Abdominal Pain (Case 19)
Case: A 54-year-old man with a history of hypertension, diabetes mellitus, and hyperlipidemia presents to the emergency department (ED) complaining of progressive epigastric pain for the last 2 days. The pain initially woke him from a deep sleep. He describes his discomfort as “sharp” and states it has worsened in intensity over the last few hours. He also complains of nausea and has had two episodes of clear vomiting. He has been unable to tolerate any solid food since the onset of the pain. He is passing gas and recalls his last bowel movement was earlier in the day. He has never had symptoms like this before. He denies any fevers or chills. He has had no sick contacts. He is not a heavy drinker and reports only drinking one glass of wine with dinner 5 days ago. He quit smoking several years ago.
On physical exam, his temperature is 100.4° F. His heart rate is 110 beats per minute (bpm) and blood pressure (BP) is 151/92 mm Hg. The patient’s sclerae are mildly icteric, but there is no overall evidence of jaundice. His abdomen is soft with mild distension. He has significant tenderness in the epigastrium and right upper quadrant (RUQ) to palpation but without any guarding or rebound.
Acute mesenteric ischemia
When evaluating a patient with abdominal pain, a detailed history about the character, duration, and quality of pain is imperative. It is important to discern exactly how and when the pain started and inquire about its location; this can give you important clues as to the underlying diagnosis. A nocturnal component to the pain often suggests an organic or serious cause. It is also important to inquire about exacerbating and alleviating factors, as well as any association of the pain with nausea, vomiting, fevers, or chills, and if ingestion of food worsens the pain.
• When evaluating a patient with abdominal pain, it is important to determine if the symptom is acute or chronic.
• A patient with a 6-month history of pain is less likely to have an acute abdomen.
• A good clinician must always be on the lookout for the possibility of an abdominal disorder requiring surgery, which would require urgent intervention; time may be critically important in these cases.
• Pain that is sudden in onset or wakes a person from sleep usually signifies an acute abdominal process. It is thus important to ask the patient what he or she was doing when the pain began.
• It is also imperative to determine if the pain was mild and progressively worsened, or if it was severe at onset.
• Ask patients to rate their pain on a scale of 1 to 10.
• Pain associated with nausea and vomiting can be seen in patients with pancreatitis.
• Fever and chills are associated with cholecystitis.
• The most urgent assessment during a physical exam is to determine if there are signs of peritonitis, including a careful assessment for rebound tenderness and guarding.
• Absent bowel sounds may also signify a more critical intra-abdominal pathology.
• The location of tenderness can be important to elucidate a particular etiology for the patient’s symptoms. For example, right lower quadrant (RLQ) pain is often seen in patients with appendicitis, and left lower quadrant (LLQ) tenderness is closely associated with diverticulitis.
• Tachycardia and hypotension can be signs of both pain and volume depletion.
Tests for Consideration
|Clinical Entities||Medical Knowledge|
This is a transmural injury of an organ resulting in perforation through the serosa. Common etiologies of perforation include ulcer disease in the duodenum or stomach, intestinal ischemia, and diverticular transmural inflammation.
Patients present with sudden onset of acute pain. On physical examination, most patients will have signs of peritonitis such as rebound or guarding. It is important to recognize these findings, as some patients will require emergent surgical intervention.
The abdominal exam is often the most telling. Patients are extremely uncomfortable and lying still. They will often have pain when going over bumps in the stretcher or ambulance. Abdominal imaging will show free air. If a CT scan is done, it can show extravasation of contrast at the point of perforation.
The treatment is surgical repair. These patients also require antibiotics (targeted principally against gram-negative bacilli and anaerobes) as well as fluid resuscitation. See Cecil Essentials 34, 37.
The hallmark of this disease is gallbladder inflammation, most often secondary to gallstones. Acute cholecystitis can be associated with cystic duct obstruction. On a pathologic spectrum, the disease can manifest as mild edema, acute inflammation, or necrosis and gangrene of the gallbladder. The clinician should be aware of the possibility of acalculous cholecystitis. This entity is clinically similar to acute cholecystitis but is not associated with gallstones. Acalculous cholecystitis is usually found in the critically ill patient.
Acute cholecystitis presents as steady RUQ pain with fever and leukocytosis. The pain can also be located in the epigastrium, and it can radiate to the patient’s right shoulder or back. The pain may be associated with nausea, vomiting, and anorexia. On exam, patients are usually ill-appearing and tachycardic. A Murphy sign may be positive.
Patients with uncomplicated cholecystitis do not always have elevated bilirubin, because the common bile duct is not obstructed. Mild elevation in serum aminotransferases can be seen. An ultrasound often shows gallbladder wall thickening >4 mm, along with gallstones and pericholecystic fluid. A hepatobiliary iminodiacetic acid (HIDA) scan may be helpful to rule out choledocholithiasis; a positive test will show no visualization of the gallbladder after IV injection of the isotope due to obstruction of the cystic duct.
The treatment of acute cholecystitis consists of IV hydration, correction of electrolyte abnormalities, and analgesia. IV antibiotics should target common biliary pathogens including Klebsiella, Enterococcus, Enterobacter, Escherichia coli, and anaerobes. Early cholecystectomy (now almost always performed laparoscopically) is ideal, and surgical consultation should be obtained. See Cecil Essentials 46.
Pain secondary to gallstones is referred to as biliary colic. It is caused by gallbladder contraction in response to hormonal or neural stimulation. Often this contraction forces a stone against the gallbladder outlet or the opening of the cystic duct, resulting in pain. The stone will often fall back from the cystic duct as the gallbladder relaxes.
The typical pattern of pain in patients with biliary colic is one of constant epigastric or RUQ discomfort that progresses over an hour and then slowly diminishes over the next several hours. The pain may radiate to the back and the right shoulder, and may be associated with nausea and vomiting. Unlike individuals with acute cholecystitis, most people with biliary colic are not ill-appearing and have no fever or leukocytosis.
The first step in diagnosis is obtaining a typical history paired with an ultrasound showing the presence of cholelithiasis. There is usually no gallbladder wall thickening or pericholecystic fluid. Elevations of serum transaminases can be seen during an acute attack.
Patients with typical biliary colic and gallstones are advised to undergo prophylactic cholecystectomy so as to avoid more serious complications such as cholangitis, pancreatitis, or Mirizzi syndrome, which is obstruction of the common bile duct caused by chronic cholecystitis and large gallstones resulting in compression of the common bile duct. The risk of further symptoms and complications in patients with biliary colic and gallstones is approximately 70% within 2 years of initial presentation. See Cecil Essentials 46.
Diverticulitis is inflammation of colonic diverticula. Diverticula form at certain points of weakness in the bowel wall. The cause is thought to be a microscopic or macroscopic perforation of a diverticulum. Erosion of the diverticular wall occurs because of increased intraluminal pressure leading to inflammation, followed by focal necrosis and eventually perforation.
The most common symptom is LLQ pain that can occur several days before presentation. The severity of symptoms is often based on the underlying inflammatory process. Pain is often accompanied by fever and elevated WBC count. Diarrhea or constipation can be seen in at least 30% of patients. Patients present with tenderness in the LLQ. A macroscopic perforation may lead to localized peritoneal signs.
In addition to the history and physical exam, the diagnosis of acute diverticulitis is established with a CT scan of the abdomen with IV and oral contrast. Findings include soft-tissue density within the pericolic fat around an area of colonic diverticula and bowel wall thickening. CT scan is also helpful in identifying the complications of diverticulitis, such as a localized abscess formation or a fistulous connection to the urinary bladder, vagina, or the abdominal wall.
For patients with uncomplicated diverticulitis, bowel rest and antibiotics are the mainstays of therapy. The antibiotic coverage is targeted at colonic anaerobic and aerobic gram-negative flora. Abscess occurs in 16% of patients with acute diverticulitis and can be managed with percutaneous drainage performed by an interventional radiologist. If there is peritonitis or perforation, surgical therapy with a two-stage procedure is recommended. See Cecil Essentials 34.
The most common physiologic mechanism for the development of appendicitis is obstruction of the appendiceal lumen. The obstruction may be secondary to follicular hyperplasia in the young, or possibly malignancy, such as carcinoid or adenocarcinoma, in the older population. A superimposed inflammatory process of the appendiceal wall then leads to ischemia, perforation, or the development of an abscess.
Many patients present with nonspecific signs and symptoms such as generalized malaise or indigestion. Pain can be produced on abdominal examination over the McBurney point, which is located one third of the distance along a line from the anterior superior iliac spine to the umbilicus. The Rovsing sign is the development of pain in the RLQ upon palpation in the LLQ. The initial pain can also be dull and constant in the epigastric or periumbilical region. Eventually the pain localizes to the RLQ once the parietal peritoneum is involved. The pain is associated with nausea and vomiting. A low-grade fever may also be present.
In addition to a thorough history and physical, a CT scan of the abdomen and pelvis may be performed if there is doubt of the clinical picture. Notable findings include thickened appendiceal walls, free fluid, and fat stranding in the RLQ. The presence of contrast or air in the appendix actually helps to exclude the diagnosis.
The definitive treatment is an appendectomy. Preoperative treatment includes hydration and perioperative antibiotics. If, however, CT scanning reveals an abscess, percutaneous drainage is needed before surgery. See Cecil Essentials 34.
Acute pancreatitis is an inflammatory condition of the pancreas characterized by abdominal pain and elevated levels of the pancreatic enzymes amylase and lipase. While there are clear etiologic conditions associated with the disease, the exact cellular pathogenesis of the disorder is not fully understood. It is thought that intra-acinar activation of pancreatic proteolytic enzymes leads to an autodigestive injury to the gland. In general, acute pancreatitis can be divided into two broad categories: edematous or mild acute pancreatitis, and necrotizing or severe acute pancreatitis. Patients with severe acute pancreatitis can develop systemic complications including acute respiratory distress syndrome, fever, renal failure, and shock.
The most common cause of acute pancreatitis in the world is gallstones—specifically, the mechanical obstruction by the stone of the pancreatic ampulla. Alcohol is another common cause of acute pancreatitis. A serum triglyceride concentration above 1000 mg/dL can also precipitate acute pancreatitis. A medication history is imperative when evaluating a patient with pancreatitis, as many medications are associated with pancreatitis, such as metronidazole, tetracycline, furosemide, thiazide diuretics, tamoxifen, valproic acid, didanosine, and pentamidine. Less common etiologies include hypercalcemia, infection (mumps, coxsackievirus), vasculitis, and, rarely, pancreatic cancer. Pancreatitis is seen in 3% of patients undergoing diagnostic endoscopic retrograde cholangiopancreatography (ERCP). A full 30% of patients with acute pancreatitis fall into the idiopathic category.
Patients typically present with acute upper abdominal pain that is in the mid-epigastrium or RUQ. Pain can also be diffuse in nature. Patients commonly describe a pain that radiates to the back in a “bandlike” fashion. The pain may improve upon bending forward. Nausea and vomiting are commonly associated symptoms. On physical exam, patients have significant tenderness in the epigastric region. Ecchymotic discoloration of the costovertebral angle (Turner sign) or the periumbilical region (Cullen sign) is seen in 1% of cases and is associated with intra-abdominal hemorrhage.
An elevation in serum amylase and lipase in the appropriate clinical setting strongly suggests a diagnosis of pancreatitis. In gallstone pancreatitis, a concomitant rise in ALT is also seen. A CT of the abdomen and pelvis is not necessary on the first day of admission if the history and biochemical markers suggest pancreatitis but should be done if the diagnosis is questionable. It is important to remember that many patients present with significant hypovolemia, and an IV contrast CT could worsen renal function. Some experts advocate a CT scan with contrast in 2–3 days after presentation following appropriate volume repletion to assess for pancreatic necrosis.
All patients should receive supportive care including vigorous fluid resuscitation, correction of electrolyte abnormalities, and adequate pain control. The use of aggressive fluid therapy cannot be stressed enough. Patients with severe pancreatitis can sequester large amounts of fluid in the injured pancreatic bed, and rates of 250 mL of IV fluids per hour may be required for the first 24–48 hours if the cardiac status permits. Inadequate fluid replacement can be evidenced by persistent hemoconcentration. Thus, the hematocrit should be measured on admission, 12 hours after admission, and 24 hours after admission to assess the adequacy of fluid resuscitation. Transfer to the intensive care unit (ICU) is warranted in patients with evidence of sustained organ failure. In mild pancreatitis, the patient can be fed orally in 3–5 days upon cessation of abdominal pain, with diets advancing from clear liquids to a more regular, but low-fat, diet. In those with severe pancreatitis, enteral feeding with a jejunal tube distal to the ligament of Treitz is preferred over total parenteral nutrition. The use of prophylactic antibiotics is recommended only in those with severe necrotizing pancreatitis. See Cecil Essentials 40, 46.
Acute Mesenteric Ischemia
Acute mesenteric ischemia is caused by a reduction in intestinal blood flow secondary to occlusion, vasospasm, or hypoperfusion of the mesenteric vasculature. Chronic mesenteric ischemia is referred to as intestinal angina and is a separate clinical entity that will not be discussed here. The intestinal blood supply consists of the celiac artery, superior mesenteric artery, inferior mesenteric artery, and an extensive network of collateral blood vessels known as the splanchnic circulation. The four major causes of acute mesenteric ischemia are superior mesenteric artery embolism, superior mesenteric artery thrombosis, mesenteric venous thrombosis, and nonocclusive ischemia. Risk factors for mesenteric arterial disease include advanced age, atherosclerosis, states of low cardiac output, cardiac arrhythmias, recent myocardial infarction (MI), and intra-abdominal malignancy. Risk factors for mesenteric venous thrombosis include hypercoagulable states, portal hypertension, abdominal infections, pancreatitis, splenectomy, and malignancy in the portal region.
Patients with acute arterial embolism have rapid onset of severe periumbilical pain that may be out of proportion to the findings on the physical exam. Arterial thrombosis or mesenteric vein thrombosis will present in a more insidious fashion, with vague abdominal pain that can be present for days to weeks before the diagnosis.
After appropriate resuscitation and supportive measures, a CT scan with IV contrast should be done to evaluate the mesenteric arterial and venous vasculature as well as assess for bowel wall ischemia and injury, which can be seen as bowel wall thickening or intestinal pneumatosis with portal vein gas. Mesenteric angiography is the gold standard diagnostic study for acute arterial ischemia and has both diagnostic and therapeutic importance. CT angiography and MR angiography are noninvasive alternatives. Laboratory evaluation may reveal an elevated serum lactate concentration.
The ultimate goal of treatment is the rapid restoration of intestinal blood flow, which requires aggressive hemodynamic monitoring and support, correction of acidosis, antibiotics, and placement of a nasogastric (NG) tube. Immediate surgery is required in those suspected of having perforation or intestinal gangrene. In those for whom surgery is not emergent, mesenteric angiography not only can be diagnostic but also can offer therapeutic options with the administration of intra-arterial vasodilators, thrombolytic agents, angioplasty, vascular stenting, or embolectomy. In acute mesenteric venous thrombosis, treatment includes anticoagulation and resection of necrotic bowel. See Cecil Essentials 35.
a. Celiac artery compression syndrome is a rare condition that occurs in healthy young and middle-aged individuals, and presents as chronic epigastric abdominal pain that occurs after eating and may be associated with an epigastric bruit and weight loss.
b. Hereditary angioedema is a disease that results from defects in the C1 inhibitor of the classical complement pathway. Patients have recurrent episodes of colicky abdominal pain associated with nausea, vomiting, and diarrhea. Diagnosis is made with blood tests that show a low C4 level and low C1 inhibitor antigen levels.
c. Acute intermittent porphyria (AIP) is an autosomal-dominant disorder resulting from a partial deficiency of porphobilinogen deaminase, previously called the third enzyme in the heme biosynthetic pathway. Abdominal pain is the most common symptom in AIP. It is usually severe, steady, and poorly localized.