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Abstract
The incidence of venomous snakebites is high in rural areas where people are engaged in agricultural activities & are in the habit of sleeping on the floor. About 40,000 people die each year from venomous snake bites (worldwide).Death can be prevented if diagnosis & management is made early in the course. Thus a high degree of clinical suspicion, a timely diagnosis & management is life saving in these cases as it happened in this case report.
Acute onset of pain abdomen in previously healthy young male adults who were sleeping on the floor, without any history of bite, were successfully treated & cured based on high index of clinical suspicion with appropriate antivenom therapy.
Key words : Venomous snake bite , Clinical suspicion, Acute abdomen, Timely diagnosis & management
Introduction
Snakebite is common in rural areas. Venomous snakenites of the families like Elapidae (Cobra, Krait ) & Viperidae (Viper) are verycommon. Clinical symptoms & signs vary with the species of snake & the amount of envenocation. Fang marks , local swelling , echymosis, blistering , necrosis , are seen at the site of bite in viper bites. Bleeding & clotting disturbances, DICC, ARF , shock are also seen inm veperbites. (Krait ) local signs are absent & the neurotoxic symptoms mostly appear within 1-2hrs after the bite (15min.-15hrs). Blurring of vision , ptosis , dysphagia, Opthalmoplegia, paralysis of muscles of respiration, alteration of consciousness, coma, convulsion occur.
But a patient with a venomous snake bite presenting with features of Acute abdomen has not been reported in neurotoxic bites except in cases of viper & colubridae bites so far. Therefore acute pain abdomen with neurotoxic signs & symptoms should prompt one to suspect snake bite & to exclude other causes of Acute pain abdomen with neurological signs , so that appropriate therapy (ASV, Neostigmine) & supportive measures can be life sving.
Case report
(1) A young male adult about 26 years tushed in to the casualty O.P.D. in early morning with complaints of acute pain abdomen, vomiting , difficulty in deglutition for 6 hrs. Family History : Similar symptoms in his mother who died 1 month back. No other specific complaint was reported by his relatives except for some weakness & frothing from mouth. For this he was treated at Sundergarh district hospitas as a case of acute pancreatitis & was referred to V.S.S Medical College, Burla as patient deteriorated,. For further evaluation & management.
Examination revealed:
Average Body built, drowsy ptosis, frothing from mouth, Restlessness because of severe pin abdomen.
Pulse – 82/min, regular,
BP – 140/90 mmHg
R.R – 20/min, Thoracoabdominal type , No pallor, Icterus, Cyanosis, Lymphadenopathy
Chest – Clinically NAD
CVS – NAD
P/A – Revealed diffuse tenderness & rigid abdomen , No organomegaly.
Bowel sounds absent – No evidence of freefluid.
CNS – Conscious, drowsy, difficulty in speech & deglutition ( both liquied + solid ) bilateral ptosis was present
No sensory, motor deficit
No meningeal sign
Plantar ( B/L Flexor )
After about 5 min. of admission in the casualty O.P.D., Surgery consultation was done who excluded any surgical, cause of acute abdomen. Necessary investigations were done immediately , which revealed DC – N80 ,E1,L18,M1, TLC- 10,200/Cumm, HB % - 11.6gm %ESR-20mm,1st hr, BI.Urea-40 mg %Sr.Cr.-0.8mg%,Sr.Na+ -137m mol/L,Sr.K+=2.6M MOL/l,Sr.LIPASE- 180 I.U./L, Whole Blood Clotting test neg. , PT – N Sr. Amylase –27UL,St. X-ray Abnormal, U.S.G. Abd. – NAD , ECG – Normal except for the presence of U. waves due to hypokalemia, chest X- ray – NAD.
The patient was finally diagnosed provisionally basing on minimal Neurotoxic sogns & symptoms as a suspected case of neurotoxic snake bite & was treated with (150ml) i.e. 15 vials of Antisnake Venom (ASV), Inj. Atropine 0.6mg I.M. Followed by Inj. Neostigmine (0.5mg) I.V. every 30 minutes for 5 doses, and repeated at 6 hrly. Other supportive care included Nil orally. Throat suction, Broad spectrum antibiotics, I.V. fluids, Hydrocortisone, Symptomatic treatment of pain & vomiting. Hypokalemia was corrected by I.V. kc! Infusion.
With the above treatment after about 2 hours, the patient’s condition started improving gradually with dimunution of pain abdomen, disappearance of ptosis, dysphagia & the patient was symptom free after 2 days & was discharged from the hospital.
(2) Interestingly another young male of 21 years with definite history of Krait bite also presented after one month with the chief complaint of pain abdomen & on examination had features of neurotoxic signs & symptoms & improved with ASV, atropine, Neostigmine. This substantiates further the fact that acute pain abdomen may be a presenting symptoms in Neurotoxic (krait) bites.
Discussion:
Snake bite is common in rural areas. Agricultural workers, hunters, & people sleeping on the floor are at risk as are evident in these cases. History of snake bite may not be present in some cases especially those bitten by krait (Neurotoxic venomous snakes) & fang marks & local signs may not be present. Signs such as early morning ptosis, dysphagia & pain abdomen should prompt one to highly suspect snake bite (Neurotoxic) & to start treatment as early as possible for a good outcome.
A delay in clinical suspicion & diagnosis & thus institution of proper therapy would have proved fatal in the case like his mother who died one month back with similar symptoms without h/o snake bite & without antivemin therapy: could be due to same environment of snakebite.
Conclusion:
Acute abdomen like presentation in neurotoxic snake bites is not yet reported in literature. However this case report suggests that Acute abdomen can be a presentation of snake bite & high clinical suspicion & appropriate therapy may save life.
References:
1. Manson’s Tropical diseases – 20th Edition.
2. Hodge III D, Snake bites. In Emergency medicine Eds. May HL, Little Brown Company, Boston, 2nd Edition 1992, 925-928.
3. Reid H.A. Snake bite in tropics British Medical Journal, 1968 3 (614): 359-362.

endocrinopathies or may a pointer towards a group of disorders. So, these skin manifestations are important in differential diagnosis of many disorders.

Diabetes mellitus, hyperthyroidism, hypothroidism, disorders of adrenals and gonads are the main endocrinopathies having skin manifestations and at time these signs help in reaching a definite diagnosis.

Certain skin lesions such as hyperpigmentation,sclerederma, xanthomas, lipomas, increased muscle mass , vesico bullous eruptions, yellow or red paules, fungal or bacterial infection, alopecia etc need the exclusion of endocrinopathies.

INTRODUCTION:
Skin is a very good reflector of internal disease in general and endocrine diseases in particular. Specific skin lesions may reflect a variety of endocrine diseases as well as manifest secondary conditions underlying metabolic disturbances. A knowledge of the same makes the diagnosis of endocrine diseases easier, which avoids delay and difficulty in diagnosis.

A timely diagnosis and early treatment spares future complications and saves the patients from their avoidable suffering. It is important that an attempt should be made to review the available literature to familiarize the treating physicians about the importance of skin markers of endocrine diseases.

These disorders are diabetes mellitus and endocrine disturbances of thyroid , adrenals , gonads and others.


I. DIABETES MELLITUS
A. PRIMARY SKIN DISEASES ASSOCIATED WITH DIABETES MELLITUS
1. Diabetes demopathy (pigmented pretibial patches, skin spots): Lesion of diabetic demopathy are less than 1 cm and are red brown , atrophic macules on the anterior shins which may begin as papules . Capillary basement membranes appear to be thickened.
2. Necrobiosis lipoidica diabeticorum (NLD): MLD lesions also characteristically appear on the anterior shins and are oval, atrophic plaques that can reach several centimeters in size. They have a raised , erythematous border and a yellow – brown, waxy central atrophic area through which telangiectatic subcutaneous vessels are easily visible. These lesions may also ulcerate.
3. Disseminated granuloma annulare (GA): Multiple small, grouped erythematous to flesh-coloured papules, which coalesce into small plaques covering the entire body surface have been associated with diabetes mellitus. However, patients with GA, even if it is extensive, do not necessarily have diabetes mellitus.
4. Lipodystrophy.:
a. The Siep-Lawrence syndrome (and related disorders with lipodystrophy) may be cogential and include insulin- dependent diabetes mellitus, hypertricosis, hyperpigmentation, increased muscle mass and somatic growth elevated trglycerides and cirrhosis of the liver.
b. Local lipoatrophy or lipohypertropy may appear at sites of insulin injection. The mechanism is unclear.
5. Insulin resistance and acanthosis nigricans: May be associated with polycystic ovaries in young women (Type A) or with antibodies to insulin receptors and other autoimmune phenomena (Type B).
6. Bullous diabeticorum: Tense blisters that appear suddenly on apparently normal skin usually on the extremities may occur in diabetes. Histologically the blister may be intraepidermla . Lesions may tend to ulcerate.
7. Eruptivexanthomas are accumulations of lipid in macriphages to form widespread yellow to red papules, which may occur in a linear fashion in response to trauma (the Koebner Phenomenon). These lesions appear in patients with poorly controlled diabetes mellitus who have massive hypertriglyceridemia.
8. Sclerederma (adultorum of Buschke) is a rare condition seen in severe insulin- dependent diabetes in which there is thickening of the collagen in the dermis and deposition of acid mucopolysaccarides between collagen bundles. The lesions are broad areas of non-pitting edema and hardening of the skin, especially on the face, neck, and upper trunk.
9. Idiopathic hemochromatosis , a disorder of excessive iron storage, consists of a triad of hepatic cirrhosis, cardiac insufficiency and diabetes. There is striking hyperpigmentation due to increased melanin deposition in the basal layer of the epidermis.

B. SECONDARY SKIN DISORDERS.
1.) Candida infection of the skin and mucous membranes occur in similar locations as described in glucocoriticoid excess.
2.) Cutaneous bacterial infections, especially staphylococcal infection such as folliculitis furinculocis and frank abscess formation may occur in poorly controlled diabetes patients.
Opportunistic infection by fungal organisms such as Mucor and Rhizopus (Phycomycosis) are rare but are seen in diabetics. Such lesions may be fatal.

II THYROID
A. HYPERTHYROIDISM.
1. General features of hyperthyroidism include warmth, increased sweating flushing and a smooth velvety texture of the skin. In sever cases there may be generalized. hyperpigmentation.
2. Hair and nails: Hair may becomethin, fine, limp and oily. There is distal onycholysis (separation of the nail plate from the nail bed). characteristically starting on the fourth finger (plummer nail).
3. Pretibial myxedema (PTM) :Localised accumulations of acid mucopolysccharides (hyaluronic acid) appear as red to brown to yellow plaque, usually on the anterior shins. There is a “peau f orange” pebbly surface with dilated hair follicles and coarse hairs. Lesions are non-pitting, cool, non-tender and may be pruritic. PTM is seen with active Graves Diseaseas well as or euthyroid “burnt out” or treated patients. High long-acting thyroid stmultor )LATS) levels have been associated with PTM.
4. Thyroid acropachy: Diffuse thickening of the distal extremities, clubbing and periosteal new bone formation with characteristic perpendicular bone spicules are seen associated with Graves Disease, often with opthalmopathy and pretibial myxedema.
B. HYPOTHYROIDISM
1. Congential signs of hypothyrodism are shubtle and should be vanishing with the advent of newly started screening programs for hypothrroidsm. General features includes cool, pale, translucent, “alabaster” skin with a yellow hue. This colour and texture are due to decreased blood flow anaeia. infiltration with mucopolysaccharides, prolonged jaundice and / or cartoenmia. Sweating is reduced. Thermal instability and frank hypothermiaare accompanied by persistent cuits marmorata (purplish discoloration), a violaceous mottling in a vascular pattern. Umbilical hernia, short proximal limbs depressed nasal bridge and large tongue complete the picture of congential hypothyroidism.
2. Acquired hypothyroidism has many of the same general feature as seen in the congential disease. Children and adults, in addition have more prominent dry and scaling skin resembling ichthyosis. Sweating is minimal as the eccrine ducts become atrophic, Generalised myxydema make the skin puffy, pale and doughy with a non-pitting edema, espically noticeable around the face and eyelids due to the accumulation of acid mucopoly saccharides.
3. Hair:Scalp hair is lost in a generalized pattern. The remain scalp hair is coarse and dry. Loss of the lateral one third of the eyebrows. (St. Ann Sign) is characteristic. Pubic and axillary hair is spares. Children may get a paradoxical hypertrichosis of arms. back and legs which is reversible with treatment.

III. ADRENAL
A. HYPOADRENALISM (Adrenocortical insufficiency. Addition’s disease)
1. Patients gradually develop generalized hyperpigmentation, there is darkening of the aerolae, genital skin preexistent nevi, palmar and plantar creases and recent scars. Blue black pigment deposit are seen on the gum at the toot margin and on the hard palate. The etiology of hyperpigmentationis probably due to excessive secretion of melanocyte –stimulating hormone (MSH).

2. 2). Hair in pubic and axillary areas becomes sparse and nails may develop hyperpigmented and linear streaks.

3. 3). Vitiligo rarely occurs in patients with Addison’s disease.

B. HYPERASRENALISM
Pituitary cushing syndrome, adrenal tumors, ad autonomous nodlar adrenal hyperplasia may have features of androgen excess as well as of the glucocorticold excess.
Iatrogenic Cushing Syndrome, resulting from systemic or topical glucocorticosteroids, does not have the androgenic features.
a). Primary features of glucocorticoid excess
1. General features include plethora, telangiectasias and increased growth of fine, downy vellus hair, especially on the sides of the face. With prolonged exposure, there is generalized atrophy of the skin and easy bruisability.
2. Striae represents both dermal and epidermal atrophy and occur in areas of skin tension. They are pigmented and red to blue because the dermal and subcutaneous blood vessels show through the translucent and atrophic skin. In some cases, they may become hyperpigmented with melanin.
3. Steriod acne appears on the upper arem, chest and back as well as on the face. The lesions are actually perifolliclar, hyperkeratotic papules, althroug in late stages these may become pustular and comedonal. The erupt at the same stage of development.
4. Redistribution of subcutaneous fat to the cheeks, upper back, buttocks and abdomen is characteristic.
5. In pituitary disease of in syndromes of ectopic adrenocorticotropic hormone (ACTH) production, there may be hyperpigmentaton, such as seen in Addition’s disease.
6. The androgenic effects from weak adrenal androgens such as dehydropiandrosterone (which may be converted to more potent androgens such as testosterone and dihydrotestosterone) produce classic acne vulgaris as well as hirsutism and male pattern hair loss in women.
h. Secondary features of glucocorticoid excess
1. Tinea versicolor appear as scaly, oval macules and patches on the upper trunk, back and arms wit variable hyperpigmentation or hypopigmentation. it is due to a superficial colonization with the fungus. Malassezia furfur.
2. Candida (Monilia) infections of the skin and mucous membranes include buccal mucosa (thrush) vaginal mucosa, nails and surrounding tissues (onychomycosis and paronychia). Interdigital webs, corners of the mouth (perleche) and intertriginous folds (intertigo).
3. There is an increased occurrence of cutaneous bacterial infections with pustules, furuncles and abscesses especially caused by Staphylococcus aureus.

C. CONGENTIALADRENAL HYPERPLASIA (CAH)
1. Infancy, severe forms of CAH are caused by enzyme defects in the to the synthesis of cortisol and may have only mild cutaneous signs, primarily hyperpigmentation of genital skin from excessive pituitary production of ACTH or MSH or both.
2. In later childhood, early onset of pubic and auxiliary hair and acne are signs of androgen excess.
3. In postpubertal adult women and perhaps in some men “mild” (or “partial” or late onset”) forms of CAH are now being recognized primarily from their skin manifestation of severe late onset or persistent acne, hair loss and hirsutism in women.
Hirustism is defined as excessive hair in androgen-dependent areas , such as upper lip, chin, areolae, linea albha and upper inner thighs. Male pattern hair loss (androgenic alopecia) is thinning of the hair over the crown of the scalp with relative sparing of the sides and back. Affected hair are of smaller diameter and grow to shoter length before entering the resting phase and falling out.
The diagnosis of CAH is made by finding elevation of the hormone that the sustrate for the deficient enzyme (e.g 17-alpha-hydroxyprogesterone in 21 hydroxylase deficiency, II-deoxycortisolin II-hydroxylase deficiency and 17-alpha- hydroxypregnenolone in 3-beta-hydroxysteroid dehydrogenase deficiency). If levels are not elevated in basal blood samples, these may be found as abnormal responses to ACTH stimulation.

IV. GONADS
A. Androgen excess: from the ovary will cause the same skin manifestations of acne, hair loss, and/or hirsutism as described above. Rarely, ovarial tumors are the cause; most grequently, polycystic ovarian disease (PCOD) is the source of hyperandrogenemia from the ovary.
B. In gonadal dysgenesis: (Turner Syndrome), there may be a few special cutaneous features such as multiple brown –black acquired nevi, a double row of eyelashes and low W-shaped posterior hairline, short fourth (and often fifth) digits on the hands and feet with dysplasia or absence of nails hyperconvexity of finger nails and toenails.

V. MISCELLANEOUS
ENDOCRINE DISORDERS
A. Mucocutaneous candidiasis has been associated with muliple endocrinopathy syndrome of autoimmune disorders, including hypoparathyroidism, Addison’s disease, premature ovarian failure, diabetes and Hashimoto’s thyroiditis. Vitiligo complete loss of pigment in patches and alopecia areata patchy hair loss which may progress to total loss of scalp hair (alopecia totails) or of al body hair (alopecia universails) have also been seen in association with these endocrinopathies.
B. Alopecia has been reported in association with vitamin –D resistant rickets in a few well-studied families.
C. Multiple mucosal neuromas are found in the multiple endocrine neoplasia (MEN) syndrome in association with a marfanoid habitus, thick lips hig calcitonin levels, medullary carcinoma of the thyroid and phenochromocytoma.
D. The glucagonoma syndrome consists of a diffuse, scaly brightly erythematous rash made up of gyrate, serpiginous plaques with clear centers and superficial scales. The lesions tend to expand, thus the name necrolytic migratory erythema. Such lesion are seen in association with malignant neoplasms of the alpha cells of the pancreas and have regressed when the tumor has been surgically removed.
E. Acanthosis nigricans (AN) has been associated with a wide variety of endocrine disorders including. Cushing syndrome, pituitary tumours, acromegaly, Addisons’s disease and polycystic ovarian disease. Most cases of AN have underlying insulin resistance.

CLINICAL FOCUS
• Many endocrinopathies involve skin as primary or secondary complication.
• Skin is a very good reflector of systemic disorders including the endocrinal diseases.
• Diabetes mellitus is commonly associated with varied dermatological lesions.
• Thyroid disorder (hyper or hypo) involve skin through various mechanisms.
• Adrenal pathology is associated with various manifestation of skin and its appendages.
• Other uncommon endocrinopathies are also someway associated with dermatopathies.


CONCLUSION
Endocrinipathies are associated with a large number of skin markers. A perfect knowledge about the pointers is mandatory for an endocrinologist or a physician.

The services of a dermatologist will be of immense help in such a situation and hence ideally in case of doubt in any cases the opinion of the dermatologist should be obtained in the greater interest of proper, diagnosis and ideal patient care.

“SUPER VASMOL 33 WITH AYUR PRASH” POISONING – A CASE REPORT

Dr. B.K. Barik, Dr. Dinabandhu Sahu, Dr. Abhiram Behera, Dr. Pusparani Das

ABSTRACT

"Super Vasmol" a commonly used hair dye containing various chemical and herbal ingradients may produce severe local and systemic manifestation when ingested. The fatality is low, the incidence is rare. Here we are reporting a case of vasmol poisoning who was thoroughly investigated and followed up till complete recovery.

KEYWORDS:
Super Vasmol, PPD, Resorcinol, Gastritis, Angioneurotic oedema.

NTRODUCTION:

`"SUPER VASMOL 33 WITH AYURPRASH" is an emulsion hair dye containing Paraphenyl Diamine (PPD), Liquid Paraffin, Cetostearyl Alcohol, Sodium Lauryl Sulphate, EDTA Disodium, Resorcinol, Propylene glycol, Herbal extracts, preservatives and perfume.

Severe angioneurotic oedema, acute renal failure (PPD); oedema, haemolysis, methemoglobinemia in infants, blue black pigmentation (Resorcinol); Acute haemolysis (Propylene glycol); headache, vomiting, gastritis (EDTA) are the serious systemic manifestations when the dye is ingested besides the local allergic reactions observed when in contact with skin in few cases.

CASE REPORT:

A 20 year female alleged to consume 'Super Vasmol 33' on previous night at 10 PM presented with vomiting , dyspnoea, dysphagia, difficulty of speech and gross swelling of neck and face below the chin and mandible (both sides) and dark urination.

The Patient was admitted to the local hospital (after 8 hours of ingestion) with worsening of above mentioned symptoms and treated with injection hydrocortisone (200 mg), injection Chlorpheniramine maleate (1 Amp) injection Cefotaxim (1gm-2 vials), injection Deriphylline (1 Amp) , injection Ranitidine (1 Amp) and oxygen inhalation. As the patient did not improve he was referred to this hospital.

At the time of admission (12 hours after ingestion) the patient was severely dyspnoeic with semi opened mouth having gross swelling of tongue and oral mucosa with salivation. The lip and gums were swollen with black pigmentation, ulceration and bleeding. There was difficulty in speech and swallowing. The urine colour was greenish black and volume was 400 ml since 12 hours. There was swelling efface (submandibular, submental and parotid region) extending to neck.

On examination the temperature was 98.8°F, Pulse 88/minute, regular , BP 126/80 mm Hg, without any localized or generalized lymphadenopathy. There was no pallor, cyanosis or icterus except black pigmentation of lip and gum. Respiration rate was 24/min, regular with vesicular breath sound without any added sound. Heart sounds, were normal without any murmur. There was no neurological deficit. The pharynx could not be examined due to oedema and ulceration of tongue & oral cavity. P/A examination revealed soft abdomen without any organomegaly. The urine was greenish black in color with suppressed volume (400 ml -12 hours). Other systemic examination were normal.

Patient was treated with gastric lavage by normal saline, O2 inhalation, injection Adrenaline - 0.6 mg (starting dose), Injection Avil, Injection Hydrocortisone (100mg) 8 hourly, injection Pantoprazole OD, injection Frusemide, injection Deriphylline 8 hourly and Cefriaxone 1 gm I/V twice daily and Tiniba infusion 500 mg daily and intravenous fluid. Patient gradually improved 3rd day onwards with decrease in mucosal swelling and face & neck swelling. There was slow improvement of the voice, dysphagia, dyspnoea and throat pain. Pharyngeal examination revealed oral mucositis with inflamed postcricoid area and presence of slough in the pyriform fossa. Gradually the colour of urine changed from greenish black to normal with increased volume. The patient was able to take orally (from liquid to solid) with supportive treatment of Xylocaine viscus, antacids.

Early investigation report shows Hb- 10.2gm%, ESR - 28mm/1st hr, TLC-13,000, DC - N 92, EO, BO, L8, MO, RBS - 148mg%, B. Urea 58mg%, S. Creatinine - 2.3mg%, S. Sodium -138 mmol/L, S.Potassium - 3.8 mmol/L, S. Bilirubin - 2.8 mg/dl (Total) 1.6 mg/dl (Direct), SCOT - 852 IU/L, SGPT - 1100 ILJ/L, Alkaline Phosphatase 290IU/L. Urine examination shows proteinurea (+), Puscells 0-3 /HPF with granular and hyaline cast. Upper Gl endoscopy (on 4th day of admission) shows erosive gastritis.

On 10th day, the patient recovered fully. The investigation parameters were normal.

DISCUSSION:

The commonly used hair dye having multiple chemical ingredients cause various complications. The fatality is low and incidence of poisoning is rare.

PPD, one of the intermediate dye used in hair colour is associated with systemic toxicities like severe angioneurotic oedema, acute renal failure and rhabdomyolysis. Liquid paraffin, a saturated hydrocarbon can produce extremely rare hypersensitivity reaction and dermatitis. Cetostearyl alcohol, the combination of aliphatic alcohol and esters act as non-ionic surfactant can produce allergic and urticaria! reaction. Sodium lauryl sulphate, an anionic surfactant used as detergent and foaming agent act as direct irritant at high concentration to the skin. 1% may cause contact dermatitis with burning, redness, tightening of skin with painful fissure and lamellar exfoliation. 2% may produce painful oral desquamation. Resorcinol can produce oedema, haemolysis and methemoglobinaemia in infants with blue-black pigmentary chages.

EDTA (0.3gm%) in excess produce headache, vomiting and gastritis. Propylene glycol is relatively nontoxic, may cause acute hemolysis. In animal when injected causes haemoglobinuric acute renal failure. It has low oral toxicity. Absorption through intact skin is minimal but the application of Propylene glycol containing compounds to infants with large areas of desquamation (e.g. Silver Sulphadizine Therapy in Toxic Epidermal necrolysis) has resulted in cardio-respiratory arrest. The kidney excretes 45% of absorbed dose unchanged and the remainder is metabolized by hepatic alcohol dehydrogenase to lactate, acetate and pyruvate. Liver metabolism produces lactic acids, which enters the glycolytic pathway and after large exposure causes an anion gap and metabolic acidosis. Used as a vehicle in oral, injectable and topical preparations, signs of alcohol intoxication seen after intake of vitamins suspended in Propylene glycol. The compound may be absorbed and produce a rise in serum osmolarity. Contact dermatitis, erythematous oedematous plaque and hypersensitivity occurs. Primarily Propylene glycol is a CMS depressant in large doses and such doses may cause hypoglycaemia, lactic acidosis and seizure in susceptible patients.

Our patient who was attended within hours of ingestion presented with some degree of renal, hepatic and haemolytic features. Local reaction, orophayngeal involvement were profound along with erosive gastritis.

REFERENCES:

1. Goldfrank's Toxicologic Emergencies - 6th Edition, Year 1998, Page Nos. 476-r, 477T, 913-915, 1057-1058.
2. Medical Toxicology Diagnosis and Treatment of Human Poisoning - Mathew J. Ellenhorn, Donald G, Barceloux, Year 1998, Page Nos. 31,32, 36, 442, 528-530,809-810,906,964.
3. Clinical Management of poisoning and drug overdose, Haddad, Shannon & Winchester, 3rd edition, Year 1998, Page No. 1170.

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