"The only real difference between medicine and poison is the dose...and intent"

- O. Hernandez MD

Today in morning report we discussed a case of a patient referred after having a fall, and being unable to ambulate. 

We discussed our own personal assumptions that arise when given consults and that we should always stay open minded and be sure not to be biased when seeing patients. Especially in this case where one might have assumed a non-urgent case that suddenly became very urgent.

Upon assessment, this patient was noticeably drowsy, lethargic, slow to answer, and according to her RN in ER, this was a change from initial presentation. 

PMH revealed bipolar affective disorder, congenital bllindness, overactive bladder and restless legs syndrome.

Meds included risperidone, quetiapine, amitriptyline, tolteradine, bupropion, clonazepam.

On exam afebrile, BP 140/70, HR 88, RR 22 but would jump up to >50. Patient was diaphoretic
Neurologic exam revealed a depressed mental status, increased tone on exam with cogwheel rigidity in the upper extremities and lower extremity rigidity. Question of tremors on exam or clonus, it was unclear. No inducible clonus, Reflexes were difficult to illicit because of the rigidity.

Labs revealed an elevated CK at 43000 and elevated liver enzymes. Imaging, ECG were all normal. 

Given this history and presentation and especially her meds, we generated a list that included:

1. NMS (Neuroleptic malignant syndrome)
2. Serotonin Syndrome
3. Anticholinergic toxicity
4. Combination

NMS is a result of dopamine blockade and is usually with typical antipsychotics, but can be with atypicals. It is an idiosyncratic reaction and can occur even with prolonged exposure. Risk factors include a change, or an increase in dose, high doses. Patients with PD and a sudden withdrawal of their meds can also get NMS. NMS is associated with fever, autonomic instability, rigidity, mental status change. Often is bradyreflexic and is usually not as acute as serotonin syndrome.

Treatment is supportive including active coolling, d/c'ing offending meds, and can consider dantrolene.

Serotonin syndrome is the result of a combination of increased release, inhibition of reuptake and/or inhibition of breakdown. We discussed MAOI's and how other medications can have MAOI effects e.g. Linezolid. Defining features include similar presentation as NMS, but often more acute, and with hyperreflexia and clonus. 

Treatment is supprotive, d/c'ing offending meds. Antidotes aim at blocking 5HT2 receptors i.e. cyproheptadine. Atypical antipsychotics also have 5HT2 blockade particularly olanzapine

Anticholinergic toxicity presents with fever, elevated BP (usually not that high), dilated pupils, confusion, and they are dry!!
We touched briefly on TCA overdoses, but mainly to state to monitor QRS, give bicarb if needed and to be careful in managing arrythmias and seizures with medications that further block Na channels. Also to avoid physostigimine in TCA overdoses because of risk of fatal bradyarrythmias. Clearly, a topic for another day.

Given her medications and presentation it was felt that this was either NMS or Serotonin Syndrome. 

Her med list favoured NMS over Serotonin syndrome as the only serotinergic medication she was on was bupropion which has small effects. Additionally she was also on quetiapine which might have given some 5HT2 blockade.

She was admitted on tele, ICU followed, psychiatry was involved and we discussed getting poison control/toxicologist in this case. 

Her course is that she is improving, starting to be more alert and admitted to taking an excess amount of pills, though this issue is currently being investigated.

Check out this review article on serotonin syndrome from the NEJM