Poisoning

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Approach to a patient with Poisoning

Treatment of Common Specific poisoning

Dr. Rozina Sultana


FCPS(Medicine)
MD(Critical Care Medicine)
Registrar

Dept. of Critical Care


Medicine
BIRDEM General Hospital & IMC
What is poison ?
➢ Substance that when introduced into, or absorbed by
a living organism destroys life or injures health.
➢ Majority of poisoning are accidental, specially in the
under 5 age group.
➢ Intentional overdoses and substance abuse are seen in
adult person.
Common poisoning cases
• Organophosphorus compound poisoning
• Benzodiazepine and abusive substance poisoning
• Paracetamol poisoning
• Methanol poisoning
• Dhatura poisoning
• Corrosive poisoning
• Kerosine poisoning
• Others ..
Comprehensive
evaluation of
poisoning
patient
Taking a history in poisoning

• What toxin(s) have been taken and how much?


• What time were they taken and by what route?
• Has alcohol or any other substance (or substances,
including drugs of misuse) been taken as well?
• Obtain details from witnesses (e.g. family, friends,
ambulance personnel) of the circumstances of the
overdose
Taking a history in poisoning (contd)
• Assess immediate suicide risk in those with apparent
self-harm (full psychiatric evaluation when patient has
recovered physically)
• Assess capacity to make decisions about accepting or
refusing treatment
• Establish past medical history, drug history and
allergies, social and family history
• Record all information carefully
Important substances involved in
poisoning
In the UK:
• Analgesics: paracetamol and non-steroidal anti-
inflammatory drugs (NSAIDs)
• Antidepressants: tricyclic antidepressants
(TCAs), selective serotonin re-uptake
inhibitors (SSRIs) and lithium Cardiovascular
agents: β-blockers, calcium channel blockers
and cardiac glycosides.
• Drugs of misuse: depressants (e.g. opiates,
benzodiazepines), stimulants and entactogens
(e.g. amphetamines, MDMA, mephedrone,
cocaine), hallucinogens (e.g. cannabis,
synthetic cannabinoid receptor agonists, LSD)
• Carbon monoxide
• Alcohol
In South and South-east Asia
• Organophosphorus and carbamate insecticides
• Aluminium and zinc phosphide
• Oleander
• Corrosives
• Snake venoms
Clinical assessment
• Start with the basics
– Airway, breathing, circulation
• Get a better history
– Get rescue person to get pill bottles, tell you what
they do know (found outside, inside, garage…)
– Call friends, family, neighbors
– Call primary physician to see what he is on
regularly
• Get him to tell you
– Always remember that suicidal patients (just like
everyone else) can lie so be skeptical of their history
➢ Address ABCDE…immediately
• A = Airway
• B = Breathing and ventilation
• C = Circulation
• D = Disability: neurological status
• E = Exposure /Environmental control
Airway - A

• Head tilt, chin lift


• Jaw trust
Airway - A

• Clearance (aspiration)

• Oral/Nasal Airway

• Intubation
Breathing - B

Look, listen and feel for


NORMAL breathing

•Symmetry
•Breathing Sounds
•Tidal Volume
•Respiratory rate
Circulation - C

• Pulse
• Rate
• Rhytme
• Arterial Pressure
• Hypertension
• Hypotension
Disability - D
• Disability is determined from the patient level
of consciousness according to the AVPU or
GCS.

A for ALERT
V for VOICE
P for PAIN
U for UNRESPONSIVE to any stimulus
Glasgow Coma Scale (GCS) assessment
Assessment of the
Glasgow Coma Scale
(GCS) score in an
obtunded patient.
Avoid using a sternal
rub, as it causes
bruising.
Bradycardia

Propanolol (β-blockers), phenylpropanolamine (a-


agonists)
Anticholinesterase drugs
Clonidine,
Ethanol / alcohols
Digoxin, Darvon (opiates)
Tachycardia

Free base (cocaine/stimulants)

Anticholinergics, antihistamines

Sympathomimetics

Theophylline (methylxanthines)
Hypotension

Clonidine, CCB
Reserpine (anti hypertensive)
Antidepressants
Sedative hypnotics
Heroin (opiates)
Treatment of Common Specific poisoning
OPC Poisoning :

➢ Organophosphorus compounds are widely used as


insecticide in agricultural sector by the farming
community in Bangladesh.
➢ Since it is easy and widely available, OPC has become
a popular method of self-harm.
➢ It is the most common poisoning found at different
level of hospitals of Bangladesh.
Clinical features:
• Smell of OPC
• Bronchorrhea (bronchial secretions)
• Bradycardia,
• Hypotension,
• Incontinence of urine & stool,
• Miosis
• Hyper salivation
Organophosphorus
compounds: Treatment by antidote:
• parathion • Inj. Atropine
• malathion • Inj.Pralidoxime
• fenthion
(if available)
• diazinon
• dichlorvos
• chlorpyrifos
• dimethoate
Signs of atropinization: Atropine toxicity features:
• Clear chest on • Restlessness
auscultation, no wheeze • Tachycardia
• Heart rate > 80 b/m • Fixed dilated pupil
• Pupils no longer pinpoint • Hyperpyrexia
• Dry axillae • Dry mouth
• Systolic B.P. >80 mmHg • Blurred vision
• Delirium, coma
• Inj. Atropine 2 amp (1.2 mg) IV stat followed by
doubling of doses every 5 mins interval until full
Atropinization occurs.
• Don’t simply repeat the initial dose; rather continue to
double each time. During this time check the five
parameters every 10 mins interval.
•Once Atropinized calculate the total amount required and
give 10-20% of it per hour through infusion (normal
saline) as maintenance.
• Review the parameters at 30 mins interval for 3 hours,
followed by hourly for 6 hours and 3-6 hourly for next
24-48 hours.

• If Atropinization is lost at any point,eg; bronchospasm,


bradycardia etc. start giving bolus dose again until
they disappear and add 20% of bolus requirement to
infusion per hour
Inj. Pralidoxime chloride:
• 1-2 g/IV stat (adult);
• 25-50 mg/kg IV over 15-30 mins (in children).

•If no improvement, repeat after 1 hour, then every 8-12


hour until improvement.
Benzodiazepine Poisoning and Poisoning by Abusive Substances

• History and Symptom


• History should include the time, dose, and intent of the
overdose.
• Determine if any co-ingestants are present or not.
• Symptoms include – Dizziness, Confusion, Drowsiness,
Blurred vision, Unresponsiveness, Anxiety and Agitation.
• The physical examination should focus on the patient's vital
signs and cardiorespiratory and neurologic function.
Clinical Features

1. Nystagmus 9. Impairment of cognition


2. Hallucinations 10. Amnesia
3. Slurred speech 11. Paradoxical agitation
4. Ataxia 12. Respiratory depression
5. Coma
6. Hypotonia
7. Weakness
8. Altered mental status
• Most patient need only supportive care.

• Antidote is rarely needed in case of severe CNS


depression (Non responding) with severe respiratory
depression or ineffective respiration.
• Flumazenil: Patient regains consciousness within 15 to 30
seconds after injection of flumazenil. If the patient becomes
unconscious again, flumazenil can be given by IV infusion
100- 400 micrograms/hour rate being adjusted according to
level of arousal.
• Adult Dose: 0.1-0.2 mg IV per/1min to a total dose of 1 mg at
one time or 3 mg in 1 h; infusion rates of 0.1 mg/min decrease
disconcerting rapid arousal.
• Pediatric Dose: 0.002-0.02 mg/kg IV per/ 1min
Contraindications of Flumazenil
• Known Hypersensitivity
• Serious cyclic-antidepressant over dosage
• Patients using benzodiazepines to control a potentially
life-threatening condition (eg, intracranial
pressure,status epilepticus);
• Chronic benzodiazepine use.
Paracetamol poisoning
• A single overdose of more than 12 g (24
tablets) or 150 mg/kg body weight can be
potentially fatal.
• In children, hepatotoxicity should be
anticipated with doses exceeding 125
mg/kg body weight.
• Patients with following conditions have a higher risk
of paracetamol induced liver damage.
• Malnutrition and eating disorders
• Chronic alcohol abuse
• Recent or ongoing viral illness
• Use of enzyme inducing drugs (e.g. Carbamazapine,
phenytoin, phenobarbitone)
Symptoms of paracetamol poisoning

Majority pt remain asymptomatic. In case of pt


presented with symptoms.
Phase- I (0‑24 hours):
• Nausea, vomiting and abdominal pain.
• Rarely, metabolic acidosis within 4 hours of
ingestion.
• Arrhythmias or bradycardia may develop
Phase- II (24‑72 hours):
• Hepatotoxicity develops with elevation of hepatic
enzymes, prothrombin time, and bilirubin.
• AST and ALT may exceed 1000 IU/1.

• There may be right upper quadrant abdominal pain.


Phase- III (72‑96 hours):
• Bleeding manifestations, portal hypertension, hepatic
encephalopathy and elevated bilirubin levels.
• Thrombocytopenia, hypoglycaernia, disseminated
intravascular coagulation, hypokalaemia, pancreatitis and
myocarditis.
• Oliguric renal failure may develop due to renal failure.
• Patient may develop coma. Death is due to hepatic
failure.
Phase- IV (96 hours‑2 weeks):
• Hepatic failure and death may occur, or
• There may be complete resolution of hepatic
damage and recovery.
Management
• Management depends on the time interval since
ingestion and the plasma paracetamol level.
• Gastric lavage
• Activated Charcoal
• Antidotes: N- Acetylecysteine (NAC) and
Methionine.
• Other supportive care
Methanol Poisoning
• Methanol is methyl alcohol also known as spirit which
consists of 90- 95% ethyl alcohol and 5-10% methyl
alcohol.
• It is used in many home chemicals, duplicating fluids,
varnishes, stains, paint thinners and dyes.
• It is easily adulterated and used as country liquor by
poor peoples who cannot afford ethyl alcohol for
drinking purpose
Clinical Features and Fatality:
• CNS Toxicity: Headache, dizziness, vertigo, dyspnoea,
cyanosis, cardiac depression and muscular weakness.
• Ocular toxicity: It is a delayed feature, which includes
blurring of vision, which gradually leads to total or
partial blindness.
• Renal toxicity
• GIT toxicity
• Respiratory toxicity
Laboratory Diagnosis:.
• Methanol produces high anion gap acidosis,
which is due to excessive production of formic
acid and lactic acid.
• In Bangladesh, methanol level can not be done
due to lack of facility but ethanol level can be
done during treatment
• Maintain airway, breathing and circulation
• IV Normal saline, O2 and Hco3 should be given if pt
presents with Metabolic acidosis
• Gut Decontamination (Gastric lavage with Normal
saline if presents within 1 hour
• Watch for worsening Sign/Symptoms
• Routine test for organ involvement
• Shock: NACL fluid± Vasoactive agents

• Ocular toxicity- Folinic acid, 50 mg i.v. 4 hourly may protect


against ocular toxicity by accelerating formate metabolism.
• Metabolic acidosis :NAHCO3± Haemodialysis

• Others:

➢ Correct electrolytes,sugar

➢ IV diazepam for convulsion

➢ 25% glucose for hypoglycaemia


• Antidote: Ethyl alcohol (whisky,Gin) Dose: 1.8
mI/kg as a loading dose, and 0.2 ml/kg/hr as
maintenance dose orally, diluted with water or fruit
juice. Maintain 2-3 days.
• Fomepizole is a direct inhibitor of alcohol
dehydrogenase. Dose: Loading dose 15mg/kg body wt
over 30 minute, four 12 hourly doses of 10mg/kg
should be given
Dhatura Poisoning..Clinical features..

• CNS muscarinic blockade: • Peripheral muscarinic


– Confusion effects:
– Agitation – Mydriasis
– Myoclonus – Anhidrosis
– Tremor – Tachycardia
– Picking movements – Urinary retention
– Abnormal speech – Ileus
– Hallucinations
– Coma
Better way to remember it. . .
• Hot as Hades - Fever
• Fast as a Hare - Tachycardia
• Dry as a Bone – Lack of diaphoresis
• Red as a Beet – Flushed skin
• Mad as a Hatter – Delerium
• Full as a Tick – Urinary retention
• Blind as a Bat – Mydriasis
Management

• Supportive care
• Stomach wash
• Airway toileting
• Antidotes: Physostigmine, prostigmin,
Pilocarpine
• Shot acting barbiturate for delirium
Corrosive poisoning
Strong acid: sulphuric acid, Nitric acid, Hydrchloric
acid, Carbolic acid
Strong Alkali :
• sodium Hydroxide
• Pottassium hydroxide
Mangement

• Supportive care:
• IV fluid
• No specific antidote
• Surgical treatment may needed
Kerosine poisoning (Clinical features)
• Asymptomatic.
• Burning sensation in the mouth and pharynges
• Nausea and vomiting.Occasional abd pain and
diarrhoea
• Fever:
– May develop within hours, up to 38-400C, subsides
within 24-48 hours. Does not warrant antibiotic
treatment.
– Temperature after 48 hours indicates infection and
antibiotic is warranted.
• Cyanosis, tachycardia, tachypnoea
• Nasal flaring
• Supraclavicular, intercostal retraction and chest-
indrawing.
• Features of bronchospasm, consolidation, crackles may
be present.
• Hypoxemia may be present and be assessed by pulse
oximetry.
• Encephalopathy may range from lethergy to convulsion
and coma.
• Rare cases may develop myocarditis.
Supportive measures

1. Control temperature
2. O2 inhalation if there is hypoxia.
3. Bag and mask ventilation, intubation and mechanical
ventilation if there is respiratory failure
4. Nutritional support
5. IV fluid
6. When infection is suspected Injection Ampicillin 200
mg/Kg/day 6 hourly for 5-7 days, Metronidazole may be
added for 5 days.
7. Steroids have no beneficial effect
TOXIDROME
TOXIDROME
Definition:
Signs, symptoms and characteristics that often occur
together in toxic exposer is called toxidromes.
• 5 Basic Toxidromes
– Sympathomimetic
– Opiate
– Anticholinergic
– Cholinergic
– Sedative Hypnotic
Toxidromes: Sympathomimetic
Sympathomimetics

• Cocaine
• Methamphetamine/Amphetamines
– Ecstasy (MDMA)/Yaba
– ADHD meds like ritalin, adderal
• Ephedrine
• Caffeine
Clinical presentation…

• Tachycardia +/- arrythmias


• Hypertension +/- ICH
• Confusion with agitation
• Seizures
• Rhabdomyolysis
– Renal failure can result
Management
• Supportive care
– Monitor airway, diagnose
ICH, rhabdo CNS
excitation
Behavioral
Agitation

– I/V for insensible loses


and volume repletion
• Benzos
• Control BP Cardiac
excitation

• NEVER GIVE BETA


BLOCKERS
Toxidrome: Opiate
Opiates / Opioids
➢ Opiate: derived directly from the opium poppy:
morphine and codeine
• Opioids: much broader class of agents that are
capable of producing opium-like effects or of
binding to opioid receptors
– Heroin
– Methadone
– meperidine
– Hydrocodone
– oxycodone
Clinical presentation…
• Coma
• Miosis
• Respiratory depression
• Peripheral vasodilation
• Orthostatic hypotension
• Bronchospasm
• Pulmonary edema
• Seizures (meperidine, propoxyphene)
Management..

• Competitive opioid antagonist: Naloxone


– Goal of return of spontanous respirations
sufficient to ventilate the patient appropriately
– May have to re-dose as opiates may act longer
than antagonist
• There are other longer acting opioid antagonists
such as nalmefene and naltrexone but these are
not often used
Toxidrome: Anticholinergic
Clinical presentation…

• CNS muscarinic blockade: • Peripheral muscarinic


– Confusion effects:
– Agitation – Mydriasis
– Myoclonus – Anhidrosis
– Tremor – Tachycardia
– Picking movements – Urinary retention
– Abnormal speech – Ileus
– Hallucinations
– Coma
Management

• Supportive care
– IVF to replace insensible losses from agitation,
hyperthermia
• Benzos to stop agitation
• Physostigmine
– Induces cholinergic effects
– Short acting
– May help with uncontrollable delirium
– Do not use if ingestion not known
• Danger with TCAs
Toxidrome: Cholinergic
Clinical presentation…

• D - Diarrhea
• U - Urination
• M - Miosis
• BBB – Bradycardia, Bronchorrhea, Bronchospasm
• E - Emesis
• L - Lacrimation
• S - Salivation
Management

• Antagonize muscarinic symptoms


– Atropine
• Stop aging of enzyme blockade
– 2-PAM
• Prevent and terminate seizures
– Diazepam
• Supportive care
Toxidrome: Sedative-Hypnotic
Clinical presentation…

• CNS depression, lethargy


• Can induce respiratory depression
• Can produce bradycardia or hypotension
Management

• Supportive care
• Be wary of the benzo “antidote” Flumazinil
– Is an antagonist at the benzo receptor
– RARELY INDICATED
– If seizures develop either because of benzo
withdrawal, a co-ingestant or metabolic
derangements, have to use 2nd line agents,
barbiturates, for seizure control
So back to our patient. ..
• Agitated, pupils 8 mm, sweaty, HR 140’s, BP 230/130
– Sympathomimetic
• Unarousable, RR 4, pupils pinpoint
– Opiate
• Confused, pupils 8mm, flushed, dry skin, no bowel sounds,
1000 cc output with Foley
– Anticholinergic
• Vomiting, urinating uncontrollably, HR 40, Pox 80% from
bronchorrhea, pupils 2 mm
– Cholinergic
• Lethargic, HR 67, BP 105/70, RR 12, pupils midpoint
– Sedative Hypnotic
So basic approach:
• Airway, breathing, circulation
• Establish IV, O2 and cardiac monitor
• Consider coma cocktail ???
– Thiamine, D50, Naloxone
• Evaluate history and a thorough physical exam
– Look at vitals, pupils, neuro, skin, bowel sounds. . .
– Gives you hints regarding the general class of toxins
– Guides your supportive care
• Draw blood / urine for testing
• Time to consider decontamination options
General management
➢ Gastrointestinal decontamination:
• Activated Charcoal
• Gastric aspiration and lavage
• Whole bowel irrigation
➢ Urinary alkalinisation
➢ Haemodialysis and haemoperfusion
➢ Lipid imulsion therapy
➢ Supportive care
➢ Antidotes
Charcoal

• Works to adsorb substances to its matrix


– Not for metals, caustics
• Generally safe, few contraindications
– Aspiration, bowel obstruction
• Dosing 1g/kg po dose, +/- single dose of
cathartic
Doesn’t adsorb

C- Caustics, Corrosives
H- Heavy metals
A- Alcohol
R- Rapid onset - cyanide
C-Chlorine
O- others ( Iron)
A- aliphatic hydrocarbon
L- lithium
Activated charcoal
Whole Bowel irrigation

• Isotonic polyethylene glycol electrolyte solutions


(GoLytely)
• Large volumes ingested “wash” the substances through
the bowel
– Especially useful for metals or other things not well
adsorbed by charcoal
• Avoid in patients with bowel obstruction or ileus
• Dose in volume sufficient to create clear rectal effluent
WBI
• Dosing:
500 – 2000 ml/hr
25cc/kg/hr peds
4-6 hours
duration
– Have to use an NG
tube
Decontamination

Skin
Remove contaminated clothing / wash skin completely with
soap water followed by repeat body wash Q4th hrly

Eyes
Hair
Decontamination

Pay special attention to


Around ears Arm pits
Eyelids Groin
Inside nose Behind knees
Inside mouth Between toes
Neck creases
Enhanced Elimination

Urinary alkalinization
Salicylates
1-2 meq/Kg bolus then 3 amps sodabicarb in
1000cc D5W
150 – 250 cc/hr
Urine pH >7.5
Watch for Hypokalemia and correct
Enhanced Elimination

Haemodialysis

Charcoal Haemoperfusion
Dialyzable poisons

Heavy metals
Alcohols
INH
Aminophyline
Paraldehyde
Barbiturates
Salicylates
Camphor
Snake bite
Carbon monoxide
antibiotics
Ethylene glycol
Haemoperfusion

Diazepam
Digoxin Phenols
OPC Phenylbutazone
Dapsone Quinidine/qunine
Chloral hydrate Salicylates
Paraquat TCA
Monitoring

Clinical observation
Pulse oximetry
ECG monitoring
Minimum 6 hours if cardio-active drug
>24 hours if delayed release preparation
Supportive care
Supportive care
Thank you

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