What is a poison?

In common usage - poisons are chemicals or chemical products that are distinctly harmful to human

More precisely - a poison is a foreign chemical (xenobiotic) that is capable of producing a harmful effect on a biologic system

What is a toxin?

It originally referred to a poison of animal or plant origin

Toxicant is the currently preferred scientific term for all poisons.

What is a toxidrome?

It is the association of several clinically recognizable features, signs, symptoms, phenomena or characteristics which often occur together, so that the presence of one feature alerts the physician to the presence of the others.

Acute poisoning is a medical emergency.

The purposes of medical practice in such case are to save lives and to relieve suffering.

In order to achieve these purposes in a poisoned patient, it is important to evaluate the severity of an exposure to a toxic substance, to make a diagnosis, to know how to approach treatment and to design an appropriate scheme of management for each patient.

I -Evaluation of the patient II-History.III- Examination. IV-Hospital disposition.V-Systemic examination.VI- Investigations.VII- Management.

ASSESSMENT & THERAPY should proceed in parallel

A-Initial assessment of all medical emergencies follows the principles of advanced cardiac life support. Establish and maintain vital functions.

1- Airway------ Ensure patent airway and protect the cervical spine.

2- Breathing-------Asses ventilation .May be with bag-valve-mask and/or intubation

Administer 100% oxygen. All unconscious or shock patients benefit from

intubation 3- Circulation-------Asses pulse: (volume-rate- rhythm). Place on ECG monitor. Establish vascular access. Obtain blood samples.4-Drugs

Personal history History of present illness Past history (Medical history) Family history

• Name • Age & sex (menstrual history in female)• Marital status.• Address (residence)• Occupation (metal toxicity, insecticide

poisoning)• Special habits.

Presenting complaint: IN patient's words (no medical terms);

analyze the Symptom (site –onset- duration –recurrence –what increase it, what decrease).

Substance (name-ingredient -regular form –slow release- enteric coated)

Amount.Time of intoxication- delay.Symptoms. (Relation between time of ingestion and

symptoms).Where - mode of intoxication-route. Pre-consultation treatment (gastric lavage - emesis-

antidotes)

Categorize the main symptoms- Ask about other symptoms- Analysis of symptoms.Respiratory symptoms: cough –wheeze –chest pain-

breathing –sputum (bloody or not) GIT symptoms: nausea -vomiting characteristics of

vomitus (odor, color, blood, tablets)-diarrhea-pain.CVS symptoms (dyspnea, pain, tightness, cough,

palpitation) Neurological symptoms (irritability, seizures, weakness,

numbness, rigidity).genitourinary symptoms (menstrual history, urine)

•

• Drug therapy- recent medication.• Similar attacks• Preexisting disease.• Trauma-accident-coma.

• Operations – blood transfusion

• Similar condition in the family.• Any familial disease (allergy-blood diseases)• Psychological troubles (child abuse- addiction-

suicidal attempts).

• Assessment of vital functions. All patients must have a complete record of initial vital signs which must be repeated and recorded frequently:

• Respiration• Pulse• Blood pressure.• Core temperature.• Examine clothing, shoes, and hat, look for

medical identification.

1. Mental and emotional state. (inability to concentrate, apathy, agitated, depressed) .

2. Pupil (size- equality-reaction to light).1. A unilateral dilated pupil means a neurological-

structural lesion, localized trauma to the eye or cataract.

2. Unilateral dilation may occur with a mydriatic drop in one eye..

3. Dilated reactive: sympathmimetic, opioid withdrawal and amphetamine.

4. Dilated irreactive: anticholinergic poisoning.5. Constricted pupil ( pin pointed): opiate overdose,

organophosphorus, carbamate insecticide toxicity and pontine lesion (no response to naloxone, confirmed by CT or MRI.)

3. Pallor: decreased visibility of oxyhemoglobin, detected in inner side of lips or palm of hands.

4. Cyanosis: Bluish discoloration of skin and mucus membrane due increased level of reduced hemoglobin > 5 gm %. Detected in tongue (under surface).

5. Jaundice: Yellowish discoloration of skin and mucus membrane due to increased bilirubin level > 3mg %. Detected in the sclera in the day light.

6. Smell of the mouth or clothes.

6. Temperature:Febrile states physiologic readjustment of

thermoregulatory set-point to a higher level (e.g. infection)..

Hyperthermia. Temperature elevation associated with toxicological causes is unregulated may be due to excess muscle activity, hypermetabolic state, interference with oxidative phosphorylation, and impaired dissipation of heat. Toxicological temperature elevations require external cooling measures and control of excess muscular activity such as convulsions. Antipyretics are not useful. It occurs in:

Anticholinergic overdose.Sympathomimetic overdose. Salicylate overdose.Hypothermia: It may occur in overdose of:Barbiturates.Narcotics.Sedative hypnotics.Alcohol.

7. Skin: Rash- eruptions – pigmentation Burns – erythema (corrosives) Sweating (salicylate, organophosphorous or hypoglycemia)Dry –flushed (anticholinergics)Cold & clammy Skin bullae( due to skin hypoxia , prolonged coma,

barbiturates, or carbon monoxide) Phlebitis (cord like fibrosed veins): drug users or

addict.8. Hands (tremors) 9. Feet (edema).10. Neck.

Guidelines for admitting adult patient to an ICU:

Need for intubation.Seizures.Unresponsive to verbal stimuli.Any rhythm except sinus arrhythmia. Systolic blood pressure less than 80 mmHg

A - Respiratory system:1- The rate; normal rate 12-20 / min.( pulse :

respiration ratio is 4 : 1).Tachypnea (increase rate) Aspiration pneumonia ( kerosene).Metabolic acidosis (methanol, salicylates).Toxic hypoxia ( CO, cyanide,

methemoglobinemia or H2S)CNS stimulants (amphetamine, cocaine,

salicylate). Bradypnea (decrease rate)May be caused by CNS depressants (opiate,

ethanol, sedative hypnotic, psychotropics or anticovulsants).

2- Depth: Hyperpnea (deep): Metabolic acidosis. Hypopnea (shallow): Pneumonia, heart failure ( rapid,

shallow) Respiratory center depression (slow,

shallow) 3-Wheezes: Dry continuous musical sounds, due to passage of air in

narrowed bronchus. e.g., cholinergic agents, foreign bodies, smoke inhalation

and irritant gases. .4- Crepitations: Moist interrupted wet sounds, due to passage of air

through fluid in bronchi or alveoli Accumulated bronchial secretions as in coma. Acute pulmonary edema or aspiration pneumonia 5-Cyanosis

1.Peripheral pulse; is a reflection of peripheral perfusion, allows estimation of stroke volume. Early sign of shock is decreased pulse volume.

2. Heart rate and heart rhythm. Sinus arrhythmia and extrasystole are common in healthy children and young adults.

a. Bradycardia (decreased heart rate): may be produced by: Digoxin Calcium channel blockers. B-blockers Opiate overdose Muscarinic effect of organophosphate poisoningb.Tachycardia (increased heart rate): may be produced by: Drugs with anticholinergic action (atropine, Tricyclic

antidepressant, Neuroleptics, Antihistaminic). Sympathomimetic drugs ( Theophylline, Amphetamine,

Cocaine) Scorpion sting Any toxic hypoxia or hypoglycemia

C. Dysrhythmia. The correction of hypoxia and metabolic disturbances (electrolyte, glucose, acid- base disturbances) will spontaneously cure many dysrhthmias. It may be due:

Digoxin.QuinidineTricyclic antidepressant.Zinc phosphide.Carbon monoxide.Sympathomimetics

3-Hypertension. It is usually initial and transient may be followed by life threatening hypotension. It may be due to:

Sympathomimetics.Anticholinergics.Scorpion sting.

4-Hypotension. Decreased peripheral vascular resistance, e.g.; (CNS depressant

poisoning – Acute metal poisoning – phenothiazine intoxication). Hypovolemia e.g. ;

Increased GIT fluid loss (food poisoning – heavy metals – colchicines – zinc phosphide – organophosphate).

Severe sweating (salicylate). Blood loss (snake bite – corrosives).

Decreased cardiac contractility ( Cardiac failure), e.g.;• B- blockers• Quinidine & quinidine like action drugs.• Dysrhythmias interfere with cardiac filling.• Scorpion myocarditis.• Substances causing cellular hypoxia (Carbon monoxide –

cyanide – methemoglobinemia). Hypoxia 2 ry to respiratory failure.

5- ECG changes: Heart block (B-blockers, digitalis)Prolonged QRS complex (tricyclic

antidepressant, quinidine).Prolonged QT interval ( neuroleptics –

tricyclic antidepressant – quinolone – organophosphate insecticides – toxin- induced hypocalcaemia)

Ischemic signs ( CO – cyanide – methemoglbinemia – scorpion myocarditis)

All patients should be evaluated with careful neurological examination. Toxins usually produce diffuse non focal manifestations.

1. Conscious status. Grading of coma.2. Orientation: Disorientation to time or distance is

characteristic for cannabis, or sedative overdose.3. Hallucinations: In overdose of; cannabis, LSD, central

anticholinergics, early picture of TCA or alcohol withdrawal.4. Agitation (uncontrollable restlessness or excessive

excitability): Sympathomimetics, anticholinergic, TCA overdose, scorpion sting or sedative hypnotic withdrawal.

5. Convulsions: CNS stimulants overdose (amphetamine, caffeine, atropine,

theophylline, anticholinergics, scorpion sting and cocaine). Strychnine produces stimulation of spinal cord. Indirect causes ( drugs produces hypoxia or hypoglycemia)

6. Tremors: lithium, cabamazipine or phenytoin.7. Fasciculations: organophosphate insecticides

poisoning.8. Numbness: ciguatera fish poisoning.9. Weakness or paralysis: Intermediate syndrome of

organophosphorus poisoning, botulism or cobra envenomation.

10. Hypertonia: sympathomimetics, neuroleptics malignant syndrome or spider sting.

11. Hypotonia: sedative hypnotic or narcotic overdose.12. Deep tendon reflexes.13. Optic Fundus: optic neuritis or atrophy may occur with

methanol toxicity.

1. Absent bowel sounds (adynamic ileus) as in anticholinergic overdose. It is a contraindication for the use of activated charcoal.

2. Epigastric tenderness: may be present with salicylates, NSAID, iron or sympathmimetic drugs overdose. Generalized abdominal tenderness is characteristic of food poisoning gastroenteritis.

3. Right hypochondrial tenderness: Hepatotoxic drugs poisoning as paracetomol, iron or zinc phosphide.

4. Abdominal rigidity: Acute abdomen in corrosive gastric perforation.

5. Determine by palpation if bladder distended or not (urinary retention) that may occur with anticholinergics.

Laboratory studies: Toxicological screening: using patient's urine, blood,

vomitus or gastric wash. Assessment of poison blood levels e.g.; salicylates,

paracetamol, theophylline and lithium. Indirect toxicological assessment:

Pseudocholinesterase ( organophosphate and carbamates insecticides)

Creatinine kinase (rhabdomyolysis).Methemoglobin ( nitrites)Erythrocyte protoporphyrin (EP) (chronic lead poisoning).

Emergency investigations (arterial blood gases, electrolytes, blood sugar, liver and renal function tests, hemoglobin and coagulation profile.

Other investigations: ECG Plain chest X-ray (aspiration pneumonia,

pulmonary edema or endotracheal tube placement)

Plain abdominal X-ray (radiocontrast poisons as iron, phenthiazines), (disk batteries) or (corrosives to exclude gasric perforation).

CT or MRI for coma of unexplained etiology.

A retired man became ill after working 3 hr in his basement workshop. He had been using a commercial paint and varnish remover to strip a piece of furniture. On admission , he complained of chest pain and discomfort. He also brought the can of paint and varnish remover with him. The product contains methylene chloride, the label did indicated that the product should be used in a well-ventilated area.

The attending physician found that the patient had an anterior wall myocardial infarction.

The physician noted the name of the ingredient, but he did not associate the victims symptoms with the use of the product.

The patient returned home 2 weeks later and continued his project. Shortly, he experienced severe chest pains. He was readmitted. This time there was severe myocardial infarction complicated by cardiogenic shock.

Six month later after recovery, the man again attempted to complete his task. Although he worked very slowly and with unnecessary effort, soon collapsed and died.

This illustrated that an uninformed health care provider fail to recognize that methylene chloride is metabolized to carbon monoxide. The resulting carboxyhemoglobin placed considerable stress on patient's CVS. Each subsequent exposure causing increased damage.

The victim could have been warned not to use these products again especially in a closed environment.

A family of five was spending a holiday in a permanently positioned camping trailer.

After the evening meal they complained of nausea, vomiting and abdominal cramping. A physician diagnosed the malady as gastroenteritis. Prochlorperazine for all members was described.

Approximately 30 hr later, a neighboring camper noticed no activity around the area for the past day. He looked inside the window and saw the father slumped on the floor. He called for help.

Three of the family members were dead. Only one small window at the end was opened, near where the father and the mother lay.

The deceased family members had bright pinkish skin. While survivors were unconscious and pale and were hyperventilating when removed from the camper.

Analysis of blood samples from survivors taken 4 hr after removal revealed 30% COHB in the mother and 27 % in the father.

Investigators learned that the heating and cooking were done with propane gas burned in a gas stove. The flue had been altered so that ventilation was poor.

When the family was found, the stove was not lit. Investigator lit it as a test and measured the CO output in the camper. The concentration quickly reached toxic levels.

A female patient of 54-year-old was brought to the hospital with chief complaint of taking large amounts of theophylline and ibuprofen with some alcohol in a suicidal attempt.

The time of ingestion was never established. In the ambulance the patient was alert, blood pressure was 110 mmHg; pulse, 176 beats/min., respirations, 28/min. Five minutes later, systemic blood pressure was 100 mmHg, pulse, 150 beats/min., respiration, 30/min. She vomited once during transport.

On admission, she was lethargic, she was given oxygen and intravenous saline

Lavage of her stomach with normal saline was done until the return was clear.

No pill fragments were seen. Fifty grams of activated charcoal followed by magnesium citrate was given. Then tube was removed.

Serum theophyline concentration was 31.1mg/L; her toxicological screen was negative for ethanol, methanol, isopropanol,salicylate, benzodiazepines, and barbiturates.

Two hours later, BP was 122/66mmHg, pulse 98 beats/min; RR 16/min. she was alert, oriented, and in no distress. She was referred to a psychiatric section of emergency department. While there, she vomited once. One hour later she was discharged.

Her family later reported that she vomited repeatedly for the next 8 hours then suddenly collapsed. Any additional ingestion was denied.

She was in cardiac arrest, when emergency medical staff arrived, and resuscitation was unsuccessful.

At autopsy, patient's serum theophylline was 190mg/L. A white , waxy mass mixed with charcoal and weighing 318.8g was found in her stomach.

Toxicological analysis of the mass revealed a content of 29g theophyline. No additional toxins were found on forensic toxicological screening.

• Take good care of the patientTake good care of the patient• Get a good historyGet a good history• Do a good physical examDo a good physical exam• Use the laboratory appropriatelyUse the laboratory appropriately• Consult with the Poison Control Center.Consult with the Poison Control Center.