Dr. ATHAL HUMO 2016

One of the most common hydrocarbon poisoning in Iraq is KEROSENE CLINICAL 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 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 1 st 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.

COMPLICATIONS 1.Pneumothorax 2.pneumatocele 3.Subcutaneous emphysema 4.Pleural effusion 5.Empyema 6.2ry bacterial infection

Lomotil 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 1. 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)

E.g. : oMetoclopramide (plasil) oChlorpromazine (largactile) oProchlorperazine (stemetil)

Clinical Findings It’s produce the s&s of toxicity by 2 reactions: extrapyramidal effect;  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/ kg Clinical 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 TEST 1.Electrolyte & glucose. 2.Arterial blood gas, urine & plasma PH. 3.Liver function test. 4.Coagulation study. 5.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 cases

insecticides. rural areas It 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: Diaphoresishypotension EmesisBronchorrrhoea TearingBronchospasm DroolingMiosis bradycardiaUrinary &fecal incontinence

 CNS S&S:  Nicotinic s&s: m. weaknessHypertensionTachy Fasiculation & tremorhypoventilationdysrrhythmia Malaisedeliriumcoma confusionSeizure 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: 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.

E.g. of TCA is imipramine which use in Rx of enursis. Toxic dose: mg/kg

CLINICAL FINDINGS TCA 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 o 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 required o 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.

Toxic dose > 60 mg/kg. CLINICAL FINDINGS 4 phases may be observed with Fe ps:  Stage I : 30 min – 6 hrs Local effect of GIT irritation Include diarrh & vomiting. Hematamesis & bloody diarrh may occur with more serious ps.  Stage II “quiescent phase” : 6-24 hr Apparent recovery hypoperfusion GI symptoms typically have resolved. However, careful clinical exam can reveal subtle signs of hypoperfusion

 Stage III : 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 1.Serum iron level, best 4 hr aft ingestion Level < 500 Mg/dl → low risk > 500 Mg/dl sig. risk 2.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.

TREATMENT 1.Good supportive & symptomatic care. 2.WBI 2.WBI, the decontamination strategy of choice. 3.Vitamin K or FFP if there is coagulation defect 4.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

SEQWA POISONING 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 POISONING CLINICAL 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.

TREATMENT prevent Once 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 occurring elimination of environmental sourc 1.Identification and elimination of environmental sources of lead exposure reduce non nutritive hand-to-mouth activity 2.Behavioral modification to reduce non nutritive hand-to-mouth activity 3.Dietary counseling calcium and iron 3.Dietary counseling to ensure sufficient intake of the essential elements calcium and iron. drug treatment enhances lead excretion. 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 with chelating agents as DMSA, EDTA, Penicillamine.