GENERAL APPROACH TO A POISONED VICTIM

GENERAL APPROACH TO A POISONED VICTIM

General principles involved in management of poisoning

The purpose of this lecture is to provide guidelines for evaluating the severity of an exposure to a potentially toxic substance, clues to the identity of the offending substance and, most importantly, how to manage the severely intoxicated victim initially.
For effective management of an acutely poisoned victim, six complementary steps are required. These are:
1. Resuscitation and initial stabilization (Emergency care)
2. Diagnostic examinations (including the type of poison)
3. Nonspecific therapy (Decontamination)
4. Specific therapy (Antidote administration)
5. Enhancement of toxicant redistribution/elimination
6. Supportive care

Resuscitation and Initial Stabilization

On arrival of a patient with poisoning, the initial priorities are:
If the patient is in a state of coma, convulsion or cardiac arrest, Determine the level of consciousness using the Glasgow Coma Scale (GCS).
Maintenance of airway, breathing and circulation (ABC).
A = AIRWAYS: clear airways of vomitus or flaccid tongue (turn the patient in lateral decubitus position).
Insert endotracheal tube (ETT), if necessary. If fluid is in the airways, aspirate it through the ETT.
B = BREATHING: maintain ventilation mechanically, if necessary (preferably with balloon)
C = CIRCULATION: maintain circulation (apply CPR if necessary; Chest compression: ventilation = 15:2)
D = DRUGS (e.g., benzodiazepine for seizure, epinephrine for cardiac arrest) and obtain venous access
If the patient has an altered level of consciousness, his cervical spine must be immobilized till an injury can be ruled out.
Hypotension in poisoned patients is most often due to loss of fluids or toxin induced vasodilatation. Hence, crystalloids (such as normal saline) are the first choice of treatment of hypotension.
Before infusing fluids, blood should be withdrawn for investigations (including sugar, urea, electrolytes and acid-base status).
Rectal temperature should be obtained in all patients with altered sensorium.
After initial resuscitation, all patients with altered sensorium should receive a coma cocktail (dextrose, thiamine, and naloxone or flumazenil).
Note:
Wernicke's syndrome results from thiamine deficiency. This is caused by malnutrition and malabsorption in the alcoholic patient, thiamine deficiency causes ATP depletion and, in turn, repolarization failure in neurons, thereby evoking the symptoms of W. syndrome = seizures + neuropathy (specially for eye muscles and for pharyngeal muscles).


II. Diagnostic examinations
History:
The history should be elicited from the patient as well as his/her relative. Occupational history and availability of potential poisons at home should also be asked for. However, it is very important not to believe the patient blindly particularly those who have ingested poison with a suicidal intent.


Physical examination:

Once the patient has been stabilized, a thorough head-to-toe examination should be conducted. The objectives of this examination is to diagnose the type of poison and to detect any associated trauma. Based on the examination findings, it may be possible to identify the type of poison involved as follows:

Vital signs (blood pressure and pulse, respiration, temperature)

 Blood pressure and pulse:
Clinical Features
Poisons

Hypertension with Tachycardia

LSD, MAO inhibitors, Marijuana, Alcohol withdrawal, Nicotine,
Antihistamines, Antipsychotic agents, phencyclidine (PCP)
Sympathomimetics, e.g., amphetamine, ketamine, MDMA (3,4 methylenedioxy-metamphetamine, Extasy), cocaine.

Hypotension with bradycardia

Cyanide, Organophosphates.
VMC depressive drugs: sedative-hypnotics, opioids
Sympatholytics: β-blockers, α2-rec agonists: clonidine and tizanidine
Ca-channel blockers (except nifedipine)

Hypotension with tachycardia

Caffeine, Disulfiram-ethanol interaction.
Theophylline, nifedipine (Mech: vasodilation → hypotension → reflex tachycardia).
TCAD, phenotiazines
(Mechanisms: Hypo: VMC depression + α1-receptor blockade in vessels
Tachy: ↓NE reupt. → β1-rec stimulation + Ach-M rec blockade.

Respiration:

Tachypnoea
Amphetamine, CO, drugs producing metab. acidosis (e.g., aspirin, isoniazid, metformin, iron; methanol, ethylene glycol)

Shallow respiration (Bradypnoea)

Opioids, α2-rec agonists (clonidine, tizanidine), barbiturates

Body temperature:

Hyperthermia
Amphetamines (Ecstasy), Antidepressants, Cocaine, Lithium, LSD, SSRIs (serotonin syndrome), MAO inhibitors, Phencyclidine, Anticholinergics, Salicylates, Antihistamines,.


Hypothermia
Narcotics and ethanol

Eye examination (pupil size and involuntary eye movements)

Miosis:
- opioids (morphine, heroin, etc.): → pinpoint pupil.
- α2-receptor agonists (clonidine and tizanidine).
- organophosphates (specially if the eye is exposed).
- in deep coma produced by sedatives.

Mydriasis: amphetamines, cocaine, LSD, atropine, terminal coma

Horizontal nystagmus: alcohol, sedative-hypnotics, phenytoin (the earliest sign of phenytoin toxicity).
Vertical + horizontal nystagmus (on conscious patients): phencyclidine (PCP), ketamine.
Oculogyric crisis (an extrapyramidal effect): phenothiazines, butyrophenones
Ptosis + ophthalmoplegia: botulism (due to paralysis of eye muscles by botulinus toxin)

Mouth

 Burns: acids, bases, mercuric salts (gray discoloration)
 Odors: - characteristic: alcoholic beverage, solvents.
- bitter almond: cyanide.
- garlic: arsenic, organophosphates.

Skin
Sweaty: organosphosphates, nicotine, Extasy.
Dry, hot and flushed: atropine (dry mouth → hoarse voice or aphonia).
Pink: CO (COHb is cherry red).
Cyanotic: -↑deoxy-Hb (due to impaired pulmonary gas exchange, e.g., gasoline aspiration)
-methemoglobinemia (although Met-Hb is chocolate brown)
Icteric (↑serum Bi): - hepatotoxicity (acetaminophen,) → ↓ bilirubin elimination
-hemolysis, e.g., arsine intoxication → ↑ bilirubin production
Abdomen
Paralytic ileus, no bowel sounds: antimuscarinic drugs (atropine), opioids, sedative- hypnotics.
Hyperactive bowel: organophosphates, theophylline, Amanita phalloides (fungus), acute intoxication with Fe (iron), As (arsenic), or thallium (Tl) compounds.


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Dextrose: 25 g i.v. (50 ml 50% sol.) because hypoglycemia causes irreversible loss of brain cells.
Naloxone: 2 mg i.v. (reverse opioid-induced respiratory depression and coma and also effective in ethanol or sedative-hypnotic overdose).
Flumazenil: 0.3 mg i.v. (reverse benzodiazepine-induced coma).
Thiamine: (Vitamin B1, 100 mg i.m.) (for alcohol-intoxicated patient - to prevent Wernicke's syndrome).

Try to obtain the history of the intoxication (causative agent, dose, time) and a sample of the toxicant. These assist in securing the diagnosis and assessing the severity of poisoning.