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65 yr old pt. Vame to us w c/o urinary incontinence amd past history of psychiatry disorder in which he was taking olanzapine and lithium and lorazepam..he was unconscious amd making sounds..we suspected NMS . And now from 2 nights he is agitated amd making loiud sounds..today there is also increasing heart rate w agitation but for few seconds..and then hr becomes normal..he is changing his posture too while agitated..what should be next step

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Clinical Assessment and Next Steps

This is a high-risk situation. Let me break it down systematically.

Current Picture - What's Happening

Your patient has:

Known NMS (suspected, on olanzapine - a classic trigger)
Now 2 nights of agitation + loud vocalizations
Paroxysmal tachycardia (episodic, then normalizes)
Postural changes during agitation
Lithium and lorazepam on board

This evolution is telling you that autonomic instability is now manifesting - the paroxysmal tachycardia with agitation is a major red flag. NMS typically progresses in this order: altered mental status → rigidity → fever → autonomic lability (last and most dangerous stage).

Immediate Next Steps (in order of priority)

1. STOP all triggering drugs NOW (if not already done)

Olanzapine - must be stopped immediately
Lithium - also stop (potentiates NMS, nephrotoxic in the setting of dehydration/rhabdomyolysis)
Lorazepam can be continued / increased - it is actually therapeutic in NMS

2. Urgent Investigations (if not yet done)

Test	Why
CK (Creatine Kinase)	Rhabdomyolysis marker - can be >1000x normal in NMS
RFT / Creatinine	Rhabdo-induced AKI
Serum electrolytes + Na	Hyper/hyponatremia common
CBC	Leukocytosis expected
LFTs	Elevated transaminases
Temperature (core)	Fever may lag 24+ hours behind other symptoms
ABG	Metabolic acidosis in severe NMS
Urine myoglobin	Myoglobinuria
Serum iron	Low serum iron is a marker of NMS severity
ECG	Paroxysmal tachycardia - rule out QTc prolongation, arrhythmia

3. Address the Agitation + Tachycardia

The agitation is driving the sympathetic surges (tachycardia). This needs to be controlled:

Lorazepam 1-2 mg IV every 2-4 hours as needed - first-line sedation in NMS. This also helps differentiate from catatonia (lorazepam-responsive catatonia will improve dramatically)
Do NOT give more antipsychotics to sedate - this will worsen NMS

4. Consider Adding Specific Pharmacotherapy

Since the patient now has autonomic instability (paroxysmal HR), upgrade to active treatment:

Bromocriptine 2.5 mg PO/NG 2-3 times daily (dopamine agonist - addresses the core DA blockade mechanism). Increase up to 45 mg/day total if needed.
- Important caveat: Before starting bromocriptine, you must rule out serotonin syndrome (it can worsen SS). Given this patient is on lithium (mild serotonergic), think about this.
Dantrolene 1.0-2.5 mg/kg IV if muscle rigidity is severe - it reduces the muscle hypermetabolism. Avoid concurrent calcium administration.
Amantadine 100 mg PO 3x daily is an alternative DA agent if bromocriptine is not available.

5. Supportive Care (Critical)

IV fluids aggressively - maintain urine output >1 mL/kg/hr to prevent renal failure from rhabdomyolysis
External cooling if febrile - fans, cool packs. Paracetamol is NOT effective for the hyperthermia of NMS (muscle-generated heat, not prostaglandin-driven)
Monitor for airway compromise - with agitation, excessive secretions, and possible rigidity worsening, have a low threshold for early intubation
- If intubation needed: use rocuronium (non-depolarizing) NOT succinylcholine (succinylcholine risk of fatal hyperkalemia in rhabdomyolysis)

A Key Diagnostic Point - Don't Miss This

The combination of psychiatric history, posturing, agitation, and vocalizations in a patient on lithium raises an important differential:

Catatonia vs NMS - These can be very difficult to distinguish and can co-exist. Catatonia features include posturing, mutism, waxy flexibility, and bizarre vocalizations - which fits your patient's current picture. Catatonia is lorazepam-responsive; NMS is not reliably so.

Give a lorazepam challenge (2 mg IV) and observe over 30-60 minutes. Marked improvement points toward catatonia. No improvement or worsening points toward NMS.

Also consider:

Serotonin Syndrome (lithium + other serotonergic combinations can contribute - onset faster, features hyperreflexia, clonus, diarrhea)
Lithium toxicity (tremor, confusion, agitation on its own - check serum lithium level urgently)

Escalation Threshold

Call for ICU transfer if:

Fever >40°C
Sustained tachycardia or other arrhythmia
Rising creatinine (rhabdomyolysis-AKI)
Decreasing SpO2 or secretion management issues
No improvement in 24-48 hours on current treatment

Summary of Immediate Actions

Stop olanzapine and lithium now
IV lorazepam 1-2 mg for agitation + diagnostic catatonia challenge
Urgent bloods: CK, RFT, electrolytes, serum iron, CBC, LFT, serum lithium level
ECG - characterize the tachycardia
IV fluids aggressively
Start bromocriptine or amantadine given autonomic instability
Monitor temperature continuously and cool actively if febrile
Plan for ICU/HDU - this patient is escalating

The paroxysmal tachycardia is telling you the autonomic nervous system is being hit - this is the most dangerous phase of NMS and needs urgent escalation of care.

Tintinalli's Emergency Medicine, pp. 1252-1253
Kaplan & Sadock's Comprehensive Textbook of Psychiatry

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