Poisoning in children
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Poisoning in children
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Poisoning in children
- 9. SYMPTOMATOLOGY IMPORTANT CAUSES 1. ODOR Kerosene, Organophosphorous, camphor etc 2. SWEATING Organophosphorous, acetaminophen, atropine 3. HYPERTHERMIA HYPOTHERMIA Salicylates, kerosene, anticholinergics Barbiturates, Phenothiazines 4. DELIRIUM Dhatura, salicylates, barbiturates 5. CONVULSIONS Organophosphorous, phenol, kerosene, phenothiazines,
- 10. 6. MIOSIS Opiates, OP, cholinergics, phenothiazines, sedative hypnotics 7. MYDRIASIS Atropine, anti histamines, sympathomimetic agents 8. NYSTAGMUS 9. TACHYCARDIA Sedative hypnotics, anticonvulsants, alcohol Atropine, theophylline 9. BRADYCARDIA Digitalis, beta blockers, OP, sedative hypnotics 10. RESPIRATORY CHANGES Hyperventilation in salicylates, CO ; depression in barbiturates, OP ; distress in kerosene
- 11. FINDING ADRENERGIC ANTICHOLINERGIC ANTI CHOLINESTERASE OPIOD HR Increased Increased Decreased Decreased Temp Increased Increased No change No change Pupils Dilated Dilated Constricted Constricte d Mucosa Wet Dry Wet No change Skin Diaphoresis Dry Diaphoresis Normal
Notas del editor
- Irrespective of the substance ingested, initial management is identical
- Vital signs, mental status, pupils, skin, bowel sounds and odors – these finding my suggest a toxidrome that can help in identifying a poison. OP – garlic smell Sweating- acetaminophen – increased, atropine - decreased
- Hypotension – Beta blockers, Iron,, narcotics, sedative hypnotics Hypertension – Anticholinergics, sympathomimetics
- Constellation of signs and symptoms that help to classify a patient into a category for toxin identification
- Hyperkalemia – Potassium, digoxin Hypokalemia – Diuretics, theophylline ECG – Wide QRS – tricyclic anti depressants, diphenhydramine,
- Once the child is in the hospital, the aim is to – prevent further absorption, enhance elimination, administer antidote and prevent re exposure GI – if the ingested poison is non toxic, the amount is small and child is asymptomatic, no evacuation is required. Cathartics / purgatives – accelerated defecation Laxatives – accelerated defecation – sorbitol, mgso4, mg citrate
- WBI – adverse effects – vomiting, abdominal pain, abdominal distension
- THESE MEASURES are indicated only in patients where the recovery would be otherwise unlikely Diuresis – for drugs that are excreted primarily through renal route
- G I absorption seen in benzene, turpentine, carbon tetrachloride
- 1 – perihilar opacities 2- bibasal infiltrations
- Those who are asymptomatic at 6 hours but shows doubtful cxr – observe for more than 1 day
- In an intubated patients – control of bronchial secretions is a useful sign ATROPINE – HIGHLY EFFECTIVE IN COUNTER ACTING MUSCARINIC SYMPTOMS. It does not reverse peripheral muscular action which is a nicotinic action PAM – oxime end reacts with the phosphorous atom attached to the esteratic site – oxime phosphonate so formed diffuses away leaving the reactivated cholinesterase.
- DDT – dichloro diphenyl trichloro ethane – spray in the houses against malaria GBH – scabies and lice infestation
- Adult - >10gram
- NAC – Enhances glutathione stores, provides glutathione substitute and provides non toxic sulphate conjugation of paracetamol in the liver
- Rumack Mathew normogram – plasma coc of acetaminophen vs time after ingestion. If AST is normal and apap level is known and the ingestion is within 24 hours , then treatment decisions are based on where the apap level falls in this normogram If AST becomes elevated then the patient moves into the next category of treatment – hepatic injury
- CNS - Acidosis worsens CNS toxicity by increasing the amount of salicylate that crosses the blood brain barrier and increases CNS tissue levels. Other signs and symptoms of CNS toxicity include nausea, vomiting, hyperpnea, and lethargy. Severe toxicity can progress to disorientation, seizures, cerebral edema, hyperthermia, coma, cardiorespiratory depression, and, eventually, death.
- Bedside ferric chloride testing: Historically, qualitative determination for the presence of salicylates was rapidly performed in the emergency department by adding a few drops of 10% ferric chloride (FeCl3) to 1 mL of urine. If salicylates are present, the solution changes to a brown/purple color. Positive results with the urine ferric chloride test only indicate that a salicylate is present; however, even very small amounts of a salicylate, such as a single ingested aspirin tablet can give a positive test result. Most emergency departments no longer perform this test and instead obtain a plasma salicylate level because these results are rapidly available from almost all hospital laboratories. Repeat testing: Repeated blood gases and serum salicylate levels should be done every 2 hours, until the acid-base status is improving, levels are falling, and the patient is clinically improving.
- Done normogram – used to predict the severity of salicylate poisoning. Starting at 6 hours post ingestion…. No longer considered a useful tool and is seldom used by clinicians
- Salicylate poisoning has been shown to cause metabolic derangements with significant inhibition of Krebs cycle enzymes.8 It also uncouples oxidative phosphorylation. Because of impaired glucose homeostasis, CNS glucose supply is sometimes lowered, which results in hypoglycorrhachia and delirium, even when serum glucose concentration is normal
- Renal excretion of salicylic acid depends on urinary pH. Because aspirin is a weak acid, it ionizes when exposed to a basic environment, such as alkaline urine. Ions are poorly reabsorbed in the tubules and are excreted more readily. This phenomenon is called ion trapping and also works well for overdoses of other weak acids, such as phenobarbital.
- Phase 1 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. This is predominantly due to direct local corrosive effects of iron on the gastric and intestinal mucosa. Phase 3 Following absorption, ferrous iron is converted to ferric iron, and an unbuffered hydrogen ion is liberated. Iron is concentrated intracellularly in mitochondria and disrupts oxidative phosphorylation, resulting in free radical formation and lipid peroxidation. This exacerbates metabolic acidosis and contributes to cell death and tissue injury at the organ level. The decrease in cardiac output may be related to a decrease in myocardial contractility exacerbated by the acidosis and hypovolemia. Free radicals from the iron absorption may induce damage and play a role in the impaired cardiac function. A coagulopathy is observed and may be due to 2 different mechanisms. Free iron may exhibit a direct inhibitory effect on the formation of thrombin and thrombin's effect on fibrinogen in vitro. This may result in a coagulopathy. Later, reduced levels of clotting factors may be secondary to hepatic failure.
- Phase 4 Iron is absorbed by Kupffer cells and hepatocytes, exceeding the storage capacity of ferritin and causing oxidative damage. Pathologic changes include cloudy swelling, periportal hepatic necrosis, and elevated transaminase levels. This may result in hepatic failure. Phase 5 late scarring of the GI tract, which causes pyloric obstruction or hepatic cirrhosis.
- Activated charcoal – does not absorb iron Desferoxamine – It removes loosely bound iron as well as that from hemosiderin and ferritin. But not from haemoglobin or mitochondria The administration of deferoxamine may be intramuscular or intravenous. The intramuscular route is not recommended because it is painful and less iron is excreted compared with the intravenous route. Other use – transfusion siderosis Adverse effects – it causes histamine release– fall in bp, flushing, itching, urticarial, rashes, ARDS DEFERIPRONE – Orally acting iron chelator. Less effective than desferoxaimnie – transfusion siderosis in thalassemia patients
- Neostigmine – ineffective.. Does not antagonize central effects
- CPZ – Schizophrenia, anti emetic, secondary drug I tetanus, intractable cough EXTRA PYRAMIDAL – These are the major dose limiting side effects – Parkinsonism. Tabbit syndrosm (rare form) – perioral tremors
- Hypersensitivuity rns – cholestatoc jaundice, photosensitivity, urticarial, skin rashes, agranulocytosis, myocarditis
- CVS – Fall in bp due to ganglionic blockade, vasomotor centre depression Reduce urine flow by decreasing BP and increasing ADH secretion
- No antidote to barbiturates Flumazenil – competes with BZD agonists for the BZD receptor Side effects – agitation, discomfort, twithdrawal seizures.
- Ppm -
- Hyperbaric o2 – use of oxygen at a pressure higher than the atmospheric pressure to increase the availability of o2 in the body ?? Acidosis corrction
- ? Osteo lathyrism…? Angio lathyrism
- Angio – clooagen cross linkin is affected making tunica media of vessel weak,
- Toxicology - wikipedia
- Burton line – pic Basophilic stippling – also in folate and b12 deficiency -- ??? Confirm it EP – blood level high but EP ios still normal – recent exposure----refer wikipedia