3: Abdominal Pain

Abdominal pain is the most common cause for hospital admission in the United States. Diagnoses range from benign entities (eg, irritable bowel syndrome [IBS]) to life-threatening diseases (eg, ruptured abdominal aortic aneurysms [AAAs]). The first pivotal step in diagnosing abdominal pain is to identify the location of the pain. The differential diagnosis can then be limited to a subset of conditions that cause pain in that particular quadrant of the abdomen (Figure 3-1).

Several other pivotal points can help narrow the differential diagnosis including (1) the time course of the pain, (2) peritoneal findings on exam, (3) unexplained hypotension, and (4) abdominal distention. Each of these is reviewed below.

The time course of the pain is a pivotal feature. Some diseases present subacutely/chronically over weeks to months or years (eg, IBS) whereas others present acutely, within hours to days of onset (eg, appendicitis). In patients with their first episode of acute severe abdominal pain, a variety of life-threatening, must not miss diagnoses must be considered (eg, AAA). Many of these diseases that cause acute abdominal pain cannot recur because patients are either treated or die of complications (eg, AAA, acute appendicitis, splenic rupture.) Since prior episodes are incompatible with many of these diagnoses, a history of such prior episodes narrows the differential diagnosis. Therefore, the differential diagnosis of abdominal pain can be organized based on whether patients are presenting with their first episode of acute abdominal pain, a recurrent episode of acute abdominal pain, or chronic/subacute abdominal pain. Table 3-1 outlines the typical time course associated with different diseases causing abdominal pain. See Table 3-2 for a summary of abdominal pain organized by location, time course, and clinical clues.

Peritoneal findings of rebound tenderness, rigidity, and guarding are pivotal features and suggest an intra-abdominal catastrophe. Typical causes include AAA, bowel infarction (due to bowel obstruction or acute mesenteric ischemia), bowel perforation (due to appendicitis, peptic ulcer disease [PUD], diverticulitis), pancreatitis, or pelvic inflammatory disease (PID).

Unexplained hypotension is yet another potential pivotal clue. While many patients with abdominal pain experience hypotension due to dehydration from nausea, vomiting, or poor oral intake, some patients with abdominal pain present with unexplained hypotension. Unexplained hypotension can suggest sepsis, retroperitoneal hemorrhage, or other diseases. Table 3-3 lists diseases associated with abdominal pain and unexplained hypotension.

Orthostatic vital signs should be taken in patients with abdominal pain. They may provide invaluable diagnostic and therapeutic information.

The final pivotal finding is significant abdominal distention, which may develop from excess air or fluid in the abdomen. Excess air may occur with bowel obstruction or bowel perforation (free air). Excess fluid may be seen in patients with ascites or hemorrhage. Percussion and shifting dullness can usually distinguish excess air from fluid in such patients. Table 3-4 lists the diagnostic considerations in patients with abdominal distention.

Other important historical points include factors that make the pain better or worse (eg, eating), radiation of the pain, and associated symptoms (nausea, vomiting, anorexia, inability to pass stool and flatus, melena, hematochezia, change in color of the urine or stool, fever, chills, weight loss, altered bowel habits, orthostatic symptoms, urinary symptoms) or prior abdominal surgeries (increasing the risk of small bowel obstruction [SBO]). Pulmonary symptoms or a cardiac history can be clues to pneumonia or myocardial infarction presenting as abdominal pain. In women, sexual and menstrual histories are important. The patient should be asked about alcohol consumption as well as prescription and over-the-counter medications.

A few final points about the physical exam are worth emphasizing. First, vital signs are just that, vital. Hypotension, fever, tachypnea, and tachycardia are critical clinical clues that must not be overlooked. The HEENT exam should look for pallor or icterus. Jaundice suggests either hepatitis or biliary disease. Careful heart and lung exams can suggest pneumonia or other extra-abdominal causes of abdominal pain.

The physical exam of a patient with abdominal pain includes more than just the abdominal exam.

Of course, the abdominal exam is key. Inspection assesses for distention as noted above. Auscultation evaluates whether bowel sounds are present. Absent bowel sounds may suggest an intra-abdominal catastrophe; high-pitched tinkling sounds and rushes suggest an intestinal obstruction. Palpation should be performed last. It is useful to distract the patient by continuing to talk with him or her during abdominal palpation. This allows the examiner to get a better appreciation of the location and severity of maximal tenderness. The clinician should palpate the painful area last. The rectal exam should be performed, and the stool tested for occult blood. Finally, the pelvic exam should be performed in adult women and the testicular exam in men.

The patient’s history is not particularly suggestive of any diagnosis. The first pivotal point determines the location of the pain. Mr. C’s pain is in the mid/upper abdomen, which limits the differential diagnosis. Common causes of mid/upper abdominal pain include appendicitis, IBS, PUD, pancreatitis, inflammatory bowel disease (IBD), SBO, or large bowel obstruction (LBO), AAA, diabetic ketoacidosis, and gastroenteritis (Figure 3-1). Several of these diagnoses are very unlikely and need not be considered further. AAA would be exceptionally rare in this age group and gastroenteritis is very unlikely in the absence of either vomiting or diarrhea. The lack of a history of diabetes would make diabetic ketoacidosis unlikely unless this was the initial presentation. A simple blood sugar could help exclude this diagnosis. Other pivotal points in patients with abdominal pain include its time course (see Table 3-1), and if present, unexplained hypotension or abdominal distention (see Tables 3-3 and 3-4). The patient reports that this is an acute episode that has not occurred previously. This makes IBD and IBS very unlikely, focusing attention on the remaining possibilities of appendicitis, PUD, pancreatitis, and bowel obstruction. Since appendicitis should always be considered in young, otherwise healthy patients with unexplained abdominal pain, this is the leading hypothesis (Table 3-5). He has neither unexplained hypotension nor distention to help focus the differential diagnosis further.

Leading Hypothesis: Appendicitis

Textbook Presentation

The classic presentation of appendicitis is abdominal pain that is initially diffuse and then intensifies and migrates toward the right lower quadrant (RLQ) to McBurney point (1.5–2 inches from the anterior superior iliac crest toward umbilicus). Patients often complain of bloating and anorexia.

Disease Highlights

1. Appendicitis is one of the most common causes of an acute abdomen, with a 7% lifetime occurrence rate.

2. It develops secondary to obstruction of the appendiceal orifice with secondary mucus accumulation, swelling, ischemia, necrosis, and perforation.

3. Initially, the pain is poorly localized. However, progressive inflammation eventually involves the parietal peritoneum, resulting in pain localized to the RLQ.

4. The risk of perforation increases steadily with age (ages 10–40, 10%; age 60, 30%; and age > 75, 50%).

Evidence-Based Diagnosis

1. The classic presentation of nausea and vomiting with pain migration from the periumbilical area to the RLQ is present in only 50–65% of patients.

2. RLQ pain is the most useful clinical finding; LR+, 7.3–8.5; LR–, 0.0–0.3

3. Most individual clinical findings have a low sensitivity for appendicitis making it difficult to rule out the diagnosis.

   1. In 1 study, guarding was completely absent in 22% of patients, and rebound was completely absent in 16% of patients with appendicitis.

   2. Fever was present in only 40% of patients with perforated appendices.

   Fever, severe tenderness, guarding, and rebound may be absent in patients with appendicitis.

4. Nonetheless, certain findings increase the likelihood of appendicitis when present (ie, rebound, guarding) (Table 3-6).

5. Symptoms are different in octogenerians than in patients aged 60–79 years.

   1. The duration of symptoms is longer prior to evaluation (48 vs 24 hours).

   2. They are less likely to report pain that migrated to the RLQ (29% vs 49%).

6. History is particularly important in women to differentiate other causes of RLQ pain (eg, PID, ruptured ectopic pregnancy, ovarian torsion, and ruptured ovarian cyst). The most useful clinical clues that suggest PID include the following:

   1. History of PID

   2. Vaginal discharge

   3. Cervical motion tenderness on pelvic exam

   Rule out ectopic pregnancy in women of childbearing age who complain of abdominal pain by testing urine for beta-HCG.

7. WBC

   1. The WBC has low discriminatory value for diagnosing acute appendicitis. One meta-analysis reported a LR+ of 2.46, LR– of 0.26 for a WBC > 10,000 /mcL.

   2. Very low WBCs (< 7000/mcL) and very high WBCs (> 17,000/mcL) substantially decrease or increase the likelihood of appendicitis respectively (see Table 3-6). Moderate elevations are less predictive.

   3. A low WBC does not exclude appendicitis in patients who have severe rebound or guarding; 80% of such patients had appendicitis even when WBC was < 8000/mcL.

   The WBC is not reliably elevated in patients with acute appendicitis.

8. C-reactive protein (CRP) levels are not highly diagnostic. For CRP > 10 mg/L, LR+ is 2.0 and LR– is 0.32.

9. One paper suggested that the combination of an elevated WBC (> 10,000/mcL) and an elevated CRP (> 12 mg/L) suggest appendicitis; LR+, 8.2 (both present); LR– 0.05 (both absent)

10. Urinalysis may be misleading and reveal pyuria and hematuria due to bladder inflammation from an adjacent appendicitis.

11. Plain radiography is useful only to detect free air or signs of another process (ie, SBO).

12. CT scanning is an accurate imaging method that is helpful when the diagnosis is uncertain.

    1. Noncontrast CT scanning

       1. 92.7% sensitive, 96% specific; LR+, 24; LR−, 0.08

       2. IV and oral contrast may increase sensitivity further

    2. A meta-analysis compared CT use with clinical evaluation alone

       1. CT scanning lowered the rate of unnecessary surgery compared with clinical evaluation alone from 16.7% to 8.6% (P < 0.001).

       2. The 2 randomized controlled trials within the meta-analysis showed similar reductions in unnecessary surgery in patients undergoing CT vs clinical evaluation without CT (2.6% vs 13.9% and 6.7% vs 27%).

    3. CT scanning has also been demonstrated to lower overall costs.

13. Ultrasonography: 78% sensitive, 83% specific; LR+, 4.5; LR−, 0.27

14. Clinical decision rules: Scoring systems to predict appendicitis have been developed (eg, the Alvardo score). However validation studies have documented a high rate of appendicitis even among patients with low scores.

15. Pregnancy

    1. Although inferior to CT, ultrasonography is recommended due to the risk of radiation to the fetus.

    2. Indeterminate studies in the third trimester are common.

    3. Unenhanced MRI

       1. An alternative option for patients with indeterminate ultrasound; sensitivity, 91%; specificity, 98%; LR+, 45; LR− 0.09

       2. Gadolinium is a pregnancy category C drug and is not advised.

    4. Surgical and gynecologic consultation are suggested.

Treatment

1. Observation is critical.

2. Monitor urinary output and vital signs.

3. IV fluid resuscitation

4. Broad-spectrum antibiotics, including gram-negative and anaerobic coverage

5. Urgent appendectomy is recommended. Trials of medical therapy (antibiotics and observation without surgery) have demonstrated both a high rate of recurrence and complications.

Mr. C’s symptoms are consistent with—but certainly not diagnostic of—appendicitis. He has no risk factors for any of the alternative diagnoses of pancreatitis, PUD, or bowel obstruction (alcohol use, NSAID ingestion, or prior abdominal surgery, respectively). Diagnostic options include obtaining a CBC (always done but clearly of limited value), continued observation and reexamination, surgical consultation, and obtaining a CT scan. Given the lack of evidence for any of the less concerning possibilities you remain concerned that the patient has early appendicitis. You elect to observe the patient, obtain a CBC and lipase, order a CT scan and ask for a surgical consult.

Frequent clinical observations are exceptionally useful when evaluating a patient with possible appendicitis.

The migration of pain to the RLQ is suggestive of appendicitis. Less likely considerations might include Crohn ileitis as well as diverticulitis or colon cancer (both unlikely in this age group). If the patient were a woman, PID and ovarian pathology (ruptured ectopic pregnancy, ovarian torsion, or ruptured ovarian cyst) would also need to be considered.

Diffuse abdominal pain that subsequently localizes and becomes more constant, suggests parietal peritoneal inflammation.

The first pivotal feature of Ms. R’s abdominal pain is its epigastric location. Common causes of epigastric pain include PUD, biliary colic, and pancreatitis (Figure 3-1). The second pivotal feature of Ms. R’s abdominal pain is its time course, with multiple acute episodes. Many diseases cause well-defined recurrent discrete episodes ofabdominal pain (Table 3-1) but of these, only pancreatitis and biliary colic tend to occur in the epigastrium. PUD is a common cause of epigastric abdominal pain and obviously needs to be considered. However, the pain in PUD is typically more chronic than acute, and not typically discrete or so severe, making this a less likely possibility. Ms. R does not have other pivotal clues such as unexplained hypotension or abdominal distention that could focus the differential. The final clinical clue is the severe crampy quality of the pain. Severe intense crampy abdominal pain (“colicky”) suggests obstruction of a hollow viscera, which can be caused by biliary, bowel, or ureteral obstruction (due to biliary obstruction, bowel obstruction, or nephrolithiasis, respectively). Taken together, the epigastric location, multiple discrete episodes, quality and intensity of the pain, biliary colic is the leading hypothesis. Table 3-7 lists the differential diagnosis.

Leading Hypothesis: Biliary Colic

Textbook Presentation

Gallstone disease may present as incidentally discovered asymptomatic cholelithiasis, biliary colic, cholecystitis, cholangitis, or pancreatitis. The pattern depends on the location of the stone andits chronicity (Figure 3-2). Biliary colic typically presents with episodes of intense abdominal pain that begin 1 hour or more after eating and commonly wake patients from sleep. The pain is usually located in the RUQ, although epigastric pain is also common. The pain may radiate to the back and may be associated with nausea and vomiting. The pain usually lasts for more than 30 minutes and may last for hours.

Disease Highlights

1. Asymptomatic cholelithiasis

   1. Predisposing factors

      1. Increasing age is the predominant risk factor. The prevalence is 8% in patients older than 40 years and 20% in those older than 60 years (Figure 3-3).

      2. Obesity

      3. Gender: women are affected more than men (risk increases during pregnancy)

      4. Gallbladder stasis (due to rapid weight loss, which may occur in patients on very low calorie diets, on total parenteral nutrition, and after surgery)

      5. Other less common risk factors include family history, Crohn disease, and hemolytic anemias (eg, thalassemia, sickle cell disease) which can lead to increased bilirubin excretion and bilirubin stones.

   2. Cholecystectomy not advised for patients with asymptomatic cholelithiasis.

      Make sure the gallstones are causing the pain before advising cholecystectomy.

   3. Annual risk of biliary colic developing in patients with asymptomatic gallstones is 1–4%.

2. Biliary colic

   1. Occurs when a gallstone becomes lodged in the cystic duct and the gallbladder contracts against the obstruction.

   2. Presents as one of the classic visceral obstructive syndromes with severe, constant, and crampy waves of pain that incapacitate the patient.

   3. Characterized by episodes of pain with pain-free intervals of weeks to years.

   4. Pain begins 1–4 hours after eating or may awaken the patient during the night. May be precipitated by fatty meals.

   5. The pain is usually associated with nausea and vomiting.

   6. The pain usually lasts < 2–4 hours. An episode that lasts longer than 4–6 hours and is accompanied by fever or marked tenderness suggests cholecystitis has developed.

   7. Resolution occurs if the stone comes out of the gallbladder neck. The intense pain improves fairly rapidly, although mild discomfort may persist for 1 to 2 days.

   8. Prognosis

      1. Biliary colic recurs in 50% of symptomatic patients.

      2. Acute cholecystitis develops if the stone remains lodged in the cystic duct.

      3. Complications (eg, pancreatitis, acute cholecystitis, or ascending cholangitis) occur in 25% of patients who have experienced biliary colic.

   9. Colic occasionally develops in patients without stones secondary to sphincter of Oddi dysfunction or scarring leading to obstruction.

Evidence-Based Diagnosis

1. Pain may localize to the RUQ (54% of patients), epigastrium (34% of patients) or may present as a band-like pain across the entire upper abdomen, or rarely in the mid-abdomen. Pain may radiate to back, right scapula, right flank, or chest.

2. Laboratory tests (liver function tests [LFTs]), lipase, urinalysis) are normal in uncomplicated biliary colic. Abnormalities suggest other diagnoses or complications (eg, stone migration into the common bile duct [CBD]).

3. Ultrasonography is the test of choice; sensitivity 89%, specificity 97%, LR+ 30, LR− 0.11 (CT scan is only 79% sensitive.)

4. Endoscopic ultrasound (EUS) is 100% sensitive and is useful in patients with a negative transabdominal ultrasound but in whom biliary colic is still strongly suspected.

Treatment

1. Cholecystectomy is recommended.

2. Lithotripsy is not advised.

3. Dissolution therapies (eg, ursodiol) are reserved for nonsurgical candidates.

Ms. R’s history suggests biliary colic. You order an ultrasound of the RUQ.

Alternative Diagnosis: PUD

See Chapter 32, Unintentional Weight Loss.

Alternative Diagnosis: Acute Pancreatitis (see below)

This episode of abdominal pain raises several possibilities. The first is that the current symptom complex is in some way related to her known cholelithiasis. The persistent pain suggests either cholecystitis (due to a stone lodged in the cystic duct), choledocholithiasis, ascending cholangitis, or pancreatitis. Of note, her dark urine is a pivotal clinical clue. Both hematuria and bilirubinuria can cause dark urine. Bilirubinuria only occurs in patients with conjugated hyperbilirubinemia which, in turn, is due to either CBD obstruction or hepatitis. In Ms. R, the preexistent biliary colic, persistent RUQ pain, and dark urine make the most likely diagnosis CBD obstruction due to migration of a stone into the CBD (choledocholithiasis) (Figure 3-2). On the other hand, in cholecystitis, only the cystic duct is obstructed. The CBD is unobstructed and therefore cholecystitis does not cause hyperbilirubinemia, bilirubinuria, dark urine, or significant increases in ALT (SGPT) or AST (SGOT). Finally, Ms. R’s fever suggests that the CBD obstruction has been complicated by ascending infection and taken together suggests ascending cholangitis, a life-threatening condition (Figure 3-4).

Dark urine suggests bilirubinuria and may precede icterus.

Rigors (defined as visible shaking or teeth chattering chills) suggests bacteremia and should increase the suspicion of a life-threatening bacterial infection.

Other considerations include hepatitis or pancreatitis (which may be caused by concomitant pancreatic duct obstruction). While hepatitis can cause RUQ pain, hyperbilirubinemia, and bilirubinuria, it would also require giving Ms. R another unrelated diagnosis and is therefore less likely. Table 3-8 lists the differential diagnosis.

Leading Hypothesis: Choledocholithiasis & Ascending Cholangitis

Textbook Presentation

Patients typically have some form of biliary obstruction (biliary colic, acute cholecystitis or gallstone pancreatitis). The presence of pain, fever, and jaundice suggest ascending cholangitis is present.

Disease Highlights

1. 5–20% of patients with symptomatic gallstones have stones within the CBD (choledocholithiasis).

2. Patients with choledocholithiasis may be asymptomatic.

3. Complications of choledocholithiasis may be the presenting manifestations.

   1. Obstruction and jaundice may be present.

   2. Fever, jaundice, and leukocytosis may be present due to ascending infection from the duodenum (ascending cholangitis). Ascending cholangitis may also occur when the CBD is obstructed due to tumors or strictures.

   3. Pancreatitis may occur if there is concomitant obstruction of the pancreatic duct.

Evidence-Based Diagnosis

1. Ascending cholangitis

   1. Clinical findings in patients with cholangitis include jaundice, 79%; temperature ≥ 38.0 °C, 77%; and RUQ pain, 68%. In various studies 42–75% of patients had all 3 (Charcot triad).

   2. There is leukocytosis in 73% of patients and elevated alkaline phosphatase and bilirubin in 91% and 87%, respectively.

   3. 74% of patients are bacteremic

   Bacteremia is exceptionally common in ascending cholangitis. Antibiotics should be administered promptly to patients in whom this diagnosis is suspected.

2. Choledocholithiasis

   1. Any of the following suggests choledocholithiasis and warrants CBD evaluation (Table 3-9):

      1. Cholangitis

      2. Jaundice

      3. Dilated CBD on ultrasound

      4. Elevated alkaline phosphatase

      5. Elevated amylase or lipase

   2. CBD stones are present in 5–8% of patients without any of the aforementioned risk factors.

   3. Transabdominal ultrasound is noninvasive but not consistently sensitive for choledocholithiasis as opposed to its performance in cholelithiasis (sensitivity 25–81%, specificity 88–91%). A dilated CBD is seen in only 25% of patients.

   4. Endoscopic retrograde cholangiopancreatography (ERCP), magnetic resonance cholangiopancreatography (MRCP), and EUS are highly accurate in detecting CBD stones. These techniques share high sensitivity (90–100%) and specificity (90–100%).

      1. ERCP

         • (1) Invasive procedure that allows direct cannulation of CBD and relieves obstruction via simultaneous stone extraction and sphincterotomy

         • (2) > 90% sensitive, 99% specific for diagnosis

         • (3) Requires sedation

         • (4) Complicated by pancreatitis in 1–5% of patients

         • (5) Preferred procedure in patients with a high pretest probability of CBD stones particularly those with jaundice and fever in whom ERCP can also permit stone extraction

         • (6) In patients less likely to have a CBD stone (ie, those with cholelithiasis and isolated elevation in alkaline phosphatase), a less invasive test (eg, MRCP or EUS) is an appropriate initial study.

      2. MRCP

         • (1) Noninvasive scan visualizes CBD and adjacent structures

         • (2) Highly accurate for CBD stones: 90–100% sensitive, 88–100% specific

      3. EUS

         • (1) Both sensitive (94–99%) and specific (94–95%) for CBD stones.

         • (2) One study reported that EUS was more sensitive than ERCP (97% vs 67%).

         • (3) A normal EUS or MRCP would obviate the need for a more invasive ERCP.

         • (4) EUS followed by selective ERCP in patients with documented CBD stones is an appropriate strategy in patients with suspected choledocholithiasis without cholangitis. Reserving ERCP for the subset of patients with documented choledocholithiasis decreased the need for ERCP by 67% and the complication rate by 12% compared with performing ERCP in all patients with suspected choledocholithiasis.

      4. CT scanning is only 75% sensitive for choledocholithiasis. Two studies suggest that multidetector CT using iotroxate (which is excreted in the biliary system) is highly accurate for choledocholithiasis (85–96% sensitive, 88–94% specific).

      5. Summary: The ASGE recommends the following based on the risk of choledocholithiasis:

         • (1) High-risk patients (> 50% risk): ERCP is recommended in patients with

           • (a) Suspected ascending cholangitis

           • (b) Documented CBD stones

           • (c) Bilirubin > 4 mg/dL

           • (d) Bilirubin levels of 1.8–4 mg/dL and dilated CBDs

         • (2) Moderate-risk patients (10–50% risk): MRCP or EUS is recommended followed by selective ERCP in patients with documented choledocholithiasis.

           • (a) Patients with dilated CBD on ultrasound

           • (b) Elevated bilirubin levels (1.8–4 mg/dL)

           • (c) Gallstone-associated pancreatitis

           • (d) Elevated LFTs

           • (e) Age > 55 years

           • (f) An alternative approach is laparoscopic cholecystectomy with intraoperative cholangiogram and postoperative ERCP in patients with choledocholithiasis.

         • (3) Low-risk patients (< 10% risk): In patients with gallstone disease and none of the aforementioned risk factors, laparoscopic cholecystectomy without other preoperative CBD evaluation is recommended.

Treatment

1. Ascending cholangitis

   1. Blood cultures, IV broad-spectrum antibiotics, and IV hydration should begin immediately

   2. Biliary drainage with ERCP should be performed urgently in patients with moderate to severe disease.

   3. Biliary drainage with ERCP should be performed

      1. Emergently in patients with persistent pain, hypotension, altered mental status, persistent high fever, WBC ≥ 20,000/mcL, and bilirubin ≥ 10 mg/dL

      2. Electively in more stable patients

   4. If ERCP is unavailable, percutaneous transhepatic drainage or surgical decompression can be used.

2. In patients who have choledocholithiasis without ascending cholangitis, CBD stones can be removed via intraoperative CBD exploration or ERCP.

3. Cholecystectomy

Neither dilation of the CBD nor CBD stone can be seen on ultrasound (but is only 25% sensitive). You still suspect choledocholithiasis because of the jaundice and increased transaminases.

Alternative Diagnosis: Acute Hepatitis

See Chapter 26, Jaundice & Abnormal Liver Enzymes.

Alternative Diagnosis: Acute Cholecystitis

Textbook Presentation

Typical symptoms of acute cholecystitis include persistent RUQ or epigastric pain, fever, nausea, and vomiting.

Disease Highlights

1. Secondary to prolonged cystic duct obstruction (> 4–6 hours)

2. Persistent obstruction results in increasing gallbladder inflammation and pain. Necrosis, infection, and gangrene may occur.

3. Jaundice and marked elevation of liver enzymes are seen only if the stone migrates into the CBD and causes obstruction.

Evidence-Based Diagnosis

1. No clinical finding is sufficiently sensitive to rule out cholecystitis.

   1. Fever: present in 0–35% of patients

   2. Murphy sign

      1. Sensitivity, 65%; specificity, 87%

      2. LR+ = 5.0, LR− = 0.4

2. Laboratory findings

   1. Leukocytosis (> 10,000/mcL) is present in 52–63% of patients.

   2. Cholecystitis does not typically cause significant increases in lipase or LFTs. Such findings suggest complications of pancreatitis and choledocholithiasis.

3. Ultrasound (by radiologists)

   1. Test of choice due to speed, cost, ability to image adjacent organs and lack of radiation.

   2. Sensitivity, 88%; specificity, 80%, LR+, 4.4; LR−, 0.15

   3. Cholelithiasis is usually present (84–99%) but is not in and of itself diagnostic of acute cholecystitis.

   4. Additional findings that suggest acute cholecystitis include gallstones with gallbladder wall thickening, pericholecystic fluid, sonographic Murphy sign, or gallbladder enlargement > 5 cm. However, more specific findings may be less sensitive (27–38%).

   5. If ultrasound is normal, and clinical suspicion is high, consider HIDA (see below).

4. Bedside ultrasound by trained non-radiologists

   1. Used with increasing frequency in emergency departments

   2. One study reported good accuracy when performed by emergency department physicians with 5 hours of training; sensitivity, 91%; specificity, 66%; LR+, 2.7; LR–, 0.14.

   3. Abnormal results should be confirmed with formal ultrasonography.

   4. Normal results are probably adequate to rule out cholecystitis in patients with low pretest probabilities but not in those for whom there is a higher suspicion of acute cholecystitis.

5. Cholescintigraphy (HIDA) scans

   1. Radioisotope is excreted by the liver into the biliary system. In normal patients, the gallbladder concentrates the isotope and is visualized.

   2. Nonvisualization of the gallbladder suggests cystic duct obstruction and is highly specific for acute cholecystitis (97% sensitive, 90% specific).

   3. Nonvisualization can also be seen in prolonged fasting, hepatitis, alcohol abuse, and prior biliary sphincterotomy.

   4. Useful when the pretest probability is high, due to persistent pain, and the ultrasound is nondiagnostic (ie, the ultrasound demonstrates stones within the gallbladder) but no clear evidence of cholecystitis is seen (eg, no stones within the cystic duct nor evidence of gallbladder wall thickening or pericholecystic fluid).

   5. Visualization of the gallbladder essentially excludes acute cholecystitis.

6. A diagnostic algorithm is shown in Figure 3-4.

Treatment

Patients with acute cholecystitis should be admitted, administered parenteral antibiotics, and undergo cholecystectomy. The precise timing of surgery (early vs delayed) is controversial.

Alternative Diagnosis: Acute Pancreatitis

Textbook Presentation

Patients with acute pancreatitis often complain of a constant and boring abdominal pain of moderate to severe intensity that develops in the epigastrium and may radiate to the back. Associated symptoms may include nausea, vomiting, low-grade fever, and abdominal distention.

Disease Highlights

1. Etiology

   1. Alcohol abuse (typically binge drinking) and choledocholithiasis (with concomitant obstruction of pancreatic outflow) cause 80% of acute pancreatitis cases.

   2. 15–25% of cases are idiopathic, many of which may be due to microlithiasis or sphincter of Oddi dysfunction.

      1. 34–67% of patients with idiopathic pancreatitis were found to have small gallstones on EUS or ERCP.

      2. Sphincter of Oddi dysfunction may be particularly common in patients with prior cholecystectomy.

   3. Post ERCP

   4. Drugs commonly associated with pancreatitis include azathioprine, didanosine, estrogens, furosemide, hydrochlorothiazide, l-asparaginase, metronidazole, opioids, pentamidine, sulfonamides, corticosteroids, tamoxifen, tetracycline, valproate, and many others.

   5. Less common causes include trauma, marked hypertriglyceridemia (> 1000 mg/dL), hypercalcemia, ischemia, HIV infection, other infection, pancreatic carcinoma, pancreatic divisum, autoimmune pancreatitis, cystic fibrosis, and organ transplantation.

   6. Regardless of the inciting event, trypsinogen is activated to trypsin, which activates other pancreatic enzymes resulting in pancreatic autodigestion and inflammation (which may become systemic and lethal). Interleukins contribute to the inflammation.

2. Complications may be local or systemic. Severe, potentially fatal pancreatitis develops in about 20% of patients.

   1. Local complications

      1. Pancreatic pseudocyst

      2. Pancreatic necrosis

      3. Infections

         • (1) Bacterial translocation from the bowel with resultant local and systemic infection

         • (2) Infected pancreatic pseudocyst (abscess)

         • (3) Infected pancreatic necrosis

         • (4) Ascending cholangitis (in patients with gallstone-associated pancreatitis [GAP])

   2. Systemic complications

      1. Hyperglycemia

      2. Hypocalcemia

      3. Acute respiratory distress syndrome

      4. Acute kidney injury

      5. Disseminated intravascular coagulation

   3. Death

      1. Usually occurs in patients with infected pancreatic necrosis and in patients in whom multiple organ dysfunction develops.

      2. Several predictive scores have been developed including the Ranson criteria as well as the Glasgow and Apache II scores. All use similar variables that increase the likelihood of organ failure, including increased age and elevated WBC, BUN, glucose, or lactate dehydrogenase. Hypoxia and hypocalcemia are also associated with an increased risk.

      3. Hemoconcentration (HCT ≥ 50%) on admission predicts severe pancreatitis; LR+ 7.5 (vs 0.4 for patients with HCT ≤ 45%).

      4. CRP > 150 mg/L at 48 hours can also predict severe pancreatitis; sensitivity, 85–86%; specificity, 74–87%; LR+, 3.2–6.6; LR−, 0.16–0.2

Evidence-Based Diagnosis

1. History and physical

   1. Low-grade fevers (< 38.3°C) are common (60%).

   2. Pain may radiate to the back (50%) and may be exacerbated in the supine position.

   3. Nausea and vomiting are usually present (75%).

   4. Rebound is rare on presentation; guarding is common (50%).

   5. Periumbilical bruising (Cullen sign) is rare.

   6. Retroperitoneal bleeding from pancreatitis or a variety of other causes (including ruptured AAA) can lead to flank bruising (Grey Turner sign), which is rare, but can be a valuable clue when present.

2. Laboratory studies

   1. Lipase

      1. 94% sensitive, 96% specific; LR+ = 23, LR− = .06

      2. Remains elevated longer than serum amylase

      3. Marked elevations suggest pancreatitis secondary to gallstones.

   2. Amylase

      1. Less sensitive and specific than lipase

      2. Should not be routinely ordered if lipase available

   3. LFTs

      1. Studies suggest that significant elevations of the bilirubin, alkaline phosphatase, ALT, or AST in patients with pancreatitis suggest etiology secondary to gallstones (GAP). These enzymes increase due to concomitant obstruction of the CBD.

         • (1) ALT or AST elevations > 100 IU/L suggest GAP (sensitivity ≈ 55%, specificity ≈ 93%; LR+ 8–9)

         • (2) AST levels < 50 IU/L make GAP unlikely (sensitivity 90%, specificity 68%; LR− 0.15).

         • (3) 10% of patients with GAP have normal levels of alkaline phosphatase, bilirubin, AST, and ALT.

      2. Patients with GAP have high risk of recurrent pancreatitis and require cholecystectomy.

   4. Imaging: A variety of imaging techniques can be used in patients with acute pancreatitis.

      1. Plain radiography is useful to rule out free air or SBO.

      2. Transabdominal ultrasound is noninvasive and should be performed in all patients with pancreatitis to determine if they have gallstones or CBD dilatation suggesting GAP.

      3. CT scanning is 87–90% sensitive and 90–92% specific for the diagnosis of acute pancreatitis but insensitive for determining whether or not patients have GAP.

         • (1) Should be performed when the diagnosis is unclear or complications are suspected (pseudocysts or pancreatic necrosis)

         • (2) Pancreatic necrosis should be suspected in patients with severe pancreatitis, when signs of sepsis are present, and in patients who do not improve in the first 72 hours.

         • (3) IV contrast is required to demonstrate necrosis.

   5. Detecting GAP

      1. GAP should be suspected in any patient with pancreatitis that is not clearly secondary to alcohol.

      2. Neither transabdominal ultrasound nor CT is sensitive at detecting choledocholithiasis (21% and 40%, respectively).

      3. MRCP is highly accurate for choledocholithiasis (80–94% sensitive) as are EUS and ERCP (≈ 96–98% sensitive).

      4. ERCP

         • (1) Can cause pancreatitis and is therefore limited to patients with persistent obstruction or cholangitis.

         • (2) Its use in patients with severe pancreatitis is controversial.

      5. Preoperatively, patients with GAP should have CBD evaluation with ERCP, MRCP, or EUS. A reasonable option in such patients is EUS followed by ERCP if stones are identified.

   6. Imaging in idiopathic pancreatitis

      1. One study suggested EUS is superior to MRCP (except in patients with prior cholecystectomy).

      2. EUS more commonly discovered microlithiasis and sludge (suggesting GAP) than MRCP.

      3. Sensitivity of EUS is 88–96%, compared with 24% of MRCP.

   7. Calcium and triglycerides should be ordered to exclude less common causes of acute pancreatitis.

   8. Figure 3-5 outlines an approach to evaluation of pancreatitis.

Treatment

1. Vital signs, orthostatic BPs, and urinary output should be carefully monitored to assess intravascular volume.

2. IV fluid is critical to maintain appropriate BP and urinary output (> 0.5 mL/kg/h).

   1. One study demonstrated lactated Ringers was superior to normal saline with a significant reduction in the incidence of systemic inflammatory response syndrome at 24 hours (absolute risk reduction ≈ 15%, NNT = 6.7).

   2. Lactated Ringers should be avoided in patients with hypercalcemia.

3. No oral intake

4. Opioids for pain relief

5. Nasogastric tube if recurrent vomiting

6. Oxygen, electrolyte, and glucose monitoring

7. ICU admission for severe pancreatitis

8. Prophylactic antibiotics for patients with pancreatic necrosis are controversial.

9. If infection is suspected (due to increasing fever, leukocytosis or deterioration) evaluate with fine-needle aspiration and culture. If infection is confirmed, broad-spectrum antibiotics should be administered and surgical debridement considered.

10. ERCP and sphincterotomy (see above)

11. GAP: Cholecystectomy and ERCP/sphincterotomy

    1. Surgery during the index admission is superior to delayed surgery or ERCP with sphincterotomy (ERCP/S) decreasing the rate of recurrent acute pancreatitis and other biliary events.

    2. Recurrent GAP was seen in 1.7% of patients receiving surgery during their index admission vs 5.3% of patients having delayed ERCP/S and 13.2% in patients without surgery.

    3. CBD evaluation (with intraoperative cholangiogram, MRCP, or EUS) is also required to ensure that the CBD is clear of stones.

12. Alcohol abstinence

13. Nutrition

    1. Enteral feeding is superior to parenteral feeding and has been shown to decrease mortality.

    2. Enteral feeding avoids a variety of IV catheter–related complications and decreases gut bacterial translocation, which may contribute to infection.

    3. Jejunal feeding tubes are preferred.

Alternative Diagnosis: Chronic Pancreatitis

See Chapter 32, Unintentional Weight Loss.

The first pivotal point for Mr. J’s abdominal pain is its periumbilical location. A variety of diseases present with pain in this location, including AAA, appendicitis (early), bowel ischemia, bowel obstruction, diabetic ketoacidosis, gastroenteritis, IBS, and IBD (Figure 3-1). The second useful pivotal point to consider is the time course of Mr. J’s abdominal pain (Table 3-1). This allows us to further limit the differential diagnosis to those diseases causing acute periumbilical pain. Many of the aforementioned diseases cause acute pain, but not typically IBS and IBD. Furthermore, diabetic ketoacidosis is unlikely (unless this is his presentation of diabetes). Gastroenteritis is also unlikely given the absence of diarrhea and the severity of the pain. Finally, Mr. J’s severe crampy abdominal pain suggests some type of visceral obstruction. The syndromes associated with pain of this quality include ureteral obstruction secondary to kidney stones, biliary obstruction, or intestinal obstruction (large or small bowel). The associated nausea and vomiting can be seen with any of those diseases. However, the combination of the location of the pain and the loud intestinal sounds that accompany the pain makes bowel obstruction the leading hypothesis. It will also be important to determine if he has unexplained hypotension or abdominal distention during his exam. Table 3-10 lists the differential diagnoses for Mr. J.

The constipation, absence of flatus, and rushing bowel sounds further increase the suspicion of bowel obstruction. The tympanitic abdominal distention is a pivotal finding suggesting accumulation of air in the abdomen, in this case most likely due to obstruction. Most cases of SBO are due to adhesions from prior surgery. Mr. J’s negative surgical history makes SBO less unlikely. However, the hematochezia raises the possibility of a malignant obstruction and large bowel obstruction. The orthostatic hypotension is most likely due to dehydration from the vomiting and lack of oral intake and does not in and of itself suggest intra-abdominal hemorrhage from an AAA.

Leading Hypothesis: Large Bowel Obstruction (LBO)

Textbook Presentation

Bowel obstruction presents with waves of severe crampy abdominal pain that the patient finds incapacitating. Vomiting is common. The pain is often diffuse and poorly localized. Initially, the patient may have several bowel movements as the bowel distal to the obstruction is emptied in the first 12–24 hours. Bowel sounds are hyperactive early in the course. Abdominal distention is often present. (Distention is less prominent in proximal SBOs.) At first, the pain is intermittent; later, the pain often becomes more constant, bowel sounds may diminish and become absent, constipation progresses and the patient becomes unable to pass flatus. If bowel infarction occurs, focal tenderness and peritoneal findings may be seen.

In patients with abdominal pain, the absence of bowel movements or flatus suggests bowel obstruction.

Disease Highlights

1. Bowel obstruction accounts for 4% of patients with abdominal pain.

2. LBO accounts for 20% of all bowel obstructions.

3. Etiology: cancer (53%), sigmoid or cecal volvulus (17%), diverticular disease (12%), extrinsic compression from metastatic cancer (6%), other (12%) (adhesions rarely cause LBO)

Evidence-Based Diagnosis

1. History and physical exam in LBO and SBO (Table 3-11)

   1. None of the expected clinical findings are very sensitive.

      1. Vomiting, 75%

      2. Abdominal distention, 63%

   2. Certain findings are fairly specific.

      1. Constipation, 95%; LR+, 8.8

      2. Prior abdominal surgery, 94%; LR+, 11.5

      3. Abdominal distention, 89%; LR+, 5.7

   3. Certain combinations are insensitive (27–48%) but highly specific.

      1. Distention associated with any of the following highly suggestive (LR+ ≈ 10): increased bowel sounds, vomiting, constipation, or prior surgery

      2. Increased bowel sounds with prior surgery or vomiting also very suggestive of obstruction (LR+ of 11 and 8, respectively)

2. A CBC and electrolytes should be obtained: Anion gap acidosis suggests bowel infarction or sepsis.

   Marked leukocytosis, left shift or anion gap acidosis in a patient with bowel obstruction is a late finding and suggests bowel infarction.

3. Plain radiography may show air-fluid levels and distention of large bowel (> 6 cm).

   1. 84% sensitive, 72% specific for presence of LBO (not etiology)

   2. Small bowel distention also occurs if ileocecal valve is incompetent.

4. Barium enema (water soluble) or colonoscopy

   1. Barium enema is highly accurate for LBO.

      1. 96% sensitive, 98% specific

      2. LR+ 48, LR− 0.04

   2. Can determine etiology preoperatively (if patient stable)

   3. Can exclude acute colonic pseudo-obstruction (distention of the cecum and colon without mechanical obstruction)

   4. Colonoscopy can decompress pseudo-obstruction and prevent cecal perforation.

5. CT scan is also accurate in the diagnosis of LBO.

   1. 91% sensitive, 91% specific

   2. LR+ 10.1, LR− 0.1

Treatment of LBO

1. Aggressive rehydration and monitoring of urinary output is vital.

2. Broad-spectrum antibiotics advised: 39% of patients have microorganisms in the mesenteric nodes.

3. Surgery, stents, and balloon dilatation have been used. Consultation is advised.

4. For patients with sigmoid volvulus, and no evidence of infarction, sigmoidoscopy allows decompression and elective surgery at a later date to prevent recurrence.

   1. Emergent indications for surgery: perforation or ischemia

   2. Nonemergent indications for surgery: increasing distention, failure to resolve

Alternative Diagnosis: SBO

Textbook Presentation

The presentation is similar to that for LBO with the exception that patients are more likely to have a history of prior abdominal surgery.

Disease Highlights

1. Bowel obstruction accounts for 4% of patients with abdominal pain.

2. SBO accounts for 80% of all bowel obstructions.

3. Etiology

   1. Postsurgical adhesions, 70%

   2. Malignant tumor, 10–20%

      1. Usually metastatic

      2. However, 39% of SBOs in patients with a prior malignancy are due to adhesions or benign causes.

   3. Hernia (ventral, inguinal, or internal), 10%

   4. IBD (with stricture), 5%

   5. Radiation

   6. Less common causes of SBO include gallstones, bezoars, and intussusception.

4. SBOs may be partial or complete.

   1. Complete SBO

      1. 20–40% progress to strangulation and infarction. Strangulation may occur secondary to mesenteric twisting cutting off the blood supply or due to increasing intraluminal pressure directly compromising perfusion.

      2. Clinical signs do not allow for identification of strangulation prior to infarction: Fever, leukocytosis, and metabolic acidosis are late signs of strangulation and suggest infarction.

      3. 50–75% of patients admitted for SBO require surgery

   2. Partial SBO

      1. Rarely progresses to strangulation or infarction

      2. Characterized by continuing ability to pass stool or flatus (> 6–12 hours after symptom onset) or passage of contrast into cecum

      3. Resolves spontaneously (without surgery) in 60–85% of patients

Evidence-Based Diagnosis

1. Ideally, tests for SBO should identify obstruction and ischemia or infarction, if present (since ischemia and infarction are indications for emergent surgery rather than further observation.) Unfortunately, even tests that successfully predict SBO do not reliably determine whether there is ischemia and infarction.

2. See test characteristics of history and physical exam under LBO.

3. Physical exam findings are insensitive at predicting infarction. However, localized tenderness, rebound, or guarding would all suggest infarction is present.

4. WBC may be normal even in presence of ischemia.

5. Plain radiographs may show ≥ 2 air-fluid levels or dilated loops of bowel proximal to obstruction (> 2.5 cm diameter of small bowel).

   1. Sensitivity for obstruction 59–93%, specificity 83%

   2. Rarely determines etiology

   3. Complete obstruction is unlikely in patients with air in the colon or rectum.

6. Bedside ultrasound

   1. Can show dilated bowel (≥ 25 mm) proximal to normal or collapsed distal bowel.

   2. One study demonstrated excellent accuracy: sensitivity, 91%; specificity, 84%; LR+, 5.7; LR–, 0.11

   3. Superior to plain films (18% sensitive, 56% specific; LR+, 0.41; LR–, 1.5)

7. CT scanning

   1. Sensitivity for determining high-grade obstruction is 80–93%.

      1. Obstruction is suggested by a transition point between bowel proximal to the obstruction, which is dilated, and bowel distal to the obstruction, which is collapsed.

      2. CT scanning should be performed prior to nasogastric suction, which may decompress the proximal small bowel and thereby decreases the sensitivity of the CT scan for SBO.

   2. May delineate etiology of obstruction

   3. Test of choice to diagnose SBO (not ischemia)

   4. Not reliably sensitive at determining the presence of ischemia and infarction (and the need for immediate surgery). Different studies have reported sensitivities ranging from 15% to 100% (specificity 85–94%).

      The absence of CT signs of ischemia in patients with SBO does not in fact rule out ischemia.

   5. CT scan only 48% sensitive for partial SBO

8. Gastrografin small bowel series

   1. Diagnosis

      1. Accurate in the diagnosis of SBO and useful to predict nonoperative resolution

      2. 97% sensitive, 96% specific. (Spontaneous resolution is likely in patients in whom contrast reaches the colon.)

      3. Unlike CT scanning, small bowel series cannot delineate etiology of SBO or demonstrate ischemic changes.

   2. Therapy

      1. Gastrografin is hyperosmolar and draws fluid into bowel lumen, potentially dilating bowel.

      2. Randomized trials of patients with presumed adhesive SBO demonstrate reduced odds of surgical intervention in patients receiving gastrografin compared to controls (0.44–0.87).

Treatment

1. Fluid resuscitation

   1. IV rehydration is important to correct the prominent intravascular dehydration from decreased oral intake, vomiting, and third spacing of fluid within the bowel.

   2. Monitor vital signs, orthostasis, and urinary output carefully.

2. Careful, frequent observation and repeated physical exam over the first 12–24 hours

3. Nasogastric suction

4. Broad-spectrum antibiotics (59% of patients have bacterial translocation to mesenteric lymph nodes)

5. Frequent plain radiographs and CBC

6. Indications for surgery include any of the following:

   1. Signs of ischemia (increased pain, fever, tenderness, peritoneal findings, acidosis, or worsening leukocytosis)

   2. CT findings of infarction

   3. SBO secondary to hernia

   4. SBO clearly not secondary to adhesion (no prior surgery)

   5. Some clinicians recommend surgery when bowel obstruction fails to resolve in 24 hours. Others suggest a small bowel study.

Alternative Diagnosis: Ischemic Bowel Secondary to Acute Mesenteric Ischemia or Ischemic Colitis

Ischemic Bowel

Three distinct clinical subtypes of ischemic bowel include chronic mesenteric ischemia (chronic small bowel ischemia), acute mesenteric ischemia (acute ischemia of small bowel), ischemic colitis (ischemia of the large bowel). Chronic mesenteric ischemia is discussed at the end of the chapter.

1. Acute Mesenteric Ischemia

Textbook Presentation

Acute mesenteric ischemia is a life-threatening condition that virtually always presents with the abrupt onset of acute severe abdominal pain that is typically out of proportion to a relatively benign physical exam. Acute mesenteric ischemia usually occurs in patients with risk factors for systemic embolization (eg, atrial fibrillation) or arterial thrombosis. Unexplained metabolic acidosis can be an important clue.

Disease Highlights

1. Etiology: Usually due to superior mesenteric artery or celiac artery embolism (50%). Other causes include thrombosis (15–25%), low flow states without obstruction (15–30%) (nonobstructive mesenteric ischemia), and mesenteric venous thrombosis (5%).

   1. Embolism

      1. Risk factors include atrial fibrillation, acute myocardial infarction, valvular heart disease, heart failure, ventricular aneurysms, angiography of abdominal aorta, and hypercoagulable states.

      2. The onset is often sudden without prior symptoms.

   2. Thrombosis

      1. Usually occurs in patients with atherosclerotic disease of the involved artery.

      2. Approximately half of such patients have a prior history of chronic mesenteric ischemia with intestinal angina.

   3. Nonobstructive mesenteric ischemia

      1. May have an insidious onset

      2. Often occurs in elderly patients with mesenteric atherosclerotic disease and superimposed hypotension (due to myocardial infarction, heart failure, dialysis, or sepsis). Alpha-agonists, digoxin, and beta-blockers may also increase the risk of nonobstructive mesenteric ischemia.

      3. Also seen in critically ill patients after cardiopulmonary bypass or other major surgery

      4. Other causes include cocaine use and following endurance exercise activities (eg, marathon, cycling).

   4. Mesenteric venous thrombosis is often secondary to portal hypertension, hypercoagulable states, and intra-abdominal inflammation.

2. Patients have acute abdominal pain that is often out of proportion to their abdominal exam. If left untreated, bowel infarction and peritoneal findings will develop.

3. Incidence: 0.1–0.3% of hospital admissions

4. Mortality is high at 30–82%.

Evidence-Based Diagnosis

1. Common presenting symptoms are abdominal pain (94%), nausea (56%), vomiting (38%), and diarrhea (31%).

2. 50% of patients have a prior history of intestinal angina.

3. The WBC is abnormal in 90% of patients and often markedly elevated (mean WBC 21.4 × 10⁹/mL).

4. Lactate level was elevated in 77–89% of patients (mean 3.3 mmol/L [normal < 2.0 mmol/L]).

   A normal lactate level does not rule out acute mesenteric ischemia.

5. Plain abdominal radiographs may reveal thickening of bowel loops or thumbprinting but are insensitive (40%).

6. Doppler ultrasonography is insensitive due to bowel distention.

7. Standard CT scanning may demonstrate superior mesenteric artery occlusion or findings suggesting ischemic and necrosis such as segmental bowel wall thickening or pneumatosis but is insensitive (64%). One study reported 100% sensitivity but patients were studied 3 days after symptom onset, when infarction may have been easier to demonstrate.

8. CT angiography is very accurate (89–96% sensitive, 97–98% specific), rapidly available and fast. It is increasingly used as the initial study prior to angiography. Magnetic resonance angiography has also been used.

9. Catheter angiography is the gold standard and can also be therapeutic. However, it is invasive, time consuming, and may not be available on an emergent basis.

Treatment

1. Emergent revascularization (via thromboembolectomy, thrombolysis, vascular bypass or angioplasty) and surgical resection of necrotic bowel are the mainstays of therapy. Prompt surgical intervention (< 12 hours) reduces mortality compared with delayed intervention (> 12 hours) (14% vs 75%).

2. Broad-spectrum antibiotics

3. Volume resuscitation

4. Preoperative and postoperative anticoagulation to prevent thrombus propagation

5. For patients with nonobstructive mesenteric ischemia, improved perfusion is paramount.

6. Intra-arterial papaverine improves mesenteric blood flow by reducing reactive mesenteric arteriolar vasoconstriction.

2. Ischemic Colitis

Textbook Presentation

Ischemic colitis typically presents with left-sided abdominal pain. Patients frequently have bloody or maroon stools or diarrhea. Profuse bleeding is unusual.

Disease Highlights

1. The most common form of intestinal ischemia

2. Usually due to nonocclusive decrease in colonic perfusion

3. Distribution: Typically involves the watershed areas of the colon, most commonly the splenic flexure, descending colon, and rectosigmoid junction. Right colonic involvement occurs occasionally. Rectal involvement is rare and points to other diseases.

4. Precipitating events may include hypotension, myocardial infarction, sepsis, heart failure, or cardiac or aortic surgery but is usually not identified.

5. Uncommon causes include vasculitis, hypercoagulable states, vasoconstrictors, cocaine, vascular surgery, drugs (eg, alosetron), and long-distance running or bicycling (presumably due to shunting and hypoperfusion).

Evidence-Based Diagnosis

1. Abdominal pain (not usually severe) is reported by 68–84% of patients.

2. Hematochezia is a helpful diagnostic clue when present but not diagnostic when absent. Sensitivity 46%, specificity 90.9%; LR+ 5.1, LR−, 0.6

3. Diarrhea is seen in approximately 40% of patients.

4. Abdominal tenderness is common (81%), but rebound tenderness is rare (15%).

5. Risk factors that increase the likelihood of ischemic colitis include age > 60 years, hemodialysis, cardiovascular disease, hypertension, diabetes mellitus, hypoalbuminemia, and medications that induce constipation.

6. Features that distinguish acute mesenteric ischemia (small bowel) from ischemic colitis are summarized in Table 3-12.

7. Colonoscopy (without preparation) is the preferred test to evaluate ischemic colitis.

8. Plain radiographs rarely demonstrate free air (perforation) or thumbprinting (specific for ischemia).

9. Ultrasound may show segmental circumferential thickening a long segment (>10cm) of the splenic flexure or sigmoid with sudden transition from abnormal to normal areas. Color flow is absent or greatly diminished in 80% of cases, helping distinguish this from IBD in which flow is increased.

10. CT scanning may demonstrate segmental circumferential wall thickening (which is nonspecific) or be normal.

11. Vascular studies are usually normal and not indicated except in the unusual case of isolated right-sided ischemic colitis.

Treatment

1. Therapy is primarily supportive, with bowel rest, IV hydration, and broad-spectrum antibiotics.

2. Colonic infarction occurs in a small percentage of patients (15–20%) and requires segmental resection.

3. Indications for surgery include peritonitis, sepsis, free air on plain radiographs, clinical deterioration (persistent fever, increasing leukocytosis, lactic acidosis), or strictures.

Mr. L has diffuse abdominal pain, which is also acute and severe. This focuses the differential diagnosis on AAA, appendicitis, bowel obstruction, bowel ischemia, diabetic ketoacidosis, nephrolithiasis, and pancreatitis. The hyperacute onset and severity are most suggestive of AAA, bowel ischemia, nephrolithiasis, and pancreatitis. The radiation to the flank increases the likelihood of AAA, nephrolithiasis, and pancreatitis. Clearly, AAA is a must not miss diagnosis. Less likely possibilities would be diverticulitis with rupture, which can cause severe sudden onset of pain, although the pain is more often in the left lower quadrant (LLQ) than diffuse. Table 3-13 lists the differential diagnoses for Mr. L.

The most dramatic and important physical finding is the presence of profound orthostatic hypotension. It is critical to appreciate that his hypotension is clearly out of proportion to dehydration since he has only vomited once and his decreased oral intake only began 1 hour ago. As noted above unexplained hypotension is a pivotal finding suggesting either intra-abdominal hemorrhage or sepsis (Table 3-3). He has no fever or chills to suggest sepsis, but this is still possible. A serious consideration must be massive intra-abdominal hemorrhage, either within the GI tract or intraperitoneal. Large volume GI hemorrhage always exits the bowel quickly resulting in hematemesis, melena, or hematochezia and is rarely subtle. Therefore, you are more concerned about intraperitoneal hemorrhage. Causes of massive intraperitoneal hemorrhage include AAA rupture, splenic rupture, or rupture of an ectopic pregnancy. The patient’s history is most suggestive of AAA rupture. You call for a stat vascular surgery consult.

Orthostatic hypotension is always important. It significantly influences the differential diagnosis and the diagnostic and management decisions, and it may be marked despite a normal supine BP and pulse.

Leading Hypothesis: AAA

Textbook Presentation

Classically, patients are men with a history of smoking who have the triad of severe abdominal pain, a pulsatile abdominal mass, and hypotension.

Disease Highlights

1. Defined as an external diameter of the infrarenal abdominal aorta of ≥ 3 cm.

2. The highest prevalence of AAA is 5.9% in white male smokers between the ages of 50 and 79 years.

3. 10,000 deaths per year in United States

4. Risk factors

   1. Smoking is the most significant risk factor (OR 5).

   2. Men are affected 4 to 5 times more often than women.

   3. Family history of AAA (OR 4.3)

   4. Increased age

   5. Hypertension (OR 1.2)

5. May present acutely with rupture and catastrophic consequences, occasionally chronically when expansion causes pain or a contained rupture, be discovered incidentally or with screening ultrasound.

   1. Ruptured AAA

      1. Mortality with rupture is 70–90%.

      2. Misdiagnosis (most commonly renal colic) occurs in 16% of cases.

      3. Hypotension is a late finding, and palpable mass is often not present.

      4. Syncope may be present.

      5. Occasionally the rupture is contained and patients may have symptoms for months or longer (see below).

      6. Rupture into the duodenum is a rare complication, is more common in patients with prior AAA graft, and may result in GI bleeding over weeks.

   2. Symptomatic, contained

      1. Rarely, patients present nonemergently with symptomatic contained rupture of the abdominal aorta. Symptoms are primarily secondary to retroperitoneal hemorrhage and are occasionally present for weeks or even several years.

      2. Manifestations include

         • (1) Abdominal pain 83%

         • (2) Flank or back pain 61–66%

         • (3) Syncope 26%

         • (4) Abdominal mass on careful exam 52% (only 18% had abdominal mass noted on routine abdominal exam)

         • (5) Hypotension or orthostasis 48%

         • (6) Leukocytosis (> 11,000/mcL) 70%

         • (7) Anemia (unusual)

   3. Inflammatory AAA

      1. Comprise about 5–10% of AAAs and usually occurs at a slightly younger age.

      2. Distinguishing characteristic is marked inflammation of aortic adventitia.

      3. Back pain or abdominal pain is usual presentation (80% of patients); rupture is rarely presenting manifestation.

      4. Symptoms of inflammation (fever, weight loss) present in 20–50% of patients.

      5. Erythrocyte sedimentation rate is elevated in 40–90% of cases.

      6. CT or MRI reveal the aneurysm and marked thickening of the aortic wall. Periaortic fat stranding may be seen.

   4. Rarely presents when intraluminal thrombus within the aneurysmal sac embolizes, leading to the blue toe syndrome

   5. Asymptomatic AAA (discovered incidentally or on screening)

      1. The risk of rupture increases markedly as the diameter of the aneurysm increases. See Table 3-14.

Evidence-Based Diagnosis

1. Physical exam is not sufficiently sensitive to rule out AAA.

2. Bruits do not contribute to diagnosis.

3. Sensitivity of focused exam for asymptomatic AAA is poor overall (31–39%) and only 82% among patients with large AAA (≥ 5 cm). The sensitivity of the physical exam is less in obese patients (53% waist circumference > 39 inches vs 91% < 39 inches).

4. Sensitivity of abdominal exam in symptomatic AAA.

   1. Abdominal pain, distention, and rupture all limit sensitivity.

   2. Distention was reported in 52–100% in different series.

   3. Palpable mass was found in 18%.

      A palpable mass is unusual in patients with a ruptured AAA.

5. Laboratory and radiologic tests

   1. CT angiography is very accurate for ruptured AAA: sensitivity, 98.3%; specificity, 94.9%; LR+, 19.3; LR–, 0.02

   2. Bedside emergency ultrasound has been demonstrated to be highly accurate: sensitivity, 96–100%; specificity, 98–100%.

   3. For screening, ultrasound is preferred: sensitivity, 95%; specificity, 100%.

   4. Preoperative evaluation prior to repair of asymptomatic AAA typically utilizes CT angiography.

Treatment

1. For ruptured AAA, proceed directly to the operating room.

2. Screening: See Chapter 2, Screening & Health Maintenance

3. Timing of elective surgery

   1. Mortality with rupture exceeds 80%. Surgery is performed to minimize the risk of rupture.

   2. The risk of rupture increases substantially with increasing AAA diameter (see above).

   3. The standard recommendation is to electively repair AAAs ≥ 5.5 cm or those that are tender or have increased in size by ≥ 1 cm in 1 year.

   4. Other risk factors for rupture include smoking (hazard ratio 2.02, 1.33–3.06) and female gender (HR 3.76, 2.58–5.47). Hypertension also increases the risk.

   5. Some authorities recommend repair in women when the AAA reaches 5.2 cm.

4. Options include open surgical repair versus endovascular stent placement. Comparing stent to open repair:

   1. 30-day mortality, length of hospital stay, and discharge to nursing home is lower with stent placement than open repair.

   2. Minor revisions are required in 2–5% per year of patients with stent placements but the overall rate of all re-interventions for complications is lower in the stent placement group (21.2% vs 25.6%).

5. Surveillance of small AAA (4.0–5.4 cm)

   1. The optimal frequency of follow-up ultrasonography has not been determined. A reasonable approach would be annual surveillance for aneurysms < 4.0 cm, every 6 months for aneurysms < 4.0–4.9 cm, and every 3 months for aneurysms 5.0–5.4 cm.

   2. CT scan may be appropriate for patients with AAA of 5–5.4 cm. One study reported that 73% of patients found to have an AAA of 5–5.4 cm on ultrasound had an aneurysm that was ≥ 5.5 cm on CT.

6. Medical management

   1. Smoking cessation and blood pressure control

   2. AAAs are considered a coronary equivalent. Aspirin and statins are recommended.

Alternative Diagnosis: Nephrolithiasis

Textbook Presentation

Patients typically experience rapid onset of excruciating back and flank pain, which may radiate to the abdomen or groin. The intensity of the pain is often dramatic as patients writhe and move about constantly (unlike peritonitis) in an unsuccessful attempt to get comfortable. The pain may be associated with nausea, vomiting, dysuria, or urinary frequency.

Abdominal tenderness is unusual in patients with nephrolithiasis and should raise the possibility of other diagnoses.

Disease Highlights

1. Incidence: Symptomatic stones develop in 7–13% of people in the United States.

   1. 35–50% recurrence at 5 years

   2. Men affected 2–3 times more often than women

   3. Positive family history increases the risk (relative risk 2.6)

2. Etiology

   1. Calcium oxalate stones 75%

   2. Calcium phosphate stones (CaPO₄) 5%

   3. Uric acid stones 5–10%

   4. Struvite stones (MgNH₄PO₄) 5–15%

   5. Other: cystine and indinavir stones

3. Pathophysiology

   1. Stones form when the concentration of salts (ie, calcium, oxalate, or uric acid) becomes supersaturated in the urine resulting in precipitation and crystallization.

   2. Supersaturation is secondary to a combination of increased urinary salt excretion combined with inadequate diluting urinary volume. Numerous mechanisms can contribute to an increase in urinary mineral excretion including:

      1. Calcium: idiopathic hypercalcuria, hypercalcemic disorders, primary hyperparathyroidism, immobilization, excessive sodium intake (which increases calcium excretion), systemic acidosis, and excessive vitamin D supplementation

      2. Uric acid: Excessive dietary purines, myeloproliferative disorders, uricosuric agents (for the treatment of gout), and metabolic syndrome. Low urine pH also contributes to uric acid stone formation. Hyperuricosuria can lead to uric acid stones or calcium stones due to heterogeneous ossification.

      3. Oxalate: Increased excretion may be secondary to excessive oxalate intake (rhubarb, spinach, chocolate, nuts, vitamin C) and/or increased oxalate absorption.

         • (1) Fat malabsorption increases oxalate absorption. The unabsorbed fat competes with oxalate to bind calcium leading to more intraluminal oxalate that is not bound to calcium. Unbound oxalate is absorbed and excreted in the urine.

         • (2) Causes of fat malabsorption include short bowel syndrome, IBD, celiac sprue, and bariatric surgery.

   3. In some patients, a decrease in urinary stone inhibitors (urinary citrate) also contribute to stone formation.

   4. Infection with urea splitting organisms (ie, Proteus) plays a key role in the formation of struvite stones (MgNH₄PO₄).

   5. Renal colic develops when stones dislodge from the kidney and obstruct urinary flow.

4. Complications

   1. Ureteral obstruction

   2. Pyelonephritis

   3. Sepsis

   4. Renal failure is rare, occurring in patients with bilateral obstruction or obstruction of a solitary functioning kidney.

Evidence-Based Diagnosis

1. The evaluation is directed at establishing the diagnosis of nephrolithiasis and its underlying etiology so that measures to prevent its recurrence can be implemented.

2. Establishing the diagnosis

   1. Hematuria is present in 80% of patients; LR− is 0.57.

      The absence of hematuria does not rule out nephrolithiasis.

   2. Radiographs (kidneys, ureters, bladder) or ultrasound are not sufficiently sensitive to rule out nephrolithiasis (sensitivity 29–68% and 32–57%, respectively).

   3. Noncontrast renal CT is the test of choice.

      1. Sensitivity 95%; specificity 98%

      2. LR+, 48; LR−, 0.05

      3. Importantly, CT scan revealed alternative diagnoses in 33% of patients clinically suspected of nephrolithiasis.

   4. In pregnant women, ultrasound is the test of choice.

3. Evaluation of documented nephrolithiasis

   1. All patients should have a urinalysis and culture and basic serum chemistries, including several measurements of serum calcium. Urine culture, pH, and chemical analysis of any retrieved stones are also recommended.

   2. A more comprehensive evaluation, including several 24-hour urine specimens for analysis of calcium, oxalate, uric acid, sodium, creatinine and citrate as well as submission of retrieved stones for chemical analysis, is recommended for patients with recurrent stones. Some experts recommend this for patients with their first stone.

Treatment

1. Pain control

   1. NSAIDs

      1. Treat pain and diminish spasm

      2. Create less dependence than opioids

      3. To be avoided 3 days before lithotripsy due to antiplatelet effects

   2. Opioids

2. Hydration (oral if tolerated, otherwise IV)

3. Hospitalization indicated for uncontrolled pain, persistent nausea or vomiting, acute kidney injury or signs of infection.

4. Sepsis or acute kidney injury due to bilateral obstruction or unilateral obstruction in a solitary kidney

   1. Necessitate emergent drainage (via percutaneous nephrostomy tube or ureteral stent)

   2. For sepsis, broad-spectrum IV antibiotics to cover gram-negative organisms and enterococcus should also be administered.

5. Stone passage

   1. Nifedipine and tamsulosin have been demonstrated to significantly increase the likelihood of stone passage by 65%.

   2. Lithotripsy or ureteroscopy can be used to remove persistent ureteral stones.

6. Secondary prevention

   1. Patients with a single calcium stone:

      1. General measures include increasing fluid intake (≥ 2 L/d)(relative risk of recurrent stones 0.45, 0.24–0.84).

      2. Reducing phosphate-containing soft drinks may decrease recurrences (relative risk 0.83, 0.71–0.98).

   2. For patients with recurrent idiopathic calcium stones other options include:

      1. Thiazide diuretics decrease urinary calcium excretion (especially when combined with potassium supplementation) (relative risk 0.52, 0.39–0.69).

      2. Citrate supplementation is effective in patients with and without hypocitraturia (relative risk 0.25, 0.14–0.44).

      3. Allopurinol in patients with concomitant hyperuricemia or hyperuricosuria (relative risk 0.59, 0.42–0.84).

   3. More specific management (ie, dietary modification) is complex and depends on the underlying etiology of the patient’s nephrolithiasis.

Alternative Diagnosis: Diverticulitis

Textbook Presentation

Patients typically complain of a constant gradually increasing LLQ abdominal pain, usually present for several days. Diarrhea or constipation and fever are often present. Guarding and rebound may be seen.

Disease Highlights

1. Diverticula are outpouchings of the colonic wall that may be asymptomatic (diverticulosis), become inflamed (diverticulitis), or hemorrhage.

2. Diverticulosis

   1. Develops in 5–10% of patients aged > 45 years, 50% in persons aged > 60 years, and 80% in those aged > 85 years.

   2. Low-fiber diets are believed to cause diverticula by decreasing stool bulk, resulting in increased intraluminal pressure causing the mucosa and submucosa to herniate through weakness in the colonic wall where vessels penetrate creating diverticula.

3. Diverticulitis

   1. Develops secondary to microscopic or frank perforation of diverticula.

   2. 85–95% of diverticulitis occurs in sigmoid or descending colon

   3. Mean age of onset is 63 years.

   4. Complications of diverticulitis

      1. Abscess

      2. Peritonitis

      3. Sepsis

      4. Colonic obstruction

      5. Fistula formation (colovesicular fistula most common)

   5. Simultaneous diverticular hemorrhage and diverticulitis are unusual; diverticular hemorrhage is discussed in Chapter 19, GI Bleeding.

Evidence-Based Diagnosis

1. LLQ tenderness increases the likelihood of diverticulitis (LR+, 3.4; LR–, 0.41).

2. Neither fever nor leukocytosis is very sensitive for diverticulitis or diverticular abscess.

   1. In patients with uncomplicated diverticulitis, only 45% had temperature of ≥ 38.0°C or WBC > 11,000/mcL.

   2. In patients with diverticular abscess, only 64% of patients had temperature of ≥ 38.0°C and 62% had WBC > 11,000/mcL.

3. Plain radiographs may demonstrate free air or obstruction.

4. CT scan is test of choice in men and non-pregnant women.

   1. CT can confirm diverticulitis (diverticula with thickened bowel wall or pericolonic fat stranding); evaluate the extent, severity, and complications (abscess formation and perforation); and diagnose other conditions.

   2. 93–97% sensitive

5. Colonoscopy

   1. Colon cancer can be mistaken for diverticulitis on CT.

   2. All patients with diverticulitis should have follow-up CT.

   3. Colonoscopy should be delayed 4–6 weeks until there is resolution of acute inflammation.

Treatment

1. Outpatient management is appropriate for patients with a mild attack (ie, patients without marked fever or marked leukocytosis, pain manageable with oral analgesics, tolerating oral intake) and without significant comorbidities, immunocompromise, or advanced age.

   1. Ciprofloxacin and metronidazole recommended for 7–10 days

   2. Liquid diet

   3. High-fiber diet after attack resolves

   4. Follow-up colonoscopy (see above)

2. Moderate to severe attack (unable to tolerate oral intake, more severe pain) necessitates inpatient treatment.

   1. Broad-spectrum IV antibiotics

   2. No oral intake

   3. CT-guided drainage for abscesses > 5 cm

   4. Emergent surgery is recommended in patients with

      1. Frank peritonitis

      2. Uncontrolled sepsis

      3. Clinical deterioration despite medical management

      4. Obstruction or large abscesses that cannot be drained or are contaminated with frank fecal contents

   5. The threshold for surgery should be lower in immunocompromised patients.

   6. High-fiber diet once the attack has resolved

Irritable Bowel Syndrome (IBS)

Textbook Presentation

Patients often complain of intermittent abdominal pain accompanied by diarrhea or constipation or both of years' duration. The diarrhea is often associated with cramps that are relieved by defecation. Pain cannot be explained by structural or biochemical abnormalities. Weight loss or anemia should alert the clinician to other possibilities.

New persistent changes in bowel habits (either diarrhea or constipation) should be thoroughly evaluated to exclude colon cancer, IBD, or other process. An assumption of IBS in such patients is inappropriate.

Disease Highlights

1. Affects 12% of adults, women 1.7 times more than men.

2. Etiology is a combination of altered motility, visceral hypersensitivity, autonomic dysfunction, and psychological factors.

3. Symptoms are often exacerbated by psychological or physical stressors.

4. Patients may have pain associated primarily with diarrhea (IBS-D) or constipation (IBS-C) or a mixed bowel pattern (IBS-M).

Evidence-Based Diagnosis

1. There are no known biochemical or structural markers for IBS.

2. A variety of symptoms are common in patients with IBS including lower abdominal pain, passage of mucous, feeling of incomplete evacuation, loose or frequent stools at onset of pain, and pain relieved by defecation. However, none of these are very predictive (LR+, 1.3–2.1 and LR–, 0.59–0.88).

3. Only abdominal pain is very sensitive (but required by the criteria).

4. Diarrhea pattern

   1. One recent study suggested that patients with diarrhea-predominant IBS were more likely to have irregularly irregular diarrhea that fluctuated over days whereas patients with inflammatory diseases (IBD and celiac disease) were more likely to have persistent diarrhea that fluctuates over months.

   2. Persistent diarrhea increased the likelihood of IBD (LR+ 4.2).

   3. A more extensive workup may be indicated in patients with persistent, constant diarrhea.

5. The diagnosis is usually made by a combination of (1) a consistent history, (2) the absence of alarm features, and (3) a limited work-up to exclude other diseases.

   1. Consistent history

      1. Although a variety of criteria have been developed (ie, Rome Criteria), a recent review by the American College of Gastroenterology suggested a consistent history was abdominal pain or discomfort that occurs in association with altered bowel habits for at least 3 months.

      2. Patients may also report a relief of pain with defecation.

   2. Alarm symptoms (suggest alternative diagnosis and necessitate evaluation)

      1. Positive fecal occult blood test or rectal bleeding

      2. Anemia

      3. Weight loss > 10 lbs

      4. Fever

      5. Family history of colorectal cancer, IBD, or celiac disease

      6. Recent antibiotic use

   3. Limited workup

      1. A CBC is appropriate to rule out anemia, which would suggest alternative diagnoses.

      2. Other diagnostic testing is not recommended for young patients without alarm features, with the exception of serologic testing for celiac sprue in patients with IBS-D.

         • (1) Although recommended by the ACG, a recent study found the incidence of confirmed celiac disease in IBS-D patients (without alarm features) to be very low (0.41%) and not different from asymptomatic patients.

         • (2) May best be reserved for the subset of IBS-D patients with other possible clues suggesting celiac disease (eg, anemia, autoimmune disease or family history)

      3. Lactose hydrogen breath testing can be considered if lactose intolerance remains a concern despite dietary lactose restriction.

      4. There is no evidence that routine flexible sigmoidoscopy or colonoscopy is necessary in young patients without alarm symptoms.

      5. Colonoscopy is recommended in patients with alarm symptoms and in those aged ≥ 50 years (if not already performed). Biopsy is also recommended in patients with IBS-D to rule out microscopic colitis.

      6. The following should also be evaluated in patients with alarm symptoms:

         • (1) Stool for occult blood

         • (2) Thyroid-stimulating hormone levels

         • (3) Basic chemistries

         • (4) Stool for Clostridium difficile toxin and presence of ova and parasites

         • (5) A variety of serum and fecal markers, including ASCA, pANCA, fecal calprotectin, and fecal lactoferrin, are useful in selected patients and can suggest bowel inflammation or IBD.

Treatment

1. Nonspecific management. A variety of treatments have been shown to be effective in IBS including:

   1. Diets low in apples, cherries, nectarines, lactose, legumes, broccoli, cauliflower, Brussels sprouts and peas

   2. Physical activity

   3. Antispasmodics (including hyoscine and peppermint oil) help decrease abdominal pain.

   4. Tricyclic antidepressants and selective serotonin reuptake inhibitors are effective. Psychological counseling may also be effective although the data are less robust.

   5. Dietary fiber (psyllium) may be effective. Studies are conflicting.

2. Specific therapy is based on predominant syndrome.

   1. Diarrhea-predominant IBS (IBS-D)

      1. Patients with IBS-D should have a trial of lactose-free diet. Such treatment in lactase-deficient individuals with IBS markedly reduces outpatient visits.

      2. Loperamide reduces diarrhea (but not abdominal pain or bloating).

      3. A single, short course of rifaximin, a nonabsorbed antibiotic is helpful. Doses have ranged from 400 mg to 550 mg twice daily for 10–14 days.

      4. Alosetron is a 5HT₃-receptor antagonist whose use is restricted to prescribing program by US Food and Drug Administration. Expert consultation recommended.

      5. Probiotic treatment with Bifidobacteria may be useful.

   2. Constipation predominant IBS (IBS-C)

      1. Lubiprostone

         • (1) A selective C-2 chloride channel activator is more effective than placebo in women.

         • (2) Women of childbearing years should have a negative pregnancy test before starting the medication and maintain contraception while taking lubiprostone.

         • (3) Not yet recommended in men

Chronic Mesenteric Ischemia

Textbook Presentation

Patients with chronic mesenteric ischemia typically complain of recurrent postprandial abdominal pain (often in the first hour and diminishing 1–2 hours later), food fear, and weight loss. Patients often have a history of tobacco use (75%), peripheral vascular disease (55%), coronary artery disease (43%), or hypertension (37%).

Disease Highlights

1. Usually secondary to near obstructive atherosclerotic disease of the superior mesenteric artery or celiac artery or both.

2. Arterial stenosis results in an imbalance between intestinal oxygen supply and demand that is accentuated after eating leading to intestinal angina resulting in food fear and weight loss.

3. Two or more vessels (ie, superior mesenteric artery and celiac artery) are involved in 91% of affected patients.

Evidence-Based Diagnosis

1. Abdominal pain

   1. Occurs in 94% and is postprandial in 88%.

   2. It is typically epigastric or periumbilical.

   3. Typically develops in the first hour after eating and diminishes 1–2 hours later.

2. Weight loss occurs in 78% of patients and is due to food aversion.

3. Diarrhea occurs in 36% of patients.

4. An epigastric bruit has been reported in 63% of patients (17–87%).

5. The abdomen is typically nontender even during a severe episode of pain.

6. Although stenoses are common (18% of population over age 65 years), symptomatic chronic ischemia is rare, and documented stenosis does not confirm the diagnosis of mesenteric ischemia. It is important to exclude more common disorders (ie, PUD and gallstone disease).

7. Duplex ultrasonography is very sensitive (> 90%) and can be used as the initial diagnostic tool. Normal results make the diagnosis very unlikely.

8. CT angiography and magnetic resonance angiography have also been used. Angiography should be considered if the results of noninvasive testing suggest vascular obstruction.

Treatment

Revascularization (surgical repair or angioplasty [with stent]) is the only treatment.