May 20, 2022: Why add Fentanyl to heroin? What causes wooden chest syndrome?


For at least 5 years, the number of deaths due to heroin have increased annually. Post-mortem evidence has revealed that these deaths were caused by fentanyl that was added to the heroin.

Fentanyl, a high-affinity mu(µ) opioid receptor (OR) agonist, is highly lipid soluble and can penetrate the blood-brain barrier more rapidly than other opioids. A synthetic opioid, fentanyl has a relatively straightforward chemistry and can be readily and cheaply produced in a clandestine lab. It is therefore much cheaper to produce than heroin as there is no need to cultivate poppy plants. As fentanyl has much greater potency than heroin, you can’t just add fentanyl or replace heroin with fentanyl. You must first add inert additives such as baking soda, talcum powder, laundry detergent or sugar (?rat poison) to heroin which significantly increase the volume but decrease the strength of the adulterated heroin. Adding a small amount of fentanyl boosts the potency. Fentanyl can also be pressed into pill form and marketed as a diverted prescription opioid. Fentanyl may be mixed with other drugs such as cocaine, marijuana, or meth.

Wooden chest syndrome (WCS) defined as laryngospasm, chest wall muscle rigidity, and rigidity of the diaphragm is unique to fentanyl. It occurs 1-2 minutes after injection. It is an uncommon response to anesthesia induction. And although anesthesiologists are aware of WCS (and manage it with paralytics and endotracheal intubation), it is less well known in the ED or on the street. Although data is conflicting regarding the etiology of WCS, there is evidence that agonism of the µ OR in the locus coeruleus (LC) activates alpha-adrenoreceptors of the LC and spinal cord which increases noradrenergic outflow. (I know that is TMI, but I couldn’t help myself. Mechanism of action is such a beautiful thing). When fentanyl is injected directly into LC, peripheral skeletal muscle rigidity occurs within 60 seconds.

So, does naloxone (competitive antagonist at µ OR) reverse the symptoms of WCS? Results are mixed. There clearly are case reports of naloxone reversal as well as case reports of lack of reversal. When naloxone doesn’t reverse the opioid symptoms (primarily respiratory depression), it is theorized that naloxone has little to do with the cholinergic or noradrenergic sites associated with WCS. When it does work, higher doses (forget the 2 or 4 mg), have been administered. The dose of naloxone may be important as fentanyl has a high affinity for the µ opioid receptor.

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Professor Emeritus
Department of Medicine

Tennessee Poison Center
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