Asphyxiant Poisoning

Asphyxiant PoisoningDr. M. Mustafa ArifLecturerDepartment of Forensic Medicine and ToxicologyToxic GasesToxic gases may be classified as:Simple Asphyxiants: Displace oxygen form ambient air and reduce Pp O2. Co2, nitrogen, noble gases e.t.cRespiratory irritants: These gases damage the respiratory tract. Ammonia and hydrogen sulfide. Systemic Asphyxiants: These gases produce toxicity by specialized mechanisms. CO, Cyanide, SmokeCarbon DioxideIt is a heavy, colorless, odorless gas, with a slightly acid taste.

It is given off in the process of respiration, combustion, fermentation and decomposition of organic mature.

Atmospheric air contains approximately 0.4% carbon dioxide

Stage%O2 SaturationSymptomsIndifferent90%Night vision is slightly decreasedCompensatory stage82%-90%R/R and Pulse increased, Alertness and performance ability decreasesDisturbance stage64%-82%Compensatory mechanisms become inadequate/. Air hunger, fatigue, Tunnel vision, Dizziness, Headache, Euphoria, Hyperventilation, cyanosis, Poor judgmentCritical Stage60-70%Deterioration in judgment an co-ordination may occur in 3-5 mins. Unconsciousness may follow leading to death.

Fatal dose:60-80%Fatal period:Instant death.

Treatment Art. Resp. & oxygen.

Maintain body warmth.

Cardio-resp. stimulants e.g. amphetamine.

Postmortem Appearances:External : Body remains warm for a longer period.

Face: pale, swollen, cyanosed, congested.

Tongue: protruded & grasped by teeth.

Froth at mouth & nose.

Pupils dlated.

Internal: Lungs, brain & its membranes & other organs are congested.

Heart: right side full of dark blood.

Small intestine: ecchymosed.

Medico legal importance: Accidental : In deep old wells, grain godowns, damp cellars, mines, refrigerating plant and lime burning.

Carbon MonoxideIt is a colorless, odorless and non irritating.

CO has 250 times more affinity for hemoglobin than oxygen, combines with it very avidly, depriving the tissues of oxygen supply (tissue anoxia).

About 15% of inhaled CO combines with extra vascular proteins like myoglobin.

Signs and symptoms:These depend upon the degree of saturation of CO in the blood.

The approximate relationship between carboxyhaemoglobin level and clinical manifestation is summarized in the following table.Signs and Symptoms:

These depend upon the degree of saturation of CO in the bloodCO Hb level %Symptoms10 to 20%Exertional dyspnea, mild frontal headache20 to 30 %Increasing dyspnea, severe headache30 to 40%Vertigo, blurred vision, confusion, nausea40 to 50 %Weakness, trismus, muscle spasms, vomiting,tachypnea50 to 60%Convulsions, respiratory failure, coma, bullous lesions commonly develop in the skinOver 60%Coma

Fatal dose50-70% saturation of blood.Fatal periodNot fixed

DiagnosisA simple test that can be done by the attending physicians isto dilute 1ml of the patient`s blood with 10ml of water in atest tube and add to it 1ml of a 5% solution of sodiumhydroxide. If carboxyhemoglobin (COHb) is present, thesolution will turnStraw yellow (20% COHb)In the case of normal blood , i.e. oxyhemoglobin, the solution turns brown in colour.COHb level in the blood measured by spectrophotometry.Diagnostic testsSpectroscopic testIf blood is examined spectroscopically two bands of COHb between D & E will be found in the yellow green region. A calibrated instrument is necessary to appreciate this difference. Spectroscopic examination of blood is negative unless the amount of carbon monoxide in the blood exceeds 20-25%Kunkel`s test or tannic acid testA sample of suspected blood is diluted with 4 times its volume of water and a few drops of 3% aqueous tannic acid solution are added to it. It is then shaken well. If carbon monoxide is present, it forms a pinkish white precipitate. Blood saturated even with 10% carbon monoxide responds to this test.Hoppe-seyler TestA sample of suspected blood is diluted with about 20 times its volume of water and 10 drops of 10% caustic soda is added to it. Normal blood produces a dirty greenish brown colour while blood containing carbon monoxide retains its bright red colour.Treatment Immediate removal from the source of exposure

Administration of 100% oxygen or hyperbaric ( oxygen under greater pressure than normal atmospheric pressure)

Monitor cardiac and respiratory status.

Watch for increased intracranial pressure. If there is increased ICP treat with corticosteroids, hyperventilation, head elevation and mannitol. Convulsions can be controlled with IV diazepam or phenytoin.

Supportive measures.

Postmortem Appearances:Cherry pink colour (body)

Pulmonary and cerebral edema

Congestion of viscera with petechia, on the lungs and heart, and sometimes in the white matter of brain.

Medico legal ImportanceAccidental: disused wells, water gas, coal gas, illuminating gas, explosion in mines, dynamites, charcoal stoves, oil heaters, oil lamps, gas heaters, car engines, exhaust gases and lime burning.

Suicidal: by Sui gas

Homicidal: very rare

Hydrogen sulphideHeavy, colorless, flammable gas with a strong rotten egg odor.Found in areas where sulphur containing organic material is undergoing decay such as sewers.

It interferences with cellular respiration by inhibiting the action of cytochrome oxidase by forming a complex bond with iron and inhibiting cellular respiration.

It also forms methhaemoglobin.

Signs and Symptoms:Acute poisoning:CNS: headache, vertigo, nystagmus, vomiting, weakness, coma.

Eye : lacrimation, photophobia, conjunctivitis.

RS : rhinitis, bronchitis, pneumonia.

CVS: arrhythmia, myocardial depression.

Chronic poisoning:Headache, weakness, nausea, weight loss, ataxia, tremor, etc.

Fatal dose:0.2% in air.Fatal period:Within few minutes.

Treatment :Remove the victim from the source of exposure.

100% oxygen inhalation, assisted ventilation, etc. hyperbaric oxygen has not been proved conclusively to be of any benefit.

Antidote: Amyl nitrite and sodium nitrite enhance the formation of methhaemoglobin which gets converted to sulfmethemoglobin, which in turn is spontaneously detoxified in the body.

Supportive measures: correction of electrolyte imbalance, pulmonary edema, etc.

Postmortem Appearances:Signs of asphyxia are present.

External :Putrefaction: begins much rapidly.

Cyanosis and bloating of body due to gas formation.

Post mortem staining is bluish green.

Internal: Offensive odour of gas on opening the body.

Blood: fluid and dark brown due to sulphmethemoglobin.

Lungs: oedematous

Medico legal importance:Accidental: mostly from sewer gas.

Chronic poisoning :In artificial silk works, sulphur dye works, gas works, tar distillation works.

Hydrocyanic Acid Hydrocyanic Acid is also known as cyanogen or prussic acid.At ordinary temp. the acid is a gas having an odour of bitter almonds. In low temp and pressure it is a liquid form.

IT IS USED TO FUMIGATE SHIPS,BUILDINGS AND CITRUS TREESHCN FORMS CYANIDES WITH METALSPOTASSIUM, SODIUM CYANIDE,MERCURIC CYANIDE AND SILVER CYANIDE ARE USED IN PHOTOGRAPHY,ELECTROPLATING,HARDENING OF STEEL,SILVER AND GOLD PROCESSING AND DYEINGCALCIUM CYANIDE IS USED IN MINING INDUSTRYMAGNESIUM CYANIDE AND CYANOGEN CHLORIDE ARE USED AS INSECTICIDESSOURCESHydrocyanic acid is a vegetable acid naturally found in many fruits : plums, peach etc. It exists in the form of glucoside amygladin which is harmless.

Enzyme emulsion can liberate the harmful gas. Also reactions with acids can also liberate it. MECHANISM OF ACTIONIT INHIBITS CYTOCHROME OXIDASE-FORMING CYTOCHROME OXIDASE CYANIDE COMPLEX-PARALYSIS OF ELECTRON TRANSPORT SYSTEM-CELLULAR HYPOXIAPYRUVATE-LACTATE-METABOLIC ACIDOSISASPHYXIA AT TISSUE LEVEL DESPITE OF AMPLE SUPPLY OF OXYGEN AND BLOOD IS SATURATED WITH OXYGENABSORPTION,FATE AND EXCRETIONLIQUID HCN CAN BE ABSORBED THROUGH ALL MUCOUS MEMBRANES AND SKINGASEOUS FORM IS READILY ABSORBED THROUGH RESP TRACTSALTS VARY IN THEIR RATE OF ABSORPTIONRAPIDITY WITH WHICH SALTS CAUSE DEATH UPON INGESTION DEPENDS UPON AMOUNT OF ACID PRESENT IN STOMACH AND SUBSEQUENT LIBERATION OF HYDROGEN CYANIDE ON REACTION WITH ACID OF STOMACH.PRESENCE OF FOOD IN STOMACH DELAYS ABSORPTIONAFTER ABSORPTION GREATER PART CONVERTED BY MITOCHONDRIAL ENZYME, RHODANASE INTO THIOCYANATE WHICH IS NON TOXICSMALL AMOUNT ELIMINATED THROUGH EXPIRED AIRMAIN ROUTE OF EXCRETION IS KIDNEY

FATAL DOSE:50-60 MG OF PURE ACID60 DROPS OF CRUDE OIL OF BITTER ALMONDS200MG OF POTASSIUM CYANIDEFATAL DOSE:DEATH IN SOME CASES IS IMMEDIATE BUT AVERAGE PERIOD IS TWO TO TEN MINUTES FOR HCN AND THIRTY MINUTES FOR SODIUM OR POTASSIUM CYANIDESIGNS AND SYMPTOMSWHEN INHALED AS A GAS SYMPTOMS OCCUR WITHIN SECONDS.MASSIVE DOSES PRODUCE SUDDEN LOSS OF CONCIOUSNESS AND PROMPT DEATH FROM RESP ARRESTAFTER INGESTION:SYMPTOMS APPEAR WITHIN MINUTES,DURING WHICH VICTIM MAY PERFORM CERTAIN VOLUNTARY ACTS AS CORKING OR THROWNING AWAY A BOTTLE OR WALKING A LITTLE DISTANCEFOLLOWING ORGANS ARE INVOLVED:GIT:BURNING TASTE,THROAT NUMBNESS,SALIVATION,FROTHING AT MOUTH,NAUSEA,VOMITING,SUBSTERNAL AND EPIGASTRIC PAIN

CNS:DIZZINESS,HEADACHE,SWEATING,ANXIETY,CONFUSION,DROWSINESS,SEIZURES,COMA,DEATH

RESP SYSTEM:INITIALLY TACHYPNOEA AND DYSPNEAIN LATER STAGE IRREGULAR RESPIRATION,PULMONARY OEDEMA,CYANOSIS AND RESP ARREST.BITTER ALMOND LIKE ODOUR IN BREATHCARDIOVASCULAR SYSTEM:INITIALLY HYPERTENSION ALONG WITH REFLEX BRADYCARDIA.FOLLOWED BY HYPOTENSION,TACHYCARDIA ,ARRHYTHMIASVENOUS OXYGEN TENSION APPROACHES THAT OF ARTERIAL OXYGEN TENSION AND BRIGHT RED IN COLOUR.

DIAGNOSISDIAGNOSIS CAN BE DONE BY:HISTORYCLINICAL EXAMINATIONMEASUREMENT OF WHOLE BLOOD CYANIDE LEVELCYANIDE ASSAYS NOT ROUTINELY AVAILABLE SO MAJOR DIAGNOSIS ON HISTORY AND CLINICAL EXAMINATIONTREATMENTSTABILIZATION:IT INCLUDES ASSISTED VANTILATION,OXYGEN ADMINISTRATION,CARDIAC MONITORING,TREATMENT OF METABOLIC ACIDOSIS,VASOPRESSORS FOR HYPOTENSION

DECONTAMINATION:IN CASE OF CUTANEOUS EXPOSURE REMOVE CLOTHING AND WASH WITH SOAP AND WATER.IN CASE OF INGESTION STOMACH WASH WITH 5%SODIUM THIOSULPHATE SOLUTION.INSTILL ACTIVATED CHARCOAL AT BEGINNING AND END OF STOMACH WASH.LAVAGE SHOULD BE DONE AFTER STABILIZING THE PATIENT AND INITAITING ANTI DOTAL THERAPY.

ANTIDOTAL THERAPY:CONSISTS OF THREE STEPS:ADMINISTRATION OF AMYL NITRATE-ONE AMPOULE OF 0.2ML-INHALED OVER 30 SEC OF EACH MINUTE AND USE FRESH AMPOULE EVERY 3MINUTES

2ND STEP:ADMINISTRATION OF SODIUM NITRITE-AS 3% SOLUTION AT A DOSE OF 300-450 MG/10-15ml SLOW IV OVER 5-10 MIN

3RD STEP:ADMINISTRATION OF SODIUM THIOSULPHATE(AS 25% SOLUTION AT A DOSE OF 12.5gm/50 ml IV,3-5 ML PER MINUTE)POSTMORTEM APPEARANCESEXTERNAL:

SKIN PRESENT VIOLET APPEARANCEPOST MORTEM STAINING IS BRIGHT RED DUE TO FORMATION OF CYAN-METHAEMOGLOBIN AND DUE TO BRIGHT RED BLOOD IN VEINSFINGERS MAY BE CLENCHED,FINGER NAILS BLUE AND FROTH AT THE MOUTH AND NOSTRILSEYES MAY BE BRIGHT,GLISTENING AND PROMINENT WITH DILATED PUPILSJAWS FIRMLY CLOSEDRIGOR MORTIS SETS EARLY AND LASTS LONGER INTERNAL FINDINGS:

CRANIALCAVITY SHOULD BE OPENED FIRST AS ODOUR IS USUALLY WELL MARKED IN BRAIN TISSUEBLOOD STAINED FROTH MAY BE PRESENT IN TRACHEA AND BRONCHIPULMONARY OEDEMA IS EVIDENTMUCOSA OF STOMACH AND INTESTINE IS CONGESTEDIN CASE OF CYANIDES LIPS AND MOUTH MAY BE CORRODEDMUCOUS MEMBRANE OF STOMACH AND DUODENUM MAY BE BRIGHT RED TO BROWN IN COLOURBRAIN LUNGS AND BLOOD IN ADDITION TO OTHER VISCERA SHOULD BE SENT FOR TOXICOLOGICAL EXAMINATIONMEDICOLEGAL ASPECTSHYDROCAYNIC ACID AND ITS SALTS ARE USED FOR SUICIDAL PURPOSES BECAUSE OF ITS QUICK ACTIONACCIDENTAL POISONING CAN OCCUR WHEN IT IS USED FOR DISINFECTING PURPOSESHCN IS ALSO USED AS CATTLE POISON.CATTLE POISONING HAS BEEN KNOWN TO HAVE OCCURRED FROM EATING KADVI JUAR AND PLANT DUE TO NATURAL DEVELOPMENT OF A CYANOGENIC GYCOSIDE WHICH MAY LIBERATE HCNUSE AS HOMICIDAL PURPOSE IS RARE

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