acute poisoning - management ayman m. kamaly, md professor of anesthesiology ain shams...

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ACUTE POISONING - MANAGEMENT Ayman M. Kamaly, MD Professor of Anesthesiology Ain Shams University [email protected]

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ACUTE POISONING -MANAGEMENT

Ayman M. Kamaly, MDProfessor of Anesthesiology

Ain Shams University

[email protected]

INTRODUCTION

• Acute poisoning is a common medical emergency in any country.

• The exact incidence of this problem in our country remains uncertain.

For effective management of an acutely poisoned victim, 5 steps are required:

I. Resuscitation and initial stabilizationII. Diagnosis of type of poisonIII. Nonspecific therapyIV. Specific therapyV. Supportive care

I. Resuscitation and Initial Stabilization

Initial management: ABCDs

• Airway• Breathing• Circulation

Lessons from History...

• A young princess ate part of an apple given to her by a wicked witch

• She was found comatose and unresponsive, as if in a deep sleep,

• Airway positioning and mouth to mouth ventilation were performed,

• and she was fully

recovered.

Lessons:

• Best Antidote = Good Supportive Care(Love’s first kiss)

• Airway issues is a still the major cause of morbidity in toxicology as in other aspects of emergency.

Circulation = Plumbing

• Pump working? Inotrope

• Enough volume (is it primed)? Hypovolemia?

IV fluid challenge

• Adequate resistance (no leaks)? Inadequate vascular resistance?

Norepinephrine, phenylephrine

Initial management: ABCDs

Treat problems as you find them!!• Airway,• Breathing,• Circulation,• Drugs, • Decontamination, • Detoxication,• Disability – GCS/AVPU and Pupils,• DON’T EVER FORGET GLUCOSE.

Don’t forget GLUCOSE

“A stroke is never a stroke until it’s had 50 of D50”

• Empiric administration of dextrose??!• Check the blood sugar using a reliable bedside

test• Administer dextrose ONLY if the RBS is <80

mg/dl.

II. Diagnosis of Type of Toxin

• What?• When?• How much? (mg/kg)• What else?• Why?

A) History Be a Detective

• Collateral history– Paramedics– Family / friends– Notes– Look in pockets – carefully!!!

Look for Clues

B) Examination

Investigations• All Patients

– Glucose– Paracetamol & Salicylate

• As indicated– LFT– RFT, Lytes– Co-ag / INR– CK– ABG / VBG

• Urine toxicology screen

Investigations• Urine toxicology screen

– Pinkish urine --->>> phenothiazine,

– Chocolate colored --->>> met-hemoglobinaemia,

– Oxalate crystals --->>> ethylene glycol,

– Ketonuria (without metab. changes) --->>> Salicylate

Investigations• Abdominal X-Ray (Radiopaque Toxins)

– Chloral hydrate, iodides,

– Heavy metals, iron,

– Sustained release pills,

– Solvents (Chloroform, CCL4)

• Aim:

– Reduce absorption of poison from the gut,

– Increase excretion of absorbed poison.

III. Non-Specific Therapy

1) Emesis

• Syrup of Ipecac• Amount of recovered toxin is highly variable • Effective within ONE hour• Contraindicated:

– Comatose/Convulsing– Ingested corrosive or hydrocarbon*

A. Reducing absorption

2) Gastric Lavage

• Lt Lat Position + head down • to prevent aspiration & ↓ pushing lavage into

duodenum.• If unconscious ETT• Effective within 1-2 hours• Contraindicated:

– Strong corrosive or – Volatile hydrocarbons

3) Activated Charcoal

• Small particle size & enormous surface area,• Bind most drugs & toxins,• Dose: 1 g/kg• Exceptions:

– Iron, Lithium, Metals,– Methanol, Ethanol, Hydrocarbons,– DDT

Activated Charcoal (cont.)

• More effective than Ipecac, Gastric Lavage• First choice for most Over Doses

4) Whole Bowel Irrigation

• Isotonic soln. of Polyethylene glycol (2 L/hr)• Not absorbed from intestine (mechanical

flush)• Good for:

– Iron, Lithium,– Sustained-release pills,– Foreign bodies,– Drug “packets”

1) Forced Alkaline Diuresis• Principle: Renal tubular epith is impermeable toionized (+) molecules. If the urinary pH is changedso as to produce more of ionized form, it is trapped in the tubular fluid & is excreted in the urine.

• Useful in: – Salicylates, – Phenobarbital,– Lithium

B. Increasing Excretion

Forced Alkaline Diuresis (Cont.)

• Method: – D5% - ½ NS + bicarbonate 20-35 mEq/L to produce

a urine output of 3-6 ml/kg/hr & a urine pH 7.5-8.5.

– Diuretics are often needed to maintain high urine flows.

– KCl is added to prevent ↓K+,

• Contraindications: – Shock,– Hypotension, CHF,– Renal failure

2) Multiple-Doses Activated Charcoal• 1 g/kg/1-4 hrs• To maintain intestinal toxin conc. near-zero

(Gastrointestinal Dialysis).• Indicated in toxins with :

– Long ½ life,– Enterohepatic circulation ( Digoxin, Phenobarbitals,

Theophylline),– Sustained-release preparations,– Massive toxin dose to be effectively adsorbed by

single charcoal dose

3) Dialysis (Peritoneal/Hemo)

• For H2O soluble & Low MW compounds.

• Useful in: – Ethanol, Methanol,– Salicylates, – Theophylline, – Ethylene glycol,– Phenobarbital – Lithium

IV. Specific Therapy

• Try to maintain functions of CNS, CVS, Renal, …

• Care for coma, seizures, hypotension, arrhythmias, hypoxia, …

V. Supportive Therapy

• Exposure to toxins could be through routes other than ingestion (Cutaneous, Ocular)

• Antidotes are NOT available for every toxin

• However; when Antidote is Present the effect is Dramatic

• The 1st sample of gastric lavage should be collected in “clean” container (Contamination !!).

• Container should be sealed using a glue paper before sending for toxicological screening.

Legal Aspects

• After sealing Blood & Urine collection tubes and bottles, pt’s information should be written on the labels & affixed @ the juncture between the cap & the bottle.

• POLICE should be informed !!

Clinical Scenarios

Paracetamol

• Very common: 40% poisons admissions• Often asymptomatic• Can be lethal – 200-300 deaths/year• Check blood level at 4 hours• Two treatment lines normal and high risk

Prescott Nomogram

Paracetamol metabolism• Metabolised by:

– Glucuronidation (60%),– Sulphation (35%) – Oxidation (10%) by Cytochrome p450

produces NAPQI (toxic hepatocellular necrosis)

• NAPQI detoxified by conjugation with glutathione.

High Risk pt.

• Increased oxidation pathway (enzyme induction)– Chronic alcohol use– Drugs

• Reduces glutathione stores– Malnutrition– Eating disorders– Chronic liver disease

N-Acetylcysteine

• Most effective within 8 hours• Precursor for glutathione production• Can cause anaphylactoid reactions !!• Consider starting before paracetamol result if:

– Presenting > 8 hrs & > 150mg/kg taken– Other accompanying overdose.

Patient 1

• 20 year old woman who takes a handful of paracetamol tablets

• No drug history• No alcohol use• Fit and well• Blood level is 80mg/L

after 4 hrs.

No need to treat

• Patient is not high risk• Level at 4 hours is below even the high risk line

Patient 2• 70 year old man• Takes 20 paracetamol 6

hours before presenting• Alcoholic• No drug history• Blood level 100mg/L

Treat

• High risk patient• Level above the high risk line

Patient 3• 17 year old

epileptic• 25 tab Panadol 2

hours before attendance

• Taking carbamazepine

• Blood level at 4 hours is 120mg/L

Treat

• High risk patient• Level above the high risk line

Patient 4

• 35 year old man who presents after taking 24 paracetamol over a period of 24 hours

• No drug history• Fit and well• Blood level 20mg/L

Treat

• Staggered overdoses are difficult• Level is above the treat-line in context to time• Need to monitor Liver function, clotting and renal

function• May need discussing with Liver Unit if abnormal

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Some Famous Historic Poisonings

Thank You .. !!