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Practice

Abstract

WE REPORT A CASE INVOLVING AN 81-YEAR-OLD man with schizoaffective disorder who presented with neuroleptic malignant syndrome (NMS) after an increase in his neuroleptic dose. NMS, a rare but potentially fatal complication of neuroleptic medications (e.g., antipsychotics, sedatives and antinauseants), is characterized by hyperthermia, muscle rigidity, an elevated creatine kinase level and autonomic instability. The syndrome often develops after a sudden increase in dosage of the neuroleptic medication or in states of dehydration. Treatment is mainly supportive and includes withdrawal of the neuroleptic medication and, possibly, administration of drugs such as dantrolene and bromocriptine. Complications of NMS include acute renal failure and acute respiratory failure. Given the widespread prescription of neuroleptics by physicians in a variety of fields, all physicians need to be able to recognize and appropriately manage NMS.

Case

An 81-year-old man with a history of schizoaffective disorder presented to hospital with increasing auditory hallucinations, persecutory delusions and depressive symptoms, including suicidal ideation. He was admitted to hospital and given loxapine (10 mg every morning, 50 mg every evening) for his psychotic symptoms and methotrimeprazine (10 mg once daily) for sleep disturbance. Two weeks earlier he had been prescribed venlafaxine by his family physician and had been experiencing some symptomatic hypotensive episodes as a result. He had also been taking levothyroxine (0.1 mg once daily) and procyclidine (2.5 mg once daily).

Within 3 days after admission, the methotrimeprazine therapy was stopped because of somnolence and the loxapine dose increased to 65 mg/d at bedtime. Twelve hours after this change, the patient had diaphoresis, tremulousness, urinary incontinence and some cognitive impairment. His temperature was elevated (38.3°C), and although normotensive (blood pressure 124/84 mm Hg) he had tachycardia (heart rate 128 beats/min) and exhibited Parkinsonian features, including tremor, rigidity and unsteady gait. An electrocardiogram revealed no acute ischemic changes. Laboratory investigation revealed mild leukocytosis (leukocyte count 11.7 х 10⁹/L), with a shift to the left (neutrophil count 9.9 х 10⁹/L). His aspartate aminotransferase level was elevated (82 U/L), and his creatine kinase (CK) level was markedly elevated (1145 U/L), with normal CK MB fraction and cardiac troponin levels. Other laboratory results, including electrolyte levels, were normal.

The patient was observed for the night. The next morning his Parkinsonian features and elevated temperature persisted, and he was found to have bilateral hyporeflexia. The loxapine therapy was stopped because neuroleptic malignant syndrome (NMS) was suspected. That afternoon the CK level climbed to 2574 U/L. The next day, the patient had increased rigidity and his temperature rose to 39.3°C. A septic workup yielded normal results, but the urine myoglobin test result was positive. A firm diagnosis of NMS was made, and therapy with dantrolene (70 mg intravenously) was started and about 24 hours later was changed to bromocriptine (2.5 mg 3 times daily).

Within a few days, the patient's NMS symptoms improved and his CK level returned to normal. As his symptoms resolved, the bromocriptine dose was tapered off. In order to control his ongoing psychotic symptoms, the patient was prescribed olanzapine (2.5 mg once daily) because of its lower reported rate of NMS. He was also given sertraline (25 mg once daily) to control his depressive symptoms. After 5 weeks, his depressive and psychotic symptoms improved considerably, and he was discharged from hospital without further complications.

Comments

NMS is an uncommon but serious complication of neuroleptic medications. It was first described in 1967 as “akinetic hypertonic syndrome.” ^,2 The frequency of the syndrome ranges from 0.07% to 2.2% among patients receiving neuroleptic medications. The mortality is 10%–30%.

NMS likely results from a complex interaction between the neuroleptic medication and a susceptible host. Two theories have been proposed to explain the syndrome: central dopamine receptor blockade and skeletal muscle defect. In the first theory, the dopaminergic receptor antagonism by neuroleptics may interfere with dopamine's normal role in central thermoregulation. Heat is produced from serotonin stimulation in the hypothalamus, and dopamine inhibits this process. Dopaminergic blockade therefore leads to less inhibition of serotonin stimulation and contributes to the hyperthermia seen in NMS. To support this theory, there have been reported cases of conditions resembling NMS in patients with Parkinson's disease who had no history of the syndrome and in whom therapy with levodopa–carbidopa and amantadine was abruptly stopped. Because central thermoregulation is mediated by noradrenergic, dopaminergic, serotoninergic and cholinergic pathways, it is unlikely that the syndrome is due to central dopaminergic blockade alone. Furthermore, dopamine may directly inhibit skeletal muscle contraction, and therefore dopamine blockade may result in increased skeletal muscle contraction.

In the second theory, NMS is believed to share a pathophysiology with malignant hyperthermia. The symptoms of hyperthermia, rigidity and elevated CK levels are common to both conditions, as is the response to the peripheral muscle relaxant, dantrolene. Furthermore, both conditions produce abnormal in vitro contractility test results.^, As has been found in patients with malignant hyperthermia, in vitro investigations of patients with NMS have revealed multiple defects in skeletal muscle, usually associated with increased calcium release from the sarcoplasmic reticulum.

Most neuroleptic medications have some risk of NMS associated with them (Box 1).^,,,,,,, Even atypical neuroleptics previously thought to have less risk, such as olanzapine^, and quetiapine, have been associated with reported cases of NMS. A rapid change in neuroleptic dose is a major risk factor for the syndrome, especially if it occurs within 5 days before the onset of symptoms, and the risk can persist for 20 days or more after discontinuing the neuroleptic therapy. NMS most often occurs after the initiation or increase in dose of neuroleptics, but rarely it can occur after the sudden discontinuation of the drug therapy. There is no demonstrable relation between the actual dose or duration of exposure of the neuroleptic and the development or fatal outcome of NMS. There seems to be no significant difference in the duration of clinical symptoms with long-acting neuroleptics compared with short-acting ones. Psychomotor agitation preceding the onset of symptoms is a significant clinical manifestation in patients who are at risk of NMS.^,19 Dehydration with the concomitant use of neuroleptics has been implicated as a risk factor for the syndrome, because the decreased blood volume induces peripheral vasoconstriction and impairs heat dissipation. NMS can often be prevented by ensuring that patients receiving neuroleptics are well hydrated. Other risk factors for NMS include stress, humidity and concomitant use of lithium, anticholinergic agents or some antidepressants.

Many diagnostic criteria have been proposed for NMS, but because of its variable presentation, no single set of criteria is used universally. Some clinical manifestations are described in Box 2.^,, The symptoms usually develop over 24 to 72 hours and can last from 1 to 44 days (about 10 days on average). There is no typical sequence of symptoms, but extrapyramidal symptoms usually occur before autonomic ones. Hyperthermia, rigidity and recent initiation of drug therapy with one or more neuroleptics are common features of NMS.

The differential diagnosis of NMS is described in Box 3.^,,,, A thorough history taking, physical examination and laboratory investigations, including leukocyte count with differential, renal function tests, and measurement of electrolyte, serum CK, urine myoglobin and serum lithium concentrations, should be performed. An electroencephalogram, CT scan of the head and lumbar puncture should also be considered to rule out other causes.

For treatment, it is essential to recognize the symptoms and to stop the neuroleptic therapy immediately. Supportive therapy, such as fever reduction, hydration and nutrition, is important until the blood levels of the neuroleptic drug decrease. It is controversial whether specific therapies are beneficial in addition to the supportive therapy. The role of intravenous dantrolene sodium therapy, used widely in malignant hyperthermia, is unclear, but it is still administered to reduce body temperature and to relax peripheral muscles by inhibiting the release of calcium from the sarcoplasmic reticulum of muscle. The recommended dose is 2 mg/kg intravenously, repeated every 10 minutes if necessary, to a maximum of 10 mg/kg daily. It is only usually given in the acute stage and not continued for more than a few days. Hepatotoxic effects may occur if the daily dose exceeds 10 mg/kg. Bromocriptine, a dopamine agonist, usually improves muscle rigidity within a few hours, followed by a reduction in temperature and an improvement in blood pressure. Doses of 2.5–10 mg up to 4 times daily have been used with some success. Hypotension is the most common adverse effect of bromocriptine therapy. It can be mild or severe, and treatment would be similar to that of other causes of hypotension. It is unknown what affects the degree of hypotension and other autonomic factors. Dantrolene and bromocriptine may be used together, without more adverse effects than with either one alone. Amantadine and levadopa–carbidopa have been used successfully to reduce hyperthermia in patients with NMS. Treatment of NMS must be continued for 2–3 weeks until symptoms remit. Because of possible exacerbation of NMS symptoms, dopamine antagonists such as metoclopramide should be avoided.

Many serious complications of NMS can arise and must be treated aggressively. Some common ones are described in Box 4.^,,, Myoglobinuria, due to rhabdomyolysis, may develop and progress to acute renal failure, which would require temporary dialysis. Renal failure is a strong predictor of death, with an associated mortality of 50%. Acute respiratory failure, due to a pulmonary embolism or aspiration pneumonia, often requires mechanical ventilation in the intensive care unit.

After an episode of NMS, neuroleptic therapy is still required to control the patient's psychiatric symptoms. Rechallenging the patient with the same neuroleptic drug at the same dose results in the syndrome recurring in 5 out of 6 cases. The use of a lower potency neuroleptic (Box 1) is safe in 9 out of 10 cases. Starting with an atypical neuroleptic such as olanzapine at a low dose and slowly increasing the dose while monitoring for signs of NMS and for control of psychotic symptoms is the safest option. The goal is to find the lowest dose necessary that will control the psychotic symptoms. It is important to prevent significant dehydration in patients taking neuroleptics in order to prevent the recurrence of NMS.

In summary, NMS is a potentially fatal complication of neuroleptic therapy regardless of the duration or dose of the drug. The mortality and morbidity associated with NMS can be decreased if one understands the role of neuroleptics in causing such a serious complication, if neuroleptic therapy is started slowly, in incremental doses, and if timely supportive therapy is provided.

Footnotes

This article has been peer reviewed.

Contributors: Dr. Chandran was the principal author and was responsible for collecting data (chart and literature reviews). Dr. Mikler was instrumental in organizing and planning the presentation of the manuscript. Dr. Keegan was the attending physician and was involved in the chart review. All authors contributed to the revision of the manuscript and approved the final version.

Competing interests: None declared.

Both the title and the content of posts must directly relate to Dungeons & Dragons. Healing word 5e.

Correspondence to: Dr. Geethan J. Chandran, 75 Leddy Cres., Saskatoon SK S7H 3Y9

References

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Abstract

In recent years, there has been an increased use of neuroleptic agents in the primary care setting. Neuroleptic malignant syndrome (NMS) is a rare complication of neuroleptic therapy that can be missed if not suspected. This manuscript reviews the diagnosis and management of NMS in the primary care setting. There is a lack of prospective data, and most of the information is obtained from case series. Physicians need to have a high index of suspicion with regard to excluding NMS in patients taking neuroleptics and presenting with hyperthermia.

The use of antipsychotic (neuroleptic) agents in the primary care setting is increasing for a variety of reasons, such as lack of access to psychiatric care; the advent of the atypical antipsychotics, which have a lower propensity for causing side effects; the increased use of the atypical antipsychotics to treat mood disorders; increased off-label use of atypical antipsychotics for anxiety disorders; and increased promotion by the pharmaceutical companies of the atypical agents in primary care and skilled nursing facilities.

Despite the fact that the atypical antipsychotics are safer and easier to use, side effects such as neuroleptic malignant syndrome (NMS) are still reported. Little is known about NMS in general (most data are from case studies rather than research), and still less is known about the nature of presentation of NMS with the atypical agents. Hence, we need to be vigilant and have a high index of suspicion when patients are taking neuroleptics. This article will provide an overview of diagnosis and management of NMS.

EPIDEMIOLOGY

Delay et al. were the first to describe neuroleptic malignant syndrome (NMS) in 1960. The incidence of NMS with conventional antipsychotics has been shown to be anywhere from 0.02% to 2.44%. Prospective studies in 2 psychiatric hospitals in the Boston area found an incidence of 0.07% to 0.9%. NMS has been reported among patients of all ages; however, most cases have occurred between the ages of 20 and 50 years, possibly due to high antipsychotic usage.

CAUSES

Although NMS is most commonly associated with antipsychotic usage, withdrawal of dopaminergic therapy such as levodopa and amantadine has also been reported to cause NMS. The syndrome has been reported with all antipsychotics, including atypicals such as clozapine, risperidone, quetiapine, and olanzapine. The use of metoclopramide and droperidol has also been implicated in the causation of NMS. Schizophrenia or affective disorders are the common diagnoses associated with NMS; however, NMS has also been reported with other conditions such as dementia, Parkinson's disease, Huntington's disease, and Wilson's disease in patients exposed to antipsychotics or dopamine-depleting agents or those who have had abrupt discontinuation of dopamine agonists.

DIAGNOSIS

One of the key interventions for decreasing the lethality in NMS is early detection. To make any early diagnosis, a high index of suspicion is required. Several diagnostic schemas have been proposed; however, there is no single set of criteria that is universally accepted. The reasons for these differences in diagnostic schemas are partly the lack of adequate prospective data on this illness and partly the fact that most of the information has been obtained from case studies. Nevertheless, there is agreement that elevated temperature (greater than or equal to 40°C, or 104°F); extrapyramidal symptoms, particularly lead-pipe rigidity; and autonomic instability (elevated or labile blood pressure, tachycardia, profuse diaphoresis, incontinence, and pallor) are considered cardinal features of NMS. Other findings that may help support the diagnosis are altered consciousness, tremor, mutism, leukocytosis, and elevated creatine phosphokinase (CPK) levels. It is important that other general medical conditions, as well as psychiatric disorders such as catatonia, are excluded prior to making the diagnosis of NMS.

The research criteria for NMS as listed in the DSM-IV¹⁶ require the presence of severe muscle rigidity and elevated temperature associated with neuroleptic medication use (Criterion A).¹⁶ In addition, the patient should have at least 2 other supportive symptoms such as diaphoresis, dysphagia, tremor, incontinence, changes in level of consciousness ranging from confusion to coma, mutism, tachycardia, elevated blood pressure, leukocytosis, or elevated CPK levels (Criterion B).¹⁶ General medical conditions and psychiatric disorders leading to NMS-like presentations should be excluded prior to making a diagnosis of NMS (Criteria C and D).¹⁶

In a study delineating symptoms of NMS, the syndrome was characterized by hyperpyrexia, muscular rigidity, alterations in the level of consciousness, autonomic dysfunction, and elevated CPK levels and white blood cell count. The alteration in consciousness runs the gamut from confusion to coma. The risk factors for NMS noted in the literature include dehydration, elevated temperature, rapid neuroleptic loading, alcoholism, previous brain injury, and treatment-resistant extrapyramidal symptoms (Table 1). NMS may manifest with varying severity.

Differential Diagnosis

1. The differential diagnosis of NMS (Table 2) includes malignant hyperthermia, which presents as clinically identical to NMS. It occurs following the administration of halogenated anesthetic agents and succinylcholine. The diagnosis of malignant hyperthermia can be made by exposing the biopsied muscle to halothane or caffeine, which results in a hypercontractile response not seen in NMS patients.

   Table 2.

   Differential Diagnosis of Neuroleptic Malignant Syndrome

2. Lethal catatonia begins with severe psychotic excitement, while NMS begins with rigidity. These 2 syndromes may be very difficult to distinguish. Neuroleptics should be stopped in both cases.

3. Heatstroke should also be considered in the differential diagnosis.

4. Central nervous system infective processes, which include meningitis, encephalitis, and neurosyphilis, should also be considered as likely causes.

5. Serotonin syndrome is an uncommon toxic, hyper-serotonergic state that needs a high index of suspicion so as to make the diagnosis. Serotonin syndrome is characterized by mental status changes, tachycardia, diaphoresis, labile blood pressure changes, shivering, tachypnea, mydriasis, and sialorrhea. Hyperthermia has been observed in 34% of NMS cases.²¹ Neurologic manifestations include tremor, myoclonus, tachycardia, hyperreflexia, ankle clonus, muscle rigidity, and incoordination. Leukocytosis, rhabdomyolysis, and elevated CPK levels are common.²¹

6. Allergic drug reactions may resemble NMS, as they also produce fever and autonomic instability.

7. Toxic encephalopathies such as tetanus, botulism, and anticholinergic delirium should also be considered when making the final diagnosis. The cerebral spinal fluid in NMS does not demonstrate the changes seen in central nervous system infections.

COMPLICATIONS

Estimates of mortality in NMS cases have ranged as high as 76%, although most reports put it between 10% and 20%, due primarily to complications such as cardiovascular collapse, arrhythmia, renal failure, and respiratory failure. At least 3 NMS-attributed deaths have been reported with the use of atypical antipsychotics—1 with olanzapine and 2 with risperidone. Rhabdomyolysis is the most serious complication associated with NMS. Dementia, parkinsonism, dyskinesias, and ataxia are some of the permanent neurologic complications that may occur in survivors.

MANAGEMENT

Pelonero and colleagues suggest 6 initial important steps to be taken: (1) stop neuroleptic therapy, (2) seek appropriate consultation, (3) transfer the patient promptly to the best care setting, (4) document a differential diagnosis plan, (5) document a treatment plan, and (6) inform the family.

General Measures

The management of a suspected or diagnosed case of NMS depends on the severity of symptoms. It would be prudent at the time of suspicion to involve the expertise of a psychiatrist for further clarification of the diagnosis and an internist for management of the patient. The family must be informed of and kept updated about the patient's condition. Mild cases may be treated on a psychiatric in-patient basis, whereas the more severe cases are treated in the medical intensive care unit. The following steps need to be undertaken with close collaboration with a psychiatrist and an internist (Table 3).

Table 3.

Nonpharmacologic Measures in Neuroleptic Malignant Syndrome

Specific Steps

1. The first and most critical step in the treatment of NMS is discontinuation of the neuroleptic medication.

2. If dopamine agonists such as amantadine are being used, they should be continued, as their sudden withdrawal may worsen symptomatology.

3. Supportive therapies, which include intravenous fluids to correct dehydration, use of antipyretics, and electric blanket for gradual reduction in temperature, are important measures to be considered. Some patients may require ventilator support if their respiratory system is involved in the rigidity. It is important to assess the gag reflex; if the reflex is lost, parenteral nutrition may be needed.

4. Deep venous thrombosis and pulmonary embolism are prevented by the use of subcutaneous heparin.

5. If renal failure occurs, dialysis may be considered.

6. The nutritional status of the patient needs to be assessed on an ongoing basis. As the patient is under considerable stress during an episode of NMS, comorbid illnesses such as diabetes may lead to ketoacidosis and need to be monitored closely.

Pharmacologic and Other Interventions

Supportive therapy is instituted first, and pharmacologic treatment may then be considered if the patient does not improve.

When? If the condition of the patient is declining (e.g., increasing rigidity, persistent hyperpyrexia, increasing symptoms), medication treatment should be started (Table 4).²⁴

Table 4.

Pharmacologic Intervention for Neuroleptic Malignant Syndrome

What? Bromocriptine is usually the drug of choice, started at a dosage of 2.5 mg 2 or 3 times daily and titrated to a maximum dosage of 45 mg per day.²⁴ Side effects to be assessed include nausea, vomiting, psychosis, and altered mental status.

Dantrolene is used in cases of severe hyperthermia. Its efficacy has been demonstrated in malignant hyperthermia. This drug is administered by bolus injection in a dosage of 1 to 10 mg/kg (oral dosage 50–600 mg) of body weight.²⁴

The 2 agents bromocriptine and dantrolene may be used in combination depending on the severity of the clinical situation. Rosebush and Stewart found that dantrolene and bromocriptine did not improve time to response compared with supportive measures, while another report was to the contrary.²⁶ In a large case analysis, medications such as bromocriptine, dantrolene, and amantadine were found to be the most effective agents for treating NMS.

Electroconvulsive therapy (ECT) has also been found to be effective for the treatment of NMS and the underlying psychiatric condition. Iron supplementation has been suggested for those individuals with iron deficiency, as low iron levels may aggravate movement disorders.

Course

NMS may run a clinical course anywhere from 2 to 14 days. In patients on depot neuroleptics, the resolution of symptoms may take up to 35 days from the last injection.

Posttreatment Plan

After the resolution of NMS, it is essential to continue treatment of the patient with the help of a psychiatrist. Therapeutic alternatives to neuroleptics, such as lithium, benzodiazepine, anticonvulsants, and ECT, should be considered after recovery from NMS. In some patients, due to the persistent nature of the symptoms, neuroleptics may be essential. In such patients, neuroleptics from a class other than the one causing NMS should be used. Atypical antipsychotics have lower affinity for the nigrostriatal D₂ receptors and hence could be considered for patients needing retreatment.

It should be noted that NMS has also been reported with atypical neuroleptics. High-potency neuroleptics have been reported to be a possible risk factor for recurrence of NMS. Rosebush and colleagues have recommended a 2-week interval between recovery and the reintroduction of neuroleptics. Despite the seriousness of the condition, neuroleptics can often be reintroduced and used safely. Anesthesia can be given safely to patients post-NMS, unlike in the case of malignant hyperthermia. Patients with a history of NMS are not good candidates for long-acting (depot) preparations.

CONCLUSION

Prospective studies of NMS are difficult to conduct because of the infrequent and serious nature of the disorder. NMS should be considered in the differential diagnosis of any patient with high fever and marked rigidity. There remain controversies about treatment specifics among leaders in the field; however, there is agreement about measures such as rapid cooling to decrease temperature, maintaining hydration, and anticoagulation.

A greater awareness of this disorder needs to be created among primary care physicians and internists, and the Neuroleptic Malignant Syndrome Information Service (NMSIS) is aiming to fill this void by collecting data. NMS is a source of malpractice litigation, especially if there is a bad outcome. For physicians seeking information or consultation about a clinical case of NMS, the NMSIS can serve as a reliable resource. The case can be discussed with one of the consultants staffing the service's hotline, which is staffed 24 hours a day year-round. The number to call is 1-888-NMS-TEMP; e-mail: gro.sismn@ofni; Web site: www.nmsis.org.

Drug names: amantadine (Symmetrel and others), bromocriptine (Parlodel and others), clozapine (Clozaril, Fazaclo, and others), dantrolene (Dantrium), droperidol (Inapsine and others), heparin (Hepflush-10, Heparin Lock Flush, and others), lithium (Lithobid, Eskalith, and others), metoclopramide (Reglan and others), olanzapine (Zyprexa), quetiapine (Seroquel), risperidone (Risperdal).

Footnotes

The authors report no financial affiliation or other relationship relevant to the subject matter of this article.

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