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    Acute abdominal pain - Feldman - Gastrointestinal and Liver Diseases, 2010 Acute abdominal pain - Feldman - Gastrointestinal and Liver Diseases, 2010 Document Transcript

    • CHAPTE R 10 Acute Abdominal Pain Frederick H. Millham CHAPTER OUTLINE Anatomy  151 Visceral Pain  151 Somatic-Parietal Pain  152 Referred Pain  152 Clinical Evaluation  153 Approach to Acute Care  154 History  154 Physical Examination  155 Laboratory Data  156 Imaging Studies  156 Other Diagnostic Tests  156 Causes  156 Acute Appendicitis  157 Acute abdominal pain is a common complaint that brings patients to emergency departments. As many as 1 in 20 emergency department visits is for abdominal pain.1 Approximately half of these patients have nonspecific findings or “gastroenteritis.”2 The other half have a more serious disorder that warrants further evaluation and treatment. A small proportion of patients has a life-threatening disease. Therefore, the evaluation of acute abdominal pain must be efficient and lead to an accurate diagnosis early in the presentation so that the treatment of patients who are seriously ill is not delayed and patients with self-limited disorders are not overtreated. This chapter discusses the anatomic factors that determine how abdominal pain is perceived, a systematic approach to the evaluation of abdominal pain, and common and special circumstances encountered in evaluating patients with acute abdominal pain. ANATOMY Physiologic determinants of pain include the nature of the stimulus, the type of receptor involved, the organization of the neural pathways from the site of injury to the central nervous system, and a complex interaction of modifying influences on the transmission, interpretation, and reaction to pain messages.3,4 Sensory neuroreceptors in abdominal organs are located in the mucosa and muscularis of hollow viscera, on serosal structures such as the peritoneum, and within the mesentery.5 In addition to nociception (the perception of noxious stimuli), sensory neuroreceptors are involved in the regulation of secretion, motility, and blood flow via local and central reflex arcs.6 Although sensory information conveyed in this manner usually is not perceived, disordered regulation of these gastrointestinal functions (secretion, motility, blood flow) can cause pain. For example, patients with irritable bowel syndrome perceive Acute Biliary Disease  157 Small Bowel Obstruction  158 Acute Diverticulitis  158 Acute Pancreatitis  158 Perforated Peptic Ulcer  159 Acute Mesenteric Ischemia  159 Abdominal Aortic Aneurysm  160 Abdominal Compartment Syndrome  160 Other Intra-Abdominal Causes  160 Extra-Abdominal Causes  160 Special Circumstances  161 Pharmacologic Management  161 pain as a result of heightened sensitivity of intestinal afferent neurons to normal endogenous stimuli that results in altered gut motility and secretion (see Chapter 118).7 Abdominal pain is transmitted by two distinct types of afferent nerve fibers, unmyelinated C fibers and myelinated A-δ fibers. These two types of nerve fibers result in the perception of two different types of abdominal pain (visceral and somatic-parietal pain, respectively); interplay between the two systems results in a third type of pain, referred pain. 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. 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 151
    • 152 Section III  Symptoms, Signs, and Biopsychosocial Issues A 1 2 3 1 2 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 3 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. 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 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. 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, welllocalized 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-d 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
    • Chapter 10  Acute Abdominal Pain Heart Midbrain Medulla Larynx Trachea Bronchi Lungs Vagus nerve C1 Superior cervical ganglion Esophagus Stomach T1 Celiac ganglion Abdominal blood vessels Liver Bile ducts Pancreas Superior mesenteric ganglion L1 Inferior mesenteric ganglion Adrenal Small intestine Large intestine S1 Kidney Pelvic nerves Bladder Reproductive organs 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 CLINICAL EVALUATION Effective evaluation of a patient with acute abdominal pain (an acute abdomen) requires careful but expeditious history taking and physical examination (often repeated serially) and, in many cases, informed use of imaging studies. When a carefully performed history and physical examination are paired with appropriate and timely imaging, an accurate diagnosis can often be determined relatively quickly. Inadequate clinical evaluation or poor selection of imaging methods leads to unnecessary delay, often resulting in a 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). To brain C B Spinal cord A Visceral afferent first-order neuron A B Spinal cord second-order neuron Somatic afferent first-order neuron C 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. 153
    • Section III  Symptoms, Signs, and Biopsychosocial Issues poor outcome. Currently, common entities such as appendicitis, cholecystitis, and diverticulitis can be diagnosed with almost complete accuracy; patients with other diseases require an orderly and efficient evaluation and judicious selection of imaging studies. 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: A: Airway: Is the patient able to maintain an airway? Does an impaired sensorium endanger the patient’s airway or pose a risk for aspiration of vomit or oral secretions? B: Breathing: How effectively is the patient breathing? Are breaths rapid and shallow? Is the use of accessory muscles evident? Does the patient appear tachypneic? C: Circulation: Circulation encompasses three areas of assessment: (1) Is the patient in shock, as suggested by pallor, cyanosis, mottling, prostration, hypotension, tachycardia, or other signs of hypoperfusion? (2) Has intravenous access been established? (3) Is there evidence of active bleeding? 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. 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., D B C Severity 154 A 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 Time 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. Table 10-1  Comparison of Common Causes of Acute Abdominal Pain Cause ONSET LOCATION CHARACTER DESCRIPTOR RADIATION Appendicitis Gradual None ++ Acute Acute Gradual Sudden Constricting Boring Ache Burning Scapula Midback None None ++ ++ to +++ Small bowel obstruction Mesenteric ischemia, infarction Ruptured abdominal aortic aneurysm Gastroenteritis Pelvic inflammatory disease Ruptured ectopic pregnancy Gradual Sudden Periumbilical area Periumbilical area Diffuse early; localized late Localized Localized Localized Localized early, diffuse late Diffuse Diffuse Ache Cholecystitis Pancreatitis Diverticulitis Perforated peptic ulcer Periumbilical area early; RLQ late RUQ Epigastrium, back LLQ Epigastrium Cramping Agonizing None None ++ +++ Sudden Abdomen, back, flank Diffuse Tearing None +++ Gradual Gradual Sudden Periumbilical area Either LQ, pelvis Either LQ, pelvis Diffuse Localized Localized Spasmodic Ache Sharp None Upper thigh None + to ++ ++ ++ + = mild; ++ = moderate; +++ = severe; LLQ = left lower quadrant; LQ = lower quadrant; RLQ = right lower quadrant; RUQ = right upper quadrant. INTENSITY +++
    • Chapter 10  Acute Abdominal Pain 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. lent vomitus suggests more distal small bowel or colonic obstruction. A constellation of findings may indicate a particular disease entity. Location Past Medical History The location of abdominal pain provides a clue to interpreting the cause. As noted, a given noxious stimulus may result in a combination of visceral, somatic-parietal, and referred pain, thereby creating confusion in interpretation unless the neuroanatomic pathways are considered. For example, the pain of diaphragmatic irritation from a left-sided subphrenic abscess may be referred to the shoulder and misinterpreted as pain from ischemic heart disease (see Fig. 10-3). Changes in location may represent progression from visceral to parietal irritation, as with appendicitis, or represent the development of diffuse peritoneal irritation, as with a perforated ulcer. Intensity and Character Acute abdominal pain usually follows one of three patterns. Pain that is prostrating, physically incapacitating the sufferer, is usually caused by a severe, life-threatening disease such as a perforated viscus, ruptured aneurysm, or severe pancreatitis. By contrast, patients with obstruction of a hollow viscus, as in intestinal obstruction, renal colic, or biliary pain, present with the gradual onset of cramping pain that follows a sinusoidal pattern of intense pain alternating with a period of relief. Nausea and vomiting are characteristic symptoms associated with this group of disorders. The obstructed viscus need not be the intestine for nausea or vomiting to occur, as in the case of a kidney stone. The third pattern is of gradually increasing discomfort, usually vague and poorly localized at the start, but becoming more localized as the pain intensifies. This picture is usually caused by inflammation, as with acute appendicitis or diverticulitis. Some disorders, such as acute cholecystitis, may start out as colicky pain but evolve into a constant pain as cystic duct obstruction leads to gallbladder inflammation. The clinician should be cautious, however, in assigning too much importance to a patient’s description of the pain; exceptions are common, and a given descriptor may be attributable to a number of conditions. Aggravating and Alleviating Factors The relationship of the pain to positional changes, meals, bowel movements, and stress may yield important diagnostic clues. Patients with peritonitis, for example, lie motionless, whereas those with renal colic may writhe in an attempt to find a comfortable position. Sometimes, certain foods exacerbate pain. A classic example is the relationship between the intake of fatty foods and the development of biliary pain. Pain associated with duodenal ulcer often is alleviated by meals. By contrast, patients with gastric ulcer or chronic mesenteric ischemia may report exacerbation of pain with eating. Patients often self-medicate to alleviate symptoms. A history of chronic antacid use or of nonsteroidal anti-inflammatory drug use, for example, may suggest the presence of peptic ulcer disease. Associated Symptoms Information regarding changes in constitutional symptoms (e.g., fever, chills, night sweats, weight loss, myalgias, arthralgias), digestive function (e.g., anorexia, nausea, vomiting, flatulence, diarrhea, constipation), jaundice, dysuria, changes in menstruation, and pregnancy should be solicited from the patient. A careful review of these symptoms may reveal important diagnostic information. For example, clear vomitus suggests gastric outlet obstruction, whereas fecu- A careful review of the patient’s other medical problems often sheds light on the presentation of acute abdominal pain. Previous experience with similar symptoms suggests a recurrent problem. Patients with a history of partial small bowel obstruction, renal calculi, or pelvic inflammatory disease are likely to have recurrences. A patient whose presentation suggests intestinal obstruction, and who has no prior surgical history, deserves special attention because of the likelihood of surgical pathology, such as a hernia or malignancy. Patients with a systemic illness such as scleroderma, systemic lupus erythematosus, nephrotic syndrome, porphyria, or sickle cell disease often have abdominal pain as a manifestation of the underlying disorder. Abdominal pain also may arise as a side effect of a medication taken for another disease. PHYSICAL EXAMINATION The physical examination of the patient with acute abdom­ inal 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 electro­ cardiogram may suggest mesenteric arterial embolus. All patients should undergo a careful, systematic examination, regardless of the differential diagnosis suggested by the history. Abdominal Examination Examination of the abdomen is central to the evaluation of a patient with acute abdominal pain and should begin with careful inspection. The entire abdomen, from the nipple line to the thighs, should be exposed. Obese patients should be asked whether the degree of protrusion of the abdominal wall is more than usual. Asthenic patients may feel distended but have relatively little apparent abdominal protrusion. Assessment for the presence of bowel sounds and their character should precede any maneuvers that will disturb the abdominal contents. Before concluding that an abdomen is silent, the examiner should listen for at least two minutes and in more than one quadrant of the abdomen. Experienced listeners will distinguish the high-pitched churning of a mechanical small intestinal obstruction from the more hollow sounds of toxic megacolon (like dripping in a cavern). The examiner should begin to palpate the abdomen with the head of the stethoscope while carefully watching the patient’s facial expression. If tenderness is detected, an assessment for rebound tenderness should be carried out next to look for evidence of peritonitis. Rebound tenderness may be elicited by jarring the patient’s bed or stretcher or by finger percussion. Palpation is performed next. If pain is emanating from one particular region, that area should be palpated last to detect involuntary guarding and muscular rigidity. Patients with a rigid abdomen rarely reveal any additional findings (such as a mass) on physical exam­ ination. Because these patients usually have a surgical 155
    • 156 Section III  Symptoms, Signs, and Biopsychosocial Issues emergency, abdominal examination can be done more completely once the patient is under anesthesia, just before laparotomy. Genital, Rectal, and Pelvic Examinations The pelvic organs and external genitalia should be examined in every patient with acute abdominal pain. The rectum and vagina provide additional avenues for gentle palpation of pelvic viscera. Gynecologic pathology should be excluded in all women with acute abdominal pain. 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 Computed Tomography The development of high-speed helical computed tomog­ raphy (CT) scanning has revolutionized the evaluation of acute abdominal pain. In many conditions, such as appendicitis, CT scanning can almost eliminate diagnostic uncertainty. In the pre-CT era, history taking and physical examination alone had a specificity of approximately 80%; by contrast, the sensitivity and specificity of CT scanning for acute appendicitis are 94% and 95%, respectively.17 A negative CT scan in the setting of acute abdo­ inal pain has m considerable value in excluding common disorders. The question arises as to whether CT scanning should be a standard part of the evaluation in all patients with acute abdominal pain. Several arguments as to why CT should not be routine have been raised. First, CT scanning can be performed in a number of ways, and the most efficacious method must be chosen in any given clinical setting. For example, a patient with suspected renal colic should have a limited, non–contrast-enhanced, renal calculus protocol CT; obtaining a standard oral and intravenous contrast CT in this case may obfuscate rather than illuminate the pathology. Alternatively, a patient in whom arterial occlusive disease is suspected should undergo CT arteriography using a bolus intravenous contrast technique. A radiologist should be consulted regarding the selection of the most appropriate CT study in a given patient. Second, some diseases, such as acute cholecystitis and cholangitis, remain relatively invisible on CT. A patient with right upper quadrant pain who is suspected of having either of these diagnoses should undergo an ultrasound examination of the right upper quadrant as the primary diagnostic test. Third, as noted earlier, a patient who is unstable or exhibits signs of shock should be evaluated by a surgeon before any imaging study is considered. In a patient with suspected trauma or hemoperitoneum, the focused abdominal sonogram for trauma (FAST; see later), which can be done at the bedside in the emergency department, is a preferable approach. The presence of shock and fluid in the abdomen is an indication for immediate laparotomy, and further diagnostic maneuvers, including CT, add little value to the patient’s care. A final consideration regarding the role of CT in the evaluation of acute abdominal pain is radiation exposure. Particularly for patients younger than 35 years and those who have required multiple examinations, abdominal CT may increase the lifetime risk of cancer.18 Additionally, unless a life-threatening condition is suspected, CT is best avoided in a pregnant patient, in whom ultrasound examination or magnetic resonance imaging (MRI) may provide a suitable alternative. Ultrasonography A FAST is a rapid, reliable, bedside test to detect fluid in the abdominal cavity. Although its main usefulness is for the evaluation of injured persons, this examination also aids in the diagnosis of any condition that results in free intraperitoneal fluid. Although not part of the formal FAST series, imaging of the aorta can be added, allowing a rapid assessment for aortic aneurysm. General beside ultrasound is likely to be used increasingly by nonradiologists in the future. A Swedish study has demonstrated that the diagnostic accuracy of emergency abdominal examinations by surgeons is increased significantly when an ultrasound examination is added to the evaluation.19 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. CAUSES Acute abdominal pain is usually defined as pain of less than one week in duration. Patients usually seek attention within the first 24 to 48 hours, although some may endure longer periods of abdominal discomfort. The most common reason for a patient to seek emergency department evaluation of abdominal pain is so-called nonspecific abdominal pain. Between 25% and 50% of all patients who visit an emergency department for abdominal pain will have no specific disease identified. The distribution of the causes of abdominal pain in patients who present to an emergency department is shown in Table 10-2.
    • Chapter 10  Acute Abdominal Pain Acute abdominal pain Most likely diagnoses Evaluation ABC Prostration; hemodynamically unstable No RLQ pain (gradual onset); RLQ tenderness, localized rebound tenderness Yes No Gradual onset of RUQ cramping pain; history of postprandial discomfort Yes Resuscitation Urgent surgical consultation Consider FAST examination Consider laparotomy Perforated viscus Severe pancreatitis Ruptured spleen/ hemoperitoneum Ruptured AAA Appendix protocol CT Appendicitis* In female patients, consider pelvic US or CT Yes Tubo-ovarian abscess Ovarian torsion Ectopic pregnancy Cholelithiasis Cholecystitis Bile duct obstruction Cholangitis RUQ ultrasound No Nausea, vomiting, obstipation, constipation, abdominal distention; prior surgery Yes Upright abdominal film or oral contrast CT scan Small bowel obstruction No Sudden onset, diffuse pain; involuntary guarding, rebound tenderness, peritonitis Yes Upright abdominal film or oral contrast CT scan Perforated viscus Diverticulitis Mesenteric infarction Acute pancreatitis Table 10-2  Causes of Acute Abdominal Pain in Patients Presenting to an Emergency Department CAUSE Nonspecific abdominal pain Appendicitis Bowel obstruction Urologic disease Biliary disease Diverticular disease Pancreatitis Medical illness Other PATIENTS (%) 35 17 15 6 5 4 2 1 15 From Irvin TT. Causes of abdominal pain in 1190 patients admitted to a British Surgical Service. Br J Surg 1989; 76:1121-5. 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 appendi­ citis, a low-grade fever to 38°C and mild leukocytosis are usually present. A higher temperature and white blood cell 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. 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 157
    • 158 Section III  Symptoms, Signs, and Biopsychosocial Issues 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 s Murphy’s sign) is essentially diagnostic of acute cholecy­ ­ titis, 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 airfluid 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, intraabdominal, 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
    • Chapter 10  Acute Abdominal Pain 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. Lapa- 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. rotomy 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). 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. 159
    • 160 Section III  Symptoms, Signs, and Biopsychosocial Issues CT is the best initial diagnostic test. Mesenteric angio­ ­ g raphy may be useful for determining the cause of intestinal ischemia and defining the extent of vascular disease. Patients with acute embolic or thrombotic intestinal ische­ mia 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 presen­ tation. 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 intraabdominal 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 highgrade ACS, particularly when renal and respiratory function is com­ romised, laparotomy and creation of an open p 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 Congestive heart failure Endocarditis Myocardial ischemia and infarction Myocarditis Thoracic Esophageal rupture (Boerhaave’s syndrome) Esophageal spasm Empyema Esophagitis Pleurodynia (Bornholm’s disease) Pneumonitis Pneumothorax Pulmonary embolism and infarction Hematologic Acute leukemia Hemolytic anemia Henoch-Schönlein purpura Sickle cell anemia Metabolic Acute adrenal insufficiency (Addison’s disease) Diabetes mellitus (especially with ketoacidosis) Hyperlipidemia Hyperparathyroidism Porphyria Uremia Toxins Hypersensitivity reactions (e.g., to insect bites, reptile venoms) Lead poisoning Infections Herpes zoster Osteomyelitis Typhoid fever Neurologic Abdominal epilepsy Radiculopathy, spinal cord or peripheral nerve tumors, degenerative arthritis of spine, herniated vertebral disk Tabes dorsalis Miscellaneous Familial Mediterranean fever Heat stroke Muscle contusion, hematoma, tumor Narcotic withdrawal Psychiatric disorders
    • Chapter 10  Acute Abdominal Pain SPECIAL CIRCUMSTANCES Extremes of Age Evaluation of acute abdominal pain in patients at the extremes of age is a challenge. Historical information and physical examination findings are often difficult to elicit or are unreliable. Similarly, laboratory data may be misleadingly normal in the face of serious intra-abdominal pathology. For these reasons, patients at the extremes of age often are diagnosed late in the course of the disease, thereby resulting in increased morbidity. For example, the perforation rate for appendicitis in the general population averages 10% but exceeds 50% in infants. A carefully obtained history, thorough physical examination, and high index of suspicion are the most useful diagnostic aids. The occurrence of acute abdominal conditions is highly variable in these populations, and a high index of suspicion is required. In the pediatric population, the causes of acute abdominal pain vary with age. In infancy, intussusception, pyelonephritis, gastroesophageal reflux, Meckel’s diverticulitis, and bacterial or viral enteritis are common. In children, Meckel’s diverticulitis, cystitis, pneumonitis, enteritis, mesenteric lymphadenitis, and inflammatory bowel disease are prevalent. In adolescents, pelvic inflammatory disease, inflammatory bowel disease, and the common adult causes of acute abdominal pain predominate. In children of all ages, two of the most common causes of pain are acute appendicitis and abdominal trauma secondary to child abuse. In the older adult population, biliary tract disease accounts for almost 25% of cases of acute abdominal pain and is followed in frequency by nonspecific abdominal pain, malignancy, intestinal obstruction, complicated peptic ulcer disease, and incarcerated hernia. Appendicitis, although rare in older patients, usually manifests late in its course and is associated with high morbidity and mortality rates. Pregnancy The gravid woman with acute abdominal pain presents a difficult diagnostic dilemma. Pregnant women develop acute appendicitis and cholecystitis at the same rate as their nonpregnant counterparts. A number of additional diag­ noses, such as placental abruption and pain related to tension on the broad ligament, must be distinguished from nonobstetric diagnoses. Furthermore, the risk of radiation injury to the developing fetus must be considered when imaging studies are planned. Surgery in pregnancy is not rare; approximately 1 in 500 pregnancies will be associated with a nonobstetric general surgical intervention.50 Primary consideration is given to the health of the mother. The middle three months of gestation are optimal for abdominal surgical intervention, because this period presents the lowest risk for teratogenicity and spontaneous labor. Emergency interventions during pregnancy carry a risk of fetal loss that varies with the type of intervention and the age of gestation. Appendicitis occurs in approximately 1 in 2000 pregnancies and is equally distributed among the three trimesters. In later stages of pregnancy, the appendix may be displaced cephalad, with consequent displacement of the signs of peritoneal irritation away from McBurney’s point. Ultrasound or, in challenging cases, MRI may be useful for establishing a diagnosis in this setting. Biliary tract disease is also common during pregnancy. Open or laparoscopic management of these diseases is safe but is associated with a rate of preterm delivery of approximately 12% for appendectomy and 11% for cholecystectomy.51 Immunocompromised Hosts In addition to diseases that occur in the general population, such as appendicitis and cholecystitis, a number of diseases unique to immunocompromised hosts may manifest with acute abdominal pain, including neutropenic enterocolitis, drug-induced pancreatitis, graft-versus-host disease, pneumatosis intestinalis, and cytomegalovirus (CMV) and fungal infections. Patients infected with human immunodeficiency virus (HIV) can present a particular challenge. When advanced, HIV infection is associated with a number of other diseases that may present as acute abdominal pain. One of the most common abdominal disorders seen in immunocompromised persons in the developing world is primary peritonitis. Affected patients have suppurative peritonitis without a definable source. Spontaneous intes­ tinal perforation, usually secondary to CMV infection, is also common in patients with advanced HIV infection. Tuberculous peritonitis is a consideration in patients from areas in which tuberculosis is common.52 In general, immunocompromised patients may lack the definitive signs of an acute abdominal crisis usually seen in immunocompetent persons; an elevated temperature, peritoneal signs, and leukocytosis may be absent in these cases. PHARMACOLOGIC MANAGEMENT An unfortunate practice in the care of patients with acute abdominal pain is the delay in administration of narcotics pending definitive surgical assessment. Sir Zachary Cope stated that “Morphine does little or nothing to stop serious intra-abdominal disease, but it puts an efficient screen in front of the symptoms.”53 The practice of delaying relief of pain in a suffering patient, however, does not appear to withstand careful clinical scrutiny. Six studies in which the early administration of analgesia was compared with administration of placebo in patients with acute abdominal pain have shown that the patients who receive analgesics are more comfortable and do not experience a delay in diagnosis.54 Patients with acute abdominal pain frequently are suffering the most intense pain that they have ever experienced and should receive appropriate opioid analgesics early in their care. Patients with acute abdominal processes frequently require antibiotic treatment for peritonitis. When appro­ priate, antibiotic therapy aimed at the likely causative pathogens should be given as soon as a putative diagnosis is reached; little benefit is derived from treating an immunocompetent patient with broad-spectrum antibiotics before a likely source is identified. Patients who are immunocompromised or neutropenic are an exception to this rule. They should receive broad-spectrum antibiotics early in the course of management for acute abdominal pain (see Chapters 37 and 91). KEY REFERENCES An G, West M. Abdominal compartment syndrome: A concise clinical review. Crit Care Med 2008; 36:1304-10. (Ref 49.) Addiss DG, Shaffer N, Fowler B, Tauxe RV. The epidemiology of appendicitis and appendectomy in the United States. Am J Epidemiol 1990; 132:910-25. (Ref 21.) Birnbaum BA, Wilson SR. Appendicitis at the millennium. Radiology 2000; 215:337-48. (Ref 23.) Bohner H, Yang Q, Franke C, et al. Simple data from history and phy­ sical examination help to exclude bowel obstruction and to avoid radiographic studies in patients with acute abdominal pain. Eur J Surg 1998; 164:777-84. (Ref 2.) 161
    • 162 Section III  Symptoms, Signs, and Biopsychosocial Issues Cotton M. The acute abdomen and HIV. Trop Doct 2006; 36:198-200. (Ref 52.) Diaz JJ, Bokhari F, Mowery NT, et al. Guidelines for management of small bowel obstruction. J Trauma 2008; 64:1651-64. (Ref 33.) Frossard JL, Steer ML, Pastor CM. Acute pancreatitis. Lancet 2008; 371:143-52. (Ref 39.) Jacobs DO. Diverticulitis. N Engl J Med 2007; 357:2057-66. (Ref 34.) Maerz L, Kaplan LJ. Abdominal compartment syndrome. Crit Care Med 2008; 36:S212-15. (Ref 48.) Manterola C, Asutdillo P, Losada H, et al. Analgesia in patients with acute abdominal pain. Cochrane Database Syst Rev 2007; (3):CD005660. (Ref 54.) McGory ML, Zingmond DS, Nanayakkara D, et al. Negative appendectomy rate: Influence of CT scans. Am Surg 2005; 71:803-8. (Ref 25.) Parangi S, Levine D, Henry A, et al. Surgical gastrointestinal disorders during pregnancy. Am J Surg 2007; 193:223-32. (Ref 50.) Peng WK, Sheikh Z, Nixon SJ, Paterson-Brown S. Role of laparoscopic cholecystectomy in the early management of acute gallbladder disease. Br J Surg 2005; 92:586-91. (Ref 30.) Silen W. Cope’s early diagnosis of the acute abdomen, 18th ed. New York: Oxford University Press; 1991. p 301. (Ref 16.) Terasawa T, Blackmore CC, Brent S, Kohlwes RJ. Systematic review: Computed tomography and ultrasonography to detect acute appen­ dicitis in adults and adolescents. Ann Intern Med 2004; 141:537-46. (Ref 17.) Full references for this chapter can be found on www.expertconsult.com.