Dr. ATHAL HUMO
2016-2017
Poisoning
HYDROCARBONS
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 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.
complications
1. Pneumothorax
2. pneumatocele
3. Subcutaneous emphysema
4. Pleural effusion
5. Empyema
6. 2ry bacterial infection
LOMOTIL
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)
PHENOTHIAZINE
E.g. :
oMetoclopramide (plasil)
oChlorpromazine (largactile)
oProchlorperazine (stemetil)
clinical findings
It’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 norepinephrine
ASPIRIN
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
ORGANOPHOSOHOROUS
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:
•Diaphoresis •hypotension
•Emesis •Bronchorrrhoea
•Tearing •Bronchospasm
•Drooling •Miosis
•bradycardia •Urinary &fecal incontinence
Nicotinic s&s:
• m. weakness •Hypertension •Tachy
•Fasiculation & tremor •hypoventilation •dysrrhythmia
CNS S&S:
•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:
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/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.
IRON
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
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 develop 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 , 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
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 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
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
1. Identification and elimination of environmental sources of lead exposure
2. Behavioral modification to reduce non nutritive hand-to-mouth activity
3. Dietary counseling to ensure sufficient intake of the essential elements 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 with chelating agents as
DMSA, EDTA, Penicillamine.