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PARACETAMOL POISONING: Hepatic damage: more than 150mg per kg Clinical feature : Nausea, vomiting, abdominal discomfort In untreated patient`s developing.

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Presentation on theme: "PARACETAMOL POISONING: Hepatic damage: more than 150mg per kg Clinical feature : Nausea, vomiting, abdominal discomfort In untreated patient`s developing."— Presentation transcript:

1 PARACETAMOL POISONING: Hepatic damage: more than 150mg per kg Clinical feature : Nausea, vomiting, abdominal discomfort In untreated patient`s developing liver damage, vomiting continues beyond 12 hrs and there is tenderness over the liver, jaundice,hepatic encephalopathy, loin pain, haematuria, proteinuria suggest renal failure. Investigation :LFTs, liver enzyme,INR(international normalised ratio)

2 Management : Paracetamol antidotes: Acetylcysteine :is given by iv infusion in 5 % dextrose. Initial dose :150mg per kg body weight in 200 ml dextrose over 15 mins, Than 50 mg per kg in 500 ml over 4 hrs, Then 100 mg per kg in 1L over 16 hrs Methionine :if acetylecysteine is not available 2.5g every 4 hrs to a total of 10 g.

3 IRON POISONING: Serious toxicity: more than 60 mgper kg body weight, Lethal dose :150-300 mg per kg. C / F: Nausea, vomiting, diarrhoea, abdominal pain Severe poisoning : haematemesis, drowsiness, convulsion, coma metabolic acidosis and shock

4 Management: Check serum iron,FBC,glucose Gastric lavage if more than 20 mg iron per kg body weight Use supportive measures if required In serious : Desferrioxamine : iv infusion (15 mg per kg per hr, max 80 mg per kg in 24 hr)

5 Salicylate poisoning(Aspirin): Mild toxicity :150mg per kg body weight Severe and fatal dose :500 mg per kg body weight

6 Clinical features Acid-base status :- Stimulate the respiratory center, leading to hyperventilation and respiratory alkalosis Interfere with the Krebs cycle, limit production of ATP, and increase lactate production, leading to ketosis and metabolic acidosis Respiratory system effects : - Causes stimulation of respiration level of 35 mg/dL or higher causes increases in both rate (tachypnea) and depth (hyperpnea) Glucose metabolism : - Hypoglycemia (increased cellular metabolic activity)

7 Cont.. Fluid and electrolyte effects : - dehydration because of increased GI tract losses (vomiting) and insensible fluid losses (hyperpnea and hyperthermia). Renal clearance of salicylate is decreased by dehydration. CNS effects : - Salicylates are neurotoxic, which manifests as tinnitus, and ingestion can lead to hearing loss at doses of 20-45 mg/dL or higher. CNS toxicity is related to the amount of drug bound to CNS tissue. Other signs and symptoms include nausea, vomiting, hyperpnea, and lethargy, which can progress to disorientation, seizures, cerebral edema, hyperthermia, coma, and, eventually, death.

8 Cont.. GI tract effects : - Nausea and vomiting are the most common effects. Hepatic effects : - Hepatitis Reye syndrome (characterized by nausea, vomiting, hypoglycemia, elevated levels of liver enzymes and ammonia, fatty infiltration of the liver, increased intracranial pressure, and coma)

9 Cont.. Hematologic effects : - Hypoprothrombinemia and platelet dysfunction are the most common effects. Bleeding (either by inhibition of vitamin K– dependent enzymes or by the formation of thromboxane A2). Musculoskeletal effects : - Rhabdomyolysis can occur because of dissipation of heat and energy resulting from oxidative phosphorylation uncoupling.

10 Management Gastric lavage Mild poisoning : plasma salicylate less than 350 mg per L than increase oral fluids Moderate : more than 350 mg per L than IV fluids to correct dehydration, sodium bicarbonate 1.26% alkalinises the urine Severe : haemodialysis.

11 KEROSENE OIL POISONING: SERIOUS PAEDIATRIC PROBLEM IN DEVELOPING COUNTRY. C / F : age between 1 and 3 years of age, common symptoms: chemical pneumonitis, fever, cough, breathlessness, abdominal distention Rarely : Convulsion, Coma,cyanosis Radiological changes: right basal infiltrates. Emphysema,pleural effusion and pneumatoceles have also been observed.

12 Management: Supportive and symptomatic : Gastric lavage :if amount ingested is massive (within 30 mins of ingestion) Oxygen if respiratory involvement Antibiotic Observation for at least 24 hrs is essential even in an asymptomatic child

13 DROWING AND NEAR DROWING: DROWING : when the victim dies NEAR DROWING :when submersion victim survives WET DROWING :aspiration of fluid into lungs C / F: Respiratory distress Cyanosis Hypothermia Coma Respiratory faliure Apnea

14 Treatment: Initial resuscitation Basic life support Diuretics (pulmonary oedema) Sodium bicarbonate (correct metabolic acidosis) Diazepam (convulsion) Adequate warming (hypothermia)

15 LEAD POISONING: TREATMENT : Symptomatic children :dimercaprol (BAL),calcium disodium edetate

16 BURNS: TREATMENT : describe under three heading Treatment of shock: General treatment : Local treatment of burn wound: TREATMENT OF SHOCK : sedative and analgesic, fluid resuscitation maintenance of airway

17 GENERAL TREATMENT : Fasciotomy Tetanus prophylaxis Antibiotics Nutritional support Gastric decompression Treatment of G.I. complication LOCAL TREATMENT : First-aid measures Burn wound care (exposure and closed method) Skin grafting Physcial therapy and rehabilitation


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