Abdominal pain is one of the top five causes for presentation to the emergency department and accounts for 18% of hospital admissions. It has one of the broadest differential diagnoses the hospitalist will confront, and therefore a methodological approach is paramount.

In order to promptly identify the underlying etiology of the abdominal pain, the historian must identify the specific characteristics of the symptoms. Factors such as history of trauma, constitutional symptoms, surgical history, relation to food intake, and appetite must be considered. In addition, one must take a careful history, taking into account the patient’s previous diagnoses, dietary habits, travel history, medication, substance, and environmental exposures.

As with symptoms of other systems and organs, one must first consider basic features to get an idea of the acuity and character of the abdominal pain, by asking questions pertaining to Frequency, Associated symptoms, Radiation, Characteristic, Onset, Location, Duration, Exacerbating factors and Relieving factors (FAR COLDER).

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The differential diagnosis for generalized abdominal pain is vast. In order to remember the various entities that cause abdominal pain, it is helpful to consider broader categories first, such as inflammation, vascular causes, obstruction, cardiac causes, superficial entities and systemic etiologies.

Inflammatory processes generally consist of cavity irritation or peritonitis or spontaneous bacterial peritonitis (SBP), intestinal inflammation or inflammatory bowel disease (IBD), gastroenteritis, Clostridium difficile, colitis, and appendicitis.

Vascular causes include, from larger to smaller vessels, abdominal aortic aneurysm, portal vein thrombosis (PVT), sickle cell disease (SCD), mesenteric ischemia, and collagen vascular disease.

Obstructive causes can include a large bowel obstruction (LBO), small bowel obstruction (SBO) and kidney stones.

Cardiac causes are usually related to congestive heart failure (CHF) (see “Congestive heart failure”).

Superficial causes arise from skin processes (see “Cellulitis”) or superficial nerve dysfunction as seen with zoster or neuropathy.

Finally, systemic causes should also be considered, such as metabolic/endocrine imbalances (hypercalcemia, hypokalemia, diabetic ketoacidosis (DKA), adrenal insufficiency, angioedema), toxins (lead poisoning, narcotic withdrawal) and depression. Less common causes such as familial Mediterranean fever, acute intermittent porphyria and abdominal migraine may also be considered once more common conditions are ruled out.

One helpful approach in diagnosing generalized abdominal pain is to start with the outer lining of the abdominal cavity considering causes for peritonitis, then move inward, considering the various organs (intestines, pancreas, appendix, etc.). Next, move on to what is most diffuse (vascular causes). Also, consider metabolic/systemic causes for abdominal pain such as hypercalcemia, hypokalemia, DKA, lead poisoning, adrenal insufficiency, narcotic withdrawal, and depression.

Generalized abdominal pain can be characterized by certain features of different disease processes.

Peritonitis is typically found in patients with a history of cirrhosis, who endorse symptoms of abdominal discomfort, subjective fever, chills, weakness, nausea, vomiting, fatigue, or other symptoms of infection and confusion (whether self-reported or witnessed). Prior history of SBP is also a risk factor for a recurrent episode.

With intestinal inflammation such as ulcerative colitis (UC) or Crohn’s disease (CD), in addition to generalized abdominal pain, diarrhea, anorexia, nausea, vomiting, weakness, or malaise are usually present. CD in particular may present with low-grade fever and abdominal pain. UC tends to present with bloody diarrhea along with purulent or mucous anal drainage.

In females, peritoneal inflammation can be caused by a ruptured ovarian cyst, although more alarming diseases, such as tubo-ovarian abscess, pelvic inflammatory disease, and ectopic pregnancy, may also cause peritonitis and abdominal pain.

C. difficile infection should be considered in someone with a history of recent antibiotic use in the past 3 months and the presence of loose stools. Advanced age (more than 64 years old) increases the risk, as does the length of hospitalization. Sometimes, presence of abdominal cramping or mucous in the stools may be present. Patients with severe C. difficile infection may present with no diarrhea if ileus or toxic dilatation is present.

When considering vascular causes for abdominal pain, starting from largest to smallest vessels, abdominal aortic aneurysms (AAA) are found in people with a history of smoking (risk correlates to number of years spent smoking), advanced age, white race, male sex, prior history of coronary artery disease (CAD), family history of AAA, and symptoms of hypotension such as weakness, postural light-headedness and possible loss of consciousness.

PVT is likely to present in someone with a history of cirrhosis or hepatocellular carcinoma (HCC), a pro-thrombotic state, recent surgical procedures, portal hypertension, abdominal malignancy, or intra-abdominal infection. The highest rate of occurrence is in patients with hepatic malignancy associated cirrhosis (one third of these patients). Symptoms will include fevers, colicky abdominal pain, lumbar back pain, non-bloody vomiting, diarrhea or abdominal distension.

Sickle cell crisis will present in someone with usually an already established diagnosis of SCD, with recent dehydration, stress, infection, or exposure to extreme temperatures. The pain is throbbing, sharp, dull, stabbing, or shooting.

Mesenteric ischemia is more likely in someone with previous aortic/cardiac surgery, medication or illicit drug use, colon carcinoma, strenuous exercise, systemic diseases, or hypercoagulable states.

Ischemic colitis should be considered in patients experiencing lower abdominal discomfort with or without bloody stools. Risk factors for ischemic colitis include age greater than 60 years, hemodialysis, hypertension, diabetes mellitus (DM), hypoalbuminemia, and constipation-inducing medications.

Acute mesenteric ischemia (AMI) presents in those with advanced age, low cardiac output states, arrhythmias, severe valvulopathy, recent myocardial infarctions (MI), severe, sudden abdominal or periumbilical pain, and possibly nausea.

Chronic mesenteric ischemia (CMI), on the other hand, presents with pain 15-60 minutes after meals, often leading to fear of eating. Patients with CMI usually have a history of atherosclerosis or severe stenosis.

Mesenteric thrombosis tends to be hereditary or an acquired disorder of hypercoagulation, but can also occur in those with oral contraceptive (OCP) use, prior history of deep vein thrombosis (DVT), or inflammatory conditions (trauma, IBD, postoperative states).

Finally, polyarteritis nodosa (PAN) tends to afflict patients aged in their 40s and 50s, of male sex, with intravenous drug use (IVDU), hepatitis B (HBV), or hepatitis C (HCV) infection, whose pain is associated with meals.

Predisposing factors for systemic lupus erythematosus (SLE) are female sex, age during childbearing years, intermittent lower abdominal pain, nausea, vomiting, anorexia, and diarrhea. Scleroderma typically manifests with early satiety, bloating and emesis.

Obstructive causes of generalized abdominal pain are broken down into SBO, LBO, pseudo-obstructions and ureteral obstruction (kidney stones).

SBOs are more likely if history of prior surgeries is present (and therefore an increased likelihood of adhesions, the most common cause for SBO), history of IBD, hernias, malignancies, intestinal malrotation, or diverticulitis.

LBOs on the other hand, are more common in those with a history of tumors or signs or symptoms suggestive of malignancy.

Pseudo-obstruction should be considered after a recent operation, trauma, infections, or cardiac disease.

Finally, kidney stones are more common in obesity, history of weight gain, family history of stones, prior stone before age 25, and colicky pain.

Metabolic or systemic causes depend on the specific problem at hand, but in general co-morbidities, such as DM, should be considered, medications that would cause electrolyte imbalances, complaints of associated malaise, fatigue, headaches, postural hypotension to suggest adrenal insufficiency, recent toxin ingestions, or symptoms suggestive of depression. Abdominal pain is a common manifestation of underlying psychiatric disease such as depression or anxiety disorder. It is important to remember to ask about new medications or dosing changes of current medications, and to elicit an environmental exposure history.

Not all disease processes have physical examination maneuvers specific to that process. However, most disease processes will have at least some physical exam finding more commonly present.

When considering peritonitis assess the abdomen for a fluid wave and rebound tenderness. Rebound tenderness is a good indication of peritoneal irritation or inflammation. When suspecting IBD, particularly in CD, perform a careful dermatologic examination looking specifically for oral aphthous ulcers, erythema nodosum, and pyoderma gangrenosum.

In suspected UC perform careful ear, nose and throat (ENT) exam looking for iritis, uveitis, episcleritis or stomatitis. Rectal exams, of course, should always be performed looking for abscesses, fistulae or fissures.

C. difficile infection will usually present with abdominal cramping, however if ileus is present, decreased, high-pitched bowel sounds, rebound or guarding may also be present.

Splenomegaly is often present in the setting of acute PVT. Ascites may not necessarily be present, nor would epigastric varices unless there is a massive clot burden. Jaundice may be present.

For AAA assess for expansile pulsatile epigastric mass by placing one finger on each side of the aorta and noting if the pulsations push the fingers outward or apart, indicating an aneurysm vs. pulsations of other etiologies (such as thin abdomens or epigastric masses overlying normal aorta).

In sickle cell crisis, abdominal distention may occasionally be present, roughly 30% of the time.

The key finding in acute mesenteric ischemia is pain out of proportion to exam in acute cases. Often there will be generalized tenderness but it can localize to the central abdomen in some cases. In chronic mesenteric ischemia an epigastric bruit is more common.

In vasculitides the most severe cases may present with signs of peritonitis or ileus. In PAN assess for livedo reticularis, testicular pain, myalgias, leg tenderness, and mono- or polyneuropathy.

Intestinal obstruction can be distinguished from pseudo-obstruction by noting presence of constitutional symptoms in addition to distention and failure to pass flatus. In pseudo-obstruction there may still be abdominal distention and failure to pass flatus, but it is highly unlikely to have absence of constitutional symptoms. Obstruction of ureters, such as in nephrolithiasis, will be most notable for patients having difficulty in finding a comfortable position. Check for accompanying costovertebral angle tenderness. Pain may be suprapubic as well.

Metabolic causes for abdominal pain will have to be specific to the disease process; look for signs of dehydration or diaphoresis in DM, hypotension for adrenal insufficiency, or flat affect in a depressed person.

Work-up for peritonitis entails paracentesis to look for SBP. Ultrasound should be used to determine if there is sufficient fluid to perform a paracentesis safely and to help locate the largest fluid collection. Fluid should be sent for cell count, protein, glucose, gram stain, cultures, and cytology. The more fluid that can be collected without compromising the hemodynamic stability of the patient the higher the sensitivity for both cultures and cytology. Abdominal flat and erect x-ray may be useful in ruling out perforation.

If suspecting IBD as an initial diagnosis, colonoscopy is indicated. However, if IBD has already been diagnosed and complications such as abscess, fistulae or strictures are considered, a computed tomography (CT) abdomen scan with contrast is recommended.

If C. difficile infection is suspected, two stool samples should be sent to evaluate for the toxin and a complete blood count (CBC) should be sent to evaluate the extent of elevation of white blood cell (WBC) count; in severe cases a CT abdomen is warranted to evaluate for toxic colitis.

Vascular causes such as PVT or AAA may be first evaluated using abdominal ultrasonography; for PVT, evaluating specifically the portal veins for presence of thrombosis, also noting flow of blood, and for AAA, assessing the size of the aneurysm. Any aneurysm larger than 5.5cm warrants a surgical consultation. If visualization of portal veins is not possible with ultrasonography, CT of abdomen with and without contrast may be considered.

When working-up SCD check a CBC to evaluate evidence of infection and anemia more severe than the patient’s baseline. Hemoglobin (Hgb) electrophoresis may be ordered to evaluate the degree of hepatocyte growth factor (HgF) to guide use of hydroxyurea. Reticulocyte count, lactate dehydrogenase (LDH) and bilirubin may ensure the presentation is consistent with sickle cell crisis and not another process (in crisis expect all to be elevated). CT may be performed if non-crisis diagnoses are seriously considered (cholecystitis, pancreatitis, appendicitis, or other intra-abdominal processes).

If mesenteric ischemia is strongly suspected colonoscopy should be considered or arteriography in severe cases. If concern for mesenteric thrombosis is high, helical CT should be considered, or alternatively magnetic resonance angiography (MRA) has also been shown to provide high-resolution angiograms. Mesenteric angiography ultimately is the gold standard.

In cases were vasculitides are suspected check anti-nucleated antibody (ANA), rheumatoid factor (RF), double-stranded deoxyribonucleic acid (dsDNA), anti-Sm, anti-Ro, anti-La, and anti-Scl-70 antibodies. If further work-up is indicated, obtain tissue biopsy.

Selective angiography of mesenteric vessels is the gold standard for acute arterial occlusion. If scleroderma is suspected, a barium enema can detect loss of haustrations and show wide mouthed diverticulae.

In intestinal obstructions radiographs are useful to rule out perforation. CT with and without contrast may help in distinguishing mechanical from pseudo-obstruction and to identify etiology of true obstruction. If evaluating for kidney stones, helical CT abdomen is recommended.

If considering metabolic or systemic causes for abdominal pain, a basic metabolic profile (BMP), cortisol stimulation test, urine toxicology, or lead level may be obtained, depending on how the history affects the likelihood of a condition being present.

SBP is diagnosed by serum-ascites albumin gradient (SAAG) less than 1.1g/dL and ascites polymorphonucleated cells (PMNs) greater than 250/mm3. If there are many red blood cells (RBCs), one PMN should be subtracted for every 250 RBCs to adjust for the presence of blood in the fluid.

Risk factors for the development of SBP include low levels of ascites protein (less than 1g/dL), elevated serum bilirubin (greater than 3.2mg/dL) and platelet count 98,000/mm3. Furthermore, an increased model for end-stage liver disease (MELD) score (calculated using international normalized ratio (INR), bilirubin and serum creatinine) corresponds to a higher risk of developing SBP, with an overall generalization that for every point of increase in the MELD score, the risk of developing SBP increases by 11%.

Secondary bacterial peritonitis should be considered if there are greater than two organisms that grow from the culture or there is no improvement on the current antibiotic regimen.

New diagnosis of IBD is dependent upon colonoscopy, however IBD complications usually rely on imaging or stool studies to rule out infectious diarrhea. C. difficile colitis or infection diagnosis is reliant upon the presence of diarrhea (three or more loose stools in the previous 24 hour period) and toxins present in stool studies or histopathologic demonstration by colonoscopy. History of recent antibiotic use is present in most cases. Response to specific treatment is also suggestive of C. difficile infection.

Vascular causes are diagnosed by imaging for the most part, with the exception of vasculitides. PVT is diagnosed by ultrasound or CT, AAA is also diagnosed by ultrasound.

Sickle cell crisis is diagnosed in the absence of another disease entity that could explain abdominal pain in a patient with documented history of SCD.

Mesenteric ischemia or thrombosis relies on CT with contrast or angiography. Vasculitides rely more on serologies supporting collagen vascular disease or tissue biopsy revealing disease process.

CT may be obtained if ischemia is suspected (except not in PAN because of small vessels); angiography is the gold standard when acute mesenteric artery occlusion is suspected (especially in PAN). For scleroderma, barium enema may highlight loss of haustra of the large intestines.

Intestinal obstruction is determined by high pre-test probability or imaging suggestive of obstruction, while pseudo-obstruction is determined by absence of mechanical obstruction on imaging. Kidney stones are confirmed by helical CT.

Metabolic or systemic etiologies are confirmed by history and abnormal lab findings pointing to etiology.

CT abdomen tends to be over-utilized in the diagnosis of peritonitis and should be ordered only if reason for suspicion of perforation on abdominal radiograph exists. There is also no data to support screening for coagulopathy prior to paracentesis and emphasis should be placed on clinical stability; paracentesis should be postponed in the context of three-dimensional ecchymosis or clinically suggestive disseminated intravascular coagulation. Ascites fluid cytology and mycobacterial cultures should only be ordered if pre-test probability is high, otherwise they are not cost-effective tests. Repeat testing for C. difficile during the same episode of diarrheal illness is of limited value.

Early intervention decreases the morbidity and mortality of patients with cirrhosis so starting antibiotics empirically is indicated while results from paracentesis are being processed. If there is copious fluid on physical exam to compromise the patient’s respiratory status, a therapeutic paracentesis should be performed concurrently with the diagnostic paracentesis if the blood pressure is stable for the patient’s normal range.

Have a low threshold for consulting the intensive care unit if the patient remains tachycardic, tachypneic or hypotensive despite initiation of antibiotics. Cefotaxime (or a similar third-generation cephalosporin) is a good choice to cover most common organisms (Escherichia coli, Enterobacter species and Streptococcus); 2g intravenous (IV) every 8 hrs for 5 days unless speciation and sensitivity allows for narrowing of spectrum coverage. For high risk patients (serum creatinine >1.0 mg/dL, serum BUN >30 mg/dL, or total bilirubin >4.0 mg/dL) albumin must be given at a dose 1.5 g per kg of body weight within 6 hours of SBP detection. On day 3 of treatment, another dose at 1.0 g per kg of body weight should be given. If there is a lack of improvement, in which case repeat paracentesis may be warranted to evaluate for secondary bacterial peritonitis or a resistant organism. Secondary peritonitis should also be considered if there is more than one bacterial species growing from culture. If a secondary cause is suspected, it is reasonable to investigate the cause with abdominal imaging, likely a CT.

Otherwise, treatment is generally for 5-7 days. Amoxicillin-clavulanic acid is also a good alternative. Fluoroquinolones (FQ) are an option for treatment provided the patient has not received them in the past. Prophylaxis against future episodes of SBP should be considered in cirrhotics with an upper gastrointestinal (GI) bleed (independent of presence of ascites), history of SBP (40-70% chance recurrence within 1 year) or ascitic fluid albumin less than 1 g/L. Caution should be taken to note the institution’s rate of resistance to FQs since FQ-resistant strains are on the rise.

Management of IBD depends on if this is a first time presentation or not. If a first time presentation, diagnosis is warranted by colonoscopy. Management entails hydration and control of diarrhea symptoms, if no infectious diarrhea is present, with an agent such as diphenoxylate/atropine (Lomotil) and pain control.

If there is a complication of IBD, such as an abscess or fistula, intravenous antibiotics are indicated and surgical consultation if the patient is unstable. Once stabilized, preparation for long-term immunosuppressive agents includes ruling out HIV and tuberculosis infection (purified protein derivative (PPD) or T-spot).

Chronic malnutrition is a natural result of IBD and supplementation with iron, vitamin B12, folate, zinc, magnesium, phosphate, calcium, and vitamin D is necessary. Low-saccharide diets (low in lactose, sucrose, maltose, isomaltose) have been used successfully. One study suggests that consumption of meat and alcohol increases relapse rates, which may be related to the sulfur ingestion. Another study suggests wheatgrass (100cc/d) decreases relapse rates.

Management of uncomplicated C. difficile infection is oral metronidazole 500mg 3 times daily (or alternatively 250mg 4 times daily) for 10-14 days. If the patient cannot tolerate oral intake, intravenous metronidazole may be used instead (every 8 hours). Metronidazole should be continued 1 week beyond the termination of antibiotics used for other concurrent infections.

If there is severe C. difficile infection, oral vancomycin is the drug of choice. Markers of disease severity include a leukocyte count greater than 15,000 cells/µL, serum creatinine more than 1.5 the baseline value, or evidence of toxic megacolon, shock, ileus, or multi-organ failure. When concerned about possible ileus, perforation or toxic colitis, surgery should be consulted. Contact precautions should be enforced (donning of gowns and gloves, separate room) and anyone who comes into contact with the patient should wash their hands with soap and water rather than use alcohol-based hand sanitizers.

PVT should be treated with anti-coagulation for at least 3 months, or indefinitely if a thrombotic risk factor exists that cannot be corrected. If complications occur, such as ischemia, surgical consultation is indicated (consider ischemia if there is evidence of thinning of intestinal mucosa on CT, presence of ascites, or presence of multi-organ failure).

Investigation for underlying HCC is advised since the incidence of PVT in patients with HCC is 13-14%. Check for pro-thrombotic conditions. Check blood cultures if fevers and chills or other signs of infection are present. If PVT is chronic, investigation of esophageal varices is indicated.

The most important factor for the presence of AAA is the stabilization of the patient; so if concern for rupture exists, immediate surgical consultation is indicated. If there is quick evolution of an already existing aneurysm (0.6-0.8cm/yr) or the aneurysm is larger than 5.5cm, surgical consultation is also indicated. Smoking cessation should be encouraged. Aim for blood pressure and lipid control similar to atherosclerotic disease. Beta-blockers may be considered to slow the rate of growth.

Management of sickle cell crisis includes ruling out an alternate diagnosis to explain the abdominal pain, then hydration is mainstay, along with pain management, hydroxyurea and transfusion if indicated.

Mesenteric ischemia/thrombosis should rely on a surgical consultation if it is acute mesenteric ischemia, however in chronic ischemia only severe cases warrant surgical consultation. Otherwise, supportive care is sufficient.

Finally, vasculitides rely on supportive care with hydration and bowel rest, and antibiotics if infection is suspected. Corticosteroids and other immunosuppressive agents may be considered with the help of rheumatologists. Other modalities may include nutritional support (fat soluble vitamins, vitamin C, medium-chained triglycerides), laxatives and pro-kinetic agents.

In scleroderma, octreotide stimulates intestinal motility, which also reduces bacterial overgrowth and improves abdominal symptoms.

The management of intestinal obstruction depends on its etiology: if it is true obstruction decompression with nasogastric tube is warranted along with fluid resuscitation and electrolyte management. Any reversible causes are to be addressed promptly, such as fecal disimpaction and cessation of causative medications (opiates, anti-cholinergics and possibly calcium-channel blockers).

Gastrografin (hypertonic water-soluble contrast) may speed the return of bowel function, decrease the length of stay and possibly decrease the need for surgical intervention. Surgical consultation is warranted if underlying etiology is a mass or conservative treatment fails.

Management of kidney stones depends on their size. If the stone is small (less than 5mm) the mainstay of treatment is hydration and analgesia, since most stones will pass spontaneously. If the patient can drink on his/her own, oral water consumption is encouraged. Non-steroidal anti-inflammatory drugs (NSAIDs) are encouraged over opiates (more effective with less side effects), however these should be avoided in patients with renal compromise or with a history of GI bleeds.

Stones 5-10mm have variable courses and stones greater than 10mm general do not pass spontaneously. For those that do not pass spontaneously urologic consultation is warranted. Magnesium supplementation in patients without renal failure is posited to assist passage of stones by its anti-spasmodic effects and arterial smooth muscle dilatation similar to calcium-channel blockers, which have been shown to facilitate stone passage. Dietary education is pivotal since high protein (high acid concentration) is lithogenic, while high fruit and vegetable intake confers alkali, and therefore protective properties.

Management of metabolic and systemic causes relies on re-balancing the underlying cause.

Take caution in the diagnosis of peritonitis to not remove too much fluid on paracentesis, and don’t delay initiation of antibiotics. Side effects of antibiotics include rash, pruritus, granulocytopenia, development of diarrhea (including C. difficile), nausea, vomiting, and colitis. In IBD it is common to neglect to address malnutrition, so nutrition consults are warranted in addition to supplementation of the minerals listed above.

Take caution in the treatment of PVT to monitor for bleeding from anticoagulation or from esophageal varices. AAA can have significantly worse outcomes (rapidly increasing rates of death) if surgical consultation is delayed for emergent cases so have a low threshold to consult vascular surgery. Monitor hemodynamics closely for any side effects of anti-hypertensives. Side effects from lipid lowering agents can also be seen.

A common mistake in sickle cell crises is to over-transfuse, with the possible development of transfusion reaction, transfusion-related acute lung injury (TRALI), alloimmunization, transfusion-related infection, and iron overload eventually leading to cirrhosis in some cases.

The most difficult aspect of mesenteric ischemia or thrombosis is lack of clinical suspicion leading to a delay in diagnosis, but also in delay in surgical consultation potentially leading to bowel infarction. Similarly, vasculitides may be overlooked due to low clinical suspicion leading to a delay in diagnosis.

There can be delays in decompression of intestinal obstructions due to not correcting the underlying problem (i.e., cessation of causative meds, rebalancing electrolytes) and a delay in nasogastric tube placement.

Take caution in pain management with kidney stones if using NSAIDs, to avoid GI bleeding. Ketorolac (Toradol) induces GI bleeding more than other NSAIDs. Also take caution to consult a urologist for larger kidney stones (greater than 10mm) or for those with complications (hydronephrosis).

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