In this article we will discuss about:- 1. Introduction to Poisoning 2. Diagnosis of Poisoning 3. Clinical Picture 4. Treatment.
Introduction to Poisoning:
In a study carried out by the authors in NRS Medical College Hospital, Calcutta (1975) it was observed that 469 cases of poisoning cases were admitted in a year, total admission from all causes being 30,287. These 469 cases were due to self-inflicted or accidental poisonings but snake bites were not included.
Although ICU’s are now available in many city hospitals, it is unfortunate that Respiratory care’ units are not available in many hospitals. For proper treatment of poisoned individuals ‘Respiratory support’ is most valuable.
Poisoning may occur due to the following causes:
(1) Accidental
(2) Suicidal or Intentional
The substances that are commonly involved are drugs like phenobarbitone, diazepam, antidepressants, aspirin, salicylates and even iron-salts as well as household substances like paraquet, carbolic acid, detergents, weed killers, rat poisons and sometimes poisonous fruits like berries etc. In Indian villages datura seeds are sometimes used. Children are often victims.
(1) Accidental Poisoning:
It appears that deaths due to suicidal poisoning have increased considerably in last 30 years and women are more often involved. Except in children, many cases which are recorded as accidental may be actually intentional. Such incorrect reporting is often made to save family prestige.
Another type of accidental poisoning may be due to industrial hazards. In the recent Bhopal tragedy in India, thousands of people were affected due to methyl isocyanate gas leak from an Union Carbide Plant (1985).
(2) Intentional Poisoning:
Patients in pathological state of mind of often indulge in self-destruction by committing suicide. Some of these patients do not really want to die but demand sympathy. Therefore they indulge in “self-poisoning” not always to really kill themselves but to threaten their relatives. This is called “para-suicide”. In self-poisoning, the patients may often take positive precautions to ensure that help will be available, although misjudgements may also occur.
Substances and methods used in intentional poisoning:
The easy availability of a number of drugs and chemicals has made this method one of the commonest modes of self-poisoning. Pesticides (e.g. TIC 20 (Sumithien) and corrosive materials (e.g. phenol and carbolic acid) are used very often.
Kerosene is often taken usually by poorer and illiterate class of people. Small children have often consumed kerosene accidently while playing in the kitchen.
Some of the drugs used are:
Morphine, opium, pethidine, methaqualone (Mandrax), tricyclic antidepressants, barbiturates, benzodiazepenes, salicylates, dextropropoxyphene in combination with paracetamol.
Corresives especially acids are also swallowed by emotionally agitated patients especially women.
The methods used for suicide often vary with sex. Females prefer drugs while males seem to indulge in self-injury such as hanging and shooting. Previously when coal-gas lines were available for domestic purposes, this method constituted an important cause in both accidental and intentional poisoning but nowadays also gas cylinders are available. Accidental coal gas poisoning is also possible.
Diagnosis of Poisoning:
Careful history taking environmental clues and clinical findings are the basis of diagnosis. No time should be lost in starting emergency care, whenever possible in an I.C.U. In most cases diagnosis is not difficult if the history and environmental circumstances are carefully taken into account. The poisoned patient may have left a note of his intention to die by taking poison. Be sure to verify his signature.
Poison-consultancy centres are not yet available as in the West. Therefore, .he clinical has to work with lots of practical difficulties. However, much good work can be done in most cases without the accurate knowledge of the poison.
A general practitioner should always refer cases of poisoning or suspected poisoning, to hospitals but unfortunately in our world even hospitals are not available within miles in many villages. So the local practitioner has to give the possible treatment, hence he should be aware of his medico-legal responsibilities.
Treatment consists of the following principles:
(1) Prevention of further absorption of poison:
If the poison has been ingested:
Try to empty the stomach by:
(a) Induction of vomiting,
(b) Gastric lavage.
This should not be done in corrosive poisoning if patient comes several hours after ingestion of poison.
(2) Minimising gastrointestinal absorption:
Neutralisation and precipitation for acids or alkalies with water, milk or a neutralizer (use of aluminium hydroxide, milk of magnesia or dilute vinegar depending on the case).
Absorption by powered activated charcoal may be helpful. Give 20 to 30 g. of charcoal or 15 to 20 ml of sorbitol it helps elimination of digoxin, pheno barbitone and theophylline.
(3) Catharsis:
Sodium sulphate in 10 to 30 g dosage is cathartic. But cathartics are contraindicated after ingestion of corrosives.
Poisoning by other routes:
If the poison has been inhaled — remove the patient to fresh air and assist ventilation. Skin contact-wash with water and soap.
No time should be lost in starting immediate emergency care, if possible in an I.C.U. In many cases diagnosis can be made if the history and environmental evidences are taken into account.
Some poisons have definite diagnostic clues as follows:
Morphine or opium — pinpoint pupil, slow and deep respiration.
Coal gas — Circumstances and its smell give clue at once.
Methaqualone (Mandrax) — Exaggerated reflexes, myoclonus and hypertonic limbs.
Tricyclic compounds (used in Psychiatry) — may cause coma presenting with dilated pupils, pyramidal signs, even cardiac arrhythmias.
Corrosive poisons — (Corrosive burnmarks can be seen in skin tongue and oral mucosa.
Clinical Picture of Poisoning:
Respiration depression:
Note if the patient is maintaining his own airway and ventilation. Respiratory depression from sleeping pills is less hazardous and resuscitation is more effective, as the B.M.R. is lowered in barbiturate poisoning and so permanent brain damage is less likely.
Cyanosis:
If cyanosis is present administer oxygen and note its effect.
Gag-Reflex:
Good gag-response is invariably coupled with the functioning pharyngeal reflexes. Minute volume (MV) — A Wright’s respirometer is used to measure minute volume (MV). If MV is satisfactory and the rate of respiration is around 16 to 18 per minute, ventilatory exchange is considered adequate. If in doubt measure arterial carbon dioxide (PCO2) and oxygen tensions (PO2) wherever possible. Normal values are PCO2 = 40 mm Hg. PO2 = 100 mm Hg.
Shock:
Clinical Appearance:
A warm pink patient with full veins indicates adequate tissue perfusion. Urine flow should be at least 30 ml per hour.
Monitoring of pulse rate — rate and depth of respiration, relationship of skin (surface) to rectal (core) temperature and acid base balance are to be noted.
Blood Pressure:
Should the systolic fall below 90 mm Hg, it is worth administering a plasma expander.
Hypothermia:
Rectal temperature below 36° C indicates a significant degree of hypothermia.
Identification of Poison:
Samples of gastric lavage, blood, urine and vomitus should be sent to the nearby Forensic Laboratory or the Regional Poisons Centre for analysis which is a must for medico-legal purposes. However, in developing countries even in large cities poison consultancy centres are not available.
Removal of absorbed poisons from the body:
Detoxification:
Enzyme induction — Certain enzymes act as cholinesterase reactivators e.g. Pralidoxime in insecticide poisoning.
Biliary Excretion:
Interruption of enterohepatic circulation.
Urinary Excretion:
Forced diuresis by administering osmotic diuretics such as mannitol or urea.
Mannitol 10 to 20 g/hr. Urea 25 to 50 gm. loading dose may increase the urinary output by one litre/hr.
Frusemide 40 mg I-V administration further increases the flow. Osmotic diuretics should not be used in presence of congestive heart failure, shock or renal failure. Forced diuresis has a beneficial effect in salicylate, barbiturate, meprobamate and glutethimide poisoning.
This method is potentially applicable to all unfiltered poisons which are passively reabsorbed.
Alteration of pH — increases renal clearance of some poisons.
Dialysis:
Peritoneal dialysis, hemodialysis, charcoal or resin haemoperfusion, exchange transfusion, as well as chelation or chemical binding are all practised. However, both peritoneal and haemodialysis are very useful in suitable cases.
Administration of Systemic Antidotes:
Chemical Agents:
Chemicals combine with toxic substance and thus reduce the concentration of the toxic substance e.g. ethylene diamine tetra-acetate with lead and dimercaprol with mercury.
Pharmacologic Antagonists:
Other systemic antidotes complete with the poison for the receptor site. e.g. Atropine with muscarine
Nallorphine and Naloxone with morphine
Vitamin K with coumarine.
Supportive Therapy:
Most chemical poisonings are reversible, self-limited diseased state. Skilful supportive therapy can keep seriously ill patients alive, detoxifying & keeping excretory functions active till the concentration of toxic agent has fallen to a safe level.
As mentioned already very few poisons have specific antidotes and it is the supportive therapy which brings them back to life.
Central Nervous System Depression:
This may result in coma but if the patient is given meticulous nursing care and is kept under close observation he will emerge from the state of unconsciousness as if from prolonged anaesthesia. Depression of medullary centre may result in respiratory and circulatory failure and this has got to be supported by chemical and mechanical means.
The use of analeptics in the treatment of poison induced central nervous system depression has been largely abandoned for the following reasons:
(1) Their effect is unpredictable and their use in intoxicated patient produces an abnormal pattern of nervous activity in which paroxysmal excitation and convulsions may be superimposed on depression.
(2) The availability of artificial ventilation and of effective measures to support the circulation has lessened the need of rapid restoration of normal medullary function.
(3) Picrotoxin and bemegride are analeptics which were commonly used in the past.
It is doubtful that analeptics shorten the duration of coma sufficiently to justify their risks, and they have not been shown to improve prognosis.
If central venous pressure is low, fluid replacement is the first therapeutic approach.
In shock resulting from central depressions vasoactive drugs are helpful. Intravenous hydrocortisone or dopamine drips may be helpful. In spite of certain disadvantages (e.g. vasoconstriction) I.V. mephentermine drip 300 mg in 5% glucose may tide over hypotensive crises, especially if dopamine is not available.
Most of the complications of poisonings are due to:
(1) Hypoxia
(2) Hypoglycaemia
(3) Metabolic disturbances.
Hypoxia may be due to lack of proper pulmonary ventilation and inadequate ventilation causes of the following:
(1) Central respiratory depression
(2) Muscular paralysis
(3) Airway obstruction
(4) Retained secretions
(5) Laryngeal oedema and
(6) Bronchospasm,
Alveolar-capillary diffusion may be impaired by e.g. pulmonary oedema.
Interference with oxygen transport may be due to:
(1) Anaemia
(2) Methemoglobinemia
(3) Carboxyhaemoglobinemia
(4) Shock.
Inhibition of cellular oxidation occurs in continued hypoxia:
(1) Cyanide poisoning
(2) Fluroacetate poisoning
(3) General protoplasmic poisons
Maintenance of an adequate airway is a must which may require frequent use of suction apparatus and insertion of an oropharyngeal airway or endotracheal tube or tracheostomy.
The following emergency equipment should be always available:
(1) Laryngoscope
(2) Cuffed endotracheal tubes
(3) Ambu bag or positive pressure breathing machine
(4) A portable mechanically or electrically operated suction machine to remove pulmonary secretions, foreign body, etc. from the upper respiratory tract.
If the patient does not breathe after the airway has been established, a positive pressure breathing (PPB) is to be utilised. A cuffed tube is desirable so that positive pressure breathing (PPB) may be accomplished if needed. The cuffed tube prevents aspiration of fluids into the lungs of an unconscious patient.
When insertion of endotracheal tube is difficult, tracheostomy may be done. In desperate emergency the trans-tracheal intubation is essential.
Transtracheal Resuscitation:
Insertion of an oxygen carrying needle into the tracheal lumen may prevent respiratory death. Hypoxaemia of arterial blood may be normalised or alleviated within minutes by this technique. However, oxygen by this route will be effective only when there is some respiratory effort by the patient. Oxygen used should be humidified.
Needle is inserted through cricothyroid membrane or by cutting a point in the trachea 2 to 3 cm. below the larynx.
Patients on artificial ventilation require careful attention to endotracheal tube. Dilute (8.4%) sodium bicarbonate is instilled into the tube to wash out the secretions if required.
Administration of high concentration of oxygen is indicated whenever tissue hypoxia occurs. When central nervous system is severely depressed oxygen administration often results in apnoea and must be combined with artificial ventilation. Hyperbaric oxygen may be helpful in some situation. The treatment of methemoglobinemia, carboxyhemoglobinemia and inhibition of cellular oxidation is discussed under the specific poisons.
Cardiac Arrhythmias:
Disturbances of cardiac impulse generation or conduction in the poisoned patient arise from the effects of certain poisons on the conductivity or due to myocardial hypoxia or metabolic disturbances. Both hypoxia and metabolic disturbances should be connected and antiarrhythmic agents administered as indicated by the nature of arrhythmia.
Pulmonary oedema-may be caused due to:
1. Depressed myocardial contractility
2. Alveolar injury from irritant gases or aspirated fluids.
This may be associated with laryngeal oedema action
(1) Suction- Clear airway
(2) O2-4L to 5L/min may raise the O2 saturation of blood. Positive pressure ventilation may be essential if the clinical state and blood gas indicates so.
(3) Aerosols of surface active agents.
(4) Bronchodilators
(5) Adrenocortical steroids
(6) Heavy doses of frusemide IM/IV
Acute Renal Insufficiency:
Oliguria and anuria as a result of renal failure may occur in poisoned patient because of:
(1) Shock
(2) Dehydration or electrolyte disturbances
(3) Nephrotoxic poisons e.g. mercury, phosphorus, carbon tetrachloride and bromate.
Treatment of Poisoning:
(1) Correction of electrolyte disturbances
(2) Fluid administration to treat shock and combat the dehydration, electrolyte and water disturbances.
Imbalances of fluid and electrolytes are common features of chemical poisoning.
They are the result of:
(1) Vomiting
(2) Diarrhoea
(3) Renal insufficiency
(4) Therapeutic manoeuvres such as catharsis, forced diuresis or dialysis.