Likely there is not a clinician in this country who has not had to deal with a patient with opioid addiction and overdose. It is a frustrating and often unsuccessful endeavor. The clinician usually treats only the initial overdose and tries to instill enough information to make a difference, but usually the patient is then discharged, only to continue using and being likely to overdose again.
Deaths from opioid overdose, particularly when heroin is mixed with fentanyl, are omnipresent, exceeding deaths from motor vehicle crashes and suicide combined. The medical system has made little progress in dealing with opioid addiction and overdose. The use of outpatient naloxone, given to patients or friends and relatives for intranasal use in overdose, is increasing and more commonly prescribed. Many pharmacies even allow patients to get naloxone intranasal kits without a prescription.
Boston researchers described a typical opioid overdose, with most of the familiar problems and ramifications of opioid addiction, and it's a good reminder of what happens to patients we see frequently.
A 36-Year-Old Man with Unintentional Opioid Overdose
Raja AS, Miller ES, et al.
New Engl J Med
This article presents a classic case of an individual who was opioid-dependent and suffered an overdose, probably unintentionally. His history before and after the ED visit is unfortunately quite typical. This 36-year-old man was first exposed to opioids when he had hand surgery and hydromorphone was prescribed by the surgeon. He sought more prescriptions after the surgery, which were denied. He then changed to intravenous heroin because it was less expensive and more easily obtained. He used heroin every day for the next few years.
He attempted methadone detoxification for only 10 days, but this failed and he returned to using heroin. He also attempted inpatient withdrawal, and he was discharged home after two weeks. This also failed, and his opioid dependence continued. Two months before this admission to the ED, the patient was released from jail and was admitted to a structured residential rehab program in which he participated in work therapy and attended Narcotics Anonymous. He underwent random urine toxicology and abstained from heroin. This was temporarily successful in quelling his opioid use, but he resumed IV heroin use three days prior to admission to the hospital.
The patient presumed that his heroin was mixed with fentanyl on the day of admission. Nonetheless, he injected the substance twice, the last dose being at 1:30 p.m. EMS was dispatched to a park a little more than an hour later where the patient was found unresponsive and lying on the ground.
His friend had administered intranasal naloxone and then called EMS. He was cyanotic when EMS first arrived, and he had a Glasgow coma scale of 3, temperature of 35.6°C, and a respiratory rate of 4 bpm. The oxygen saturation was 80% on room air. He had pinpoint pupils, and his glucose was normal. EMS delivered a second dose of intranasal naloxone. An oropharyngeal airway was placed, and he was delivered bag mask oxygen. Soon after the administration of naloxone and ventilation, the patient woke up and was said to be alert and oriented, with a respiratory rate of 16 bpm minute. He continued nasal oxygen at a rate of 6 liters per minute and was transferred to the ED.
The patient admitted to the overdose in the ED, and said it was unintentional and that he had never overdosed before. He again requested help with managing his opioid addiction. He was otherwise healthy and took no other medications. As is common, he was unemployed, and had family stress. He had no psychiatric history.
The patient was alert and fully oriented with relatively normal vital signs, except mild hypothermia. His oxygen saturation while breathing oxygen at 6 liters per minute was only 93%. The PC02 was 68 mm Hg. The pinpoint pupils were gone, and now were equally round and reactive. Scattered crackles were heard throughout the lungs. Blood tests were essentially normal except for a positive test for hepatitis C. He had persistent hypoxia in the hospital. A chest x-ray revealed cephalization of the pulmonary vasculature, fluid in the minor fissure, both consistent with interstitial pulmonary edema. A urine drug screen was negative, including an expanded panel for buprenorphine, oxycodone, methadone, and 6-monoacetylmorphine, opiates not detected by routine immunoassay.
The clinicians initially suspected aspiration while the patient was unconscious, a common occurrence in opioid overdose. He did not have a fever or cough, and was not treated with antibiotics. Aspiration and community-acquired pneumonia were subsequently ruled out. The chest x-ray was interpreted, along with the clinical findings, to demonstrate opioid-induced noncardiogenic pulmonary edema (NCPE). The patient normalized within 48 hours. He was given buprenorphine at discharge, but failed to follow up at an addiction clinic.
The patient resumed heroin and subsequently presented to the hospital with narcotic withdrawal. He was given clonidine and again referred to an addiction clinic, which he did not attend. He was subsequently incarcerated and lost to follow-up.
Comment: This is a very typical and classic description of an opioid addict who did well until an opioid overdose landed him in the ED with hypoxemia. All patients resuscitated from opioid coma should be evaluated for pneumonia, pulmonary edema, and pulmonary aspiration. Community-acquired pneumonia is 10 times more common in those who use IV drugs, but it was not the diagnosis in this patient. NCPE develops in one to two percent of patients with opioid overdose. It is mild to life-threatening, generally reversible within one or two days, and requires oxygen and occasionally assisted ventilation. The standard drugs used to treat cardiogenic pulmonary edema are not helpful. NCPE results from increased pulmonary capillary pressure and increased permeability of the pulmonary capillaries. It can sometimes be difficult to distinguish opioid pulmonary edema from cardiogenic pulmonary edema, and the two may coexist. NCPE occurs very quickly, sometimes with the needle still in the arm, but occasionally may be delayed for up to three to four hours.
This patient did not use alcohol, cocaine, or other opioids, and fentanyl was not looked for in the urine drug test. Hospital labs usually cannot find fentanyl, although now it is commonly mixed with street heroin. Attempts to decrease opioid use by limiting prescriptions has resulted in an increase in heroin use. Street heroin, now almost always mixed with fentanyl or its derivatives, is still inexpensive and very easy to find. Hospital testing will not find heroin in the urine or blood test in most cases, but the 6-monoacetylmorphine metabolite is unique to heroin. Most hospitals cannot identify this metabolite either, and it only exists in urine for a day or two. Heroin, which is metabolized to morphine, can be found in the blood for only 10 to 15 minutes. Morphine was not found in this case, so the patient probably used only fentanyl with no heroin. There are currently at least 30 fentanyl derivatives that are mixed with or substituted for heroin. Only reference labs can find them.
This case, in addition to its classic medical complications, describes the life of most chronic opioid users in this country. They are in and out of jail, often unemployed, have intermittent and usually unsuccessful attempts at detoxification, and may attempt to remain heroin-free by using methadone or buprenorphine. Fortunately, this patient was saved by intranasal naloxone, but that is not always the case. The classic presentation of coma, decreased respirations, hypoxemia, and pinpoint pupils is certainly a tipoff to an opioid overdose. The miotic pupils will be reversed with naloxone, and concurrent use of stimulants can also reverse meiosis.
There is some controversy about the best dose of naloxone to be given in the ED. Generally, it is best to avoid respiratory depression and not precipitate opioid withdrawal. Fentanyl may be more difficult to reverse than heroin. It has been suggested that patients who do not have respiratory arrest be given a lower dose of naloxone, such as 0.04 to 0.4 mg to increase the respiratory rate and improve ventilation without reversing all the effects and precipitating withdrawal. It's difficult to work with the very small doses of naloxone so I always use at least 0.4 mg.
It's unclear whether this individual would have been an opioid addict without the physician prescription. All physicians are under increasing scrutiny and criticism for giving patients opioids when other medications can be used, but few alternatives are available for severe pain.
Unfortunately, access to opioid treatment centers and opioid agonist therapy programs remains quite limited. One needs to have a special license to prescribe buprenorphine, and few physicians are certified. The authors noted that opioid users are often under the stigma of having a self-induced disorder, and using methadone and buprenorphine only replaces one addiction with another. There is still a long way to go to address opioid abuse in this country.
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Dear Dr. Roberts: I enjoyed reading your column about spinal cord compression. (EMN 2017;39:12; http://bit.ly/2kyQl3F.) As an EP with an additional practice in sports medicine, I would add one other “pink flag” in general for back pain, perhaps not always an acute compression but a more insidious one: a patient who says massage made her back pain much worse. I saw a woman who had been to several other doctors, had negative x-rays (several sets), and did not get better with physical therapy. She threw up her hands that anything could help and went out a got a massage, and felt much worse. She then saw me about a week later. I thought it was odd that a massage would make her so much worse. Unfortunately, her MRI showed bone-only breast cancer metastasis from a very, very remote cancer that was thought cured. Her spine was covered; I'm not sure why x-rays did not reveal it, but perhaps the mets had similar density to bone? Anyway, a patient getting worse after a massage will always be a pink flag (not quite to the potency of red) for my practice to get further evaluation or imaging in the nontrauma patient. — Ellen Smith, MD, Olney, MD
Dr. Roberts responds: Good pickup on your part, Dr. Smith. I assume your patient had thoracic back pain, not just low back pain, because the thoracic spine is where most badness occurs. Palpating the midline spine often defines an area of a musculoskeletal problem because musculoskeletal pain is usually paravertebral, not midline, and without point tenderness. I too have unfortunately seen metastatic cancer in patients who had been cancer-free for many years (lung, breast, prostate, thyroid, and kidney in particular). Regarding plain x-rays, I think plain films are a waste of time in anything but trauma, especially attempting to evaluate the hard-to-interpret thoracic spine films. In a patient such as yours, an MRI is clearly the best choice, better than a CT scan. Spontaneous thoracic back pain scares me, and just remember that patients often make up some minor preceding trauma to explain their pain.
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