Poisoning

Drug overdose(Poisoning)

Dr Hayder Hadi AlMusawi

Drug Overdose

It is the ingestion or application of a drug or other substance in a quantity greater than that recommended or generally practiced.
An overdose may result in a toxic state or death.
The word "overdose" implies that there is a common safe dosage and usage for the drug; therefore, the term is commonly only applied to drugs, not poisons.

Salicylate overdose(poisoning)

Aspirin is the trade name for acetylsalicylic acid.
It is the oldest known analgesic and antipyretic with anti inflammatory properties and anti platelet functions.
Mild (150 mg/kg), Moderate (150–300 mg/kg), and Severe (300–500 mg/kg).
Either acute or chronic.






Pathophysiology & Clinical Features
Phase I: Characterized by hyperventilation resulting from direct respiratory center stimulation, leading to respiratory alkalosis and compensatory alkaline-uria.. This phase may last as long as 12 hours.
Phase II: Characterized by paradoxic aciduria, with continued respiratory alkalosis. This phase may begin within hours and may last 12–24 hours.
Phase III: Characterized by dehydration, hypokalemia, and progressive metabolic acidosis. This phase may begin 4–6 hours after ingestion in a young infant or 24 hours or more after ingestion in an adolescent or adult.

Diagnosis

History of overdose aspirin containing drug ingestion.
measurement of plasma salicylate, the active metabolite of aspirin.

Treatment

Immediate hospital admission & poison center notification.
Activated charcoal, which adsorbs the aspirin in GIT.
whole bowel irrigation (WBI), with laxatives.
Gastric lavage, if ingestion has occurred less than 1 hr.
Vomiting induction & ipecac syrup, have no role.

Intravenous fluids containing dextrose, are recommended to keep a good urine output.

Alkalinization of urine, Sodium bicarbonate is given in a significant aspirin overdose regardless of the serum pH, as it enhances elimination of aspirin in the urine.
No specific antidote.
Hemodialysis, can be used to enhance the removal of salicylate from the blood.


Indications of hemodialysis:
significant neurotoxicity (agitation, coma, and convulsions).
Renal failure.
Pulmonary edema.
Cardiovascular instability.

Lead poisoning

It is also called plumbism or painter`s colic.
Lead is a very strong poison, either through swallowing or inhalation.
sources, such as: gasoline, house paints, toys and storage batteries.
Acute poisoning may require emergency measures with sever symptoms.
Chronic exposure may have an insidious onset with no evident symptoms early.

symptoms

Abdominal pain and cramping (usually the first sign of a high, toxic dose of lead poison)
Aggressive behavior
Constipation
Anemia
Irritability
Loss of previous developmental skills
Signs of renal failure.


Diagnosis
History of exposure may not be evident.
Blood lead level, higher than 10 µg/dL.
CBC, hypochromic microcytic anemia with basophilic RBC stippling.
Erythrocyte protoporphyrin, increased.
X- ray: lead lines (hyperdense) at the metaphysis of long bones of a growing child, especially at the knees. OR:Abdominal x-ray may reveal lead-containing foreign materials such as paint chips in the gastrointestinal tract.
Fecal lead content over a few days to estimate the overall amount of childhood lead intake.

Treatment

The mainstay of treatment is the removal of lead source (prevention).
Chelation therapy, for high blood levels.
Treatment of associated iron, calcium, and zinc deficiencies.
When lead-containing materials are present in the gastrointestinal tract (as evidenced by abdominal X-rays), whole bowel irrigation, endoscopy, or even surgical removal may be needed.

If lead encephalopathy is present, anticonvulsants may be given with corticosteroids and mannitol.
Chelation therapy, to excrete lead in urine with a very high rate, such as:
Edetate calcium disodium

Indications of Chelation:

Acute poisoning.
Sever poisoning.
Lead encephalopathy.


Prognosis
Outcome is related to the extent and duration of lead exposure.
Effects of lead on the physiology of the kidneys and blood are generally reversible; its effects on the central nervous system are not.

Kerosin Poisoning

Kerosin is belonged to Hydrocarbons, a group of substances that contain only hydrogen and carbon.
It is a fuel used for heating and cooking.
Mechanism of poisoning:
• Swallowing.
• Inhalation.
• Direct skin absorption.

Clinical Features

Airways and lungs:
• Dyspnea (from inhalation)
• Throat swelling (may also cause breathing difficulty)
• Eyes, ears, nose, and throat:
• Pain
• Vision loss

Clinical Features

Gastrointestinal system:
• Abdominal pain
• Bloody stools
• Vomiting, possibly hematemesis.
Heart and blood:
• Collapse
• Hypotention -- develops rapidly


Clinical Features
Nervous system:
• Convulsions
• Disturbed level of consciousness.
Skin:
• Burns
• Irritation

Diagnosis

Chest radiography :
A chest radiograph must be obtained in all symptomatic patients.
Initially, the chest radiographic results may be normal, but positive findings may develop over the first few hours after ingestion
Common findings include :
• fine perihilar opacities.
• bibasilar infiltrates.
• atelectasis.

Diagnosis

If discharge is being considered for an asymptomatic patient, a chest radiograph should be obtained 6 hours after the ingestion to document the negative findings.
Blood gas analysis :
To detect hypoxemia.


Treatment
ABC.
Take all precautions to minimize the patient's risk of vomiting and further aspiration.
A trial of bronchodilators may prove useful in patients with suspected bronchospasm.
Cutaneous decontamination in cases of cutaneous exposure.
Gastric decontamination : by ipecac syrup or gastric lavage), it is only indicated in :
• Large ingestions.
• Increased risk of systemic toxicity.

Treatment

I/V fluid in maintenance doses.
Antipyretics.
No specific antidotes are available for hydrocarbon poisoning. Treatment with corticosteroids and prophylactic antibiotics is not beneficial.

Complications

Pulmonary :
Aspiration pneumonitis and Pneumothorax.
CNS :
seizures, encephalopathy, and memory loss.
CVS :
myocarditis and cardiomyopathy.


Iron Toxicity
It is a common toxicologic emergency in young children, due to the availability of iron tablets and their candylike appearance.
Children may show signs of toxicity with ingestions of 10-20 mg/kg of elemental iron.
Serious toxicity is likely with ingestions of more than 60 mg/kg of elemental iron.
Ferrous gluconate : 12% elemental iron.
Ferrous sulfate : 20%.
Ferrous fumarate : 33%.

Pathophysiology & Clinical Features

Phase 1 :
initial toxicity, predominantly manifests as GI effects. This phase begins during the first 6 hours postingestion and is associated with hemorrhagic vomiting, diarrhea, and abdominal pain.
Phase 2 :
is known as the latent phase and typically occurs 4-12 hours postingestion. It is usually associated with an improvement in symptoms.

Phase 3 :

begins within 12-24 hours postingestion, characterized by multisystem damage,hypovolemic shock, fits and acidosis with impaired cardiac function.
Phase 4 :
occur 2-3 days postingestion, characterized by liver injury and failure.
Phase 5 :
occurs 2-6 weeks postingestion and is characterized by late scarring of the GI tract, which causes pyloric obstruction or hepatic cirrhosis.


Treatment
Supportive care, with particular attention paid to fluid balance and cardiovascular stabilization.
Ipecac-induced emesis & gastric lavage are not recommended, while Whole Bowl Irrigation (WBI) with laxatives has a limited value.
Desferrioxamine (Desferal) by I/V infusion is the iron-chelating agent of choice.
Surgery for GIT perforation, bleeding or obstruction.

Complications

• Infectious -Yersinia enterocolitica septicemia, so pay attention for :
Abdominal pain.
Diarrhea.
Fever.
• Pulmonary - Acute respiratory distress syndrome (ARDS).
• Gastrointestinal - Fulminant hepatic failure, hepatic cirrhosis, pyloric or duodenal stenosis.

Organophosphate poisoning

one of the most common causes of poisoning worldwide.
usually results from exposure to insecticides or nerve gases..
The primary mechanism of action is inhibition of carboxyl ester hydrolases, particularly acetylcholinesterase (AChE).
ACh is found in the central and peripheral nervous system, neuromuscular junctions, and red blood cells (RBCs).


Clinical presentation
Divided into 3 major categories:
• Muscarinic effects:
SLUDGE (salivation, lacrimation, urination, diarrhea, GI upset, emesis) .
DUMBELS (diaphoresis and diarrhea; urination; miosis; bradycardia, bronchospasm, bronchorrhea; emesis; excess lacrimation; and salivation) .

2. Nicotinic effects:

muscle fasciculations, cramping, weakness, and diaphragmatic failure.
Autonomic nicotinic effects include hypertension, tachycardia, mydriasis, and pallor.
3. CNS effects: most common in pediatrics, such as:
Anxiety
Emotional lability
Restlessness
Confusion
Ataxia
Tremors
Seizures
Coma

Paralysis: 3 types;

A. Acute.
B. Intermediate:
develop 24-96 hours after resolution of acute organophosphate poisoning symptoms.
persists for 4-18 days, and may include respiratory muscles paralysis.
C. delayed polyneuropathy:
occurs 2-3 weeks after exposure to large doses.
Recovery can take up to 12 months


Diagnosis
Organophosphate (OP) toxicity is a clinical diagnosis.
Red blood cell (RBC), which is the best, and plasma (pseudo) cholinesterase (PChE) levels can both be used to confirm the diagnosis.

Treatment

ABC.
Decontamination: Remove all clothing and gently cleanse patients with soap and water.
Drugs: like atropine (as muscarinic antidote) , pralidoxime, glycopyrrolate, and benzodiazepines (eg, diazepam).