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Postoperative movement disorders are often secondary to the polypharmacy of the perioperative period.
Extrapyramidal symptoms (e.g. dystonic reactions) are the most frequent movement disorders observed after surgery.
Most postoperative movement disorders are transient and may be successfully managed with appropriate pharmacological intervention and reassurance to the affected patient and his or her family.
A variety of movement disorders may be encountered in the early postoperative setting. They range from benign to serious and from transient to long-term. Although most movement disorders seen in the Post-Anesthesia Care Unit (PACU) are more bothersome to the patient than they are life-threatening, some do place the airway at risk, and emergent airway management may be necessary. When evaluating patients with movement disorders, the focus should be on managing acute emergencies and uncovering the etiology, so that the disorder may be treated appropriately and future complications may be avoided. Many of the movement disorders encountered in the PACU often have an iatrogenic etiology from drugs given prior to, during, or after surgery. The movement disorders discussed in this chapter include: extrapyramidal symptoms (EPS), with a focus on dystonic reactions, myoclonus, and other drug-induced symptoms; restless legs syndrome (RLS); nystagmus; and shivering.
Extrapyramidal symptoms
Extrapyramidal symptoms include a wide range of signs and symptoms including acute dystonic reactions, akathisia, motor tics, myoclonus, and tardive dyskinesia. Patients may experience any one or a combination of these.
The type of reaction should be distinguished upon evaluation.
Acute dystonic reactions display involuntary muscle contractions resulting in increased muscle tone, repetitive movements, or movements that result in twisting, pulling, or squeezing.[1]
Akathisia is defined by both subjective and objective signs and symptoms; subjectively the patient may express feelings of restlessness, tension, or distress, and the patient may objectively display motor restlessness. It may be easily misdiagnosed as anxiety.[1]
Motor tics are spastic muscle contractions, tonic or clonic, generally involving the face, neck, and/or shoulders.[1]
Myoclonus can include involuntary muscle twitching, lightning-like jerks, or clonic spasm of a single muscle or group of muscles.[1,2]
Tardive dyskinesia includes slow, rhythmic, stereotypical motor movements of the head, tongue, neck, arm, and/or upper trunk.[1]
Patients at risk for EPS include young women, pediatric patients, elderly patients, diabetics, patients with a history of neurological disorders, and patients receiving concurrent neuroleptics.[1] Case reports have also revealed EPS after uneventful anesthetics in healthy patients.
Dystonic reactions: Dystonic reactions following general anesthesia are rare. The differential diagnosis includes: adverse drug reaction, local anesthetic reaction, emergence delirium, hysterical response, and shivering. Case reports have demonstrated dystonic reactions following propofol and ondansetron. Most reported cases of abnormal movements following propofol occur following induction, emergence, or shortly thereafter with patients being fully awake and aware of the involuntary movements. Ondansetron has also been reported to result in EPS, with jerky movements of the head, neck, torso, and limbs, occurring in close proximity to drug administration.[3]
Rhythmic movement disorder (RMD) is classified as a sleep–wake transition disorder seen most commonly in infants and usually disappears by age 4 to 5, with a few cases presenting at a later age. Movements occur most frequently when falling asleep or between sleep stages. Movements most commonly seen with RMD include: head banging, head rolling, body rocking, and body rolling. The etiology is unknown, but the disorder has been shown to be benign, and usually resolves without intervention. A 2012 case report demonstrated RMD in a 10-year-old girl that developed in the PACU 30 minutes after a dose of IV ondansetron.[3]
Myoclonus: The differential diagnosis of the etiology of myoclonus is extensive, including drug reactions, essential myoclonus (idiopathic or hereditary), seizure, central nervous system (CNS) disease, infection, metabolic disorders, and nutritional deficiencies.[2] These should be considered upon evaluation of a patient demonstrating myoclonus in the PACU, with particular attention to drug reactions, as outlined below.
Postoperative myoclonic symptoms have been reported after the use of several inhalational anesthetic agents, induction drugs, and narcotics. Reviews reveal that postoperative myoclonic symptoms are frequently but not always associated with the use of central excitatory drugs, such as propofol and etomidate, and are associated with the use of potent narcotics.[4]
Myoclonus is a common side effect of induction with etomidate, thought to be due to subcortical disinhibition, with an incidence of 50–80% of patients who are not premedicated prior to induction with medications that inhibit subcortical activity, like benzodiazepines and fentanyl.[5] Both tonic and myoclonic muscle activity are well-known side effects of induction with opioids, including morphine, fentanyl, and fentanyl analogs. Cases report tonic rigidity and generalized myoclonus developing minutes to hours postoperatively, with successful naloxone termination of symptoms.[6]
Opisthotonus (spinal hyperextension and spasticity) has been reported to occur after anesthesia with propofol. One case even reported opisthotonus in association with torticollis, vertical nystagmus, obtundation, and periodic apnea, following an anesthetic that did not include propofol or drugs known to produce EPS symptoms. Symptomatic relief of the idiosyncratic reaction was achieved with administration of physostigmine, and the reaction was postulated to be due to central anticholinergic syndrome caused by fentanyl administration.[4]
Although rare, spinal myoclonus may be seen following intrathecal or epidural anesthesia. It is usually restricted to a limb or a few muscles of a limb, is not affected by peripheral stimuli, often persists in sleep, and is responsive to medical therapy with benzodiazepines, sodium valproate, and carbamazepine. Although symptoms may be demonstrated with conventional dosing, it is important to note that local anesthetic neurotoxicity has also been demonstrated as a possible etiology.[2]
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