Pφ

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.

TP

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.

Dx

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.

Pφ

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.

TP

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.

Dx

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.

Pφ

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.

TP

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.

Dx

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.

Pφ

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.

TP

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.

Dx

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.

Pφ

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.

TP

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.

Dx

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.

Pφ

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.

TP

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.

Dx

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.

Pφ

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.

TP

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.

Dx

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.