Dr. ATHAL HUMO 2016
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 of exposure in patients who have aspiration. CXR can remain abnormal long after the patient 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… accordinglyNeither 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.
COMPLICATIONS
Pneumothorax pneumatocele Subcutaneous emphysema Pleural effusion Empyema 2ry bacterial infectionLomotil antidiarrhoeal agent, composed of: Diphenoxylate hydrochloride + Atropine (Narcotic) Contraindication: < 2 yr
Clinical 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 be dilated 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 & convulsion
Treatment Life supportive care (ABCDE). Gastric decontamination: emesis & gastric lavage can done at any time even after 12 hrs because the drug impair gastric motility. Antidote for narcotic effect: naloxone 0.1 mg/kg up to 2mg ( can repeate the dose as needed)
E.g. : Metoclopramide (plasil) Chlorpromazine (largactile) Prochlorperazine (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, respiratory depression, & 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 norepinephrine
Toxic dose: > 150 mg/ kgClinical Findings(1). Classic finding:Hyperventilation→ aspirin directly stim the resp centerDiaphoresisTinnitusacid _ 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 TEST
Electrolyte & glucose. Arterial blood gas, urine & plasma PH. Liver function test. Coagulation study. Serial serum salicylate levels should be closely monitored.TREATMENT
Supportive care. Gastric decontamination: with AC Aggressive volume resuscitation & electrolyte correction Urinary alkalinization to enhance excretion of aspirin, by administration of a sodium bicarbonate infusion Dialysis: in severe casesIt is one of the most commonly used insecticides. Most pediatric ps occur as the result of accidental exposure to these substance esp in rural areas. Pathophysiology The toxin bind cholinesterase enz, preventing the degradation of acetylcholine, resulting in its accumulation in: Peripheral nicotinic & muscarinic synapses. CNS.
CLINICAL FINDINGS
Clin 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 incontinence
CNS S&S:
Nicotinic s&s:m. weakness
Hypertension
Tachy
Fasiculation & tremor
hypoventilation
dysrrhythmia
Malaise
delirium
coma
confusion
Seizure
SLUDGE * Salivation * lacrimation * Urination * Defecation * GI cramps * Emesis
TREATMENT
Basic supp care: O2, suction, fl & elect replacement & intubation with mech ventilation if required.Basic decontamination:Washing the skin.Gastric decontamination: charcoal.Antidote:Atropine: block Ach receptor, 0.05 mg/kg repated every 5 – 10 min untill full atropinization occur (flushed, feverish, dilated pupil)Pralidoxime: breaks the bond between the toxin & enz lead to liberation of the enzyme.E.g. of TCA is imipramine which use in Rx of enursis. Toxic dose: 5- 20 mg/kg
CLINICAL FINDINGSTCA primarily affect CVS & CNS, sympt typically develop within 1-2 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.
TREATMENT
ABC include ET if indicated. Prevent absorption → use AC. emesis C.I. bec risk of aspiration due to CNS dep & seizure.NaHCO3 : to Rx & prevent arrhythmia.Antiarrhythmic agent : e.g lidocaine.Hypotension: fluid, NE may be requiredHypertension: transient, need no Rx.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.Toxic dose > 60 mg/kg.
CLINICAL FINDINGS4 phases may be observed with Fe ps: Stage I : 30 min – 6 hrs Local effect of GIT irritationInclude diarrh & vomiting. Hematamesis & bloody diarrh may occur with more serious ps. Stage II “quiescent phase” : 6-24 hr Apparent recovery GI symptoms typically have resolved. However, careful clinical exam can reveal subtle signs of hypoperfusion
Stage III : 12-36 hr Multisystem organ failure shock, hepatic and cardiac dysfunction, acute lung injury or ARDS, and profound metabolic acidosis. Death occurs most commonly during this stage. Stage IV : 4-6 wk Pyloric stenosis In patients who survive, the 4th stage, usually develope strictures and signs of GI obstruction.
INVESTIGATIONS
Serum iron level , best 4 hr aft ingestionLevel < 500 Mg/dl → low risk > 500 Mg/dl sig. riskAbd X- ray: bec iron radiopaque, but –ve result not role out ps. lab evaluation in the ill patient should include arterial blood gas, complete blood count, serum glucose level, liver function tests, and coagulation parameters.TREATMENT
Good supportive & symptomatic care.WBI , the decontamination strategy of choice.Vitamin K or FFP if there is coagulation defectDeferoxamine (Desferal): chelate free iron in the blood.I.V. infusion → 15 mg/kg/hr (max 6g/24 hr)Indication: Moderate – severe symptomsIron level > 500 Mg/dl
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.