Acute Abdominal Pain PDF 2006

Prim Care Clin Office Pract 33 (2006) 659–684 Acute Abdominal Pain Mark H. Flasar, MDa,b,*, Raymond Cross, MDa,b, Eric Goldberg, MDa,b a Division of Gastroenterology and Hepatology, Department of Medicine, University of Maryland Medical Center, 22 South Greene Street, Baltimore, MD 21201, USA b Veterans Aﬀairs, Maryland Health Care System, 10 North Greene Street, Baltimore, MD 21201, USA Abdominal pain is a complaint seen commonly in the outpatient setting. Many etiologies, both acute and chronic, can be evaluated on an outpatient basis. However, several causes of abdominal pain necessitate prompt, fo- cused, and structured evaluation, given associated morbidity and mortality. The diﬀerential diagnosis of a patient presenting with acute abdominal pain is exhaustive, necessitating that the physician understand not only the un- derlying pathophysiology of the pain, but also the clinical presentation, course, and initial management of more harmful causes. A focused history, physical examination, and adjunctive testing strategy will allow for those pa- tients with concerning presentations to be identiﬁed, initially managed, and appropriately referred for continued care. Abdominal pain is an extremely common complaint in all settings of medical practice. In primary care practices in 2002, abdominal pain was a complaint in more than 13.5 million patient visits. Oftentimes, patients with severe abdominal pain will self-triage to an emergency department, hospital, or contact emergency medical services. However, some patients with potentially life-threatening abdominal catastrophes will initially pres- ent to the primary care physician. Ease of access to the primary care physi- cian and preexisting appointments occurring shortly after the pain onset oﬀer some explanation. Abdominal pain may often be a symptom of a disease process with a benign course, but it may also herald a severe, life-threatening condition that demands prompt recognition and management. The purpose of this re- view is to provide the practitioner with a framework for understanding * Corresponding author. E-mail address: [email protected] (M.H. Flasar). 0095-4543/06/$ - see front matter Ó 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.pop.2006.06.004 primarycare.theclinics.com 660 FLASAR et al abdominal pain, so that they may determine those patients that need a more expedited evaluation. Furthermore, the pathophysiologic mechanisms un- derlying abdominal pain will be reviewed. A general approach to the patient with acute abdominal pain will be outlined, and several gastrointestinal eti- ologies of abdominal pain will be considered in detail, focusing on the most severe and commonly encountered. A general understanding of abdominal anatomy, physiology, and patho- physiology is vital when formulating a diﬀerential diagnosis for abdominal pain. In addition, it is important to understand how abdominal pain is gen- erated and perceived by the patient. The abdominal viscera are innervated with nocioceptive aﬀerents within the mesentery, on peritoneal surfaces, and within the mucosa and muscularis of hollow organs. These aﬀerents re- spond to both mechanical and chemical stimuli producing dull, crampy, poorly localized pain sensations. The principal mechanical stimulus is stretch, while a variety of chemical stimuli including substance P, serotonin, prostaglandins, and hydrogen ions are perceived as noxious by visceral che- moreceptors. Abdominal pain occurs in three broad patterns: visceral, parietal, and referred. Visceral nocioception typically involves stretch and distension of the abdominal organs, although torsion, and contraction also contribute. The pain stimulus is carried on slow-conducting C-ﬁbers. Patients often describe pain of visceral origin as a dull ache. The location of visceral pain is often midline, because visceral innervation of abdominal organs is typically bilateral. Pain location corresponds to those dermatomes that match the innervation of the injured organ. Generally, visceral pain from organs proximal to the Ligament of Treitz, including the hepatobiliary organs and spleen, is felt in the epigastrum. Visceral pain from abdominal organs between the Ligament of Treitz and the hepatic ﬂexure of the colon is felt in the periumbilical region. Visceral pain generated from organs distal to the hepatic ﬂexure is perceived in the midline lower abdomen. Parietal pain is typically sharp and well localized, resulting from the direct irritation of the peritoneal lining. Parietal peritoneal aﬀerents are A-d ﬁbers, with a rapid conduction velocity and result in sharp pain sensation similar to skin and muscle pain. Because parietal innervation is unilateral, lateralization of pain occurs. Referred pain occurs when visceral aﬀerents carrying stimuli from a diseased organ enter the spinal cord at the same level as somatic aﬀerents from a remote anatomic location. It is typically well lo- calized. A single diseased organ may produce all three types of pain. For ex- ample, when a patient develops cholecystitis, gallbladder inﬂammation is initially experienced as a visceral pain in the epigastric region. Eventually, the inﬂammation extends to the parietal peritoneum, and the patient will ex- perience parietal pain that lateralizes to the right upper quadrant. Gallblad- der pain may also refer to the right shoulder. Awareness of the anatomy and innervation of the abdominal viscera al- lows one to formulate a diﬀerential diagnosis of abdominal pain based on the location and distribution of the pain (Table 1). However, there is ACUTE ABDOMINAL PAIN 661 signiﬁcant overlap between abdominal pain presentations. Furthermore, disease processes from organs outside of the abdominal cavity can present with abdominal pain. To considerably narrow the diﬀerential diagnosis, it is crucial to approach each patient in a systematic, logical, and deliberate manner. Having already elicited a chief complaint of abdominal pain, this begins with the patient’s history and physical examination. The history should not only include a thorough assessment of the present condition, but also a detailed assessment of underlying medical problems, medications, family history, substance abuse history, recent travel history and occupational history. Important clues to the etiology of the pain should be determined in the patient’s history by inquiring about the nature of the pain, which includes its quality, location, rapidity of onset, chronicity, radi- ation, intensity, exacerbating factors, alleviating factors, and associated symptoms. Chronicity of symptoms is an important factor in evaluating ab- dominal pain. Generally, patients with chronic symptoms can be evaluated on an outpatient basis, as the process underlying the pain rarely requires acute intervention. On the other hand, patients with new-onset of symptoms are more likely to have a signiﬁcant disease process that can bring them harm in the hours to days ahead. An exception to this is an acute worsening of chronic or intermittent abdominal pain symptoms. Examples include acute mesenteric ischemia superimposed on a history of chronic intestinal angina or development of acute cholecystitis in a patient with a history of biliary colic. Additionally, identifying high-risk patients such as the elderly, pregnant, and those with immunodeﬁciency syndromes proves invaluable in triaging patients. Following a thorough history, a focused physical examination should be performed. The generation of a diﬀerential diagnosis will help the practi- tioner tailor the examination, whose purpose is to provide conﬁrmatory or contradictory data for each disease process on their diﬀerential. Although centered on the abdomen, the examination should also focus on extraabdo- minal organ systems when indicated. For example, a patient with suspected mesenteric ischemia should have a cardiovascular examination assessing for arrhythmias and evidence of atherosclerotic disease. Overall, the abdominal examination should begin with general observa- tion of the patient, followed by abdominal inspection. A patient with peri- tonitis often lies completely still as movement further irritates the peritoneum. Their abdomen will be visually rigid. On the other hand, a pa- tient with renal colic may writhe in pain, may not be able to be consoled to comfort, and have a nonrigid abdomen. Once initial observation is com- plete, a review of the vital signs is imperative. Any signiﬁcant abnormality of vital signs should prompt the physician to consider a more life threaten- ing process. Auscultation of the abdomen determines whether intestinal peristalsis is appropriate and whether any abdominal bruits are present. Next, palpation of the abdomen should be performed to distinguish pain, a subjective sensation, from tenderness, which is an objective ﬁnding. 662 FLASAR et al Table 1 Diagnosis of abdominal pain based on location and distribution Right upper quadrant Middle upper abdomen Left upper quadrant Peptic ulcer disease Peptic ulcer disease Peptic ulcer disease Biliary disease Pancreatitic disease Splenic disease Biliary colic Pancreatitis Splenic rupture Choledocholithiasis Pancreatic neoplasm Splenic infarct Cholecystitis Biliary disease Pancreatic disease Cholangitis Biliary colic Pancreatitis Liver disease Choledocholithiasis Pancreatic neoplasm Hepatitis Cholecystitis Lung disease Neoplasm Cholangitis Pneumonia Abscess Esophageal disease Subphrenic abscess Congestive hepatopathy Reﬂux esophagitis Pulmonary embolism Lung disease Infectious esophagitis Pneumothorax Pneumonia Pill esophagitis Kidney disease Subphrenic abscess Cardiac disease Pyelonephritis Pulmonary embolism Myocardial ischemia Perinephric abscess Pneumothorax or infarction Nephrolithiasis Abdominal wall Pericarditis Herpes zoster AAA rupture/aortic Muscular Stain dissection Kidney disease Mesenteric ischemia Pyelonephritis Perinephric abscess Nephrolithiasis Colonic causes Colitis Right sided diverticulitis Periumbilical Appendicitis (early) Small bowel obstruction Gastroenteritis Mesenteric ischemia AAA rupture Aortic dissection Right lower quadrant Suprapubic Left lower quadrant Appendicitis Inﬂammatory bowel disease Inﬂammatory bowel disease Inﬂammatory bowel disease OB-GYN causes OB-GYN causes OB-GYN causes Ovarian tumor Ovarian tumor Ovarian tumor Ovarian torsion Ovarian torsion Ovarian torsion Ectopic pregnancy Ectopic pregnancy Ectopic pregnancy PID PID Pelvic inﬂammatory disease (PID) Dysmenorrhea Kidney disease Kidney disease Colonic disease Pyelonephritis Pyelonephritis Proctocolitis Perinephric abscess Perinephric abscess Diverticulitis Nephrolithiasis Nephrolithiasis Urinary tract disease Intestinal disease Intestinal disease Cystitis Sigmoid diverticulitis Right sided diverticulitis Nephrolithiasis Ileocolitis Ileocolitis Prostatitis Gastroenteritis Gastroenteritis Hernia Hernia ACUTE ABDOMINAL PAIN 663 Table 1 (continued) Diﬀuse Gastroenteritis Bowel obstruction Peritonitis Mesenteric ischemia Inﬂammatory bowel disease Diabetic ketoacidosis Porphyria Uremia Hypercalcemia Sickle cell crisis Vasculitis Heavy metal intoxication Opiate wihdrawal Familial mediterranean fever Hereditary angioedema When performing palpation, the location of tenderness should be used to narrow the diﬀerential diagnosis. Additionally, the presence of guarding or rebound tenderness should be noted, as these ﬁndings imply peritoneal irritation. Furthermore, palpation can determine the presence of visceral en- largement, masses, or ﬂuid. It is often useful to begin the abdominal exam- ination by palpating distant from, then working toward the site of pain, palpating with the ﬁngertips. It is helpful to keep the patient’s hips and knees in a ﬂexed position during a supine examination to help relax the ab- dominal musculature. Techniques such as patient distraction during exami- nation or palpation during auscultation with the stethoscope head may help discriminate functional from organic pain. The importance of a properly executed history and physical examination cannot be underestimated. Although the sensitivity and speciﬁcity of a his- tory and physical may not match that of an abdominal CT scan, there is no risk, minimal time required, and essentially no cost. In fact, one observa- tional study revealed that, based on history and physical alone, physicians were able to correctly diﬀerentiate between organic and nonorganic causes of abdominal pain nearly 80% of the time. Furthermore, historic features such as pain location have been shown in prospective investigation to be speciﬁc for certain disease states. Once the history and physical is com- pleted, the practitioner will usually be armed with suﬃcient information to sharply narrow the diﬀerential diagnosis in the majority of patients pre- senting with abdominal pain. The detection of the warning signs of a life-threatening process in a pa- tient with abdominal pain is often up to the primary physician long before the emergency room physician, surgeon, gastroenterologist, or other special- ist encounters the patient. Certain historic and examination ﬁndings should raise red ﬂags that a life-threatening abdominal process is present, and 664 FLASAR et al prompt early triage to an emergency department or inpatient hospital bed (Table 2). Red ﬂags from the history include fever, vomiting, inability to move the bowels (obstipation), syncope, concomitant chest or back pain, re- spiratory distress, excessive acute vaginal bleeding, and overt gastrointesti- nal bleeding. Red ﬂags from the physical examination include any signiﬁcant abnormality of the vital signs, mental status changes, involuntary guarding, rebound abdominal tenderness, complete absence of bowel sounds, and pain out of proportion to abdominal tenderness on physical examination. In patients without signs or symptoms of an acute abdominal catastro- phe, an acute expedited outpatient evaluation should be performed. Selec- tion of initial laboratory and imaging studies to evaluate abdominal pain should be guided by the diﬀerential diagnoses generated from the primary evaluation. Historically, plain abdominal radiographs have been the initial imaging test of choice. They can be obtained rapidly at a relatively low cost, and are often available to primary practitioners in the oﬃce. However, with the evolution of more sensitive and speciﬁc modalities such as CT and ultrasound, the utility of the plain abdominal series has been debated. None- theless, the authors feel that plain ﬁlms should still be the initial imaging modality in patients with suspected visceral perforation or obstruction. The abdominal plain ﬁlm series should include supine and upright ab- dominal ﬁlms in conjunction with an upright chest (or lateral decubitus ab- dominal) ﬁlm. Plain abdominal imaging has been estimated to be diagnostic in up to 60% of cases of suspected small bowel obstruction , although sensitivity is more limited in cases of low-grade obstruction. The location, volume, and distribution of intraluminal air, presence and distribution of air–ﬂuid levels, and luminal diameter can often be helpful in diﬀerentiating between an obstructive and nonobstructive process, such as partial or com- plete bowel obstruction, ileus, or intestinal pseudoobstruction. Unfortu- nately, overlap in the radiographic appearance of obstructive and nonobstructive processes limits the sensitivity and speciﬁcity of plain ﬁlms in this setting. The ability of plain ﬁlms to detect free air depends on the volume of free air within the peritoneal cavity. For the detection of large volumes, as would be expected with a perforated viscus, sensitivity of plain ﬁlms is reported to be as high as 100%. Sensitivity is maximized if the patient is placed in the upright or decubitus position for 5 to 10 minutes before obtaining an up- right chest or lateral decubitus ﬁlm. This allows small volumes of air to re- distribute to and collect within nondependent areas. Detection of volumes as small as 1 to 2 cc of air has been reported using this method [6,7]. CT is an imaging tool that is sensitive for the diagnosis of many etiologies of abdominal pain. Because of its widespread availability, CT is often acces- sible to primary care providers in the outpatient setting for same-day inter- pretation. With newer rapid helical scanning methods, advances in intravenous and oral contrast agents, three-dimensional reformatting, and Table 2 Red ﬂags in abdominal pain History Physical exam Labs Radiography * Inability to maintain po intake * Pathologic changes in vital signs * Renal failure * Abdominal free air ACUTE ABDOMINAL PAIN * Projectile vomiting * Bloody, maroon, or melanotic stool * Metabolic acidosis * Gallbladder wall thickening * Overt gastrointestinal blood loss * Hernia (incarcerated and tender) * Leukocytosis * Pericholecystic ﬂuid * Syncope * Hypoxia * Elevated transaminases * Dilated biliary tree * Pregnancy * Cyanosis * Elevated alkaline phosphatase and * Bowel obstruction * Recent surgery or endoscopic * Altered mentation bilirubin * Dilated small bowel loops procedure * Jaundice * Anemia or polycythemia air ﬂuid levels * Fever * Peritoneal signs * Hyperlipasemia/hyperamylasemia * Intraabdominal abscess * Caustic or foreign body ingestion * Abdominal pain out of proportion * Hyperglycemia/hypoglycemia * Bowel wall thickening to examination * Air in the portal venous system * Pneumatosis intestinalis 665 666 FLASAR et al other advanced software capabilities, CT has become the initial imaging mo- dality of choice for the evaluation of most presentations of acute abdominal pain. For example, CT diagnoses acute appendicitis with a reported sensitiv- ity and speciﬁcity as high as 98% and 97%, respectively. In fact, the su- perior diagnostic capability of CT is rendering plain ﬁlms obsolete. Even in situations where plain ﬁlms have proven diagnostic accuracy, such as perfo- rated viscus or small bowel obstruction, many physicians now opt for CT as the initial imaging study. Computed tomography has proven to be more sensitive and speciﬁc for nearly all etiologies of acute abdominal pain [9–11]. In patients with abdominal pain suspected to be from a hepatobiliary source, abdominal ultrasonography should be considered as an initial imag- ing option. It is accurate for the detection of gallstones and dilation of the biliary tree. However, ultrasound is less sensitive for stones in the common bile duct. Although MRI can be highly accurate in the diagnosis of acute abdominal pain, high cost and lack of immediate availability limit its use in the primary care setting. Following clinical evaluation of patients with abdominal pain, the pri- mary physician must appropriately triage the patient. In addition to red ﬂags revealed by the history and physical examination, there are laboratory and radiographic ‘‘red ﬂags’’ that should alert the physician of a potentially more serious cause of the abdominal pain (Table 2). Although cardiac, pulmonary, urologic, musculoskeletal, and gyneco- logic causes of abdominal pain will not be speciﬁcally addressed in this re- view, it is important to keep these extraabdominal disease processes in the diﬀerential diagnosis of abdominal pain. Red ﬂags that a life-threatening ex- traabdominal cause of abdominal pain is present include chest pain, back pain, shortness of breath, vaginal bleeding, and hemodynamic instability. Finally, there is a spectrum of systemic medical disorders, such as adrenal insuﬃciency, diabetic ketoacidosis, porphyria, and sickle cell pain crisis, that can present with abdominal pain. Evidence of these disorders in the past medical history, medications, or physical examination should prompt their consideration as the cause of the patient’s pain. Although a detailed discussion of all of the potential etiologies of acute abdominal pain is be- yond the scope of this review, there are some etiologies that merit a more detailed discussion. What follows is an overview of those gastrointestinal etiologies of abdominal pain that can often be seen in adults in the out- patient setting, with a focus on those etiologies prone to more serious or life-threatening complications. Hepatopancreatobiliary Biliary colic When patients with cholelithiasis present with abdominal pain, they will most commonly have biliary colic as the cause. Biliary colic occurs when ACUTE ABDOMINAL PAIN 667 then one or more gallstones transiently occlude the cystic duct. Tonic cystic duct spasm ensues, causing pain. Patients typically experience visceral epi- gastric or right upper quadrant abdominal pain, often with radiation to the right shoulder or scapula. The pain is sometimes postprandial, but often there is no trigger; it is not uncommon for patients to have nocturnal pain. The term biliary colic is a misnomer, as the pain is not colicky in nature. The classic time course of pain from biliary colic is one that builds over 15 to 60 minutes, lasting up to several hours before slowly dissipating. Physical ex- amination is typically benign, with tenderness sometimes elicited in the epi- gastrum or right upper quadrant of the abdomen. Patients suspected of having biliary colic should have further evaluation with liver function tests and abdominal ultrasonography. Transaminases, bilirubin, and alkaline phosphatase are usually normal, and an ultrasound can verify the presence of gallstones. Although biliary colic usually resolves without sequelae, it identiﬁes those patients whom are at higher risk for complications of gall- stone disease, such as pancreatitis or cholangitis. Therefore, referral to a gen- eral surgeon for elective cholecystectomy is recommended. Cholecystitis More than 90% of cases of acute cholecystitis are caused by gallstones. The remainder of cases are termed acalculous cholecystitis, typically occur in critically ill patients, and are rarely seen in the outpatient setting. Acute cholecystitis is most commonly caused by the obstruction of the cystic duct by the oﬀending gallstone. Prolonged obstruction of the cystic duct (O6 hours) impairs gallbladder emptying, leading to inﬂammation of the gallbladder mucosa. Secondary bacterial infection of the gallbladder may ensue, leading to possible empyema, gallbladder necrosis, and perforation. Acute cholecystitis results in gallbladder perforation in up to 12% of cases, with a subsequent mortality rate of 20%. Emphysematous cholecystitis, characterized by air in the wall of the gallbladder, is most often seen in pa- tients with diabetes mellitus. Approximately 75% of patients who develop acute cholecystitis have a prior history of biliary colic. The pain is sim- ilar to that of biliary colic, but with a longer duration. Pain lasting longer than 6 hours signiﬁes cholecystitis rather than biliary colic. As acute gall- bladder inﬂammation irritates the parietal peritoneum, the pain may shift from the epigastrum to the right upper quadrant. The physical examination of patients with acute cholecystitis reveals right upper quadrant tenderness. An inspiratory arrest during deep right upper quadrant palpation is referred to as Murphy’s sign. Laboratory abnormalities include leukocytosis with a predominance of neutrophils, and elevation of alkaline phosphatase, and transaminases. Hy- perbilirubinemia generally does not occur with acute cholecystitis owing to the unimpeded ﬂow of bile through the common bile duct. An exception is Mirizzi’s syndrome, where a large stone in the cystic duct compresses or 668 FLASAR et al erodes into the common hepatic duct, resulting in variable degrees of biliary obstruction. Right upper quadrant ultrasonography is the test of choice to diagnose acute cholecystitis, with reported sensitivity, speciﬁcity, and accu- racy approaching 95%. Common ﬁndings include cholelithiasis, gallblad- der wall thickening, pericholecystic ﬂuid, and a sonographic Murphy’s sign. The latter ﬁnding occurs when ultrasound transducer pressure on the gall- bladder results in tenderness. The ﬁnding of cholelithiasis and a positive so- nographic Murphy’s sign has a positive predictive value of 92% for acute cholecystitis. Conversely, when both of these ﬁndings are absent, the nega- tive predictive value is 95%. Radionuclude cholescintigraphy scans, such as the HIDA scan, can be used to conﬁrm the diagnosis of acute cholecys- titis when ultrasound ﬁndings are equivocal. The sensitivity, speciﬁcity, and positive predictive value for acute cholecystitis are 95%, 99%, and 97%, respectively. Patients with suspected acute cholecystitis should have an expedited eval- uation with early surgical consultation. Cholecystectomy within 24 to 48 hours of presentation has been shown to reduce mortality and shorten length of hospital stay, compared with surgery performed after weeks of conservative management aimed at ‘‘cooling oﬀ’’ the gallbladder [16–18]. The beneﬁts of early cholecystectomy have been prospectively validated for the laparoscopic approach as well [19–23]. Cholangitis Ascending cholangitis is a potentially lethal entity that occurs when the bile duct become obstructed. Once bile ﬂow is impeded, superinfection of the stagnant bile occurs. As pus builds up under pressure, the infection can rapidly ascend into the liver and spread into the blood stream. Common pathogens include Escherichia coli, Klebsiella species, Bacteroides, Entero- coccus, and other enteric pathogens. The most common cause of ob- struction in the United States is choledocholithiasis, accounting for approximately 85% of cases. Benign biliary strictures, choledochal cysts, bil- iary parasites, and neoplasms are less common causes of cholangitis. The classic presentation of cholangitis is fever, jaundice, and right upper quadrant pain. These ﬁndings are collectively referred to as Charcot’s triad, which has a reported sensitivity for cholangitis as high as 75%. If the obstruction is not relieved, mental obtundation and shock can occur. The combination of Charcot’s triad with these ﬁndings is known as Reynold’s pentad, which is associated with a higher morbidity and mortality rate. Laboratory ﬁndings include leukocytosis with a predominance of neutro- phils, elevated alkaline phosphatase, and elevation of the transaminases. An elevation of pancreatic enzymes can be seen in about one third of patients, especially with concomitant gallstone pancreatitis. As the pathophysiol- ogy of this disorder involves common bile duct obstruction, conjugated hy- perbilirubinemia is invariably present. ACUTE ABDOMINAL PAIN 669 The diagnosis of cholangitis is often made clinically, and should be con- ﬁrmed with cholangiography. Although ultrasonography may suggest the presence of biliary obstruction, its sensitivity for choledocholithiasis is poor. Therefore, when the clinical diagnosis of ascending cholangitis is suspected, patients should undergo cholangiography even in the setting of an unremarkable right upper quadrant ultrasound. Patients suspected of having acute cholangitis should be referred quickly to an emergency department or hospitalized, as the clinical course can be rapidly progressive and fatal if left untreated. Patients with suspected chol- angitis should have blood cultures drawn at presentation, so that therapy can be directed toward the oﬀending pathogen. The deﬁnitive therapy for cholangitis is decompression of the obstructed biliary system. Endoscopic retrograde cholangiopancreatography (ERCP) is the diagnostic and thera- peutic procedure of choice, and is successful in relieving the obstruction in more than 95% of cases. This is typically accomplished by stone ex- traction or placement of a stent into the common bile duct. In cases where therapeutic ERCP is not available or is unsuccessful, options include per- cutaneous transhepatic cholangiography or surgical decompression. If choledocholithiasis is the cause of ascending cholangitis, patients should un- dergo elective cholecystectomy once the infection resolves. Acute pancreatitis Acute pancreatitis is an inﬂammatory disease of the pancreas that not only may cause signiﬁcant morbidity but also carries a case fatality rate of 5% to 9%. Gallstones and alcohol account for more than 80% of cases in the United States. Less common causes of pancreatitis include medications, trauma, hypercalcemia, severe hypertriglyceridemia (O1000 mg/dL), malignancy, sphincter of Oddi dysfunction, infections, iatrogenic (ERCP), and congenital abnormalities of the pancreas such as pancreas di- visum. The remainder are termed idiopathic, although as many as 75% of cases of idiopathic pancreatitis may actually be due to biliary sludge or mi- crolithiasis. Regardless of the etiology, diﬀuse pancreatic inﬂammation and edema develop. In severe cases, necrosis of pancreatic and peripancre- atic tissue occurs, and multiorgan failure may ensue. Necrotizing pancreati- tis occurs in up to 25% of patients with pancreatitis and has a mortality rate of 15% to 20% [28,30]. Patients typically present with the acute onset of ab- dominal pain, nausea, and vomiting. The pain is steady and usually in the epigastrium, although patients may also note discomfort in the right or left upper quadrants of the abdomen. Pain is classically described as a boring sensation that radiates into the back. Patients are often unable to get com- fortable when lying supine, and they will lean forward in an attempt to ﬁnd relief. Because of marked ﬂuid shifts, patients may become severely volume depleted. Resultant tachycardia and hypotension with orthostatic changes may develop. Other vital sign abnormalities include low-grade fever and 670 FLASAR et al tachypnea. The latter is a poor prognostic sign, and may herald the develop- ment of sepsis or acute respiratory distress syndrome. The abdominal examination may reveal distension and diminished or ab- sent bowel sounds secondary to the development of a paralytic ileus. With palpation, focal tenderness in the epigastrum is seen, although the abdomen may also be diﬀusely tender. With more severe cases, voluntary guarding and rebound tenderness may also be appreciated. Signs of hemorrhagic pan- creatitis such as Gray Turner’s sign (ﬂank ecchymosis), Cullen’s sign (peri- umbilical ecchymosis), or Fox’s sign (inguinal ecchymosis) are seen in less than 1% of cases. When acute pancreatitis is suspected clinically, levels of serum amylase or lipase should be determined. In the setting of suspected acute pancreatitis, levels greater than three times the normal values have a high speciﬁcity for acute pancreatitis. Serum lipase remains elevated for longer durations than serum amylase and is more speciﬁc for acute pancre- atitis. It is important to note that the magnitude of serum amylase and lipase elevation does not correlate well with disease severity. Because of the marked intravascular volume depletion secondary to third spacing, hemo- concentration often occurs in acute pancreatitis. Hematocrit levels higher than 44% are associated with a worse prognosis, indicating potentially dangerous ﬂuid shifts. Hyperbilirubinemia, elevations of the alkaline phosphatase, and alanine aminotransferase levels O150 mg/dL suggest gallstones as the etiologic cause of the pancreatitis. Because of marked ﬂuid shifts that occur with acute pancreatitis, blood urea nitrogren, creati- nine, and serum electrolytes including calcium should be assessed. Imaging of the pancreas with CT can conﬁrm the diagnosis of acute pan- creatitis, but is not necessary in all cases. The authors feel that CT scanning should be reserved for patients in whom the diagnosis is in question, in cases of suspected pancreatic necrosis, or in cases of clinical deterioration despite adequate medical therapy. Use of intravenous contrast is highly recommen- ded, and CT should therefore be deferred until the patient has received ad- equate volume resuscitation to prevent nephrotoxicity. Because the care of patients with acute pancreatitis is complicated by the diﬃculty in diﬀerentiating whether a patient’s course will be mild or severe, several scoring systems have been developed to assess the severity in acute pancreatitis and determine prognosis. The most well known of these criteria is Ranson’s criteria, which was originally developed for alcoholic pancreati- tis and later modiﬁed and validated for gallstone pancreatitis. Ranson’s cri- teria has limited clinical value because it takes 48 hours to determine. The Imrie/Glasgow criteria and APACHE II score are two other prospective sys- tems, but both are cumbersome to perform. A prognostic CT scoring sys- tem, known as the Balthazar criteria, has been validated for predicting severity in acute pancreatitis. The score is heavily weighted on the presence of pancreatic necrosis. The cornerstone of therapy in acute pancreatitis is intravenous volume resuscitation coupled with the prevention of pancre- atic stimulation. Patients should be kept strictly nothing by mouth, and ACUTE ABDOMINAL PAIN 671 therefore require a hospital setting for treatment. Very aggressive intrave- nous ﬂuid repletion is necessary to maintain intravascular volume and allow adequate perfusion of the pancreas and extrapancreatic organs such as the kidneys. Luminal and vascular disorders Acute appendicitis Acute appendicitis is the most common abdominal surgical emergency in the United States, with over 250,000 appendectomies performed annually. Most cases of appendicitis are believed to result from obstruction of the appendiceal lumen by fecaliths. Following obstruction, increased intra- luminal pressure causes local ischemia, leading to transmural inﬂammation. Secondary bacterial infection occurs, and gangrene and perforation of the appendix may result. A thorough history and physical examination are all that is required to make a clinical diagnosis of appendicitis, thereby height- ening the importance of the initial care provider’s assessment. As a result of appendiceal hypertension and distension, a crampy visceral type pain is ini- tially felt in the peri-umbilical region. There is often associated nausea, vom- iting, and fever. As the inﬂammatory process progresses, and directly irritates the parietal peritoneum, the quality of the pain becomes sharp and shifts to the right lower quadrant (RLQ). Almost all patients with ap- pendicitis will lose their appetite, and if a patient exhibits hunger, the clinical diagnosis of appendicitis should be questioned. Auscultation of the abdomen reveals diminished or absent bowel sounds. Classically, the examination of patients with appendicitis reveals tenderness to palpation at McBurney’s point, anatomically located two thirds of the way from the umbilicus to the anterior superior iliac spine. Guarding, rigid- ity, and rebound tenderness may be present from peritoneal irritation. Rovs- ing’s sign may be present, which is RLQ pain upon left lower quadrant palpation. The obturator and iliopsoas signs can be elicited by internal ro- tation of the right hip and extension of the right hip, respectively. The ﬁnd- ing of abdominal pain during either maneuver occurs as a result of the inﬂammatory process, irritating the respective muscles during passive movement. Patients who present with acute abdominal pain that migrates from the umbilicus to the right lower quadrant, whom also exhibits RLQ tenderness on palpation, should be referred for emergent appendectomy. The accuracy of the clinical diagnosis in this situation has been estimated to be nearly 95%. However, this classic presentation of appendicitis occurs only in two thirds of patients. Atypical presentations account for the remain- der. They result from either anomalous appendiceal anatomy, or certain populations of patients that are more prone to atypical presentations of common diseases, such as the elderly, immunocompromised, or pregnant 672 FLASAR et al patients. For example, a retrocecal appendix that becomes inﬂamed may produce right ﬂank rather than abdominal pain. Patients older than 55 years of age may present with vague symptoms and exhibit more subtle examina- tion ﬁndings, thereby causing a delay in diagnosis. This delay can result in a higher rate of perforation compared with their younger counterparts. Finally, misdiagnosis is more common in premenopausal women owing to a broadened gynecologic diﬀerential diagnosis and confusing presentations. Therefore, the importance of considering this diagnosis at any age re- mains important. Patients with suspected appendicitis should be made nothing by mouth (NPO) and started on intravenous ﬂuids. The prophylactic use of antibiotics is not supported by the literature, and should only be used in cases of sus- pected perforation. Because of the potential perforation risk, patients with a clinical diagnosis of appendicitis should undergo emergent surgical inter- vention. Historically, a 20% presurgical false positive rate has been consid- ered acceptable. In patients where the clinical diagnosis is uncertain, imaging studies and observation admissions for serial abdominal examina- tions may decrease this false positive rate. In any woman of childbearing age, pregnancy should be ruled out with a serum or urinary b-human cho- rionic gonadotropin (b-HCG) test before imaging or appendectomy. Diverticulitis Nearly a third of patients over the age of 50, and two thirds by the age of 80 have diverticular disease. Diverticulitis, a complication caused by the perforation of a diverticulum, aﬀects up to 25% of patients with diverticular disease. Inspissated food, stool, and increased intraluminal pressure are believed to be involved in the pathogenesis of diverticular perforation. The clinical presentation of patients with diverticulitis is dependent on the extent of the perforation. Small perforations are walled oﬀ by surrounding mesen- tery and pericolonic fat, while larger perforations can result in extensive in- traperitoneal abscess formation and frank peritonitis. The location of abdominal pain in patients symptomatic with diverticulitis is dependent on the location of the perforated diverticulum. Diverticular disease most commonly aﬀects the sigmoid colon, so patients most often present with crampy, left lower quadrant abdominal pain. However, patients with a re- dundant sigmoid colon or diverticular disease involving the right colon may complain of RLQ abdominal pain. Patients may additionally com- plain of nausea, vomiting, fever, and anorexia. Physical examination often reveals tenderness over the inﬂamed area, and an inﬂammatory mass may be palpable in some patients. In patients with free perforation, peritoneal signs such as rebound, guarding, and rigidity may be present. Although the diagnosis can often be made on clinical grounds alone, an imaging study should be performed during a patient’s initial presentation to conﬁrm the presence of diverticula. This can be done as an outpatient, ACUTE ABDOMINAL PAIN 673 provided none of the aforementioned red ﬂags are present. CT of the abdo- men and pelvis with intravenous and oral contrast is the diagnostic modality of choice, with a reported sensitivity as high as 98%. Colonoscopy should not be performed in patients with suspected diverticulitis, as perfora- tion is a contraindication for endoscopy. Management of mild, uncomplicated diverticulitis can occur on an out- patient basis, and consists of a clear liquid diet and the administration of oral antibiotics that cover typical gastrointestinal pathogens. Complicated diverticulitis occurs when patients develop intraabdominal abscesses, ﬁstula, free perforation, or intestinal obstruction. Patients with complicated diver- ticulitis or those with mild disease who fail to respond to above therapies require hospitalization. Patients should be started on intravenous antibi- otics, made NPO, and be evaluated by a surgeon. Intraabdominal abscesses can often be managed with percutaneous drainage catheters, but surgery is sometimes required. Free perforation or intestinal obstruction usually mandates emergent surgery. Obstruction Bowel obstruction occurs when the normal ﬂow of intestinal contents is interrupted by a mechanical blockage. In patients with a history of abdom- inal surgery, nearly 75% of cases of small bowel obstruction (SBO) are the result of adhesive peritoneal bands [44–46]. In fact, up to 15% of patients who undergo laparotomy will be readmitted within 2 years with SBO from adhesions, while up to 3% will require operative intervention as a result. Furthermore, it is estimated that the 10-year risk of developing recur- rent SBO from adhesions is around 40%. Hernias are the second most common cause of SBO, and account for up to 25% of cases. The re- mainder of cases of SBO result from a number of etiologies, including Crohn’s disease, volvulus, neoplasm, intussusception, gallstones, and ische- mia. The clinical presentation of large bowel obstruction (LBO) is very sim- ilar to that of SBO. Nearly 60% of cases of LBO are the result of malignancy, with colon cancer being the most common. Other causes in- clude diverticular strictures and colonic volvulus. The cecum and the sigmoid colon are the most common locations of colonic volvulus. Once the bowel is obstructed, the segment of bowel proximal to the obstruc- tion becomes increasingly distended by swallowed air, gas from bacterial fermentation, and luminal secretions. Bacterial overgrowth, bowel edema, and loss of absorptive function follow. If the obstruction is not promptly treated, then ischemia, necrosis and perforation may occur. The pain caused by SBO is a colicky, diﬀuse pain that waxes and wanes over 5- minute intervals. Nausea, vomiting, distention, and obstipation are often associated with the abdominal pain. Emesis is often feculent due to bacterial overgrowth. The passage of stool and ﬂatus do not eliminate SBO from the diﬀerential diagnosis, as luminal contents distal to the 674 FLASAR et al blockage can still pass. Patients will often exhibit physical signs of volume depletion. Abdominal examination reveals a distended abdomen with either hyperactive high-pitched or hypoactive bowel sounds. Rushes of luminal ﬂuid can often be heard. The abdomen is usually diﬀusely tender, with ﬁnd- ings of rigidity, rebound tenderness, or guarding suggesting peritonitis. A ventral, inguinal, or periumbilical hernia should be sought as a potential eti- ology for the obstruction. Laboratory analysis is usually nonspeciﬁc, but common abnormalities include hemoconcentration, leukocytosis, and elec- trolyte imbalances. An abdominal plain ﬁlm series should be the initial diagnostic imaging test in patients with suspected obstruction. Typical ﬁndings include air–ﬂuid levels, small bowel distention, and a paucity of air in the rectal vault. In ad- dition, evidence of complications such as intraperitoneal free air can be seen. Although most diagnoses can be made clinically with the conﬁrmatory assis- tance of plain ﬁlms, there are instances where plain ﬁlms are not suﬃcient. In these instances, CT may be helpful for both diagnosing SBO and deter- mining the etiology, with a reported sensitivity of 100% and accuracy of 90% [51,52]. Patients with evidence of bowel obstruction should be admitted to the hospital, both for decompression and observation. Patients are initially managed with strict restriction of oral intake, nasogastric tube decompres- sion, intravenous ﬂuids, and electrolyte repletion. Early surgical evaluation is mandatory given the perforation risk if left unattended. The philosophy that ‘‘the sun should neither rise nor set on a bowel obstruction,’’ still remains true today. Peptic ulcer disease Peptic ulcer disease (PUD) is a common aﬄiction that signiﬁcantly im- pacts quality of life. In 1989, more than 5 billion dollars were spent on the care of patients with PUD. Helicobacter pylori infection, the most common cause of PUD, has been associated with 75% to 95% of duodenal ulcers (DU) and 65% to 95% of gastric ulcers (GU) [54–56]. Nonsteroidal anti-inﬂammatory medications (NSAIDs) are the second most common cause of PUD, with an estimated yearly incidence of clinically signiﬁcant gastric or duodenal ulceration of approximately 1.5%. Use of NSAIDs presents a particular challenge, as up to 40% of patients will not report the use of NSAIDs. Acid hypersecretory syndromes such as Zollinger Elli- son syndrome accounts for the majority of the remaining cases. The clinical presentation of PUD depends on the location of the ulcer, and whether com- plications from the ulcer develop. Complications of PUD include bleeding, obstruction, perforation, and penetration into adjacent structures. Patients with uncomplicated peptic ulcers may be asymptomatic, or they may present with pain in the upper abdomen [59,60]. The pain is typically described as a burning or gnawing pain, but patients may occasionally describe it as ACUTE ABDOMINAL PAIN 675 crampy. Nausea and vomiting may also be seen. Relation of pain to meals is unreliable to diﬀerentiate DU from GU. Bleeding from PUD may present with melena, hematochezia, or hema- temesis, with or without hemodynamic compromise. Bleeding can generally be managed medically with intravenous ﬂuid, blood transfusions, antisecre- tory therapy, and endoscopic therapy. Endoscopy is also useful to determine the risk for recurrent bleeding. Surgical or angiographic intervention is reserved for bleeding refractory to endoscopic therapies. Pyloric channel and duodenal bulb ulcers may cause gastric outlet obstruction. In addition to epigastric pain, patients with outlet obstruction may present with nausea, projectile vomiting, early satiety, anorexia, and weight loss. Conservative measures are often successful, although many patients will require surgery or endoscopic dilatation therapy [62,63]. Most ulcers that perforate are lo- cated in the duodenal bulb, and are often associated with NSAID use [64,65]. Patients present with the sudden onset of epigastric pain that quickly becomes diﬀuse as generalized peritonitis ensues. Patients can sometimes de- velop paradoxic improvement in their pain following perforation despite a markedly rigid and diﬀusely tender abdomen. Plain ﬁlms are usually ade- quate to conﬁrm the diagnosis of ulcer perforation. Perforations require im- mediate surgical evaluation. Ulcer penetration into adjacent structures occurs in up to 20% of cases of PUD, but only a small proportion become clinically apparent. The most common sites of ulcer penetration include the pancreas, omentum, hepatobiliary system, colon, and adjacent vascula- ture. Patient presentation reﬂects the structure that is involved, and the ther- apy is site-speciﬁc. Ischemic bowel disease Depending on the location, degree, and acuity of the vascular compro- mise, ischemic bowel disease is classiﬁed into three distinct syndromes: acute mesenteric ischemia, chronic mesenteric ischemia, and colonic ischemia. Acute mesenteric ischemia results from the rapid loss of blood supply to the portion of the intestines supplied by the celiac, superior mesenteric, or inferior mesenteric arteries. The cause is most commonly thromboembolic disease. The consequences of acute mesenteric ischemia are severe, and in- clude bowel necrosis, infarction, and death. Chronic mesenteric ischemia re- sults from the gradual loss of blood supply to the portion of the intestines supplied by the celiac, superior mesenteric, or inferior mesenteric arteries. The cause is usually atherosclerosis. Patients with chronic mesenteric ische- mia present with chronic postprandial abdominal pain, which is termed in- testinal angina. Because eating worsens the pain, patients develop a fear of eating (sitophobia), and signiﬁcant weight loss may occur. Colonic ischemia, also known as ischemic colitis, is the most commonly encountered intestinal vascular disorder. Colonic ischemia occurs when there is a decrease in colonic mucosal oxygenation. In the vast majority of patients, colonic 676 FLASAR et al ischemia does not result from an occlusive vascular process, but rather oc- curs when the oxygen requirements to a speciﬁc portion of the colon are not met by the vascular supply. Colonic ischemia occurs in the portions of the colon where blood ﬂow is least redundant, such as the splenic ﬂexure, and rectosigmoid junction. Lower gastrointestinal bleeding, rather than abdom- inal pain, is the most common presenting symptom. The disorder is self-lim- ited in the majority of cases, and the prognosis is good. Of the three ischemic bowel syndromes, acute mesenteric ischemia is the disease that presents with acute abdominal pain, and will be further discussed below. Acute interruption of blood supply in the mesenteric vasculature results from either thromboembolic disease or vasospasm. The major risk factors include advanced age, hypercoaguability, vascular disease, and cardiac dis- orders such as atrial ﬁbrillation or valvular disease. Once the blood supply to the mesenteric vascular is interrupted, acute ischemia ensues. If the vas- cular compromise persists, bowel infarction, necrosis, and perforation may occur. Patients with acute mesenteric ischemia present with acute onset, severe periumbilical abdominal pain. Early in the disease course, the pain is often out of proportion to tenderness produced during the physical exami- nation. If the patient presents after bowel infarction has already occurred, peritoneal signs may develop. The stool may be positive for occult blood, but hematochezia is uncommon with acute mesenteric ischemia. Common laboratory abnormalities seen with acute mesenteric ischemia include leuko- cytosis and an elevated hematocrit from hemoconcentration. A low serum bicarbonate, metabolic acidosis, and elevated lactate level are seen once bowel infarction has occurred. Retrospective studies evaluating the role of elevated plasma D-dimer levels in the diagnosis of early mesenteric ischemia showed initial promise, although subsequent prospective evaluations have shown D-dimer to be less helpful [68,69]. Several imaging modalities, including plain ﬁlms, Doppler ultrasound, conventional CT, and MRI have been studied for the diagnosis of acute mesenteric ischemia. Unfortunately, these imaging techniques lack sensitiv- ity and speciﬁcity to accurately make the diagnosis. Mesenteric angiog- raphy is the ‘‘gold standard’’ test for diagnosing occlusive arterial mesenteric ischemia. Its sensitivity and speciﬁcity are 75% to 100% and 100%, respectively. In addition to its diagnostic capabilities, angiogra- phy oﬀers the potential for treatment. Several studies demonstrate a de- creased mortality in patients who undergo angiography for suspected occlusive mesenteric arterial ischemia [71,72]. The mortality rate for patients with acute mesenteric ischemia in whom the diagnosis is not made before the onset of bowel infarction is reported to be as high as 90%. Therefore, early diagnosis is crucial. Because laboratory ﬁndings may be nonspeciﬁc early in the disease course, a high index of suspicion, based upon predispos- ing risk factors, and clinical presentation is required. Patients with suspected acute mesenteric ischemia should have prompt angiography and surgical evaluation. ACUTE ABDOMINAL PAIN 677 Abdominal aortic aneurysm It is estimated that as many as 10% of patients over the age of 65 have an abdominal aortic aneurysm (AAA). Rupture of the AAA carries an overall mortality rate of nearly 90%, which only falls to 70% if patients survive to reach the operating room [74,75]. Because of such high mortality and rapid course, a ruptured AAA is unlikely to present in an outpatient clinic. However, any severe abdominal pain complaint in a patient with a known AAA mandates immediate referral to an emergency department for evaluation. Inﬂammatory bowel disease Inﬂammatory bowel disease (IBD) encompasses ulcerative colitis (UC), Crohn’s disease (CD), and indeterminate colitis. All three disorders are chronic, characterized by disease-free intervals, followed by ﬂares of disease. These disorders are generally managed in the outpatient setting, and abdom- inal pain is often a component of active disease. Nonetheless, there are sev- eral acute, potentially life-threatening complications from IBD that may present as abdominal pain in the outpatient setting. These include fulminate colitis, toxic megacolon, bowel obstruction, bowel perforation, and abscess formation. Fulminate colitis is typically associated with UC, and is the initial pre- senting scenario in up to 10% of patients with UC [76–78]. It is deﬁned as abdominal pain, O10 bloody bowel movements per day, volume deple- tion, anemia, and any two of the following: white blood count O10,500 cells/mL, fever O38.6 C, tachycardia, and hypoalbuminemia. Patients with known UC will complain of increasingly severe, crampy, generalized abdominal pain in addition to the typical complaints of bloody diarrhea, ur- gency, and tenesmus. Toxic megacolon occurs in colitis patients when there is pathologically di- lated large bowel in conjunction with evidence of systemic toxicity. Early se- ries reported mortality rates of 19%, although more recent series estimate overall mortality approaching 0%, owing to earlier recognition and im- proved management strategies [80–82]. Toxic megacolon was originally de- scribed, and is most commonly seen in the setting of UC, but can also occur with Crohn’s colitis, infectious colitis (especially Clostridium diﬃcile), ische- mic colitis, diverticulitis, and colon cancer. Toxic megacolon generally oc- curs early in the course of UC, with 30% of cases occurring within the ﬁrst 3 months of diagnosis and 60% of cases within 3 years of diagnosis. Physical examination classically reveals abdominal distension with tympany to percussion, as well as tenderness above the underlying colon. However, examination ﬁndings are less reliable in the setting of active cor- ticosteroid therapy. In patients with peritoneal signs, perforation should be strongly suspected. The diagnosis is made based on the presence of colonic distension (O6 cm) on imaging plus any three of the following: fever 678 FLASAR et al (O38.6 C), leukocytosis (O10,500 cells/mL), anemia, or tachycardia (O120 beats/min), plus any one of the following: altered mental status, volume depletion, hypotension, or electrolyte abnormalities. The patient with either fulminate colitis or toxic megacolon should be hospitalized immedi- ately for aggressive medical care and surgical evaluation. They should be made NPO, started on intravenous hydration with appropriate electrolyte repletion, and in cases of toxic megacolon, should have a nasogastric tube placed to facilitate decompression. Bowel obstruction is common in CD, and is most frequently seen in the terminal ileum. Obstruction most commonly results from active inﬂam- matory intestinal strictures, postinﬂammatory ﬁbrotic intestinal strictures, or peritoneal adhesive disease resulting from previous abdominal surgeries. Although far more common in CD, strictures occur in about 5% of patients with UC, with up to 30% representing malignant disease. Perforation can occur both with CD and UC. In patients with UC, it is most commonly the result of toxic megacolon, and carries a mortality rate as high as 50%. In patients with CD, perforation results from unrelieved small bowel obstructions. Because of the powerful immunosuppressive med- ications that IBD patients are frequently taking, the clinical severity of a per- foration may be muted. Therefore, a high index of suspicion is needed. Intraabdominal abscess formation is common in CD, occurring in ap- proximately 25% of patients [88–90]. They result from microperforations in patients with penetrating or stricturing disease. Patients typically present with fever, leukocytosis, and abdominal pain. Additionally, they may expe- rience back or groin pain if the abscess involves the ileopsoas or pelvic struc- tures, respectively. A special subset of abscess patients includes those with perianal disease, where the abscess occurs in the perirectal fascia, muscula- ture, or adipose tissue. Approximately 30% of patients with perianal ﬁstul- izing CD will develop a perirectal abscess. These patients may note low pelvic/perineal pain, defecatory urgency, or tenesmus in addition to consti- tutional symptoms. Severity may be blunted secondary to concomitant im- munosuppressive medications. Regardless, patients with suspected perirectal or intraabdominal abscess with a history of CD warrant hospital admission for antibiotics, surgical evaluation, and advancement of medical therapy when appropriate. Irritable bowel syndrome Irritable bowel syndrome (IBS) has an estimated prevalence in the United States as high as 22%, though only one third will ever present for medical evaluation. It is estimated to account for 12% of primary care visits. The hallmark of the disorder is chronic abdominal pain or discomfort that is associated with altered bowel movements. The pathogenesis is not fully understood, but altered motility, visceral hypersensitivity, luminal fac- tors, and psychologic etiologies are felt to all play a role. Aﬀected patients ACUTE ABDOMINAL PAIN 679 exhibit variation in the description of the abdominal pain, including cramp- ing, bloating, aching, and even sharp localized pain. Although IBS is trou- bling to the patient and detrimental to everyday functioning and quality of life, IBS is not a life-threatening process. Therefore, it should be managed on an outpatient basis. Associated abnormalities such as anemia, poor nu- tritional status, weight loss, evidence of infection, fever, and electrolyte or metabolic abnormalities suggest an alternative diagnosis. Special populations There are several populations of patients who warrant special consider- ation when presenting with abdominal pain because of either underlying processes that are unique to these groups, or because presentations tend to be atypical in these groups. These include the elderly, immunosuppressed (including patients with AIDS), patients on analgesics, women of childbear- ing age, and pregnant women. Additionally, patients presenting under the inﬂuence of alcohol or illicit substances often exhibit atypical presentations of common disorders. Patients O65 years of age represent the fastest growing population demo- graphic in the United States [94–97]. The elderly often delay seeking medical care, causing them to present at a potentially more dangerous point in their disease course. Compounding this, the history and physical examination have less reliability in the elderly. Many factors contribute to this, including underlying central nervous system disorders, fear of losing independence, hearing loss, depression, complex medical histories, vague description of the discomfort, polypharmacy, and change in normal physiology (eg, inabil- ity to mount leukocytosis or pyrexic response to infection). As a result, di- agnostic accuracy has been reported as low as 40% in elderly patients with acute abdominal pain. An important point to consider when evaluating elderly patients is that common disorders may manifest with uncommon presentations. For example, both coronary ischemia and urinary tract infec- tions have been well-described causes of abdominal pain in the elderly. Also, it is not uncommon for an elderly patient to present with altered mental sta- tus as the lone sign of an acute abdominal process. Immunosuppressed patients and patients with immunodeﬁciency syn- dromes who present with abdominal pain generate a more expansive diﬀer- ential diagnosis (especially infectious causes) for their pain owing to their inability to mount a normal immune response. As in the elderly, the physical examination may be less accurate owing to an abnormal inﬂammatory re- sponse to pathologic processes. The diﬀerential diagnosis and evaluation of gynecologic and obstetric processes manifesting as acute abdominal pain are beyond the scope of this review. However, a few points need to be stressed. All women of child- bearing age require a pelvic examination and evaluation for elevated b-HCG in the workup of acute abdominal pain. 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