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Recurrent Abdominal Pain and Vomiting A SELF-TEST IM BOARD REVIEW ON A CME EDUCATIONAL OBJECTIVE: Readers will be aware of narcotic bowel syndrome as a consequence CLINICAL CREDIT of prolonged narcotic use. CASE MARKUS AGITO, MD MAGED RIZK, MD Department of Internal Medicine, Quality Improvement Officer, Digestive Akron General Medical Center, Disease Institute, Cleveland Clinic; Assistant Akron, OH Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH Recurrent abdominal pain and vomiting 32-year-old man presents to the emer- Based on the information available, which A gency department with excruciating is the least likely cause of his symptoms? abdominal pain associated with multiple epi- 1 sodes of vomiting for the past 2 days. He re- □ Acute pancreatitis ports no fevers, headaches, diarrhea, constipa- □ Cyclic vomiting syndrome tion, hematochezia, melena, musculoskeletal □ Acute intermittent porphyria symptoms, or weight loss. His abdominal pain □ Gastroparesis is generalized and crampy. It does not radiate Acute pancreatitis and has no precipitating factors. The pain is Acute pancreatitis is the least likely cause of relieved only with intravenous narcotics. his symptoms. It is commonly caused by gall- stones, alcohol, hypertriglyceridemia, and cer- See related editorial, page 441 tain drugs.1 The associated abdominal pain is usually epigastric, radiates to the back, and is He does not smoke, drink alcohol, or use accompanied by nausea or vomiting, or both. illicit drugs. He has no known drug or food The onset of pain is sudden and rapidly increas- allergies. He says that his current condition es in severity within 30 minutes. CT shows en- causes him emotional stress that affects his largement of the pancreas with diffuse edema, A year ago, performance at work. heterogeneity of pancreatic parenchyma, peri- after a About a year ago, after a complicated sur- pancreatic stranding, and peripancreatic fluid gical procedure, he needed chronic high-dose collections.1 The diagnosis is based on two of complicated narcotics. A few months later, he developed the following three criteria: abdominal pain surgical multiple bouts of abdominal pain and vomit- characteristic of acute pancreatitis; a serum procedure, ing that required hospital visits. He now takes amylase or lipase concentration three or more oral oxycodone 10–15 mg every 4–6 hours. times the upper limit of normal; and character- he needed On admission, his vital signs are stable, but istic findings of acute pancreatitis on CT.1 chronic high he is in excruciating pain. He is alert and ori- ented to person, place, and time. His sclera are Cyclic vomiting syndrome doses anicteric, and the pupils are equal, round, and Cyclic vomiting syndrome is thought to be of narcotics reactive to light. Lung and heart examinations caused by episodic dysautonomia, mitochondri- are normal. The abdomen is soft and nondis- al DNA mutations, and hypothalamic emetic tended but tender in all four quadrants without response oversensitivity,2–4 but the exact patho- guarding; the liver and spleen are not palpable, genesis is unknown. The syndrome has been and no abdominal masses are detected. He has strongly linked to migraine and to the chronic no skin rash, joint swelling or tenderness, or excessive use of cannabinoids.5–9 The Rome III peripheral edema. The neurologic examination diagnostic criteria10 are the following: the vom- is normal. Computed tomography (CT) of the iting episodes are stereotypical, ie, they are acute abdomen with contrast shows no signs of bowel and last for less than 1 week; the patient has had obstruction, pancreatic calcifications or edema, three or more episodes in the previous year; and cholecystitis, or hepatobiliary disease. Results the patient has no nausea or vomiting between of initial laboratory testing are shown in TABLE 1. episodes. The patient must meet all three crite- ria. A history of migraine or a family history of doi:10.3949/ccjm.80a.12148 migraine further supports the diagnosis. 436 CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 80 • NUMBER 7 JULY 2013 Downloaded from www.ccjm.org on September 27, 2021. For personal use only. All other uses require permission. AGITO AND RIZK Acute intermittent porphyria TABLE 1 Acute intermittent porphyria is characterized by neurovisceral symptoms such as convul- Laboratory testing results at admission sions, paresis, autonomic dysfunction, con- TEST RESULT REFERENCE RANGE stipation, and diarrhea that result from the overproduction of porphyrin precursors and Complete blood cell count deficiency of porphobilinogen deaminase.11 Most patients have poorly localized, se- Hemoglobin 13.4 g/dL 13.2–17.4 vere, steady abdominal pain that develops Leukocytes 12.3 x 109/L* 4.4–9.7 over hours to days and that may persist for days Platelets 283 x 109/L 150–370 to weeks.11 Since the pain is neuropathic, ab- dominal tenderness is usually minimal during Comprehensive metabolic panel an acute attack. Other clues include signs of Sodium 139 mEq/L 136–145 ileus, such as constipation, nausea, abdominal Potassium 3.2 mEq/L* 3.5–5.1 distention, or decreased bowel sounds; blad- der dysfunction, eg, urinary retention, incon- Chloride 104 mEq/L 98–107 tinence, or dysuria; reddish-brown urine; and Bicarbonate 28 mEq/L 21–32 sensory neuropathy of the chest, back, and ex- Blood urea nitrogen 4 mg/dL* 7.0–18 tremities.11 Blistering skin lesions are usually Creatinine 0.9 mg/dL 0.8–1.3 not seen. The presence of porphobilinogen in the urine confirms the diagnosis.11 Glucose 109 mg/dL* 74–106 Alanine aminotransferase 55 U/L 30–65 Gastroparesis Aspartate aminotransferase 19 U/L 15–37 Gastroparesis is a result of discoordination Alkaline phosphatase 110 U/L 50–136 between the sympathetic and parasympa- thetic nervous systems, neurons, and smooth Total protein 6.2 g/dL* 6.4–8.2 muscles within the stomach, causing a de- Total bilirubin 0.8 mg/dL 0–1.0 crease in gastric motility. Common causes Lipase 231 U/L 114–286 12 13 are diabetes, scleroderma, and neurologic Amylase 35 U/L 25–115 disorders.14 It can also be iatrogenic,15 re- sulting from visceral nerve injury and drug *Value outside the reference range treatment with narcotics, calcium channel blockers, muscarinic cholinergic antago- Esophagogastroduodenoscopy shows antral gas- nists, or certain antidepressants. Symptoms tritis, but the esophagus and duodenum appear are related to gastric stasis, ie, abdominal normal, and colonoscopy is normal as well. His- pain from gastric distention, bloating, vom- tologic study of biopsy specimens obtained dur- iting, and early satiety.15 Abdominal pain ing endoscopy is unrevealing. A gastric-empty- may worsen after eating, and vomitus usu- ing study shows delayed emptying. The patient’s ally consists of recently ingested food. These abdominal pain and vomiting persist with the patients may have abdominal distension or initial dose of intravenous narcotic but resolve tenderness and succussion splash. After ex- with escalating doses. When asked, the patient cluding possible mechanical obstruction, a denies an excessive need for hot baths. gastric-emptying study may be necessary to 15 make the diagnosis. Which is the most likely diagnosis at this 2point? ■ CASE CONTINUED □ Narcotic bowel syndrome A serum and urine drug screen in our patient □ Opioid withdrawal is positive only for opioids. Urine measures of □ Crohn disease delta-aminolevulinic acid and porphobilinogen □ Chronic pancreatitis are normal. CT angiography of the abdomen □ Chronic mesenteric ischemia shows no signs of mesenteric vascular occlusion. □ Cannabinoid hyperemesis CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 80 • NUMBER 7 JULY 2013 437 Downloaded from www.ccjm.org on September 27, 2021. For personal use only. All other uses require permission. ABDOMINAL PAIN Narcotic bowel syndrome hypersensitivity, these patients perceive more Narcotic bowel syndrome is the most likely severe abdominal pain than patients with gas- diagnosis. Grunkemeier et al16 described troparesis alone. it as chronic or frequently recurring ab- dominal pain that is treated with narcot- Opioid withdrawal ics, either chronically or acutely with high Symptoms of opioid withdrawal may appear doses, and that includes all the following as soon as 6 to 24 hours after cessation of the features16: opioid in patients known to be dependent on • The pain worsens or resolves incompletely opioids. These patients present with crampy with continued or increasing doses of nar- abdominal pain with nausea.18 Other symp- cotics toms include agitation, rhinorrhea, lacrima- • The pain markedly worsens when the tion, excessive yawning, arthralgias, papillary narcotic dose is decreased, and decreases dilation, and piloerection.18 when the drug is reinstituted (the “soar- Our patient did not have the typical signs and-crash” effect) of opioid withdrawal. • The frequency, duration, and intensity of the pain episodes gradually increase Crohn disease • The nature of the pain and its intensity are Crohn disease is a multisystem disorder with not explained by a current or previous gas- specific clinical and pathologic features. It trointestinal diagnosis.16 is characterized by focal, asymmetric, trans- This syndrome is common in patients mural, and occasionally granulomatous in- who receive high doses of narcotics for post- flammation primarily affecting the gastro- operative pain or for other, nonmalignant intestinal tract.19 Characteristic symptoms causes of pain. Patients eventually become include abdominal pain, chronic diarrhea dependent on the drugs but are not aware with or without rectal bleeding, and weight that chronic use activates and facilitates ar- loss. Extraintestinal signs may include ane- eas in the brain that enhance the perception mia and inflammatory changes in the eyes, Laboratory of pain.16 A study of a rat model of narcotic skin, and joints. The diagnosis is based on tests are bowel syndrome17 showed that morphine- endoscopic, radiographic, and pathologic induced hyperalgesia depends on central findings.19 usually normal; sensitization involving the activation of Our patient did not have diarrhea or signs imaging may spinal microglia.
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