intoxicación por fosfato de aluminio

8/13/2019 Intoxicación por fosfato de aluminio

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Intoxicación por fosfuro de

aluminio



Fosfuro de aluminioRodenticida altamente toxico de bajo costo

Veneno mitocondrial.

NO HAY ANTIDOTO.

Hay dos tipos de intoxicacion aguda:• Inhalacion indirecta• Ingestion directa

India 66.8% muertes no naturales causadas por envenenamiento suicida

Libera gas de fosfino se absorve rapidamente por:• Inhalacion• Piel• Via GI.



Gas fosfino

La mezcla de fosfato dealuminio y aire

produce gas fosfino(hidrogeno fosfado,trihidrido de fosforo,PH3) que es la formaactiva del pesticida

Se une alcitocromooxidasa ycambia las valencias

del componente hemde la hemoglobina.

Induce estrés oxidativo

Aumenta la liberacionde radicales libres

extramitocondriales

que produceperoxidacion lipidica ydesnaturalizacion de

las proteinas de lamembrana celular.

Disminuye la actividadde la actividad de la

colinesterasadependiendo de laconcectracion del

fosfato.

Reduce al glutation

(una de las principalesdefensasantioxidantes).



Toxicidad orgánicaDosis letal 0.5g

Síntomas tempranos

• Nauseas• Vomito• Dolor epigastrico y retroesternal• Disnea• Ansiedad• Agitacion

• Aliento a ajo.

Sigos de toxicidad fatal (90-100%):• Choque• Falla circulatoria periférica

Cambioshistopatologicos:• Congestion venosa central• Degeneracion de hepatocitos

• Infiltracion mononuclear• Adelgazamientos de alveolos

y dilatacion de capilares enpulmon

• Degeneracion de los granulosde Nissl en el cerebro

• Congestion glomerular e

intaparenquimatosa renal



Toxicidad

gastrointestinalSintomas tempranos hematemesis,

vomito y dolor epigastrico.

Endoscopia:

• Lesiones corrosivas dl esofago y estomago• Erosiones gastricas y duodenales severas.• Contracturas esofagicas o fistulas.• Dysphagia is a common late complication.

Se absorve In vitro como particulasmicroscopicas no hidrolizadas queinteractuan permanentemente con la hblibre, haemoglobin and haemoglobin inintact erythrocytes (rat and human) toproduce a haemichrome (amethaemoglobin derivative resulting fromdistorted protein conformation).

Potter et al. report that Heinz bodies (denaturedhaemoglobin aggregates) are formed whenphosphide concentration in vitro exceeds 1.25μ g mL-1.

Reports of in vivo phosphide poisoning showedintravascular complications such as haemolysisand methaemoglobinaemia, which support theinvolvement of erythrocytes in thebiotransformation of phosphine in humans.

Phosphine is excreted in the urine ashypophosphite and is also exhaled in theunchanged form.



Toxicidad hepática

Algunas veces se observa ictericia.• Puede ser una manifestacion of another

disturbances such as intravascular haemolysis.A more common finding is transient elevationof serum AST y ALT.

The main histopathological findings inthe liver at autopsy of fatal phosphinepoisoning include:• Cytoplasmic vacuolisation of hepatocytes and

sinusoidal congestion.• Nuclear fragmentation and sinusoidal clusters

of polymorphonuclear leukocytes in the liver.



Toxicidad respiratoria

Taquipnea, dirsnea,crepitantes y roncus.

Respiratory distress

syndrome and othertypes of pulmonaryoedema are

common in adults,accompanied byprotein-rich orhaemorrhagic

pleural effusions.



Toxicidad cardiaca

Post-mortem reports heart failure, profound and refractory hypotension, heart congestion,subendocardial infarction or pericarditis, separation of myocardial fibres by oedema, fragmentation ofthe fibres, non-specific vacuolation of myocytes, focal necrosis, and neutrophil and eosinophil

infiltration.

Other signs and symptoms include: increased left ventricle, hypokinesia of the left ventricleand septum, akinesia, lower ejection fraction, severe hypotension, raised systemic venouspressure, normal pulmonary artery wedge pressure, inadequate systemic vasoconstriction,and electrocardiographic (ECG) abnormalities such as dysrhythmia, ST-T wave changes and

conduction defects.

Sinus tachycardia dominates in the first three to six hours of poisoning, followedby ST-T changes and conduction disturbances between hour 6 and twelve, and

then by arrhythmias.

Siwach et al. found ventricular tachycardia in 40 %, ventricular fibrillation in 23.3%, supraventricular tachycardia in 46.7 %, and atrial flutter/fibrillation in 20 % of

AlP-poisoned patients.



Tratamiento

• Treatment with magnesium sulphate has been reported to reducemortality by up to 50 %.

• Magnesium stabilises the cell membrane and acts as an anti-oxidant. Astudy published in 1994 compared treatments of AlP poisoned patientsand concluded that the survival rate of those who receivedsupplemental magnesium was not significantly better than of thosewho did not (42 % vs. 40 %, respectively).

• In contrast, in another case control study , magnesium improved

survival of patients who ingested high doses of AlP.• Moreover, a recent study on a rat model showed that 25Mg2 +-

carrying nanoparticle (25MgPMC16) significantly increased bloodpressure and heart rate of rats poisoned with AlP. This study alsodemonstrated that 25MgPMC16 increased intracardiac magnesiumlevels, reduced lipid peroxidation, and improved mitochondrial

function.

Suplemento de magnesio



Tratamiento

• Different studies in ratsand humans have revealedthat N-acetylcysteine canhelp as it replenishescellular glutathione andmagnesium, in addition to

its antioxidant properties.In rats exposed to AlP, N-acetylcysteine increasedsurvival time and reducedmyocardial oxidative injury

N acetil cisteina

• Some authors propose thata combination ofhyperinsulinaemia-euglycaemia andhyperventilationoxygenation is worthy of

more extensive evaluationas a therapy for AlPpoisoning

Hiperinsulinemia-euglicemia



TratamientoAceite de almendras y coco

• There are reports of the positive clinical effects of coconut oil against AlPpoisoning in humans. Its mechanism of action is unclear, but it may form aprotective layer around the gastric mucosa and prevent the absorption ofphosphine gas. In addition, coconut oil may dilute HCl in the stomach andreduce the breakdown of phosphide. Saidi and Shoajaie reported thatintragastric lavage with sweet almond oil considerably reduced the mortalityof rats poisoned with AlP. It also significantly lowered plasma cholinesteraselevels.

• The authors suggested that sweet almond oil should be given orallyimmediately after AlP ingestion, but this has yet to be confirmed in humans.

Oxigenacion hiperbarica



TratamientoNepal:

Lavado gastrico aceite vegetal.

Iran:

Lavado gastrico Solucion de permanganato de potasio

Administracion oral de sorbitol y aceite de coco.

Bicarbonato de sodio, Sulfato de magnesio, Gluconato de calcio IV.



Tratamiento

• Leakege of (IABP) is a good way to mechanicallysupport the heart, especially in toxic myocarditiswith refractory shock. Trimetazidine has also

proven itself effective recently in stoppingventricular ectopic beats and preservingoxidative metabolism. In addition, digoxin can beused to stabilise the left ventricular heart failure.

Hidroxietil starch



Tratamiento

Early diagnosis of organ damageis another important aspect in

the management, as AlPpoisoning affects virtually all

organs in the body. Acute lunginjury may need endotracheal

intubation and mechanicalventilation.

Cyanosis not responding tooxygen therapy may be a sign of

methaemoglobinaemia thatrequires therapy with intravenousmethylene blue (1% solution) inthe dose of 2 mg kg-1 of body

weight over fi ve minutes.

For metabolic acidosis,

intravenous sodium bicarbonateshould be considered, whereas

severe acidosis, volume overloador renal failure may require

haemodialysis.

However, haemodialysis isprobably not very effective in

removing phosphine.



PronosticoThe mortality in adults who haveingested 500 mg of AlP or over is

between 30% and 100 %. The higherthe blood phosphine, the higher the

mortality. Patients having bloodphosphine levels equal to or less than1.067±0.16 mg survived, and this dose

seems to be the lethal threshold ofphosphine toxicity.

Survival may increase if a verysmall amount of AlP is

ingested or the tablet hasexpired or was exposed to air.Vomiting and early supportivecare also increase the survival

rate.

Poor prognosis is indicated byhyperglycaemia, high simplified acute

physiology score (SAPS II),hypotension, acidosis, leukocytosis,

hyperuraemia, ECG abnormalities, highacute physiology and chronic health

evaluation score (APACHE II), lowGlasgow coma scale, acute renalfailure, low prothrombin rate,

hyperleukocytosis,methaemoglobinaemia, use of

vasoactive drugs, lack of vomiting afteringestion, and use of mechanical

ventilation.



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intoxicación por fosfato de aluminio

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