poisons

2. CORROSIVE POISONS:
• A corrosive poison fixes, destroyes and erodes the surface with
which it comes in contact.
• They act by extracting water from the tissues and coagulate
cellular protiens and convert hemoglobin tohematin.

3. CORROSIVE POISON:
HCL

4. CHARACTERISTICS
• COLORLESS
• VOLATILE
• ODORLESS LIQUID
• HAS A BURNING SOUR TASTE
SOURCES
• INDUSTRIES
• COMMERCE
• LABORATORIES, ETC. (A NORMAL DIGESTIVE FLUID OF STOMACH)

5. MODE OF ACTION
• INFLAMMATION OF RESPIRATORY TRACT DUE TO INHALATION OF FUMES.
• INDIRECTLY—SHOCK DUE TO SEVERE PAIN
• GASTRIC NECROSIS
• CAUSES LESS SEVERE EFFECTS BECAUSE IT IS PRESENT IN OUR BODY
FATAL DOSE AND FATAL PERIOD
• FATAL DOSE: 15–20 ML (CONC.)
• FATAL PERIOD: 18–36 H
Gastric necrosis

6. SIGNS AND SYMPTOMS
• BURNING PAIN IN MOUTH ,THROAT, ESOPHAGUS AND STOMACH, SPREADING OVER THE
ABDOMEN
• USUALLY NO EROSION OF SKIN.
• EROSION OF MUCOUS MEMBRANE OF MOUTH AND TONGUE
• DIFFICULTY IN SPEECH AND SWALLOWING (AS THE MOUTH IS FILLED WITH SALIVA,
MUCUS AND CORRODED MATTER)
• ERUCTATION
• THIRST PRESENT
• VOMITING
• ALTERED BLOOD PRESENT
• TENESMUS MAY BE PRESENT
• TENDERNESS OVER ABDOMEN

7. • STIFFNESS OF ABDOMEN: MAY BE DUE TO DISTENSION OF THE
STOMACH
• PERFORATION OR RUPTURE OF STOMACH : UNCOMMON
• URINATION: SUPPRESSED
CAUSE OF DEATH
• SHOCK
• LARYNGEAL SPASM
• PULMONARY EDEMA DUE TO TRICKLING OF ACID OR VOMITUS OR
INHALATION OF VAPOR OF THE ACID

8. POSTMORTEM APPEARANCES
• THERE MAY NOT BE MUCH CORROSION OF THE SKIN. THERE MAY BE DAMAGE OF THE
SKIN OVER THESE AREAS WITH BROWNISH PARCHMENTIZATION.
• THE MUCOUS MEMBRANES OF THE MOUTH AND TONGUE SHOW REDDISH BROWN
CORROSION.
• SIMILAR CHANGES MAY BE SEEN ON THE INNER SURFACE OF ESOPHAGUS.
• THE STOMACH IS SOFT, SWOLLEN WITH CONGESTION, DESQUAMATION,
HEMORRHAGIC POINTS AND ULCERATION OF THE INNER SURFACE. IT CONTAINS
ALTERED BLOOD WITH MUCOUS SHREDS.
• PERFORATION IS UNCOMMON
• THE UPPER PART OF THE SMALL INTESTINE SHOWS SIGNS OF IRRITATION.
• IN CASE THE VAPORS ARE INHALED, THERE OCCURS CONGESTION OF THE RESPIRATORY
TRACT WITH CONGESTION AND EDEMA OF THE LUNGS. SIMILARLY, IF VOMITUS IS
INHALED, SAME FINDINGS USUALLY OCCUR

9. MATERIALS TO BE PRESERVED FROM
THE DEAD
• STOMACH WITH CONTENTS A LOOP OF UPPER PART OF THE SMALL
INTESTINE,
• HALF OF LIVER
• HALF OF EACH KIDNEY ARE PRESERVED IN ONE CONTAINER CORRODED
AREAS OF SKIN ARE PRESERVED IN ANOTHER CONTAINER.
• ACID-STAINED CLOTHES ARE PRESERVED SEPARATELY
PRESERVATIVES
• VISCERA AND SKIN ARE PRESERVED IN ABSOLUTE ALCOHOL OR
RECTIFIED SPIRIT,
• THE CLOTHES ARE SENT WITHOUT ANY PRESERVATION

10. • DO NOT ADMINISTER EMETICS TO A PATIENT WHO HAS INGESTED A
CORROSIVE AGENT.
• DO NOT PERFORM A GASTRIC LAVAGE, AS IT MAY LEAD TO PERFORATION OF
THE STOMACH OR OESOPHAGUS.
• DO NOT GIVE THE PATIENT ANYTHING ORALLY FOR 2–3 DAYS AFTER THE
INITIAL ADMINISTRATION OF WATER OR MILK. LATER ON, FLUIDS AND
ELECTROLYTES MAY BE GIVEN.
• CONCOMITANT PROPHYLACTIC BROAD-SPECTRUM ANTIBIOTIC USE IS
RECOMMENDED.
• OESOPHAGEAL STRICTURE OR GASTRIC OUTLET OBSTRUCTION MAY REQUIRE
TREATMENT

11. • THE ROLE OF GLUCOCORTICOIDS IS CONTROVERSIAL.
• LAPAROTOMY IS REQUIRED FOR PATIENTS WITH GASTRIC PERFORATION AND PERITONITIS.
• SKIN LESIONS NEED TO BE WASHED WITH SOAP AND WATER FOLLOWED BY APPLICATION OF
SOME OINTMENT.
• EYE INVOLVEMENT NECESSITATES COPIOUS IRRIGATION WITH WATER OR NORMAL SALINE.
REFERRAL TO AN OPHTHALMOLOGIST IS ADVISABLE.

12. MEDICO-LEGAL ASPECTS
• ACCIDENTAL POISONING
• SUICIDAL POISONING IS RARE
• ACUTE EXPOSURE TO THE VAPOURS IN THE INDUSTRIES MAY LEAD TO DEATH DUE TO
RESPIRATORY DISTRESS.
• PROLONGED EXPOSURE TO THE VAPOURS IN INDUSTRIES MAY LEAD TO RESPIRATORY
COMPLICATIONS.
• IN FATAL CASES OF POISONING BY THESE ACIDS, NO TRACE OF THE POISON MAY BE
DISCOVERABLE IN THE VISCERA, ESPECIALLY IF THE VICTIM HAD SURVIVED FOR A COUPLE OF
DAYS OR MORE
• THE QUANTITY OF FREE ACID PRESENT IS SPECIALLY IMPORTANT IN HCL POISONING, AS THIS
ACID IS CONTAINED UNCOMBINED WITH BASES IN THE GASTRIC JUICE TO THE EXTENT OF
ABOUT 0.2% OR MORE.
• SOMETIMES, DISPOSAL OF THE DEAD BODY MAY BE EFFECTED BY THROWING THE DEAD

13. CORROSIVE POISON:
SULPHURIC ACID

14. CHARACTERISTICS
• OIL OF VITRIOL
• ODOURLESS, COLOURLESS, NON-FUMING, HYGROSCOPIC
OILY LIQUID
• COMMERCIAL ACID IS BROWN OR DARK IN COLOUR
• CAUSES SUPERFICIAL BURNS AFTER 1 SEC CONTACT AND
FULL THICKNESS BURNS AFTER 30 SEC

15. SIGNS AND SYMPTOMS
• LIPS -SWOLLEN AND EXCORIATED
• BROWN OR BLACK STREAKS FOUND EXTENDING FROM THE
ANGLE OF MOUTH TO THE SIDE OF CHIN AND SOMETIMES
FRONT OF THE NECK DUE TO FLOW OF ACID
• CORROSION OF MUCUS MEMBRANE OF MOUTH , THROAT AND
OESOPHAGUS
• STRIDOR , DROOLING , ODYNOPHAGIA ,DYSPHAGIA
• EPIGASTRIC PAIN SOON SPREAD OVER ABDOMEN AND
THORAX

16. • PHARYNGEAL PAIN
• ERUCTATION, NAUSEA, VOMITING, INTENSE THIRST
• VOMIT IS BROWN OR BLACK, MUCOID ,STRONGLY ACID AND MAY CONTAIN SHREDS OF
CHARRED WALLS OF STOMACH
• IMMEDIATE DEATH CAN OCCUR DUE TO CIRCULATORY COLLAPSE OR ASPHYXIA(DUE TO
OEDEMA OF GLOTTIS)
• TEETH-CHALKY WHITE, TONGUE-SWOLLEN, SODDEN AND BLACK
• DISTENDED ABDOMEN, SEVERE CONSTIPATION
• VOICE TURNS HOARSE AND HUSKY
• SUNKEN EYES AND DILATED PUPIL
• IF THE PERSON RECOVER LATE OESOPHAGEAL, GASTRIC AND PYLORIC STRICTURE AND
STENOSIS MAY DEVELOP

19. CAUSE OF DEATH
• CIRCULATORY COLLAPSE
• SPASM OR OEDEMA OF GLOTTIS
• COLLAPSE DUE TO PERFORATION OF STOMACH
• TOXAEMIA
• DELAYED DEATH DUE TO HYPOSTATIC PNEUMONIA, SECONDARY
INFECTION, RENAL FAILURE OR STARVATION

20. POSTMORTEM APPEARANCE
EXTERNAL
• NECROTIC AREAS ARE FIRST GREYISH WHITE SOON TURN BROWN-
BLACK AND LEATHERY
• CORROSION OF MUCOUS MEMBRANES OF LIPS, MOUTH, THROAT
AND OF THE SKIN OVER THE CHIN, ANGLES OF MOUTH AND HAND
• CLOTHING SHOULD BE EXAMINED FOR BURNS AND STAINS

21. INTERNAL-
• UPPER DIGESTIVE TRACT IS INFLAMED, SWOLLEN AND
PRESENCE OF SEVERE INTERSTITIAL HAEMORRHAGE
• IF THE ACID IS TAKEN FROM A SPOON MOUTH AND LIP ESCAPES
INJURY
• ACIDS PRODUCES THEIR MAJOR EFFECT ON COLUMNAR
EPITHELIUM OF STOMACH THAN THE SQUAMOUS EPITHELIUM
OF OESOPHAGUS
• STOMACH IS CONVERTED INTO SOFT, SPONGY, BLACK MASS
WHICH DISINTEGRATES ON TOUCHING
• SOMETIMES ONLY PYLORIC REGION IS INVOLVED

22. • MORE DAMAGE TO MUCOSAL RIDGES THAN
INTERVENING FURROWS
• MUCOSA OR EVEN THE WHOLE THICKNESS OF STOMACH
TURNS BLACK-BROWN
• STOMACH CONTAIN ALTERED BLOOD FROM DAMAGED
MUCOSA WHICH IS BLACK OR BROWN -DUE TO ACID
HAEMATIN FORMATION
• CALCIUM OXALATE CRYSTALS MAY BE PRESENT IN
STOMACH CONTENT OR IN SCRAPINGS FROM MUCOSA
• PERFORATION OCCURS WITH THE ESCAPE OF GASTRIC
CONTENT TO PERITONEAL CAVITY-PERITONITIS(IF THE
PERSON SURVIVES)
• PERFORATION OF DIAPHRAGM MAY ALSO OCCUR

23. • LITTLE OR NO ACIDS MAY BE FOUND IN VISCERAAS THEY WILL
BE CONVERTED NORMALLY PRESENT SUBSTANCES-IF THE
VICTIM SURVIVED FOR 2 OR MORE DAYS
• CORROSION OR INFLAMMATION OF TRACHEAAND LARYNX
• SECONDARY TOXIC SWELLING OF LIVER AND KIDNEY

25. TIME COURSE OF THE INJURY
• ACUTE INFLAMMATORY STAGE- 4-7 DAYS
PERFORATION & ACIDOSIS
• GRANULATION STAGE- 4-7 DAYS
• PERFORATION-7-21 DAYS( WEAKEST TISSUE)
• CICATRISATION STAGE-STARTS AT 3 WEEKS TO YEARS
OVER PRODUCTION OF SCAR TISSUE RESULT IN STRICTURE
FORMATION

26. TESTS-
• ANALYSIS OF MATERIAL PRESENT I STOMACH
• STRONG ACID CHARS ORGANIC MATTER
• BARIUM NITRATE OR CHLORIDE SOLN PRODUCE WHITE
PRECIPITATE
CIRCUMSTANCE OF POISONING-
• ACCIDENTAL-MISTAKEN FOR CASTOR OIL, GLYCERINE OR
VAPOUR INHALATION IN FACTORIES
• SUICIDAL
• INJECTED IN TO VAGINAAS ABORTIFACIENT

27. VITRIOLAGE
• VITRIOL THROWING
• THROWING OF SULPHURIC ACID ON ANOTHER
INDIVIDUAL
• PENETRATING BURNS WHICH PREDISPOSE TO
INFECTION
• SLOW REPAIR
• BLINDNESS MAY OCCUR, IF EYES IS INVOLVED
• DEATH MAY BE DUE TO SHOCK OR TOXAEMIA

28. TREATMENT
• AVOID GASTRIC LAVAGE
• IMMEDIATE DILUTION AND NEUTRALIZATION BY GIVING ONE FOURTH LITRE OF
WATER OR MILK O MAGNESIA OR MILK
• ALKALINE CARBONATES AND BICARBONATES LIBERATING CARBON DIOXIDE
SHOULD BE AVOIDED
• GIVE A DEMULCENT
• PREDNISOLONE 60MG/DAY-PREVENT OESOPHAGEAL STRICTURE
• CORRECT CIRCULATORY SHOCK
• TRACHEOSTOMY-IN CASES OF OEDEMA OF GLOTTIS
• NUTRIENT SUBSTANCES SHOULD BE GIVEN VIA I.V NOT BY MOUTH
• SKIN BURNS-WASH WITH WATER AND APPLY MG HYDROXIDE OR SOD.
BICARBONATE
• EYE BURN- WASH WITH WATER AND INSTIL SOD. BICARBONATE

29. NITRICACID
• Strong Acid(Inorganic).
• Physical properties - Pure ,colourless,fuming, heavy liquid with a peculiar and
choking odour.
• Chemical property – Xanthoproteic reaction(concentrated acid combines
with protein to produce picric acid imparting yellow colour)
• Sources: Industrial, Commercial & ChemicalLaboratories
• Local action –
• corrosion on the area of directcontact
• Respiratory distress if fumes areinhaled
• Indirect action – shock due to pain
• Fatal dose : 10-15 ml (conc.)
• Fatal period: 12-24 HR or more

30. SIGNSAND SYMPTOMS
• Burning pain in mouth, throat, oesophagus and stomach spreading over the abdomen.
• Erosion of the skin over ankles of mouth, lips and fingers with yellowishdiscoloration
• Erosion of mucous membranes of mouth and tongue
• Difficulty in speech and swallowing due to the presence of saliva, mucous and corroded matter.
• Teeth develops yellowish surface coating.
• Eructation &thirst
• Inhalation of fumes causes lachrymation, photophobia, irritation of air passages and lungs producing
sneezing, coughing, dyspnoea andasphyxia.
• Vomiting is seen and the vomitus reaction is strongly acidic with altered blood and mucous shreds.
• Stiffness of the stomach may be due to distension or rupture (less common) of the stomach.
• Tenderness of abdomen and abdominal distension are usually seen.
• Perforation of stomach maybe seen sometimes but it is less common.
• Stool with mucous and alteredblood.
• Tenesmus (constant urge to evacuate an empty bowel)
• Suppressed urination and brown urine

31. CAUSE FOR DEATH
• Shock
• Laryngeal spasm due to trickling of acid or vomitus or inhalation of vapour.
• Perforation ofstomach.
• Peritonitis.
• Pneumonia due to inhalation of fumes.
• Glottic edema.
Materials to be preserved from death
Preservatives
• Viscera and skin are preserved in absolute alcohol or rectified spirit
• Clothes are sent without any preservation.
• stomach with contents
• a loop of upper part of the small intestine Preserved in one
• half of liver
• half of each kidney
• corroded areas of skin are preserved in another container.
• Acid-stained clothes are preserved separately .
container

32. Dark brown
urine
CORROSIVE BURNS AROUND THE LIPS,
ON THE CHIN AND ON THE RIGHT SIDE
OF THE NECK.
Suicidal ingestion of lysol. Spillage
around the mouth has run down to the
neck and onto the chest

34. POST-MORTEMAPPEARANCES
• They are similar to post-mortem findings of sulfuric acid but there are some
things only seen in nitric acid poisoning.
• Xanthoproteic reaction causes a yellowish discolouration of theskin
of the affected area, mucous membranes of mouth, tongue and oesophagus.
• Stomach wall-
• swollen and soft with desquamation, haemorrhage andulceration.
• Xanthoproteic reaction is not prominent due to altered blood (acid hematin) that
causes dark brown discolouration of its mucous membrane.
• Perforation (less common than sulfuric acid) leads to leakage of acid and corrosion of
the nearby organs and tissues withthe development of chemical
peritonitis
• Upper part of the small intestine shows signs of irritation.
• Inhalation of vapours or vomitus can lead to the congestion of the larynx,
trachea and bronchial tubes &oedema of the lungs.

35. MECHANISM OFACTION
• Extent and severity of action on GIT depends upon 3factors
• Corrosive nature of Ingested Substance
• Quantity and Conc of Ingested Substance
• Duration of Contact
• Initially when the agents come in contact with body, there occurs an intense inflammatory
reaction in first 4-7 days.
• If he survives,granulation stage will follow- fibroplasia and formation of collagen starts.
• During second and third week, chance of perforation isthere.
• At third week, the cicatrisation stage starts and excessive formation of scar tissue will result
instricture.
• Action is characterized by
• extraction of water from tissues
• coagulation of cellular proteins
• conversion of Hbinto haematin
• Nitric acid acts as-
• corrosive agent in concentrated form
• diluted, act as irritants
• very much diluted and taken by mouth, some of them act as stimulants to digestive process

36. TREATMENT
TO DO
• Administration of weak acid(carbonated beverage or citrus juice).
• Administration of base ( antacid) is alsoacceptable.
• Secure the airway.
• Administration of H2 blockers.
• Monitor acid base and electrolytesstatus.
NOTTO DO
• GASTRIC LAVAGE : Risk of perforation.
• Administration of EMETICS:Leads to new exposure and risk of
aspiration.
• Any Neutralization agents: Leads to heat production and moreinjury.
• Activated Charcoal : Obscures endoscopic view.
• Do not give patients anything orally for 2 -3days after initial
administration of water or milk.

37. OTHER TREATMENTS
• Concomitant prophylactic broad spectrum antibiotics use is
recommended.
• Oesophagial strictures or gastric outlet obstruction may require
subsequent dilatation or surgical reconstruction.
• Laparotomy is recommended for patients with gastric perforation and
peritonitis.
• Skin lesions need to be washed with soap and water followed by
application of a thick paste of magnesium oxide or carbonate
• Eyesif involved are washed with water and irrigated with a dilute sodium
bicarbonate solution. Later few drops of olive oil or castor oil are instilled
into the eyes. Referral to an ophthalmologist is advisable

38. MEDICO LEGALASPECTS
• Accidental poisoning very rare since it is a yellow fluid giving off irritating
fumes.
• Not much used for homicides since the effects are too immediate and violent.
• In a suicidal attempt, intense pain on swallowingthe acid may result in
spluttering and consequent staining about the mouth, chin and clothing.
• Acute exposure to vapours in industries– death due to respiratory
distress
• Prolonged exposure to vapours in industries – respiratory complications
• In fatal cases of poisoning, no trace of the poison may be discoverable in the
viscera, especially if the victim had survived for a couple of days or more. Salts
of these acids being common constituents of food and medicine, it is important
to ascertain whether any of these acids is present in the free condition.
• John George Haigh – a.k.aacid-bath murderer – disposed corpses into sulfuric
acid to degrade. The attempt was not completely successful and the sketchy
remains, viz., a part of the left foot, a few bone fragments,

39. Organic acids as poisons
Organic acids differ from inorganic acids in two major
respects: (i ) they are weaker in action and (ii ) they are
usually
absorbed into circulation and so have both local and
remote
action

40. CARBOLISM

41. PHYSICAL CHARACTERISTICS
 Carbolic acid consists of long, colourless, prismatic,
needle-like crystals, which turn pink on exposure to
light.
◾has characteristic carbolic orphenolic smell
◾slightly soluble in water andfreely soluble in glycerine, ether,
alcoholand benzene
 Commercial carbolic acid- dark brown liq.
 Household car. Acid- 5% phenol in water
 Used as disinfectant and antiseptic( past)

42. FATAL DOSE: 10-15G ;20ML
FATAL PERIOD: 3-4 HRS
CLINICAL FEATURES
 ON SKIN EXPOSURE: BURNING SENSATION FOLLOWED BY
TINGLING & ANAESTHESIA
 INHALATION OF VAPOURS : CAUSES RESPIRATORY TRACT
LIKE PULMONARY EDEMA AND LARYNGEAL EDEMA: CAUSING
BREATHING DISTRESS
 INGESTION: STRONG CARBOLIC ODOUR IN MOUTH, BURNING
SENSATION IN MOUTH, THROAT; VOMITING& ABDOMINAL PAIN;

43.  DUE TO RAPID ABSORPTION CNS & CVS SYMPTOMS ARE SHOWN
GIDDINESS
INSENSIBILITY DEEPENING COMA
PUPILS CONSTRICTS
TEMPERATURE DROPS
PULSE: SMALL , THREAD
RESPIRATION: SLOW
 METABOLIC ACIDOSIS IN SEVERE CASES
 RENAL FAILURE DUE TO DIRECT TOXICITY OR CAN BE DUE TO HYPOTENSION
AND HEMOLYSIS
URINARY FINDINGS IN CARBOLISM( CARBOLURIA)
• CONTAINS TRACE OF FREE CARBOLIC ACID AND THE METABOLIC PRODUCTS OF PHENOL
• TURNING IT TO A DARK, SMOKY GREEN COLOUR ON STANDING( OXIDATION).

44. • a white opaque eschar which is painless
and falls off in a few days and leaves a
brown stain.

46. CHRONIC POISONING (PHENOL
MARASMUS)
◾Characterised by-- Anorexia, weightloss, headache,
vertigo, dark urine and pigmentation of skin and sclera.
◾Hydroquinone and pyrocatecholmay cause
pigmentation in the cornea and various cartilages, a
conditioncalled oochronosis.
◾This is associated with alkaptonuria

47. Cause of death
◾Syncope
◾Asphyxia
▪️edema of glottis
▪️complications-bronchopneumonia
Diagnosis
The urine may show red blood cells, proteins and casts.
 Add a few drops of 10% ferric chloride in urine. A violet or blue colour indicates
presence of phenolic compounds.
 The urine containing carbolic acid also reduces Benedict and Fehling solution

48. POST-MORTEM
APPEARANCE
EXTERNALLY:
 THE CONTAMINATED AREAS OF THE SKIN MAY APPEAR REDDISH, NECROSED AND
SOMETIMES DENUDED AND ULCERATED.
 THE MUCOUS MEMBRANE OF MOUTH IS HYPERAEMIC WITH DESQUAMATION AND
HAEMORRHAGIC POINTS.
 PHENOLIC ODOUR IS PERCEPTIBLE.
INTERNALLY
 THE OESOPHAGUS MAY APPEAR REDDISH AND PARCHMENTIZED.
 THE MUCOUS MEMBRANE OF THE STOMACH SHOWS PROMINENT RUGAE; IT IS THICKENED,
MORE OR LESS BROWNISH IN COLOUR AND LOOKS LEATHERY.
 THE CONTENTS APPEAR DARK BROWN MIXED WITH MUCUS, IMPARTING SMELL LIKE THAT
OF PHENOL.

49.  SIGNS OF IRRITATION WILL BE SEEN IN THE STOMACH EVEN WHEN THE ACID IS NOT
SWALLOWED BUT ABSORBED FROM THE MUCOUS OR SKIN SURFACE.
 SIMILAR CHANGES MAY BE NOTICED IN THE UPPER PART OF THE SMALL INTESTINE.
 THE HEART MAY APPEAR FLABBY.
 DEGENERATIVE CHANGES BECOME APPARENT IN THE LIVER AND THE KIDNEY, IF THE DEATH IS
PROLONGED

50. TREATMENT &
MANAGEMENT
• THE AREA SHOULD BE THOROUGHLY WASHED WITH SOAP SOLUTION OR 25% ALCOHOLIC SOLUTION AND
BE TREATED WITH SOME VEGETABLE OIL
• WHEN INGESTED, CAUTIOUS GASTRIC LAVAGE IS RECOMMENDED
 MAY BE CARRIED OUT WITH 20% ALCOHOL OR GLYCEROL OR WITH SOME VEGETABLE OIL.
 ALCOHOL HAS AN ADVANTAGE IN THAT IT DISSOLVES THE AMOUNT OF PHENOL FROM THE MUCOUS MEMBRANE AND
SUBMUCOUS LAYER OF THE STOMACH. BUT IT MAKES THE ABSORPTION OF THE PHENOL EASY AND AS SUCH NEEDS TO BE
EXCRETED OUT QUICKLY
 SODIUM OR MAGNESIUM SULPHATE SOLUTION CAN BE USED FOR THE LAVAGE
 DEMULCENT DRINKS LIKE MILK, BARLEY WATER OR EGG ALBUMIN ARE ALSO ADVOCATED
 FOR EFFICIENT EXCRETION, INTRAVENOUS INFUSION OF FLUID WITH SODIUM BICARBONATE SOLUTION
MAY BE GIVEN.
 SALINE+7G OF SODIUM CARBONATE IV-TO COMBATE CIRCULATORY DEPRESSION TO DILUTE CARBOLIC
ACID CONTENT OF BLOOD.
 HAEMODIALYSIS (RENAL FAILURE)
 METHYLENE BLUE IV (METHEMOGLOBINEMIA)
 IF PHENOL FALLS ON BODY CONTAMINATED CLOTHING MUST BE REMOVED,SKIN WASHED WITH
UNDILUTED POLYETHENE GLYCOL. IF NOT WASH WITH SOAP AND WATER FOR 15 MINUTES

51. MEDICOLEGAL ASPECTS
• BEING EASILY AVAILABLE, PHENOL WAS AT TIME A POPULAR SUICIDAL AGENT
• ACCIDENTAL POISONING CAN OCCUR ( CHILDREN) AS IT IS A DISINFECTANT
• CHRONIC INTOXICATION MAY OCCUR FROM INHALATION OF VAPOUR FROM INDUSTRIAL
SOURCES.
• PHENOL IN DILUTION OR MIXED WITH SOME OTHER AGENT MAY BE USED TO CAUSE
ABORTION
• CARBOLIC ACID MAY NORMALLY OCCUR IN THE URINE IN TRACES IN THE FORM OF
PHENOL-SULPHONATE OF POTASSIUM
• ENGEL ESTIMATED THAT THE QUANTITY OF CARBOLIC ACID EXCRETED BY A HEALTHY MAN
LIVING ON A MIXED DIET IS 15 MG IN 24 HOURS.

52. OXALIC ACID POISONING:

53. PHYSICAL
CHARACTERISTICS
• COLOURLESS
• BITTER IN TASTE
• SOLUBLE IN WATER
• VAPORISES ON HEATING AND SUBLIMATES ON COOLING OF THE VAPOUR.
SOURCES
• METAL CLEANING AGENTS AND STAIN REMOVERS
• LEATHER, DYE AND BOOK BINDING INDUSTRY.
• RHUBARB (PARTICULARLY LEAVES), SPINACH, LICHEN, ONION, CABBAGE

54. MECHANISM OF
ACTION
• GIVEN IN A STRONG SOLUTION, IT EXERTS A CORROSIVE ACTION ON THE MUCOUS MEMBRANES.
• AFTER ABSORPTION, IT PRODUCE HYPOCALCAEMIA, NEPHROTOXICITY, ETC
• IT COMBINES WITH SERUM CALCIUM TO FORM INSOLUBLE CALCIUM OXALATE THEREBY
RESULTING IN HYPOCALCAEMIA.
• IT LEADS TO MUSCULAR STIMULATION WITH CONVULSIONS AND ULTIMATELY LEADING TO
COLLAPSE.
FATAL DOSE
• 15–20 GM USUALLY CAUSES FULMINATING POISONING AND DEATH.
FATAL PERIOD
• IN CASE OF FULMINATING POISONING, DEATH MAY OCCUR WITHIN A COUPLE OF HOURS.
• IN CASE OF HYPOCALCAEMIA, DEATH MAY OCCUR WITHIN 12 HOURS.

55. CLINICAL
FEATURES
• DOES NOT CAUSE MUCH CORROSION OF THE SKIN
• A SOUR TASTE IN THE MOUTH,
• BURNING IN THE THROAT AND STOMACH WITHIN A SHORT TIME
• VOMITING IS SEVERE AND BLACK IN COLOUR DUE TO ALTERED BLOOD.
• LARGE DOSES MAY CAUSE RAPID DEATH FROM SHOCK( INTESTINAL TRACT NOT AFFECTED)
• PAIN AND TENDERNESS OVER THE ABDOMEN,AND TENESMUS MAY APPEAR
• HYPOCALCAEMIA CAUSES TINGLING AND NUMBNESS OF FINGERS AND LIMBS.
• THERE IS MUSCULAR TENDERNESS, IRRITATION AND TETANIC CONVULSIONS.
• RESPIRATION IS SLOW.
• THERE IS BRADYCARDIA WITH WEAK, IRREGULAR PULSE.
• VENTRICULAR FIBRILLATION MAY LEAD TO DEATH

56. • IF THE PATIENT SURVIVES HYPOCALCAEMIA, THERE MAY BE TOXIC NEPHRITIS.
• IN SUCH CASES, THERE IS URAEMIA WITH SCANTY URINATION, HAEMATURIA,
ALBUMINURIA, OXALURIA

58. TREATMENT &
MANAGEMENT
• A SOFT STOMACH TUBE CAN BE PASSED WITH CARE AND THE STOMACH WASHED OUT USING
CALCIUM LACTATE
• DEMULCENT DRINKS SHOULD BE GIVEN TO PROTECT THE MUCOUS MEMBRANE OF THE
STOMACH
• BOWEL WASH BY ENEMA AND PURGATIVES TO REMOVE THE UNABSORBED POISON FROM THE
GUT.
• CALCIUM GLUCONATE MAY BE GIVEN ORAL OR 10 ML OF A 10% SOLUTION SLOWLY
INTRAVENOUSLY, WHICH COMBINES WITH THE OXALIC ACID IN THE CIRCULATION THUS SAVE
THE CALCIUM OF THE BLOOD.
• IN SEVERE CASES, PARATHYROID EXTRACT MAY BE GIVEN.
• URINARY OUTPUT SHOULD BE CHECKED TO DETECT THE POSSIBILITY OF RENAL DAMAGE AND
FLUID INTAKE CONTROLLED.

59. POST-MORTEM
APPEARANCES
• DEPENDS ON THE CONC. OF ACID
EXTERNALLY:
• MUCOUS MEMBRANE OF THE MOUTH AND TONGUE ARE CORRODED, SWOLLEN, SODDEN,
BLEACHED OR BROWNISH WITH OCCASIONAL DESQUAMATION AND HAEMORRHAGIC POINTS
INTERNALLY
• THE STOMACH IS SWOLLEN AND SOFT
• THE WALL IS REDDENED OR BLEACHED.
• NUMEROUS DARK BROWN OR BLACK STREAKS MAY BE FOUND ALONG THE LENGTH OF THE
STOMACH, OFTEN FORMING A NETWORK OVER THE SURFACE.( DUE TO THE ACTION OF THE ACID IN
THE VESSELS OF WALL)
• THE PRESENCE OF THIS BROWNISH STREAK IN THE STOMACH WALL HELPS TO FIND THE CAUSE OF DEATH IS OXALIC ACID
POISONING
• DESQUAMATION AND HAEMORRHAGES MAY BE FOUND
• PERFORATION IS RARE.

60. • STOMACH MAY CONTAIN GLAIRY, BROWNISH, GELATINOUS MUCUS MIXED WITH ALTERED
BLOOD.
• THE UPPER PART OF THE SMALL INTESTINE & KIDNEYS MAY SHOW SIGNS OF IRRITATION.
• THERE MAY BE EVIDENCE OF TOXIC NEPHRITIS
Stomach in oxalic acid poisoningBrownish streaks

61. MEDICO-LEGAL ASPECTS
• OXALIC ACID AND ITS SALTS ARE USED IN INDUSTRY IN BLEACHING MATERIALS FOR STRAW HATS
AND VEGETABLE FIBRES, WOOD, LEATHER, INK STAINS, ETC., AND FOR DISCHARGING DYES IN
CALICO PRINTING..
• SINCE EASILY AVAILABLE USES AS SUICIDAL PURPOSES
• HOMICIDAL RARE DUE TO ITS TASTE AND EARLY ONSET OY SYMPTOMS
• ACCIDENTAL POISONING CAN OCCUR( CHILDREN)
• TWO POTASSIUM SALTS OF THE ACID ARE IN COMMON USE IN ARTS, VIZ., BINOXALATE AND
QUADROXALATE (‘SALT OF SORREL’ AND ‘ESSENTIAL SALT OF LEMONS’), AND BOTH ARE NEARLY AS
POISONOUS AS OXALIC ACID
• OXALIC ACID CAN GAIN ACCESS TO THE BODY THROUGH FOOD AND DRUGS OF VEGETABLE
ORIGIN( SOURCES)
• URINE CONSTITUENT: .02GM EXCRETED 24HRS

63. INTRODUCTION
FORMIC ACID IS A
 Colorless liquid with pungent, penetrating odour.
 Used in electroplating, tanning, rubber, textile & paper
industry, airplane, glue , stain remover etc.

64. ACTION
 Corrosive action (coagulation necrosis) on G. I
mucousa
 Causes hemolysis leading to acute renal failure.
 ATP synthesis is diminished.
 FATAL DOSE : 50 – 200ml

65. SIGNS AND SYMPTOMS
GASTROINTESTINAL TRACT
 Burning pain
 Salivation
 Vomiting
 Mucosal ulceration and corrosion
 Haematemisis

66. RESPIRATORY
SYSYTEM
 Acute respiratory
distress
BLOOD
 Hemolysis
CVS
 Tachycardia or bradycardia
 Hypertension or hypotension
CNS
 Drowsiness
 Dilated pupil
 Coma
SKIN
 Blisters
 Metabolic acidosis
 Shock and death

71. TREATMENT
 Milk is given for dilution of acid
 Gastric lavage and emetics are contraindicated
 Folinic acid 1mg/kg i. v at 4 hourly interval 6
doses
 Dialysis for exchange transfusion

72. POSTMORTEM APPEARANCE
 Corrosion and blackening of gastric mucousa
 Pulmonary edema
 MEDICOLEGAL: Poisoning is accidental or suicidal

73. BY
AKHIL SHIROZ
KARUNA MEDICAL
COLLEGE