Dr. ATHAL HUMO2016
Poisoning HYDROCARBONSOne of the most common hydrocarbon poisoning in Iraq is KEROSENEclinical manifestations:Hydrocarbons can cause symptoms after ingestion, inhalation, dermal or ophthalmic exposures.• Lung: the most important manifestation of hydrocarbon toxicity is aspiration pneumonitis. Aspiration usually occurs during coughing and gagging at the time of ingestion or vomiting after the ingestion. Respiratory symptoms can remain mild or progress rapidly to ARDS and respiratory failure. Only small quantities (<1 mL) of low-viscosity hydrocarbons need be aspirated to produce significant injury.• GIT: gastric irritation.• CNS: transient, mild CNS depression is common after hydrocarbon ingestion or inhalation• CVS: after inhalational exposures to halogenated hydrocarbons, patients can present with ventricular dysrhythmias, often refractory to conventional management.• Renal: recurrent inhalation of the aromatic hydrocarbon toluene can lead to renal tubular acidosis.• Blood: benzene is known to cause cancer, most commonly AML, after long-term exposure.investigation• CXR: may initially be normal, but they often show abnormalities within 6 hr ofexposure in patients who have aspiration .CXR can remain abnormal long after thepatient is clinically normal. Pneumatoceles can appear on the chest radiograph 2-3 wk after exposure.treatment: Observation in EU for any symptoms, if not develop any symptoms withen 1st 6 hrs & CXR normal, discharge home. If hydrocarbon-induced pneumonitis develops:• Supportive treatment: O2, hydration , antipyretics… accordingly• Neither corticosteroids nor prophylactic antibiotics have shown any clear benefit.• Mechanical ventilation, and ECMO have all been used to manage the respiratory failure and ARDS associated with severe hydrocarbon-induced pneumonitis. Patients with dysrhythmias in the setting of halogenated hydrocarbon inhalation should be treated with β blockers. In case of dermal exposure, affected skin should be decontaminated as soon as possible.NOTE:• Activated charcoal is not useful because it does not bind the common hydrocarbons and can also induce vomiting.• Emesis and lavage are contraindicated given the risk of aspiration. If large amount of kerosene ingested & conscious affected, lavage can done only after saving the airway with cuffed endotracheal intubation.complications1. Pneumothorax2. pneumatocele3. Subcutaneous emphysema4. Pleural effusion5. Empyema6. 2ry bacterial infection
LOMOTIL
Lomotil antidiarrhoeal agent, composed of:Diphenoxylate hydrochloride + Atropine (Narcotic)Contraindication: < 2 yrclinical findings Early signs: are due to anticholinergic effect of atropine and consist of facial flushing, fever, dry skin, urinary retension, paralytic ileus. The pupil may bedilated or not due to narcotic effect which lead to miosis. Late signs: are due to the narcotic effect which is most serious and may be prolonged, it include hypothermia, hypotension, loss of facial flushing,respiratory depression, CNS dep & convulsiontreatment1. Life supportive care (ABCDE).2. Gastric decontamination: emesis & gastric lavage can done at any time even after 12 hrs because the drug impair gastric motility.3. Antidote for narcotic effect: naloxone 0.1 mg/kg up to 2mg ( can repeate the dose as needed)
PHENOTHIAZINE
E.g. :oMetoclopramide (plasil)oChlorpromazine (largactile)oProchlorperazine (stemetil)clinical findingsIt’s produce the s&s of toxicity by 2 reactions: Idiosyncrasy: this reaction is not dose related that can occur even with very small dose of the drug & include extrapyramidal effect; these are oculogyric crisis, torticolis, dystonia, stiff body, spastic, poor speech & inability to communicate. Over dose: lethargy, hypotension, respiratorydepression, & deep coma.treatment Etrapyramidal crisis: the antidote is diphenhydramine I.V. slowly 5 mg/kg q 8 hr valium also can be used Over dose: I.V. fluid Gastric lavage In severe cases norepinephrineASPIRIN
Toxic dose: > 150 mg/ kgclinical findings(1). Classic finding:• Hyperventilation→ aspirin directly stim the resp center• Diaphoresis• Tinnitus• acid _ base disturbance(2). Other symp & signs:• Nausea, vom, abd pain, gastric irritation, hemorrhagic gastritis in sv ps.• Fever.• Resp alkalosis, latter on resp acidosis.• Metabolic & lactic acidosis.• Hepatotoxicity in large acute ingestion or chr use.• CNS: agitation, restlessness, confusion, lethargy, coma.• Hyperglycemia or hypoglycemia.• Electrolyte abnormalities• Antiplatelet: bleeding tendency.lab test1. Electrolyte & glucose.2. Arterial blood gas, urine & plasma PH.3. Liver function test.4. Coagulation study.5. Serial serum salicylate levels should beclosely monitored.treatment Supportive care. Gastric decontamination: with AC Aggressive volume resuscitation & electrolyte correction Urinary alkalinization to enhance excretion of aspirin, byadministration of a sodium bicarbonate infusion Dialysis: in severe cases
ORGANOPHOSOHOROUS
It is one of the most commonly used insecticides. Most pediatric ps occur as theresult of accidental exposure to these substance esp in rural areas.pathophysiologyThe toxin bind cholinesterase enz, preventing the degradation of acetylcholine, resulting in its accumulation in:• Peripheral nicotinic & muscarinic synapses.• CNS.clinical findingsClin manifestation related to the accum of Ach at nicotinic, muscarinic receptor & CNS.Muscarinic s & s:•Diaphoresis •hypotension•Emesis •Bronchorrrhoea•Tearing •Bronchospasm•Drooling •Miosis•bradycardia •Urinary &fecal incontinenceNicotinic s&s:• m. weakness •Hypertension •Tachy•Fasiculation & tremor •hypoventilation •dysrrhythmiaCNS S&S:
•Malaise •delirium •coma•confusion •SeizureSLUDGE* Salivation * lacrimation * Urination * Defecation * GI cramps * Emesistreatment Basic supp care: O2, suction, fl & elect replacement & intubation with mechventilation if required. Basic decontamination:• Washing the skin.• Gastric decontamination: charcoal. Antidote:A. Atropine: block Ach receptor, 0.05 mg/kg repated every 5 – 10 min untill full atropinization occur (flushed, feverish, dilated pupil)B. Pralidoxime: breaks the bond between the toxin & enz lead to liberation of the enzyme.
TRI-CYCLIC ANTIDEPRESSANT
E.g. of TCA is imipramine which use in Rx of enursis.Toxic dose: 5- 20 mg/kgclinical findingsTCA primarily affect CVS & CNS, sympt typically develop within1-2 hr of ingestion, serious sympt withen 6 hrs.CNS: drowsy, lethargy, coma, seizure, agitation, choreiform movement & twitching.CVS: Tachy, hypertension, hypotension, arrhythmia & complete heart block.(ECG:prolongation of the QRS complex & QT interval). Refractory hypotension is a poor prognostic indicator and is the most common cause of death in TCA overdose.Antichol: tachy, fever, flushing, urinary retension, ↓ bowel sound, hallucination & mydriasis.treatmento ABC include ET if indicated.o Prevent absorption → use AC.• emesis C.I. bec risk of aspiration due to CNS dep & seizure.o NaHCO3 : to Rx & prevent arrhythmia.o Antiarrhythmic agent : e.g lidocaine.o Hypotension: fluid, NE may be requiredo Hypertension: transient, need no Rx.o Seizure → valium. Asymptomatic children should receive appropriate decontamination & be observed with continuous cardiac monitoring and serial ECGs for at least 6 hr. If any manifestations of toxicity develop, the child should be admitted to a monitored setting. Children who remain completely asymptomatic with normal serial ECGs may be candidates for discharge after 6 hr of close observation.
IRON
Toxic dose > 60 mg/kg.clinical findings4 phases may be observed with Fe ps:Stage I : 30 min – 6 hrsLocal effect of GIT irritationInclude diarrh & vomiting. Hematamesis & bloody diarrh may occur with more serious ps.Stage II “quiescent phase” : 6-24 hrApparent recovery GI symptoms typically have resolved. However, careful clinical exam can reveal subtle signs of hypoperfusionStage III : 12-36 hrMultisystem organ failureshock, hepatic and cardiac dysfunction, acute lung injury or ARDS, and profound metabolic acidosis. Death occurs most commonly during this stage.Stage IV : 4-6 wkPyloric stenosisIn patients who survive, the 4th stage, usually develop strictures and signs of GI obstruction.investigations1. Serum iron level , best 4 hr aft ingestionLevel < 500 Mg/dl → low risk> 500 Mg/dl sig. risk2. Abd X- ray: bec iron radiopaque, but –ve result not role out ps.3. lab evaluation in the ill patient should include arterial blood gas, complete blood count, serum glucose level, liver function tests, and coagulation parameters.treatment1. Good supportive & symptomatic care.2. WBI , the decontamination strategy of choice.3. Vitamin K or FFP if there is coagulation defect4. Deferoxamine (Desferal): chelate free iron in the blood.• I.V. infusion → 15 mg/kg/hr (max 6g/24 hr)Indication:• Moderate – severe symptoms• Iron level > 500 Mg/dl
LEAD
Several hundred products contain lead, including batteries, cable sheathing, cosmetics, mineral supplements, plastics, toys, paint chips dust, soil …E.g. of lead poisoning in Iraq: SEQWA POISONINGclinical features:GIT: anorexia, abdominal pain, vomiting, and constipation.CNS: related to worsening cerebral edema and increased intracranial pressure. Headaches, change in mentation, lethargy, papilledema, seizures, and coma leading to death.RENAL: renal tubular dysfunction.BLOOD: reversible Fanconi syndrome & hemolytic anemia.treatmentOnce lead is in bone, it is released slowly and is difficult to remove even with chelating agents. Because the cognitive/behavioral effects of lead may be irreversible, the main effort in treating lead poisoning is to prevent it from occurring1. Identification and elimination of environmental sources of leadexposure2. Behavioral modification to reduce non nutritive hand-to-mouthactivity3. Dietary counseling to ensure sufficient intake of the essentialelements calcium and iron.4. For the small minority of children with more-severe lead poisoning,drug treatment is available that enhances lead excretion.A child with a venous BLL of 45 μg/dL or higher should be treated withchelating agents as DMSA, EDTA, Penicillamine.