General Management of Poisoning
General Management of Poisoning
1, 2 Clinical Toxicology
Stabilizations
Symptoms of airway obstruction include dyspnoea, air hunger, and hoarseness. Signs comprise
stridor, intercostal and substernal retractions, cyanosis, sweating, and tachypnoea.
Normal oxygen delivery requires adequate haemoglobin oxygen saturation, adequate haemoglobin
levels, normal oxygen unloading mechanisms, and an adequate cardiac output. Increasing
metabolic acidosis in the presence of a normal PaO2 suggests a toxin or condition that either
decreases oxygen carrying capacity (e.g. carbon monoxide, methaemoglobinaemia), or reduces
tissue oxygen (e.g. cyanide, hydrogen sulfide).
Some drugs stimulate the respiratory center: amphetamines, atropine, cocaine, and salicylates.
Some drugs are associated with non-cardiogenic pulmonary oedema, characterized by severe
hypoxaemia, bilateral infiltrates on chest X-ray, and normal pulmonary capillary wedge pressure.
Some drugs cause or exacerbate asthma. The most important among them include NSAIDs,
antibiotics like penicillins, cephalosporins, tetracycline, and nitrofurantoin, cholinergic drugs,
chemotherapeutic drugs, and some diuretics.
Several drugs produce changes in pulse rate and blood pressure, while others induce cardiac
arrhythmias and heart block.
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Dr. Ahmed Sudan Alhusseini Lec. 1, 2 Clinical Toxicology
There are numerous causes for coma of which one of the most important is acute poisoning. A
number of substances can induce coma, and it will require a great deal of astuteness and expertise
to pinpoint the poison. Before proceeding to an elaborate exercise in diagnosis however, it may be
desirable to first ascertain for sure that the patient is really comatose and not just pretending
(psychogenic or hysterical coma). This is often encountered in cases of “suicide gesture” in contrast
to “attempted suicide”.
How does the doctor humanely determine whether the coma is true or fake? Several methods have
been recommended of which the following constitute barbaric acts and must never be employed:
Management
Respiratory insufficiency: Oxygen therapy is done to raise the PaO2 to at least 45–55 mmHg.
Begin with 28% oxygen mask. Depending on the response as assessed by periodic arterial gas
analysis, either continues with 28% or progress to 35%. If the condition is relentlessly
deteriorating, consider assisted ventilation.
Circulatory Failure:
Correct acidaemia, if present.
Elevate foot end of the bed (Trendelenberg position).
Insert a large bore peripheral IV line (16 gauge or
larger), and administer a fluid challenge of 200 ml of
saline (10 ml/kg in children). Observe for
improvement in blood pressure over minutes. Repeat
the fluid bolus if BP fails to normalize and assess for signs of fluid overload.
Haemodynamic monitoring should be considered in those adult patients who do not
respond to 2 liters of infusion and short-term low-dose vasopressors such as dopamine
and noradrenaline.
Obtain an ECG in hypotensive patients and note rate ,rhythm, arrhythmias, and
conduction delays.
Vasopressors of choice include dopamine and norepinephrine.
Cardiac Arrhythmias:
Obtain an ECG, institute continuous cardiac monitoring and administer oxygen.
Evaluate for hypoxia, acidosis, and electrolyte disturbances )especially hypokalaemia,
hypocalcaemia, and hypomagnesaemia(.
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Dr. Ahmed Sudan Alhusseini Lec. 1, 2 Clinical Toxicology
Lignocaine and amiodarone are generally first line agents for stable monomorphic
ventricular tachycardia, particularly in patients with underlying impaired cardiac function.
Sotalol is an alternative for stable monomorphic ventricular tachycardia. Amiodarone and
sotalol should be used with caution if a substance that prolongs the QT interval and/or
causes torsades de pointes is involved in the overdose.
Unstable rhythms require cardioversion.
Atropine may be used when severe bradycardia is present.
CNS Depression:- It was recommended that in every case where the identity of the poison was
not known, the following three antidotes (called the Coma Cocktail) must be administered
intravenously:
1. Dextrose—100 ml of 50% solution
2. Thiamine (Vitamin B1)—100 mg
3. Naloxone—2 mg
Evaluation
A. Hypothermia
Some common drugs which produce hypothermia are barbiturates, benzodiazepines, opiates and
antidepressants. It is essential to use a low reading rectal thermometer. Electronic thermometers
with flexible probes are best which can also be used to record the esophageal and bladder
temperatures.
Treatment (Rewarming):
For mild cases, a warm water bath (46o C) is sufficient until the core temperature rises to
34o C, when the patient is placed in a bed with warm blankets.
Heating the inspired air is recommended by some as very effective in raising the core
temperature.
B. Hyperthermia
Oral temperature above 39o C is referred to as hyperthermia. If it exceeds 41o C (which is very rare),
there is imminent danger of encephalopathy. In a few individuals there is a genetic susceptibility to
hyperthermia, especially on exposure to skeletal muscle relaxants, inhalation anaesthetics, and
even local anaesthetics—malignant hyperthermia. This should be distinguished from neuroleptic
malignant syndrome, which is also characterized by high fever apart from other neurological signs,
but is the result of adverse reaction to antipsychotic or neuroleptic drugs, and has no genetic basis.
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Dr. Ahmed Sudan Alhusseini Lec. 1, 2 Clinical Toxicology
Treatment
Remove all clothes, and pack the neck and groin with ice.
Immersion in cold water bath (25oC) is very effective but dangerous in the elderly and in
heart patients.
Stop cooling measures when core temperature falls below 39oC, and nurse the patient in
bed in a cool room.
Administration of dantrolene may be beneficial in some cases.
Do not use antipyretic drugs like paracetamol. They are ineffective.
C. Acid-Base Disorders
The diagnosis of these acid-base disorders is based on arterial blood gas, pH, and PaCO2,
bicarbonate, and serum electrolyte disturbances. It must be first determined as to which
abnormalities are primary and which are compensatory, based on the PH. If the pH is less than 7.40,
respiratory or metabolic alkalosis is primary.
In the case of metabolic acidosis, it is necessary to calculate the anion gap. The anion gap is
calculated as follows:
If the anion gap is greater than 20 mmol/L, a metabolic acidosis is present regardless of the pH or
serum bicarbonate concentration.
The drug of choice is sodium bicarbonate. It is widely considered to be the best antidote for acidosis
of almost any aetiology.
D. Agitation
Several drugs and poisons are associated with increased aggression which may sometimes progress
to psychosis and violent behavior. This is especially likely if there are other predisposing factors
such as existing mental disorder, hypoglycaemia, hypoxia, head injury, and even anaemia and
vitamin deficiencies.
Delirium is the term which is often used to denote such acute psychotic episodes, and is
characterized by disorientation, irrational fears, hyper-excitability, hallucinations, and violence.
Dementia refers to a more gradual decline in mental processes mainly resulting in confusion and
memory loss, and though it is often organic in nature due to degenerative diseases, there are some
drugs which can cause this especially on chronic exposure. Elderly patients are more vulnerable.
Dementia due to drugs is usually reversible.
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Dr. Ahmed Sudan Alhusseini Lec. 1, 2 Clinical Toxicology
Decontamination
EYE
GUT
The various methods of poison removal from the gastrointestinal tract include:
a. Emesis
b. Gastric lavage
c. Catharsis
d. Activated charcoal
e. Whole bowel irrigation.
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Dr. Ahmed Sudan Alhusseini Lec. 1, 2 Clinical Toxicology
Lavage should be considered only if a patient has ingested a life-threatening amount of a poison
and presents to the hospital within 1 to 2 hours of ingestion. Some authorities still recommend
lavage up to 6 to 12 hours post-ingestion in the case of salicylates, tricyclics, carbamazepine, and
barbiturates.
Contra-indications:
Complications:-
Aspiration pneumonia.
Laryngospasm.
Sinus bradycardia and ST elevation on the ECG.
Perforation of stomach or oesophagus (rare).
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Dr. Ahmed Sudan Alhusseini Lec. 1, 2 Clinical Toxicology
Activated charcoal is a fine, black, odourless, tasteless powder made from burning wood, coconut
shell, bone, sucrose, or rice starch, followed by treatment with an activating agent (steam, carbon
dioxide, etc.). The resulting particles are extremely small, but have an extremely large surface area.
Mode of action: - Decreases the absorption of various poisons by adsorbing them on to its surface.
Activated charcoal is effective to varying extent, depending on the nature of substance ingested.
Disadvantages:-
Unpleasant taste
Provocation of vomiting
Constipation/diarrhoea
Pulmonary aspiration
Intestinal obstruction (especially with multiple-dose activated charcoal).
Contraindications:-
This is a method that is being increasingly recommended for late presenting overdoses when
several hours have elapsed since ingestion. It involves the
instillation of large volumes of a suitable solution into the
stomach in a nasogastric tube over a period of 2 to 6 hours
producing voluminous diarrhea. Previously, saline was
recommended for the procedure but it resulted in
electrolyte and fluid imbalance. Today, special solutions
are used such as PEG-ELS (i.e. polyethylene glycol and
electrolytes lavage solution combined together, which is an
isosmolar electrolyte solution), and PEG-3350 (high
molecular weight polyethylene glycol) which are safe and
efficacious, without producing any significant changes in
serum electrolytes, serum osmolality, body weight, or haematocrit.
Indications:-
Ingestion of large amounts of toxic drugs in patients presenting late ( > 4 hours post-exposure)
Overdose with sustained-release preparations.
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Dr. Ahmed Sudan Alhusseini Lec. 1, 2 Clinical Toxicology
Complications—
Vomiting
Abdominal distension and cramps
Anal irritation.
Contra-indications—