Abstract
Purpose: The patient is a 46-year-old male with past medical history significant for cardiac sarcoidosis, systolic heart failure (EF 30%), type 2 diabetes mellitus, compression deformities secondary to chronic steroid use, and chronic constipation secondary to opioid use, who presented with a ventricular tachycardia storm. The patient was admitted and placed on an amiodarone drip and then transitioned to po amiodarone. During his admission, the patient complained that his back pain had worsened over the past couple of months. He was started on Morphine SA 30mg BID and Oxicodone 10mg. He was started on senna and colace for bowel movements (BMs), which initially regulated his BMs, but later became constipated again. Miralax and eventually lactulose were started. Again, he started having regular BMs, but the regimen was less effective as his need for opioid increased. Subsequently, he was started on soap enema prn. This slightly helped, but the constipation did not resolve. He was then given a fleet enema and the patient's BMs slightly improved. A couple of days later, the constipation returned. We tried to decrease his pain medication, but he complained of significant pain. He wanted to start fleet enemas again. After getting the fleet enema, he did not have a large BM, but six hours later, he started to complain of fatigue and confusion. Blood work was sent, which showed a Na 153, Ca of 5.2, PO4 12.4, and BUN/Cr of 45/3. He was transferred to the ICU, where he was given IV fluids. Patient started becoming bradycardiac, became unresponsive, and went into PEA arrest. ACLS protocol was followed but was unsuccessful. Physicians often use opioids to treat moderate to severe pain, but opioids induce constipation. Opioid-induced constipation is mediated by gastrointestinal μ-opioid receptors. Limiting opioid therapy can decrease the severity of opioid-induced constipation, but analgesia is worsened. Frequently, phosphate-containing enemas are widely used to combat opioid-induced constipation. The laxative action is created through fluid movement into the rectosigmoid induced by sodium phosphate. Normally, the response occurs within minutes, resulting in little absorption of the enema. However, phosphate can be absorbed by the colon following normal doses of fleet enema in humans if not excreted. Clinical manifestations of fleet enema intoxication include volume depletion, acute renal failure, hypernatremia, hyperphosphatemia with reciprocal hypocalcemia. Initial fluid resuscitation is mandatory. Hemodialysis is indicated if metabolic derangements and oligoanuria are present. Methylnaltrexone is a selective antagonism of peripheral μ-opioid receptors and helps relieve opioid-induced constipation, but maintains analgesia.
Published Version
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