You are just started your night shift 😢 , a 23-year-old lady with no significant past medical history was brought to the emergency department after being found unresponsive at home. Her family found medication strips of paracetamol and diclofenac beside her.
Her initial vital signs at presentation were as follows: pulse rate of 95 beats per minutes, regular; blood pressure is 109/83 mmHg; respiratory rate 25 breaths per minute and temperature of 370 c.
Her initial physical exam was unremarkable apart from low Glasgow coma scale of 7/15 with normal size reactive pupils. Due to her CNS depression, she was intubated and mechanically ventilated.
Initial ECG at presentation
Few hours later she went into multiple episodes of ventricular fibrillation refractory to the ACLS.
Q1 What is your DD and how you will proceed?
Q2 What you will give this patient ?
Nice comments all
Again I liked the broad DD
although the told story is paracetamol and diclofenac and non of which will give you this clinical presentation marked by CNS Depression and CVS toxicity
Lets us think of it
CNS sedative –Hypnotics
1- Benzodiazepine
2- Barbiturate
3-non BDZ non barbiturate drugs ( e.g Zolpidem), alcohol
4- Hydrocarbons( chloral hydrate )
5. Others drugs like antidepressant and antipschotics
CNS& then Cardiotxocity
1.Cardio active drugs unlikely( usually brady/hypotension, less cns depression)
2. TCA and sodium channel blockage( u expect wide QRS and sodium channel blockage effect
3 Antidepressant and antipsychotics that cause prolong QT and Tdp
4. Hydrocarbons(chloral hydrate CH)
CT brain was negative and tox screen was negative
Clinical toxicologist was consulted and due to the combination of cardiotoxicity and sedation; hydrocarbon poisoning was considered. Esmolol (b blocker) infusion was started with a dose of 150 microgram/kg/min following intermittent bolus dose of 30 mg to a total bolus dose of 150 mg. and shortly after that, she reverted back to sinus rhythm.
Later her sister brought the patient’s bag that had pinkish fluid in bottle of water, smelling like CH. . Over the next 36 hours, patient’s neurological and cardiac status had normalized and she was extubated successfully and was weaned off from phenylephrine and Esmolol infusion. She was discharged from the hospital in excellent condition on day 5 after psychiatric review. She confirmed the ingestion of around 30-35 grams of CH.
So what is chloral hydrate ?
Chloral hydrate is a halogenated hydrocarbon. The life threatening dysrhythmias seen are the result of increased sensitivity to endogenous catecholamines, much like we see in patients abusing inhaled hydrocarbons. Potentially lethal dysrhythmias can occur at doses very close to therapeutic doses.
Chloral hydrate (CH) is a hydrocarbon that was historically used as a sedative – hypnotic and anxiolytic agent mainly in radiological imaging procedures. Cardiac arrhythmias have been reported even in therapeutic doses of CH with risk of sudden death. Acute poisoning with CH causes significant central nervous system (CNS) depression, respiratory failure, and tachyarrhythmias
The CH induced cardiac arrhythmias are usually refractory, which are unresponsive to standard anti-arrhythmic drugs including amiodarone and lidocaine .However, b blockers have been reported to be an effective treatment of hydrocarbon-induced cardiotoxicity, including CH
Mechanism of action
1. Active metabolite trichloroethanol (TCE) Binds the GABA-A receptor in CNS
CNS depression and sedation results from potentiation of the effects of endogenous GABA
2. Catecholamine-hypersensitivity leading to tachydysrhythmias
3. Corrosive effects on the gastrointestinal mucosa
4.Hepatotoxicity and nephrotoxicity
Management
Airway compromise intubate and ventilate.
Hypotension :crystalloid boluses
Avoid catecholaminergic agents if possible due to risk of catecholamine-induced dysrhythmias.
Ventricular dysrhythmias (especially VT and VF)
Manage according ACLS guidelines but avoid catecholaminergic agents if possible.
Corect hypoxia, acidosis and electrolyte disturbances (e.g. hypokalaemia, hypomagnesaemia).
Administer beta blockers – e.g. propanolol 1-2 mg IV or metoprolol 5mg IV (0.1mg/kg in children) or esmolol infusion
Summary:
1.Always look at toxidromes
2.Always think broad DD
3.Always when in doubt stay calm and call Toxicologist 😎
References :
Goldfrank’s Toxicology
https://first10em.com/chloral-hydrate-toxicity
And of course during the resuscitations i will check the electrolytes , RBS and calcium to correct if any abnormality found
A young lady with no PMH came unresponsive, the top differential diagnosis is toxin induce but taking non toxin cause in consideration as well.
neither paracetamol nor ibuprofen toxicity will explain her condition as both of them will mainly present with GI symptoms rather than CNS and cardiac symptoms . and even in massive doses they may present with milder form of CNS disturbance. thus we need to think a bout a toxin can cause both CNS and cardiac toxicity and the first ddx came to my mind is TCA
although some recreational drugs may cause similar edfect but usually there will be some toxidrome which is absent in this pt ( almost normal vitals)
some gases may cause similar effect as well for example H2S but usually victims respond to regular care once removed from the source
and to support my thoughts About TCA is the fact that her VF is refractory to shock
so what I will do is other than ACLS protocol I will bolus this pt with sodium bicarbonate
if pt did not respond will consider ECMO ( if available)
if pt revived will cont the whole workup to rule out non toxin and other toxin causes and will keep her on Nahco3 infusion
ddx ( consider CNS and cardiotoxicity induce toxin) :
- sympathomimetics.
-hydrocarbons(less likely as no pulmonary signs or symptoms).
- digoxin toxicity.
- cholral hydrate
also non toxic possibilities must be taken into consideration:
- maybe she is having SAH or ICH resulted in depressed CNS and induced arrythemia
- cardiac ischemia.
i will proceed by:
- continue CPR according to ACLS protocol.
-in view of possibility of toxicity induced arrythemia then arrest, i will hold epinepherine, and substiute it with beta blocker/lidocaine.
-send paracetamol at 4hours.
-urine tox screen.
-digoxin level.
- send electrolyte and CK ( to look for rhabdomylsis due to prolong unconscious)
-cardiac enzymes.
-ABG.
-CT head
-ask family member to search her room and her belongings for any medications, bottels , needles.
- search pt belongings, bocket for any pills or medications
From history we should think about
1- paracetamol toxic
2- diclofinc toxic
but those rare cause LOW GCs and cause CVs instability unless massive dose ???
so we need more history
3- electrolyte imbalance
4- intracranial trauma
5- CNs infection
6- hypoglycemia
7-we should strongly think about sedative hypnotics because pt have low GCS like barbiturates, benzodiazepines , diphenhydramine and chloral hydrate because those can cause low gcs , respiratory depression, and increase catecholamine sensitivity which may cause dysthymia
the management: I think ACLS protocol to be followed but with some change as pt is in V.tachy I will give beta blocker
ABG need if pt is acidosis to give Na Hco3
the case is challenging we need more history
DD: electrolyate disturbance , paracetamol cardiotoxicity , myocardial ischaemia
I will dfibrillation her , and I will give Amidarone 300mg or lidocaine 1.5 mg/kg, I will ask to continue CPR
I will send blood for U&E , magnificent level , cardiac enzymes , paracetamol level