Suxamethonium and Critical Illness Polyneuropathy

Hughes, Mark; Is, Grant; Biccard, Bruce; Nimmo, Graham R.

doi:10.1177/0310057x9902700614

Cited by 28 publications

(5 citation statements)

References 10 publications

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“…Its use requires extensive education of critical care physicians to ensure their understanding of the contraindications for use of the drug. One survey study 109 observed that there was a poor understanding among critical care physicians of the risks of succinylcholine for patients with critical illness polyneuropathy. Succinylcholine is given in a dose of 1.5 mg/kg for intubation because a lower dose may induce relaxation of the central laryngeal muscles before peripheral musculature.…”

Section: Depolarizing Agents: Succinylcholinementioning

confidence: 99%

Airway Management of the Critically Ill Patient^*

Reynolds

Heffner²

2005

Chest

109

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Section: Depolarizing Agents: Succinylcholinementioning

confidence: 99%

Airway Management of the Critically Ill Patient^*

Reynolds

Heffner²

2005

Chest

109

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“…In order to distinguish these syndromes it may be necessary to measure serum creatine kinase levels, conduct repetitive stimulation studies, and perform a muscle biopsy. Caution is advised with respect to the administration of suxamethonium in patients with CIP because of the risk for hyperkalaemic cardic arrest [25].…”

Section: S Electrodiagnostic Featuresmentioning

confidence: 99%

Neurological complications of sepsis: critical illness polyneuropathy and myopathy

Hund

2001

J Neurol

148

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Sepsis may cause not only failure of parenchymal organs but can also cause damage to peripheral nerves and skeletal muscles. It is now recognized that sepsis-mediated disorders of the peripheral nerves and the muscle, called critical illness polyneuropathy (CIP) and critical illness myopathy, are responsible for weakness and muscle atrophy occurring de novo in intensively treated patients. CIP represents an acute axonal neuropathy that develops during treatment of severely ill patients and remits spontaneously, once the critical condition is under control. The course is monophasic and self-limiting. Among the critical illness myopathies, three main types have been identified: a non-necrotizing "cachectic" myopathy (critical illness myopathy in the strict sense), a myopathy with selective loss of myosin filaments ("thick filament myopathy") and an acute necrotizing myopathy of intensive care. Clinical manifestations of both critical illness myopathies and CIP include delayed weaning from the respirator, muscle weakness, and prolonging of the mobilization phase. The pathogenesis of these neuromuscular complications of sepsis is not understood in detail but most authors assume that the inflammatory factors that mediate systemic inflammatory response and multiple organ failure are closely involved. In thick filament myopathy and acute necrotizing myopathy, administration of steroids and neuromuscular blocking agents may act as triggers. Specific therapies have not been discovered. Stabilization of the underlying critical condition and elimination of sepsis appear to be of major importance. Steroids and muscle relaxants should be avoided or administered at the lowest dose possible.

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“…e number of fatalities which can be definitively linked to suxamethonium is few in the ICU, where possible causes of hemodynamic collapse during intubation are numerous. is may explain why some ICU physicians are unaware of suxamethonium-induced hyperkalemia [44]. e first case report of a Scandinavian COVID-19 patient experiencing lethal hyperkalemia following suxamethonium administration has been published [22].…”

Section: Discussionmentioning

confidence: 99%

Suxamethonium-Induced Hyperkalemia: A Short Review of Causes and Recommendations for Clinical Applications

Hovgaard

Juhl-Olsen

2021

Critical Care Research and Practice

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After the introduction of suxamethonium in 1953, cases of cardiac arrest during induction of anesthesia were recorded. In the following years, hyperkalemia was identified as the cause, and the connection to acetylcholine receptor modulation as the underlying molecular mechanism was made. Activation of the acetylcholine receptor with suxamethonium, acetylcholine, or choline causes an efflux of potassium to the extracellular space. However, certain pathological conditions cause acetylcholine receptor proliferation and the emergence of immature receptors capable of a larger potassium efflux to the bloodstream. These pathologic conditions include upper and lower neuron injuries, major burns, trauma, immobility, muscle tumors, muscular dystrophy, and prolonged critical illness. The latter is more important and relevant than ever due to the increasing number of COVID-19 patients requiring prolonged respiratory support and consequent immobilization. Suxamethonium can be used safely in the vast majority of patients. Still, reports of lethal hyperkalemic responses to suxamethonium continue to emerge. This review serves as a reminder of the pathophysiology behind extensive potassium release. Proficiency in the use of suxamethonium includes identification of patients at risk, and selection of an alternative neuromuscular blocking agent is imperative.

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Suxamethonium and Critical Illness Polyneuropathy

Cited by 28 publications

References 10 publications

Airway Management of the Critically Ill Patient^*

Airway Management of the Critically Ill Patient^*

Neurological complications of sepsis: critical illness polyneuropathy and myopathy

Suxamethonium-Induced Hyperkalemia: A Short Review of Causes and Recommendations for Clinical Applications

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Suxamethonium and Critical Illness Polyneuropathy

Cited by 28 publications

References 10 publications

Airway Management of the Critically Ill Patient*

Airway Management of the Critically Ill Patient*

Neurological complications of sepsis: critical illness polyneuropathy and myopathy

Suxamethonium-Induced Hyperkalemia: A Short Review of Causes and Recommendations for Clinical Applications

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Product

Resources

About

Airway Management of the Critically Ill Patient^*

Airway Management of the Critically Ill Patient^*