A 21-year-old woman presents to the emergency department at 2 a.m. with severe periumbilical abdominal pain. The nurse informs you that this patient has had several emergency department visits over the last six months for similar pain and that nothing has been found despite extensive evaluations. Looking at her triage paperwork, you see that the woman is mildly tachycardic but has otherwise normal vital signs. She is on an oral contraceptive, an antidepressant, and a short-acting anxiolytic. She says she is “allergic” to trimethoprim/sulfamethoxazole and doxycycline, which make her “sick.” The nurse has charted that she has a history of anxiety, depression, and nephrolithiasis. You walk into the examining room braced for what could be a long and challenging evaluation.

Abdominal pain is one of the most frequent complaints encountered in the emergency department. As with other types of pain, patients with abdominal pain may have a difficult time describing their symptoms, and the symptoms they do describe may have many different underlying causes. While it is important to rule out potentially life-threatening causes of abdominal pain, there are less emergent etiologies that produce significant morbidity and can prove frustrating for both the physician and patient. Many patients have undergone extensive diagnostic procedures, such as computed tomography (CT) and endoscopy, without the etiology of the pain being elucidated. Often, this reflects the absence of an adequate differential diagnosis rather than a psychogenic cause of the pain.

The pattern and timing of abdominal pain are critical pieces of information in the evaluation of this complaint. Cyclical abdominal pain may be related to menstrual and gynecologic problems; that is less likely to be the case with sporadic, random pain. Relationship to meals and other exacerbating and mitigating factors are also important. In addition, a family history of abdominal pain, a thorough social history, and dietary history can be very helpful.

In this article, we will review some of the less common causes of recurrent abdominal pain in the acute care setting and provide an approach toward their evaluation.

Cyclical vomiting is a disorder that was previously thought to affect only the pediatric population. However, we now know that it can affect adults as well. The incidence of this syndrome is thought to be between 0.4% and 2% of children in the general population; the incidence in adults is unknown. There seems to be a slight female preponderance of 1.3:1.0. The mean age at onset is 4.8 years in children and 35 years in adults. Up to three quarters of patients with cyclical vomiting have a family history of migraines. The disorder is often misdiagnosed as viral gastroenteritis, food poisoning or, in children, severe gastroesophageal reflux.

Patients with cyclical vomiting generally have a prodromal episode lasting approximately 90 minutes, during which they experience pallor, fatigue, and nausea prior to the onset of frequent explosive vomiting. The vomiting usually lasts about 24 hours in children and an average of 72 hours in adults. Most patients have up to six episodes of emesis per hour and an average of 15 episodes per day. Occasionally, the emesis is bilious or contains blood, raising the specter of a bowel obstruction or upper gastroesophageal bleeding. Not surprisingly, many of these patients exhibit esophagitis and prolapse gastropathy on endoscopy.

After the last episode of emesis has subsided, the patient can usually tolerate enteral fluids about six hours later. The patient then experiences a period of normal health and relative well-being that usually lasts from several days to several months before experiencing another attack.

Attacks can be precipitated by a multitude of triggers, including stress, upper respiratory infection, sleep deprivation, dietary intake, menstrual periods, motion sickness, asthma attacks, or environmental allergies. Many of these patients (58% of children, 100% of adults) require intravenous (IV) fluids during their attacks. Abortive medications that can be given in the emergency department include the entire spectrum of antiemetic and antimigraine agents available. Many experts recommend IV fluids containing dextrose to help terminate ketosis, 5HT3 antagonists, and a benzodiazepine; phenothiazines, such as prochlorperazine or haloperidol, may also be used.

Many patients who suffer from cyclical vomiting will see a resolution of their symptoms after a decade or so. However, a significant number will go on to develop migraine headaches, a fact that further supports the link between cyclical vomiting and migraine-related cephalgia.


Abdominal migraines are thought to be very similar to cyclical vomiting. In fact, they are widely considered to be part of the same spectrum of disease. Both involve cyclical abdominal pain with periods of complete well-being between attacks. In either condition, patients can experience pallor, diaphoresis, anorexia, and headaches. The conditions occur in the same demographic groups and are both seen in patients with a personal or family history of migraines. Both tend to be self-limited, but the majority of patients will develop migraines in the future. They both respond to antimigraine treatments.

The main difference between abdominal migraines and cyclical vomiting is emesis. While emesis is a prominent finding in the presentation of cyclical vomiting, it is much more rarely seen in abdominal migraines, where pain is the predominant symptom.


Abdominal wall trigger points are a very common cause of cryptogenic abdominal pain. Trigger points are small, discrete areas of hyperirritable, taut, skeletal muscle bands that are painful on compression. Myofascial trigger points can often be palpated as a knot; there is chronic contraction of several continuous sarcomeres within these myofibrils that create the knot. It is thought that these contractions are a result of excessive acetylcholine release from local motor end plates. This can be demonstrated by electromyography (EMG) as localized spontaneous electrical activity that is absent in the surrounding myofibrils just 1 to 2 mm away. Other painful trigger points may occur in surgical scars.

Occasionally the trigger point itself is tender. However, many of these areas produce referred pain, motor dysfunction, or referred autonomic anomalies, such as urinary retention, detrusor muscle spasm, diarrhea, or constipation.

Trigger points are often divided into two categories, based on when the patient is symptomatic. Latent trigger points are quiescent and do not cause pain unless they are palpated or mechanically irritated. Active trigger points cause pain at rest. In both types, a patient’s symptoms will be reproduced when the band of irritated muscle is palpated or manipulated. Pain from trigger points can be local, occurring in the immediate vicinity of the trigger point, or referred proximally to or distally from the trigger point.

Trigger points appear to be slightly more common in women than in men. One study found that 54% of otherwise young, healthy, asymptomatic women and 45% of asymptomatic men, also young and healthy, had a latent trigger point that would elicit pain when manipulated. In women, pain from trigger points worsens during the second half of the menstrual cycle, implying that there may be a hormonal influence. People who are normally very active are less commonly affected by myofascial pain syndromes than people who lead more sedentary lifestyles.

Myofascial trigger points can be perpetuated by a host of systemic factors, including metabolic and nutritional deficiencies, anemia, gout, infection, and mechanical, physiologic, or psychological stresses. Clinically, patients usually present with a recurrent and characteristic pain that is often brought on by a certain position or movement. However, the patient may also have continuous pain that is unrelenting. The pain should have a distribution and quality that is distinct and consistent with each episode and usually aggravated by a change in the weather, repeated use of the muscles, or pressure over the trigger point. It is typically alleviated by rest or light activity, moist heat, or slow, steady, passive stretching.

Pain from myofascial trigger points can manifest as abdominal wall pain that is easily localized. However, trigger points may also involve visceral nerves. These trigger points will produce somatovisceral symptoms that may include anorexia, nausea, diarrhea, bladder spasm, urinary retention, and intestinal colic. Often, this pain will be diffuse and difficult for the patient to localize. Unilateral trigger points can cause bilateral symptoms; some may cause symptoms that are very similar to appendicitis, cholelithiasis, and endometritis in quality and distribution.

Diagnosis is purely clinical; laboratory tests and imaging are useful only in ruling out other possible etiologies for the pain. There are no specific diagnostic criteria for the use of EMG.

Treatment of trigger points can target any of the perpetuating factors mentioned above—for example, correcting electrolyte imbalances, treating any underlying infection, or resting muscle groups that are chronically stressed or overused. Short courses of analgesics, hypnotics to help with resting, and muscle relaxants are often used. Additionally, many practitioners use antidepressants, neuroleptics, or nonsteroidal anti-inflammatory drugs as chronic therapy for these patients.

Once a trigger point is isolated, nonpharmacologic treatments are also often employed. Despite the fact that the efficacy of some of these treatments has not been well studied, there is a large body of anecdotal evidence available and these techniques are routinely used by practitioners in pain clinics.

The “stretch and spray” procedure, for example, involves passively stretching the affected muscle and then spraying the area with a cooling agent such as dichlorodifluoromethane-trichloromonofluoromethane or ethyl chloride. The theory behind this technique is that the spinal stretch reflex and higher pain centers are inhibited by the temporary anesthesia provided by the topical spray. This allows the myofibrils to be stretched to a normal resting length, relieving the spasm, restoring local blood flow, and inactivating the trigger point.

Similar benefit may be derived from injection of trigger points with a local anesthetic, such as bupivacaine or lidocaine. Interestingly, one study showed equivalent pain relief with injection of a local anesthetic compared to needling the trigger point with a dry needle. Local instillation of a steroid (for example, triamcinolone 20 mg) may also be of benefit. This demonstrates the importance of mechanically disrupting the contraction knots. It should be noted that in the above study, postinjection soreness was more prevalent in the patients that underwent dry needling.

Patients may also be treated with physical therapy, passive stretching, and gentle full range-of-motion exercises, although it may take several days to see results. These exercises are important, regardless of the therapy that the patients undergo, to prevent shortening of the muscle and reformation of contraction bands. The paramount importance of these exercises should be emphasized during discharge.


Patients with acute porphyrias often present with such intense abdominal pain that it is not uncommon for them to undergo unnecessary exploratory laparotomy. Their symptoms result from the defective biosynthesis of heme and its precursors. Porphyrins accumulate when there is an enzymatic defect in the metabolic pathway of heme synthesis. Some of these porphyrins interact with light to produce free oxygen radicals; other types of precursors are thought to be neurotoxic, either through an interaction with gamma-aminobutyric acid receptors or through some direct effect on the nerves themselves. Clinical manifestations of porphyrias, therefore, usually involve the skin or neurologic dysfunction in the form of neurovisceral symptoms, most often manifesting as intense abdominal pain.

Porphyria occurs in five out of every 100,000 people in the United States. The most common form of the disease is porphyria cutanea tarda (PCT), which manifests primarily with a photosensitive skin rash. Additionally, there are several different types of acute porphyria that may present with abdominal pain, including acute intermittent porphyria (AIP), the most common acute porphyria in the United States. It is caused by an autosomal-dominant defect with variable penetrance. Generally, patients must have less than 50% of functioning porphobilinogen deaminase, the defective enzyme. The condition is seen more often in women than in men, with a peak incidence of onset in the second decade of life for women and the third decade for men. Attacks may be precipitated by alcohol, fasting, infections or other illness, surgery, and certain drugs. Some women suffer symptoms in relation to the hormonal changes that occur during the menstrual cycle.

In additional to abdominal pain, these patients often complain of extremity pain or paresthesias, constipation, vomiting, or diarrhea, and they may present with diaphoresis, tachycardia, or hypotension. Frequently, neuropsychiatric symptoms such as confusion, depression, anxiety, or hallucinations occur, increasing the likelihood that patients will be thought to be malingering. Other neurologic symptoms include motor neuropathies with symmetric proximal muscle weakness and attenuation or loss of deep tendon reflexes.

These findings, as well as other neurologic findings, often fluctuate irregularly, which may confuse the clinician. Other upper motor neuron symptoms, such as fasciculations, are usually absent. One study noted that up to 15% of people suffering an attack of AIP may have a seizure, but it was also observed that these patients were more likely to have associated hyponatremia. Patients occasionally have signs of sympathetic hyperactivity, including labile hypertension and tachycardia.

There are no cutaneous findings in AIP. Although the abdominal pain is often severe, the abdomen remains soft, without rebound or guarding. Most textbooks state that people with AIP have dark-colored urine. However, in one study only one of 10 patients diagnosed with acute porphyria in the emergency department had dark-colored urine. As mentioned above, some patients may have hyponatremia. Other laboratory abnormalities that may be observed include hypochloremia, hypokalemia, hypomagnesemia, and azotemia.

Porphyrias are all treated in essentially the same way. All potentially harmful drugs must be discontinued. The patient must avoid fasting and maintain an adequate intake of carbohydrates (300 gm/day). Fluid replacement to treat or prevent dehydration and correction of any electrolyte imbalance is indicated. Patients should receive IV hematin (3 to 5 mg/kg/day for three to five days) to slow the body’s endogenous heme production. A search for and treatment of a precipitating infectious process is warranted.

Patients should be given symptomatic relief from their pain and anxiety. Some authors recommend meperidine, but this should be used very cautiously in patients who are already prone to seizures; morphine is an alternative for pain control and chlorpromazine is helpful for agitation. Sympathetic hyperactivity, if not improved with control of pain and anxiety, can be treated with beta blockers.

The prognosis for AIP is good once patients learn how to avoid exacerbating factors and triggering phenomena. Most neurologic deficits resolve spontaneously.


Hypercalcemia is often found incidentally during a diagnostic evaluation, but it may be an important cause of abdominal pain. Calcium is a key element in preserving homeostasis and is closely regulated, mainly by parathyroid hormone (PTH), vitamin D, and calcitonin. About 98% of the body’s calcium is stored in the skeletal system; 1% circulates bound to albumin, globulin, and other proteins. The remaining 1% is in ionized (free) form. This ionized calcium is responsible for the majority of calcium’s physiologic effects.

Because of calcium’s ubiquitous presence, it is not surprising that hypercalcemia affects nearly every system in the body. In hypercalcemia, nerve conduction velocity slows, the cycle of muscle contraction and relaxation is impaired, vascular tone increases, cardiac conduction is abnormal, renal reabsorption of fluid and gastrointestinal motility are decreased, and digestive agents such as gastrin, hydrochloric acid, and pancreatic enzymes are released at a more rapid rate.

A mnemonic learned by every medical student sums up the typical patient with hypercalcemia: “stones, bones, abdominal moans, and psychiatric groans.” The abdominal pain in hypercalcemia may be multifactorial. Intestinal ileus often occurs, causing the abdominal pain, as well as constipation, bloating, anorexia, nausea, and vomiting. In addition, these patients frequently suffer from gastritis due to the higher levels of gastrin and lower pH in the stomach. The increased secretion of pancreatic enzymes predisposes the patient with hypercalcemia to pancreatic autodigestion and pancreatitis. The altered tubular reabsorption of fluids and electrolytes may lead to nephrolithiasis.

More than 90% of cases of hypercalcemia are due to primary hyperparathyroidism (55%) or malignancy (35%). Hypercalcemia of malignancy is usually a preterminal event that carries a life expectancy of only weeks, while primary hyperparathyroidism is relatively benign. Obviously, it is important to be expeditious when trying to differentiate between these two etiologies.

The history should focus on symptoms of hypercalcemia, constitutional symptoms of malignancy, any recent surgery or immobilization, medications that may be contributing to the condition, risk factors for malignancy, and a family history of malignancy or hypercalcemia. Primary hyperparathyroidism is usually from a single parathyroid adenoma, but hyperplasia of all of the parathyroid glands may also be the underlying cause. Rarely, the patient may have parathyroid carcinoma, in which case an intact PTH level will be within the normal range, which would be inappropriately elevated in the setting of hypercalcemia.

Generally, parathyroid adenomas are indolent and grow very slowly. In most cases of malignancy-associated hypercalcemia, a hormone that is identical to PTH at the amino terminus is produced by the tumor. This PTH-related peptide binds to the PTH receptor and mimics its physiologic effects. This is the mechanism by which most solid tumors cause hypercalcemia. Other tumors may cause hypercalcemia through bone metastasis, invasion, and lysis or, in the case of Hodgkin’s lymphoma, through the increased production of calcitriol. In all of these instances, the serum PTH level should be very low.

Medications can also lead to hypercalcemia. Thiazide diuretics cause renal calcium resorption that can induce a mild hypercalcemia. When taken in excess, antacids containing calcium carbonate can lead to a constellation of renal insufficiency, alkalosis, and hypercalcemia, also known as milk-alkali syndrome. Lithium can cause hypercalcemia by making the parathyroids less sensitive to calcium, in which case they will require a higher serum calcium concentration before they stop excreting PTH. Hypervitaminosis A and D can develop in individuals who are taking dietary supplements; both vitamins are fat soluble and are stored in the body for long periods of time. Vitamin A increases serum calcium by increasing bone resorption. Vitamin D also may increase bone resorption, but it exerts its major effect through increasing absorption of calcium from the gastrointestinal tract.


Superior mesenteric artery (SMA) syndrome is an uncommon cause of abdominal pain that can be difficult to diagnose. The SMA branches off of the aorta at about the level of the first lumbar vertebra; at this level it is encased in mesenteric fat and lymphatic tissue. The third portion of the duodenum is held beneath the SMA (between the SMA and the aorta) by the ligament of Treitz. The angle that the SMA makes with the aorta is acute, normally between 20 and 50 degrees. Superior mesenteric artery syndrome develops as the result of an abnormal narrowing of the aortomesenteric angle or other anatomical variation that causes the third portion of the duodenum to be compressed by the SMA, leading to intermittent bowel obstruction (see illustration).

Patients normally present with postprandial abdominal pain, abdominal distension, bilious emesis, and weight loss. Physical examination will frequently reveal a mid-epigastric bruit. The pain may be positional, being exacerbated by the supine position and somewhat improved by lying in the left lateral decubitus position, prone position, or knee-chest position. Symptoms usually develop after a precipitating event. Common precipitants include significant weight loss that ameliorates the fat pad supporting the SMA, surgery, lying prone, or body casting. Weight loss leading to SMA syndrome can be the result of malabsorption, anorexia nervosa, or HIV infection.

Other anatomic abnormalities can also predispose to SMA syndrome. It has been reported in cases associated with aortic aneurysm and in multiple cases following surgery to correct scoliosis. Patients may have chronic symptoms or may present more acutely. Complications that have been reported from SMA syndrome include acute gastric dilation, gastric rupture, aspiration pneumonia, and cardiovascular collapse. Mortality has been reported to be as high as 33%.

The diagnosis is made based on clinical suspicion and after other causes of bowel obstruction or surgical problems have been ruled out. The syndrome can be diagnosed with a barium swallow, CT with oral and IV contrast, CT angiography, standard angiography, or ultrasound, which would show an increased velocity of flow through the SMA. There is no role for plain abdominal films in the diagnosis of SMA syndrome. A barium swallow classically demonstrates gastric dilation, dilation of the proximal duodenum, and a linear filling defect that crosses the third portion of the duodenum with minimal contrast moving beyond that point. However, these findings are only variably present and are therefore not very sensitive.

Computed tomography and ultrasound can both demonstrate an acute angle formed by the SMA and the descending aorta. An angle of less than 22 degrees is believed to be consistent with SMA syndrome. The distance between the SMA and the descending aorta at the level where the duodenum passes between them is also a reliable indicator of SMA syndrome. In control patients, this distance was normally greater than 8 mm, whereas a value of less than 8 mm was very sensitive and specific for SMA syndrome. Furthermore, in one study, the degree of decreased angle or decreased SMA-to-aorta distance seemed to correlate with the severity of symptoms.

The initial therapy for SMA syndrome is conservative, with surgery as an option should medical therapy fail. The patient should be rehydrated and any electrolyte abnormalities should be corrected. Nutritional support should be provided either through a nasojejunostomy tube that is passed beyond the obstruction or via IV nutrition. The patient should be encouraged to stay prone or in the left lateral decubitus position after any oral intake to facilitate passage of intraluminal material past the obstruction. Symptoms often resolve once weight is regained and the fat pad is reconstituted. If patients fail to improve, a variety of open or laparoscopic surgeries are available to definitively treat the condition.


The epiploic appendixes are pedunculated projections of adipose tissue that project from the antimesenteric side of the colon. There are approximately 100 of them that extend in two rows from the cecum to the sigmoid, but they tend to be clustered at either end of the colon. They are an average of 3 cm in length but have been reported to be up to 15 cm long. They are normally fed by one or two arteries that stem from the colonic vasa recta and are drained by a single central vein. The physiologic function of the epiploic appendixes is not understood.

Epiploic appendagitis (EA) is an inflammation of these structures. The appendages can undergo torsion on their stalks, becoming ischemic and necrotic. This is the usual etiology for symptoms related to EA. Additional pathologic processes include vascular thrombosis, lymphoid hyperplasia, or spread of inflammation and infection from an adjacent diverticulitis.

Several case series have been published examining the symptoms related to EA. It is a disease process that is often difficult to differentiate from other surgical pathologies and, in fact, is often mistaken for diverticulitis, appendicitis, or acute cholecystitis. However, patients with epiploic appendagitis tend to be younger than patients with those conditions (35 vs 55 years), with a more rapid onset of pain in the left lower quadrant. The primary historical feature that differentiates EA from appendicitis is the fact that the pain is well localized and does not migrate. The typical patient is nontoxic, feels well otherwise, and reports normal bowel movements and a normal appetite. Nausea and vomiting are present in a minority of patients. It is also uncommon for these patients to have a fever. The physical exam usually demonstrates a soft abdomen. Voluntary guarding and localized rebound are variably present. One study reported a palpable mass in 10% to 30% of patients.

There are no laboratory test results that are helpful in making the diagnosis of EA. The white blood cell count is usually normal to mildly elevated and the rest of the test results are most often normal.

The primary mode of diagnosis is radiologic imaging. Computed tomography reveals paracolonic inflammation with fat stranding and a hyperattenuated 2- to 3-cm oval-shaped fat density or mass. There is usually not thickening of the bowel wall, which helps to differentiate EA from diverticulitis. Ultrasound has also been useful in the diagnosis. Typically, what is seen on ultrasound is a solid, noncompressible, hyperechoic ovoid mass with a subtle hypoechoic rim. This is demonstrated at the point of maximal tenderness.

Treatment of EA is conservative. The pain is generally well controlled with nonsteroidal anti-inflammatory drugs, although occasionally narcotics are required. In all of the case series mentioned above, the pain resolved within one to four weeks and no surgical intervention was required. There have been reported complications related to the formation of adhesions or the development of an abscess, but these are rare.


Sexual or physical abuse is often a contributor to recurrent abdominal pain. However, it frequently goes unrecognized. A typical history is of recurrent abdominal pain and dyspareunia, as well as a previous extensive evaluation that was inconclusive. Many patients have had multiple abdominal surgeries with only temporary relief of their pain. To complicate matters, the abuse may have occurred when the patient was a child or teenager. In 1998, the Department of Justice estimated that nearly one million instances of intimate partner domestic violence occurred annually in the United States. There are almost 3 million reports of possible child maltreatment to the authorities each year. On further investigation, evidence of abuse is found in one out of every three of these cases.

As staggering as these numbers are, abuse is still thought to be under-reported. Somewhere between 20% and 50% of victims of abuse seek medical treatment. In fact, some studies show that of the 1000 to 1200 women who die every year from intimate partner violence, only half of them had sought medical attention within the previous year.

Occasionally, the abuse victim’s complaint is specific and she will be willing to discuss the details of what happened, but more often her complaints will be nonspecific. They often include headache, insomnia, depression, and abdominal pain. Keeping a high index of suspicion, interviewing the patient alone, and asking specific questions such as “Do you feel safe at home?” and “Has anyone ever hit, kicked, or punched you in the last year?” can yield critical information. It is also important to perform a thorough physical exam, looking for ecchymosis or abrasions that are unusual or difficult for the patient to explain.

Lastly, cyclical abdominal pain is pain that occurs at regular intervals and often with characteristics that are consistent from one episode to the next.


The patient we presented at the beginning of this article has no family or personal history of migraines and she has not been having headaches. She has not been vomiting, despite her severe pain. She denies any recent weight loss, night sweats, bone pain, or fevers. She is not taking any extra vitamins. When questioned in private, she states that she feels safe in her current relationship. Physical examination reveals severe diffuse abdominal pain without rebound or guarding. Her bowel sounds are slightly decreased. There is no abdominal bruit. She has no skin lesions. Her patellar reflexes are slightly attenuated. Her urine, however, does have a reddish tinge to it, and a urine screen for porphobilinogens is positive. (A positive screening test is found in 50% to 95% of patients with AIP, depending on the test used.)

On further questioning, the patient does admit to having skipped dinner that night, opting instead to go out and have a few drinks with a friend. The patient’s condition improves greatly after a liter of normal saline and 4 mg of morphine are administered intravenously. You advise her to take in at least 300 grams of carbohydrates per day and to ensure adequate oral hydration. You arrange outpatient follow-up one week later with a hematologist for further evaluation and hematin therapy.