“Psychiatric Emergencies and Capacity”

“Psychiatric Emergencies and Capacity”
Edwin Meresh, MD Associate Professor of Psychiatry

Delirium-DSM 5 Criteria
Disturbance in attention Disturbance develops over a short period of time, is distinctly different from baseline and tends to fluctuate Has an additional disturbance in cognition (e.g., memory deficit, disorientation, language, visuospatial ability, or perception) Not accounted for by dementia Caused by a general medical condition Delay in 1960 observed this syndrome of a rapidly progressive neurovegatative state that preceded cardio-vascular collapse and death during the early clinical trials of haloperidol and coined the term syndrome malin des neuroleptiques. Prior to the 1960s, clinical descriptions resembling NMS associated with phenothiazines were not formally diagnosed as NMS. Caroff in 1980 published the first review of the sixty cases reported in the world literature. He estimated that NMS occurs in as many as 1% of neuroleptic treated patients and may have a mortality rate of 20%. Reference Caroff SN. The neuroleptic malignant syndrome. J Clin Psychiatry (3):79-83.

DSM 5 Criteria Classification of delirium
Delirium due to another medical condition Substance intoxication delirium Substance withdrawal delirium Delirium due to multiple etiologies Medication induced delirium Delirium not otherwise specified Delay in 1960 observed this syndrome of a rapidly progressive neurovegatative state that preceded cardio-vascular collapse and death during the early clinical trials of haloperidol and coined the term syndrome malin des neuroleptiques. Prior to the 1960s, clinical descriptions resembling NMS associated with phenothiazines were not formally diagnosed as NMS. Caroff in 1980 published the first review of the sixty cases reported in the world literature. He estimated that NMS occurs in as many as 1% of neuroleptic treated patients and may have a mortality rate of 20%. Reference Caroff SN. The neuroleptic malignant syndrome. J Clin Psychiatry (3):79-83.

DSM 5 Criteria Further Specifiers Time Level of activity
Acute : Hours/Days Persistent: Weeks/Months Level of activity Hyperactive Hypoactive Mixed level of activity Academy of Consultation Liaison Psychiatry (ACLP) website

Motoric Subtypes of Delirium
Hypoactive Decreased activity Lethargy Apathy Hyperactive Increased activity Delusions Hyperalert Mixed

Prevalence Adapted from Brown and Boyle 2002
Emergency department patients: 10-15% Hospitalized medically ill: 10-30% Hospitalized elderly patients: 10-40% Intensive care unit patients: 30% Hospitalized cancer patients: 25% Post operative patients: 30-40% Post CABG: 51% Post repair of fractured hip: 50% Terminally ill patients: 80% Adapted from Brown and Boyle 2002

Consequences Increased risk of complications
Increased Mortality 3-year mortality for hospitalized elderly with index episode of delirium was 75% vs. 51% for non-delirious controls (Curyto et al 2001)‏ No difference in pre-hospital levels of depression, global cognitive performance, physical functioning or medical comorbidity Delirious patients experienced an adjusted risk of death of almost 2.0 compared to nondelirious controls (Inouye et al 1998)‏ Even after controlling for age, gender, ADL, dementia and APACHE II Increased Morbidity Poor functional recovery Possible future cognitive decline Increased risk of complications Increased nursing home placement Increased costs and LOS

Increased or decreased
Recognition Delirium Dementia Depression Onset Abrupt Slow and insidious Variable Daily Course Fluctuating Usually stable Length Hours to weeks Years Consciousness Reduced Clear Alertness Increased or decreased Usually normal Normal Activity Attention Impaired Orientation 8 8

Etiology Intoxication with drugs Withdrawal syndromes Metabolic causes
Many drugs implicated especially anticholinergic agents, NSAIDs, antiparkinsonism agents, antimicrobials, steroids, opiates, sedative- hypnotics, and illicit drugs Withdrawal syndromes Alcohol, sedative-hypnotics, and barbiturates Metabolic causes Hepatic, renal or pulmonary insufficiency

Endocrinopathies such as hypothyroidism, hyperthyroidism, hypopituitarism or hypoglycemia
Disorders of fluid and electrolyte balance

Life Threatening Causes of Delirium (Caplan and Stern, 2008)‏
W: Wernicke's encephalopathy; withdrawl (alcohol or BZDs)‏ H: Hypoglycemia; hypoxia; hypoperfusion of CNS; hypertensive crisis I: Infections; intracranial processes M: Metabolic derangements; Meningitis P: Poisons S: Seizures

Etiology Infections Head trauma Epilepsy Neoplastic disease
Sepsis, meningitis, pneumonia, and urinary tract infection Head trauma Subdural hematoma Epilepsy Neoplastic disease CNS metastasis or limbic encephalopathy Vascular disorders

Cerebrovascular Cardiovascular

Assessment Additional tests Basic laboratory test Blood chemistries
Complete blood count Hepatic function panel TSH B12 and folate RPR Serum drug levels Urinalysis and collection for culture Additional tests ECG Cardiac enzymes HIV Chest X-ray ANA Lumbar puncture

Treatment Two important aspects
Identify and reverse the reason(s) for the delirium Reduce psychiatric or behavioral symptoms of delirium Environmental manipulation Medication

Treatment Typical Antipsychotics Low potency Not recommended
High potency - Haloperidol the “gold standard” Virtually no anticholinergic properties Little risk of hypotension Does not suppress respiration Can be given IV Not FDA approved Little cardiotoxicity Concern of QTc prolongation Fast acting N.B. IV haloperidol precipitates with phenytoin and heparin

Treatment Haloperidol starting dose Elderly Young adult
Mild agitation: 0.5mg Moderate agitation: 1mg Severe agitation: 2mg Young adult Mild agitation: 1-2mg Moderate agitation: 2-5mg Severe agitation: 5-10mg Dose may be repeated at regular intervals until patient is calm

Treatment Atypical antipsychotics
Increasingly more randomized, prospective studies evaluating efficacy Use partially supported on the basis of clinical experience, case reports and small case studies Theoretical lower risk of extrapyramidal side effects Acute dystonic reactions Drug-induced parkinsonism Akathisia Continued risk of QTc prolongation

Treatment Atypical antipsychotics (continued)‏ Quetiapine (Seroquel)‏
Better than placebo in randomized control study Only oral formulation Dosage Starting dose 12.5mg-25mg qhs and titrate to effect Can also use 12.5mg-25mg q6h prn Aripiprazole (Abilify)‏ No randomized prospective studies available Multiple formulations Oral tablet, oral tablet (disintegrating), oral solution, and intramuscular ???

Mania/agitation Cannot leave AMA Security/Elopement precautions
Hospital Gown 1:1 Sitter Haldol/Ativan prn Restrain as needed

Treatment approaches must be comprehensive
Treatment approaches must be comprehensive. Besides indispensable drug treatment, non-pharmacological, behavioral and environmental interventions for acute agitation are employed . All objects near the patient that could be used as weapons (ashtrays, chairs, etc.) have to be removed, a safe passage to the secure area secured, and a sufficient number of the staff must be available. As the situation can be aggravated by overstimulation, it is helpful to screen the patient from others and turn off television and radio. We should never turn back to the agitated patient. Patients should be approached with confidence and spoken to in a soft, calm but authoritative tone. They should be allowed, asked questions designed to encourage them, to ventilate their needs. While eye contact is important, it should be broken if it makes the patient uncomfortable. The tone of the intervention is set in the first few minutes: Pavel Mohr et al. Neuroendocrinology Letters No.4 August Vol.26, 2005

Emergency Medications
PO, IM, IV, SL, ODT, Intra Nasal, Sprinkles, NG tube, Syrup

Ativan: PO, IM, IV Clonazepam: PO, ODT Diazepam: PO, IV Haldol: PO, IM, IV Saphris: SL Zyprexa: PO, ODT, IM

Seroquel: PO Abilify: PO, ODT, IM Geodon: PO, IM Risperdal: PO, ODT Adasuve (loxapine): Intra nasal

Haloperidal Haloperidal 2-5mg po/im/iv q4h prn for agiation along with ativan 1-2mg po/im/iv q4h prn. Cogentin no need to be given along with haldol for all patients, so no need to be in the initial order set. If EPS sets in, should be given. Individual cases, haldol IM 10mg can be given. Unlike geodon or zyprexa, there are extensive experience in even giving haldol 10mg IM frequently.

Geodon oral is not the best for acute agitation atleast initially
Geodon oral is not the best for acute agitation atleast initially. it is not available as IV. So, Geodon 5-10mg IM every 6 hours as needed. This will be clear as maximum dose in 24 hours is 40mg. Now, there are other ways of giving geodon-(10mg every 2hrs; or 20mg every 4hrs); but still,maximum dose is 40mg in 24 hours. This dosing is case by case variation, especially if patient has known history of EPS from haldol and patient is extremely combative, then, 20mg can be given every 4 hours (again, maximum 40mg in 24 hours) Monitor Qtc

Zyprexa: 2.5 to 5mg po q4h Order set for IM should be Zyprexa 5mg IM q4h. Again, case to case variation. In severe combative situation, higher dose is needed. Maxium dose in 24 hours is 30mg. In those cases, 2.5mg–10mg IM q4h. (not to exceed 30mg in 24 hours) The safety of total daily doses greater than 30 mg, or 10 mg injections given more frequently than 2 hours after the initial dose, and 4 hours after the second dose have not been evaluated in clinical trials. So, based on above, haldol can be given more liberally while for geodon and zyprexa, frequency and ceiling doses need a closer look.

Monitor for: EPS NMS Qtc Sedation Hypotension

Seizure threshold Masquerade: LBD Black box warnings Metabolism IM Zyprexa and IM/IV Ativan-Increased risk of respiratory depression

Serotonin Syndrome Serotonin syndrome can be a serious complication of treatment with selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants, monoamine oxidase inhibitors (MAOIs), and other serotonergic medications. It usually occurs when 2 or more serotonin-modifying agents are used in combination. Cases have been reported after single agent therapy. Academy of Consultation Liaison Psychiatry (ACLP) website

Serotonin Syndrome Pathophysiology
Enhanced central serotonergic activity The excessive serotonergic activity may influence other parts of the CNS Dopamine Norepinephrine Receptors Hyperstimulation of the 5-HT1A receptors Noradrenergic CNS hyperactivity may play a critical role in the pathophysiology of serotonin syndrome. CNS norepinephrine concentrations are increased in the serotonin syndrome may correlate with the clinical outcome.

Serotonin Syndrome Clinical characteristics (Physical) Clinical triad
Cognitive/behavioral alterations Confusion  Delirium Agitation Lethargy  Coma Autonomic instability Hyperthermia Tachycardia Diaphoresis Dilated pupils Neuromuscular abnormalities Myoclonus Hyperreflexia Rigidity Cognitive Confusion 41-77% Agitation 37-43% ANS Hyperthermia 27-34% Tachycardia 44% Nausea/Vomitting 27% Diaphoresis 49% Neuromuscular Myoclonus 49-63% Hyperreflexia 41-44% Restlessness 29% Tremor 17-61% Adapted from Mason et al XXXX Reference Mason PJ, Morris VA, Balcezak TJ. Serotonin syndrome. Presentation of 2 cases and review of the literature. Medicine (Baltimore). 2000;79(4):201-9.

Serotonin Syndrome Risk factors Prevention
Administration of 2 or more serotonergic medications Rarely with monotherapy Prevention Awareness of risk when prescribing medications that may lead to increased levels of serotonin in the CNS Pharmacodynamic interactions Pharmacokinetic interactions Avoidance of these interactions whenever possible

Serotonin Syndrome The most common drug combinations causing the serotonin syndrome MAOIs and SSRIs, MAOIs and TCAs MAOIs and tryptophan MAOIs and meperidine

Serotonin Syndrome Clinical course and outcome Rapid onset
Serotonin syndrome is usually self-limited, with an uneventful resolution, once the offending agent has been discontinued. The onset of symptoms is usually rapid Approximately 60 percent of patients with the serotonin syndrome present within six hours after initial use of medication, an overdose, or a change in dosing. Patients with mild manifestations may present with chronic subacute symptoms. The serotonin syndrome is not believed to resolve spontaneously as long as precipitating agents continue to be administered.

Serotonin Syndrome Treatment
No standardized treatment of serotonin syndrome exists. Management starts with early recognition of the syndrome, and supportive care. The basic treatment of serotonin syndrome consists of Discontinuation of the causative drugs Supportive therapy Hydration Cooling Medications Management of the serotonin syndrome involves several steps The removal of the precipitating drugs The provision of supportive care The control of agitation The administration of 5-HT 2a antagonists The control of autonomic instability and hyperthermia.

Serotonin Syndrome Pharmacologic Treatment
Several drugs have been used to treat serotonin syndrome. Cyproheptadine Propranolol Chlorpromazine As in NMS the intensity of therapy depends on the severity of illness. Mild cases (e.g., with hyperreflexia and tremor but no fever) can usually be managed with supportive care, removal of the precipitating drugs, and treatment with benzodiazepines. Moderately to severely ill patients should have all physiologic abnormalities (autonomic instability and hyperthermia) aggressively corrected and may benefit from the administration of 5-HT 2A antagonists in addition to the above measures.

Serotonin Syndrome Pharmacologic Treatment Benzodiazepines
Control of agitation May blunt the hyperadrenergic component of the syndrome Control of the agitation often present in serotonin syndrome with benzodiazepines is often necessary. Benzodiazepines such as diazepam improve survival in animal models and blunt the hyperadrenergic component of serotonin syndrome.

Serotonin Syndrome Pharmacologic Treatment Cyproheptadine
First-generation antihistamine Shown in animal studies to prevent the onset of experimentally induced serotonin syndrome. While no randomized control trials have been conducted to evaluate fully the efficacy of cyproheptadine, its use in the treatment of serotonin syndrome has been documented. Mechanism 5-HT1A and 5-HT2 receptor antagonists (McDaniel, 2001). Dose (Boyer and Shannon, 2005) May consider an initial dose of 12mg followed by 2mg every 2 hours if symptoms continue Maintenance dosage is 8mg every 6 hours Cyproheptadine is the recommended therapy for the serotonin syndrome, although its efficacy has not been rigorously established. Treatment of the serotonin syndrome in adults may require 12 to 32 mg of the drug during a 24-hour period, a dose that binds 85 to 95 percent of serotonin receptors. References Graudins A, Stearman A, Chan B. Treatment of the serotonin syndrome with cyproheptadine. J Emerg Med. 1998;16(4):615-9. McDaniel WW. Serotonin syndrome: early management with cyproheptadine. Ann Pharmacother. 2001;35(7-8):870-3. Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med Mar 17;352(11):

Neuroleptic Malignant Syndrome
NMS versus 5HT Syndrome Neuroleptic Malignant Syndrome Serotonin Syndrome Precipitated by Dopamine antagonists Serotoninergic agents Onset Variable (1-3 days) Variable (<1d) Vital Signs Hypertension, tachycardia, tachypnea Temperature Hyperthermia Mucosa Sialorrhea Skin Diaphoresis Mental Status Delirium Muscles “Lead pipe” rigidity Increased tone Reflexes Hyporeflexia Hyperreflexia, clonus Pupils Normal Dilated References Birmes P, Coppin D, Schmitt L, et al. Serotonin syndrome: a brief review. CMAJ. 2003;168(11): Adapted from Birmes et al, CMAJ 2003

NMS: Incidence Typical antipsychotics Atypical antipsychotics
Best estimate % (Caroff and Mann, 1996) Wide variance in estimates % Atypical antipsychotics It remains unclear whether atypical antipsychotics are less likely to cause NMS compared to typical antipsychotics (Troller, et al., 2009) Academy of Consultation Liaison Psychiatry (ACLP) website This estimate is produced by pooling the results of studies reporting the occurrence of NMS among large numbers of patients treated with antipsychotics at a particular center. The wide variance is thought secondary to variance in diagnostic criteria, survey techniques and clinical settings. NMS can result from treatment with atypical antipsychotics, and that it often presents with the classic features and course of illness reported previously in associated with typical antipsychotics. Only 30%, however, met the strict criteria for NMS in a case review by Carloff and Mann in 2000 the rest presented with an incomplete picture Reference Caroff SN, Mann SC. Neuroleptic malignant syndrome. Med Clin North AM 1993; 77(1): Trollor JN, Chen X, Sachdev PS. Neuroleptic malignant syndrome associated with atypical antipsychotic drugs. CNS Drugs. 2009;23(6): Sachdev P, Kruk J ,Kneebone M, et al. Clozapine-induced neuroleptic malignant syndrome: review and report of new cases. J Clin Psychopharmacol Oct;15(5): Residual catatonic state following neuroleptic malignant syndrome. Caroff SN, Mann SC, Keck PE Jr, Francis A. J Clin Psychopharmacol Apr;20(2):257-9.

Clinical Characteristics
Early signs Change in mental status Extrapyramidal symptoms unresponsive to antiparkinsonian agents Autonomic dysfunction Changes in mental status Obtundation New onset catatonia Extrapyraminal symptoms Dysarthria Dysphagia Myoclonus Tremor Rigidity Autonomic system dysfunction Episodic tachycardia Hypertension Study of the pattern of system development in 153 clinical case reports. Mental status changes or rigidity constituted the initial signs of the disorder in 82.3% of the cases . (Velamoor et al. 1994) References Velamoor VR, Norman RM, Caroff SN, et al. Progression of symptoms in neuroleptic malignant syndrome. J Nerv Ment Dis Mar;182(3):

Signs and Symptoms Hyperthermia 98% Muscle rigidity - “lead pipe rigidity” 97% Mental status changes - delirium and catatonia Hyperthermia Hyperthermia and profuse sweating occurs in 98% of reported NMS cases >38C in 87% >40C in 40% Usually develops as a late manifestation of the full blown syndrome Most distinguishing feature of NMS Sets it apart from other neuroleptic related conditions such as EPS. Need to rule out other potential sources of hyperthermia such as febrile illness do to infection. Possible sources of hyperthermia: Neuroleptic induced inhibition of central dopaminergic thermoregulatory mechanisms Increased heat production derived from neuroleptic effects on skeletal muscle tone Increased heat production resulting from increased metabolism Muscle rigidity Unresponsive to antiparkinsonian medications Generalized rigidity, described as “lead pipe” in its most severe form, is reported in 97% Rigidity may be a less impressive sign when NMS is associated with atypical antipsychotics. Mental status changes Reported in 97% of the cases Manifestations delirium catatonia

Signs and symptoms (continued) Autonomic dysfunction Tachycardia 88% Profuse diaphoresis Labile blood pressure 61% Tachycardia or labile blood pressure 95%

Laboratory findings Rhabdomyolysis Leukocytosis Low serum iron Metabolic acidosis Electroencephalogram Neuroimaging Several laboratory abnormalities are common in NMS but are either nonspecific or reflect complications of the syndrome. Rhabdomyolysis Results from myonecrosis from rigidity, hyperthermia, and ischemia CPK elevations may occur in up to 95% of cases Myoglobinuria may occur as a consequence in 67% of the cases. Leukocytosis Nonspecific No left shift Present in 98% of the cases Low serum iron Metabolic acidosis Present in 75% of examined cases Electroencephalogram Abnormal EEG present in 50% of cases Nonfocal, generalized, nonspecific slowing which is consistent with encephalopathy Neuroimaging Usually normal If abnormal the findings usually represent pre-existing pathology (atrophy or trauma) not and acute change related to NMS

Diagnostic Criteria Caroff’s Criteria for NMS
Treatment with neuroleptics Hyperthermia (>38C) Muscle rigidity Five of the following Change in mental status Tachycardia Labile blood pressure Diaphoresis Tremor Incontinence CK elevation Leukocytosis Metabolic acidosis Exclusion of other causes

Risk Factors Pharmacologic variables
Exposure to drugs that block dopamine D2 receptors High potency High dosage Rapid dose escalation (Shalev & Munitz 1988) Study of 56 NMS cases 1 episode with decreased dose 4 episodes with steady state dosing 51 cases with dose escalation Range chlorpromazine equivalents/day Average of mg chlorpromazine/day Virtually all classes of D2 dopamine receptor antagonists have been associated with NMS. The adverse effects of drugs with neuroleptic properties used in non-psychiatric settings are often neglected and under-recognized by non-psychiatric clinicians. Prochlorperazine  nausea Metoclopramide  peristalsis Droperidol  anesthesia Promethazine  sedation High-potency Cases often complicated by patients receiving more than one antipsychotic, making it difficult to distinguish the effects of individual drugs. Most cases of NMS, however, have been reported in patient’s receiving high-potency neuroleptics. Atypical antipsychotics with reduced D2 receptor affinity may mitigate extrapyramidal dysfunction. Available data suggest that the incidence of NMS with atypical drugs may be the same or less than with typical antipsychotics. However, reports of NMS may be elevated with atypicals because of the rush to publish reports and patients switched to atypical agents may be more susceptible to NMS. High dosage Rapid dose escalation Loading rate rather than total dose appears to represent more of a risk factor (Shalev & Munitz 1988) 56 NMS Cases 1 episode with decreased neuroleptic dose 4 episodes with steady state dosing 51 cases with dose escalation Range of increase 40 – 6000mg chlorpromazine per day Without extreme schedules the average rate of change is mg per day A possible explanation is that NMS is likely to occur as a reaction to the sudden and significant down regulation of dopamine transmission. References Shalev A, Hermesh H, Munitz H. The role of loading rate in neuroleptic malignant syndrome. Am J Psychiatry Aug;143(8):1059. Shalev A, Munitz H. The neuroleptic malignant syndrome: agent and host interaction. Acta Psychiatr Scand Apr;73(4):

Differential Diagnosis
Systemic disorders (continued) Heatstroke Exertional heat stroke Classical heat stroke Drugs Malignant hyperthermia Serotonin syndrome Dopaminergic withdrawal Levodopa withdrawal Freezing episodes in Parkinson’s disease Exertional Heat Stroke During hot weather agitated patients are at risk for exertional heatstroke. Caused by excessive accumulation of metabolically produced heat due to environmentally induced feature of heat dissipation. High temperatures Sweating Hypotension Rhabdomyolysis Classic Heat Stroke Occurs in elderly, inactive persons, involves inadequate host heat-defense responses, and is most probably a consequence of impaired heat dissipation (SNS failure) with aging. Exposure to neuroleptics and anticholinergic agents may impair thermoregulation and increase the risk of classical heatstroke. Not related to exertion Anhidrosis Respiratory alkalosis

Differential Diagnosis
Central Nervous System Disorders Infections Structural pathology Seizures Malignant catatonia Unchecked hyperactivity leading to exhaustion, stupor, hyperthermia, and death Reported prior to the advent of neuroleptics NMS may represent an iatrogenic form of malignant catatonia Malignant Catatonia The potentially lethal progression of catatonic states in psychotic disorders has been well described for over a century. In these cases, unchecked hyperactivity can lead to exhaustion, stupor, hyperthermia, and death. Differential diagnosis of malignant catatonia from NMS in the stuporous patient treated with neuroleptics can be difficult. NMS may represent an iatrogenic form of lethal catatonia. NMS is to lethal catatonia what neuroleptic induced catatonia is to simple catatonia.

Outcomes Morbidity Renal insufficiency/failure Respiratory failure
16-25% Respiratory failure Cardiac morbidity Cognitive sequelae (?) Renal insufficiency/failure myoglobinuric renal failure occurs on 16-25% of cases Etiology of myoglobinuria in NMS: Muscle necrosis due to severe rigidity Direct drug myotoxicity (?) Dehydration Hyperthermia Ischemia Hypoxia Catatonic posturing Respiratory failure In one study 19% of patients with NMS required ventilator support (Levenson 1985). Etiology: Aspiration pneumonia Pulmonary emboli Necrosis of respiratory muscles due to myonecrosis Cardiac morbidity Arrhythmias due to electrolyte abnormalities Ischemia secondary to hypoxia or metabolic hyperactivity Cognitive sequelae Long term cognitive effects appear rare. Prolonged hyperthermia Extreme hyperthermia Prolonged hypoxia

Treatment Basics Early recognition Cessation of neuroleptics Hydration
Temperature reduction Intensive monitoring Supportive care Nonspecific treatment consists of supportive measures and prevention of complications. Intensive monitoring (telemetry and pulse oximetry) Supportive care DVT prophylaxis Medication discontinuation Immediate discontinuation of antipsychotics are essential in managing NMS. Lithium should be discontinued. It may be hazardous to continue lithium in dehydrated patient due to concerns of toxicity. Anticholinergic medications should be discontinued do to their ability to impair heat loss and inhibit sweating, thereby exacerbating hyperthermia. However, abrupt withdrawal of dopamine agonists may predispose or exacerbate NMS Hydration Prevent hypovolemia, hypotension, shock, and renal failure. Correct electrolyte imbalance. Temperature reduction Higher temperatures are predictive of increased morbidity and mortality.

Treatments Specific treatments Benzodiazepines Dantrolene
NMS may represent an iatrogenic malignant catatonia Dantrolene 81% of patients benefited 1-10mg/kg/day in divided doses Optimal length of treatment not established May cause hepatic and respiratory compromise Benzodiazepines Use of benzodiazepines may be effective in mild cases of NMS Theory NMS may represent a drug induced form of malignant catatonia. GABA-A agonists could inhibit the pars reticulata inhibitory GABA-B neurons which may result in disinhibition of neighboring pars compacta DA cells with resulting striatal DA agonism. Dosage A trial of lorazepam 1-2 mg IV may be warranted in mild cases with close monitoring of the patient’s respiratory status. Dantrolene Inhibits contraction and heat production in muscle. It acts by inhibiting the excitation-contraction mechanism in skeletal muscles through the sequestration of calcium in the sarcoplasmic reticulum. It is not specific for malignant hyperthermia (MH). Maybe most helpful in cases of NMS with extreme temperature elevations (>40C), rhabdomyolysis and rigidity. Side effects May cause hepatic and respiratory compromise. Cardiovascular collapse may occur when coadministered with calcium channel antagonists. Sakkas and Davis (1991) 100 cases 81% of patients were helped Benefit evident within a few hours 1mg-10mg/kg/day in divided doses 1mg/kg every 6 hours for 48 hours for MH Duration of treatment is unclear

Treatments Specific treatments (continued) Dopaminergic medications
Theory Amantadine 63% found benefit as monotherapy mg/day Bromocriptine 94% found benefit as monotherapy Shortened time to clinical response 2,5mg tid - 15mg tid Levodopa Dopamine agonists Theory dopaminergic agents may reduce the probable acute hypo-dopaminergic state in NMS. Amantadine Sakkas and Davis et al(1991) 34 patients 63% of clinicians reported beneficial when amantadine used as monotherapy. Symptoms worsened in 6 patients when discontinued. Dosage mg/day in divided doses Bromocriptine Sakkas (1991) 100 patients 94% of patients benefits from monotherapy. 24-18% of patients experienced a return of NMS symptoms when discontinued after initial effectiveness. Mortality rate was decreased by 50% when added to supportive therapy alone. Rosenberg & Green (1989) 67 published cases Shortened time to clinical response (1.03 +/ days) compared with supportive treatment alone (6.80 +/ days). 2.5mg tid May increase up to 45 mg/day if necessary References Sakkas P, Davis JM, Janicak PG, et al. Drug treatment of the neuroleptic malignant syndrome. Psychopharmacol Bull. 1991;27(3):381-4.

Treatments Specific treatments (continued) ECT
May increase dopamine synthesis and release ECT considered if… Unresponsive to pharmacologic treatment Catatonia cannot be ruled out Residual catatonia develops Psychosis develops following NMS Mean time to response is / days ECT Theory Effective in catatonia and Parkinson’s disease ECT may increase dopamine synthesis and release ECT should be considered if: Patients unresponsive to pharmacological and supportive measures Catatonia cannot be ruled out Residual catatonic state develops following NMS Psychosis develops following NMS ECT offers the unique advantage of treating the NMS and potentially addressing the underlying psychiatric disorder. Patients with NMS are not considered to be at an increased risk for MH during ECT. Mean time to clinic response following ECT 1.46+/-2.38 days. Most patients responded in three days

Rough Treatment Guidelines
Mild or early NMS Supportive care and benzodiazepines Moderate NMS (rigidity and temperatures 38-40) Dopamine agonist Severe NMS (rigidity, hypermetabolism, temperatures >40) Dantrolene Rough Guidelines Mild or early NMS Discontinuation of dopamine antagonists, supportive care and benzodiazepines Moderate NMS (rigidity and temperatures 38-40) Add dopamine agonist to above treatment Severe NMS (rigidity, hypermetabolism, temperatures >40) Add dantrolene to above treatments Strawn JR, Keck PE Jr, Caroff SN. Am J Psychiatry Jun;164(6):870-6.

Antipsychotic Rechallenge
Guidelines for rechallenge Reduce potential risk factors Two weeks from resolution of NMS Gradual titration of low starting doses Low potency or atypical antipsychotics Ideally rechallenge should occur in a hospital Wells (1988) Recurrence of symptoms doubled when neuroleptics were reintroduced within five days of recovery. Susman and Addonizio (1988) Retreatment before two weeks elapsed after recovery increased the risk of recurrence. Reference Wells AJ, Sommi RW, Crismon ML. Neuroleptic rechallenge after neuroleptic malignant syndrome: case report and literature review. Drug Intell Clin Pharm Jun;22(6): Susman VL, Addonizio G. Recurrence of neuroleptic malignant syndrome. J Nerv Ment Dis Apr;176(4):

Catatonia

Catatonia TREATMENT OF CATATONIA: ECT/Lorazepam
In the 1980s, several case reports and case series began to report successful treatment of catatonia with benzodiazepines.

In an open trial of 13 patients, Bush et al
In an open trial of 13 patients, Bush et al. (1996) reported lorazepam 2mg IV reduced catatonic phenomena by 60% as measured with the BFCRS within 10 minutes of administration. 202 • Payee et al. (1999), in a prospective open trial of lorazepam (dose range 3mg/day on day 1 up to 8mg/day on day 5) demonstrated a 70% response rate in 30 psychiatric patients with catatonia.

Patients who responded to lorazepam had a mean drop in their baseline BFCRS of 17.63% by the end of day one compared to 10.85% in non-responders, which was statistically significant. 8 of the 9 lorazepam non-responders would later respond to ECT. • A retrospective literature review by Hawkins et al. (1995) collected 70 publications comprising a total of 178 patients.204 Benzodiazepines were effective in 70% of cases treated, ECT was effective in 85% of cases treated, and antipsychotics demonstrated poor efficacy

Capacity evaluation Who can determine capacity? What are the Illinois laws? difference between capacity and competence

Determinations of medical decision-making capacity are intended to:
uphold patients’ right to make their own medical decisions at the same time protecting them from their decisions when their capacity is compromised. Capacity is attached to a particular medical decision (e.g., consent to treatment, participation in research) at a particular time A person lacking capacity for one medical decision may have capacity for other decisions; or a person lacking capacity at one time may have capacity to make a decision at a later point Assessing capacity can be subjective and confusing for clinicians, particularly when patients refuse a recommended treatment or the treatment involves substantial risk.

certificates for, who can fill them out, and what do they mean legally?

Certificate A person with mental illness who, because of his or her illness is reasonably expected, unless treated on an inpatient basis, to engage in conduct placing such person or another in physical harm or in reasonable expectation of being physically harmed; A person with mental illness who, because of his or her illness is unable to provide for his or her basic physical needs so as to guard himself or herself from serious harm, without the assistance of family or others, unless treated on an inpatient basis;

A person with mental illness who: refuses treatment or is not adhering adequately to prescribed treatment; because of the nature of his or her illness is unable to understand his or her need for treatment; and if not treated on an inpatient basis, is reasonably expected based on his or her behavioral history, to suffer mental or emotional deterioration and is reasonably expected, after such deterioration, to meet the criteria of either paragraph one or paragraph two above;

I base my opinion on the following (including clinical observations, factual information): Involuntary inpatient admission and is not in need of immediate hospitalization Involuntary inpatient admission and is in need of immediate hospitalization Date: Signature: Title: Printed Name: Is in need of immediate hospitalization for the prevention of such harm.

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