Editing Suxamethonium chloride (section)

==Side effects==
[[Adverse drug reaction|Side effects]] include [[malignant hyperthermia]], muscle pains, acute [[rhabdomyolysis]] with [[hyperkalemia|high blood levels of potassium]],<ref name="Flower2011"/> transient [[ocular hypertension]], [[constipation]]<ref>{{cite book | vauthors = DiPiro JT, Talbert RL, Yee GC | title = Matzke Pharmacotherapy: A Pathophysiologicḣ Approach | edition = 6th | publisher = McGraw-Hill | date = 2005 | pages = 685 }}</ref> and changes in cardiac rhythm, including [[bradycardia|slow heart rate]], and [[cardiac arrest]]. In people with neuromuscular disease or [[burn]]s, an injection of suxamethonium can lead to a large release of [[potassium]] from [[skeletal muscles]], potentially resulting in cardiac arrest. Conditions having susceptibility to suxamethonium-induced high blood potassium are burns, [[closed head injury]], [[acidosis]], [[Guillain–Barré syndrome]], cerebral [[stroke]], [[drowning]], severe intra-abdominal [[sepsis]], massive [[Trauma (medicine)|trauma]], [[myopathy]], and [[tetanus]].

Suxamethonium does not produce [[unconsciousness]] or [[anesthesia]], and its effects may cause considerable psychological distress while simultaneously making it impossible for a patient to communicate. Therefore, administration of the drug to a conscious patient is contraindicated.{{medical citation needed|date=January 2020}}

===Hyperkalemia===
The side effect of high blood potassium may occur because the acetylcholine [[Cell surface receptor|receptor]] is propped open, allowing continued flow of potassium ions into the [[extracellular fluid]]. A typical increase of potassium ion serum concentration on administration of suxamethonium is 0.5&nbsp;[[mmol]] per [[liter]].The increase is transient in otherwise healthy patients. The normal range of potassium is 3.5 to 5 mEq per liter. High blood potassium does not generally result in adverse effects below a concentration of 6.5 to 7 [[mEq]] per liter. Therefore, the increase in serum potassium level is usually not catastrophic in otherwise healthy patients. Severely high blood levels of potassium can cause changes in [[cardiac electrophysiology]], which, if severe, can result in [[arrhythmia]]s and even [[cardiac arrest]].<ref name = StatPearls84>{{cite web | url=https://www.ncbi.nlm.nih.gov/books/NBK499984/ | pmid=29763160 | year=2022 | vauthors = Hager HH, Burns B | title=Succinylcholine Chloride | publisher=StatPearls }}</ref><ref>{{cite journal | vauthors = Martyn JA, Richtsfeld M | title = Succinylcholine-induced hyperkalemia in acquired pathologic states: etiologic factors and molecular mechanisms | journal = Anesthesiology | volume = 104 | issue = 1 | pages = 158–169 | date = January 2006 | pmid = 16394702 | doi = 10.1097/00000542-200601000-00022 | s2cid = 4556150 | doi-access = free }}</ref>

===Malignant hyperthermia===
{{unreferenced section|date=January 2020}}
[[Malignant hyperthermia]] (MH) from suxamethonium administration can result in a drastic and uncontrolled increase in skeletal muscle [[oxidative metabolism]]. This overwhelms the body's capacity to supply [[oxygen]], remove [[carbon dioxide]], and regulate body temperature, eventually leading to circulatory collapse and death if not treated quickly.

Susceptibility to malignant hyperthermia is often inherited as an [[autosomal dominant]] disorder, for which there are at least six [[gene|genetic loci]] of interest, the most prominent being the [[ryanodine]] receptor gene (RYR1). MH susceptibility is [[phenotypically|phenotype]] and genetically related to [[central core disease]] (CCD), an autosomal dominant disorder characterized both by MH symptoms and by [[myopathy]]. MH is usually unmasked by [[anesthesia]], or when a family member develops the symptoms. There is no simple, straightforward test to diagnose the condition. When MH develops during a procedure, treatment with [[dantrolene]] sodium is usually initiated; dantrolene and the avoidance of suxamethonium administration in susceptible people have markedly reduced the mortality from this condition.

===Apnea===
{{See also|Pseudocholinesterase deficiency}}

The normal short duration of action of suxamethonium is due to the rapid metabolism of the drug by non-specific plasma cholinesterases. However, plasma cholinesterase activity is reduced in some people due to either genetic variation or acquired conditions, which results in a prolonged duration of neuromuscular block. Genetically, ninety six percent of the population have a normal (Eu:Eu) genotype and block duration; however, some people have atypical genes (Ea, Es, Ef) which can be found in varying combinations with the Eu gene, or other atypical genes (see [[Pseudocholinesterase deficiency]]). Such genes will result in a longer duration of action of the drug, ranging from 20 minutes up to several hours. Acquired factors that affect plasma cholinesterase activity include pregnancy, liver disease, kidney failure, [[heart failure]], [[thyrotoxicosis]], and cancer, as well as a number of other drugs.<ref>{{cite book | vauthors = Peck TE, Hill SA, Williams M | title = Pharmacology for Anaesthesia and Intensive Care | edition = 2nd | publisher = Greenwich Medical Media Limited | location = London, UK | date = 2003 | isbn = 1-84110-166-4 }}</ref>

If unrecognized by a clinician it could lead to awareness if anesthesia is discontinued whilst still paralyzed or hypoxemia (and potentially fatal consequences) if artificial ventilation is not maintained. Normal treatment is to maintain sedation and ventilate the patient on an intensive care unit until muscle function has returned. Blood testing for cholinesterase function can be performed.{{medical citation needed|date=January 2020}}

[[Mivacurium]], a non-depolarizing neuromuscular blocking drug, is also metabolized via the same route with a similar clinical effect in patients deficient in plasma cholinesterase activity.{{medical citation needed|date=January 2020}}

Deliberate induction of conscious apnea using this drug led to its use as a form of [[aversion therapy]] in the 1960s and 1970s in some prison and institutional settings.<ref>{{cite journal | vauthors = Reimringer MJ, Morgan SW, Bramwell PF | year = 1970 | title = Succinylcholine as a modifier of acting-out behavior | journal = Clinical Medicine | volume = 77 | issue = 7| page = 28 }}</ref><ref>{{cite news | author-link = Nicholas von Hoffman | vauthors = von Hoffman N | title = A Bit of 'Clockwork Orange,' California-Style | newspaper = Washington Post | date = 5 April 1972 | url = https://news.google.com/newspapers?nid=1755&dat=19720408&id=rLkqAAAAIBAJ&pg=7180%2C2668925 }}</ref><ref>{{cite book | vauthors = Sansweet RJ | date = 1975 | title = The Punishment Cure | location = New York | publisher = Mason/Charter | isbn = 0-88405-118-8 }}</ref> This use was discontinued after negative publicity concerning the terrifying effects on subjects of this treatment and ethical questions about the punitive use of painful aversion.{{citation needed|date=November 2014}}