1 / 20

Neuroleptic Malignant Syndrome (NMS)

Neuroleptic Malignant Syndrome (NMS). Sue Henderson. Definition. Rare adverse reaction to dopamine receptor antagonists (blockers) Leading to autonomic dysfunction Can be fatal if not recognized early. Commonly associated with:. haloperidol (Serenace) fluphenazine (Prolixin)

clarencegomez
Télécharger la présentation

Neuroleptic Malignant Syndrome (NMS)

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Neuroleptic Malignant Syndrome (NMS) Sue Henderson

  2. Definition • Rare adverse reaction to dopamine receptor antagonists (blockers) • Leading to autonomic dysfunction • Can be fatal if not recognized early

  3. Commonly associated with: • haloperidol (Serenace) • fluphenazine (Prolixin) • chlorpromazine (Largactil)

  4. Less commonly associated with: atypicals: • quetiapine (Seroquel) • risperidone (Risperdal) • olanzapine (Zyprexa) dopamine receptor antagonists: • prochlorperazine (Stemetil) • metoclopramide (Maxalon) • promethazine (Phenergan)

  5. Pathophysiology • Not fully understood • Probably dopaminergic blockade or depletion in CNS • May be a drug induced malignant catatonia (? same underlying pathophysiology) (Fink, 1996, as cited in Strawn, Keck & Caroff, 2007). • Genetics may be involved

  6. Incidence • 0.5% to 3% of all patients treated with traditional antipsychotics • Recent 0.01% to 0.02% (Stubner, 2004, as cited in Strawn, Keck & Caroff, 2007). (? Due to atypical use) • Haloperidol implicated in ½ cases (potency, widespread use)Death in 10% of cases (Strawn, Keck & Caroff, 2007).

  7. Risk Factors • previous history of NMS/EPSE • dehydration • discontinuation of antiparkinsonian • withdrawal of benzodiazepines • history of organic brain syndrome • use of high potency agents • iron deficiency

  8. Onset At any time - can develop rapidly Most cases when: • drug started • dosage increased • rapidly titrated Mild to severe - depending on individual

  9. Clinical manifestations Sudden change in mental status Muscle rigidity Fever

  10. Sudden change in mental status Mental state changes precede other signs in 80% of cases Clouding of consciousness ranging from: • confusion to stupor or coma • agitation, • delirium, and • catatonia

  11. Fever • Hyperpyrexia > 38 °C of unknown origin (? caused by dopamine blockade in hypothalamus causing temperature dysregulation and profuse sweating)

  12. Muscle Rigidity • Dystonia abrupt onset stiffening and rigidity in large muscles (especially head & neck) • Severe muscle rigidity produces excess body heat contributing to hyperpyrexia • Sometimes difficulty swallowing or a sensation of tongue thickening that rapidly worsens

  13. Rigidity As the syndrome progresses: • increasing muscle rigidity can lead to diminished chest wall compliance, hypoventilation, and even respiratory failure. Other • EPSEs: parkinsonian tremors, akathisia • elevated or labile blood pressure • tachycardia, tachypnea, tremor, and urinary incontinence

  14. Laboratory • Raised Creatine kinase (muscle enzyme) • Raise Myoglobinuria (muscle protein) • Creatine kinase rises 2 – 4 hours after muscle injury (indicator degree muscle damage), continued rise may indicate onset : • Rhabdomyolysis (skeletal muscle break down) releases myoglobin into circulation. • Once myoglobin in kidneys, it precipitates in renal tubules causing kidney damage and subsequent renal failure.

  15. Lab: other • proteinuria secondary to stress/tissue damage • elevated white blood cell count • Arterial blood gas analysis - assess for adequate oxygenation and metabolic acidosis (Harrison & McErlane, 2008).

  16. Prevention • Conservative use of antipsychotics • Reduction of risk factors • Early diagnosis • Prompt discontinuation of offending medications

  17. Medical Management Depending on symptom severity and complications: • See table in handout (Woodbury & Woodbury, 1992 cited in Strawn, Keck & Caroff, 2007). • See video Brvar and Bunc (2007) pre and post Dantrolene

  18. Re-challenge Anti-psychotics • 30% risk of developing again • Check reports on previous episodes for accuracy • Clearly documented indications for antipsychotics • Consider alternative medications • Reduce risk factors • Rechallenge at least 2/52 after recovery from NMS • Use low doses of low-potency conventional antipsychotics or atypical antipsychotics • Titrate gradually after a test dose • Monitor for early signs of NMS • Obtain informed consent from patients/family regarding benefits of antipsychotic versus risk recurrence(Strawn, Keck, & Caroff, 2007).

  19. Resources Neuroleptic Malignant Syndrome Information Service www.nmsis.org

  20. References Brvar, M., & Bunc, M. (2007). Video of dantrolene effectiveness on neuroleptic malignant syndrome associated muscular rigidity and tremor. Critical Care 11(3), 415. Fink, M. (1996). Neuroleptic malignant syndrome and catatonia: One entity or two? . Biological Psychiatry, 39, 1-4. Harrison, P. A., & McErlane, K. S. (2008 ). Neuroleptic malignant syndrome American Journal of Nursing, 108(7), 35-38. Strawn, J. R., Keck, P. E., & Caroff, S. N. (2007). Neuroleptic malignant syndrome. American Journal of Psychiatry, 164(6), 870-876.

More Related