital mortality rate in a Veterans Administration population,⁴⁴ and Imhof and associates,⁴⁵ reporting on a series of German patients with perforated peptic ulcer, found an in-hospital mortality rate of 12.1%, a one-year mortality rate of 28.7%, and a five-year mortality rate of 46.8% (see also Chapters 52 and 53).

Figure 10-6. This upright chest film of an 80-year-old man with the acute onset of severe epigastric pain demonstrates free intra-abdominal air under the right hemidiaphragm. The patient has pneumoperitoneum as a result of a perforated viscus. At surgery, an anterior duodenal ulcer perforation was found.

ACUTE MESENTERIC ISCHEMIA

Acute mesenteric ischemia can result from occlusion of a mesenteric vessel arising from an embolus, which may emanate from an atheroma of the aorta or cardiac mural thrombus, or from primary thrombosis of a mesenteric vessel, usually at a site of atherosclerotic stenosis. Embolic occlusion is more common in the superior mesenteric artery than the celiac or inferior mesenteric artery, presumably because of the less acute angle of the superior mesenteric artery off the abdominal aorta. Nonocclusive mesenteric ischemia results from inadequate visceral perfusion and can also lead to intestinal ischemia and infarction. Such cases are usually consequent to catastrophic systemic illnesses such as cardiogenic or septic shock. Acute mesenteric embolism, mesenteric thrombosis, and nonocclusive mesenteric ischemia each account for approximately one third of cases of acute mesenteric ischemia and have a combined mortality rate of 60% to 100%.⁴⁶

The hallmark of the diagnosis of acute mesenteric ischemia is the abrupt onset of intense cramping epigastric and periumbilical pain out of proportion to the findings on abdominal examination. Other symptoms may include diarrhea, vomiting, bloating, and melena. On physical examination, most patients appear acutely ill, but the presentation may be subtle. Shock is present in about 25% of cases.

CT is the best initial diagnostic test. Mesenteric angiography may be useful for determining the cause of intestinal ischemia and defining the extent of vascular disease. Patients with acute embolic or thrombotic intestinal ischemia should be referred for immediate revascularization and bowel resection.⁴⁷ Patients with nonocclusive mesenteric ischemia are best managed by treatment of the underlying shock state. For those with persistent symptoms, laparotomy for resection of infarcted intestine may be necessary. Transcatheter vasodilator therapy may be helpful for patients who are found to have vasospasm on visceral arteriography (see also Chapter 114).⁴⁷

ABDOMINAL AORTIC ANEURYSM

Rupture of an abdominal aortic aneurysm is heralded by the sudden onset of acute, severe abdominal pain localized to the midabdomen or paravertebral or flank areas. The pain is tearing in nature and associated with prostration, lightheadedness, and diaphoresis. If the patient survives transit to the hospital, shock is the most common presentation. Physical examination reveals a pulsatile, tender abdominal mass in about 90% of cases. The classic triad of hypotension, a pulsatile mass, and abdominal pain is present in 75% of cases and mandates immediate surgical intervention.⁴⁷

ABDOMINAL COMPARTMENT SYNDROME

Although not usually presenting as acute abdominal pain, abdominal compartment syndrome (ACS) warrants consideration in any patient with an abdominal emergency. First reported in the setting of massive intra-abdominal trauma, ACS, defined as pathologic elevation of intra-abdominal pressure, is now recognized as a frequent complication of many severe disease processes. An elevated intra-abdominal pressure may develop in a patient who survives massive volume resuscitation with resulting visceral edema or who has a disease such as severe pancreatitis that can cause visceral or retroperitoneal edema. The elevated intra-abdominal pressure in turn compromises visceral perfusion, with resulting injury and additional edema. The kidney is particularly prone to underperfusion in this setting, and kidney failure may be the first sign of ACS.⁴⁸

Intra-abdominal pressure can be measured simply by connecting a transducer to a urinary catheter, with the zero reference point at the midaxillary line in a supine patient. The World Society for Abdominal Compartment Syndrome has established a consensus grading scheme for ACS based on the measured bladder pressure. A normal value for bladder pressure is less than 7 mm Hg. Grade I ACS is defined as a pressure of 12 to 15 mm Hg, grade II as 16 to 20 mm Hg, grade III as 21 to 25 mm Hg, and grade IV as greater than 25 mm Hg. Nonsurgical options for treating low-grade ACS include gastric decompression, sedation, neuromuscular blockade, placing the patient in a reverse Trendelenburg position while allowing the hips to remain in a neutral position, and diuretics. In a patient with high-grade ACS, particularly when renal and respiratory function is compromised, laparotomy and creation of an open abdomen is most effective. Management of the open abdomen requires specific surgical expertise usually found in referral medical centers.⁴⁹

OTHER INTRA-ABDOMINAL CAUSES

Other intra-abdominal causes of acute abdominal pain include the following: gynecologic conditions such as endometritis, acute salpingitis with or without tubo-ovarian abscess, ovarian cysts or torsion, and ectopic pregnancy; spontaneous bacterial peritonitis (Chapter 91); functional dyspepsia and peptic ulcer disease (Chapters 13 and 52); infectious gastroenteritis (Chapters 107 and 108); viral hepatitis and other liver infections (Chapters 77 to 82); pyelonephritis; cystitis; mesenteric lymphadenitis; inflammatory bowel disease (Chapters 111 and 112); and functional abnormalities such as irritable bowel syndrome (Chapter 118) and intestinal pseudo-obstruction (Chapter 120).

EXTRA-ABDOMINAL CAUSES

Acute abdominal pain may arise from disorders involving extra-abdominal organs and systemic illnesses. Examples are listed in Table 10-3. Surgical intervention for patients with acute abdominal pain arising from an extra-abdominal or systemic illness is seldom required except in cases of pneumothorax, empyema, and esophageal perforation. Esophageal perforation may be iatrogenic, result from blunt or penetrating trauma, or occur spontaneously (Boerhaave’s syndrome; see also Chapter 45).

Table 10-3 Extra-Abdominal Causes of Acute Abdominal Pain

Cardiac

Thoracic

Hematologic

Metabolic

Toxins

Infections

Miscellaneous

SPECIAL CIRCUMSTANCES