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bullous skin lesions and necrosis of eccrine sweat glands have been described in drug induced coma .
the commonest reported cause is barbiturates ; alcohol is a rare cause . a previously reported patient with alcohol induced coma and bullous skin lesions had biochemical evidence of rhabdomyolysis .
coma due to barbiturate toxicity is perhaps the most widely known setting in which such lesions develop .
though , mostly reported in association with drug induced coma , it has been postulated that bullous lesions associated with sweat gland necrosis can occur in comatose states due to any cause .
a 42-year - old male with normal previous medical history was brought to the casualty with altered sensorium and numerous bullae and erosions on the skin .
he was found lying unconscious on the floor of a cramped room , after a prolonged bout of alcohol consumption . on examination
, he was drowsy and had multiple , bilateral , asymmetrically distributed vesicles , hemorrhagic bullae and erosions of irregular shapes on the front of trunk , forearms , legs , and face ; mostly limited to areas in contact with the floor while he was lying unconscious [ figures 1 and 2 ] .
irregular and bizarre - shaped bullae and erosions on anterior trunk close - up view of bullous skin lesions urine was dark red in colour and showed albuminuria , numerous rbcs , and granular casts .
blood urea was 108 mg / dl and serum creatinine 3.1 mg / dl , which rose to 140 mg / dl and 5.6 mg / dl , respectively on the subsequent days .
prothrombin time ( pt ) was 15.7 s ( control : 11.9 ) with international normalized ratio ( inr ) 1.3 and activated partial thromboplastin time ( aptt ) 35.8 s ( control : 30.2 ) .
serum glutamic oxaloacetic transaminase ( sgot ) was 450 iu / l ( control : 5 - 40 ) , serum glutamic pyruvic transaminase ( sgpt ) 295 iu / l ( control : 5 - 50 ) and serum creatine phosphokinase ( cpk ) was 14,120 iu / l ( control : 40 - 320 ) .
ultrasonogram of abdomen showed hepatomegaly with coarse parenchyma , hyperechoic kidneys with minimal corticomedullary differentiation , and mild ascites .
vesicles on erythematous and edematous skin on the lateral aspect of forearm histopathological examination of the skin on the edge of the erosions using hematoxylin and eosin ( h and e ) stain showed mild acanthosis , spongiosis , intraepidermal vesiculation ; and focal lymphocytic infiltrate particularly around eccrine sweat glands , extravasated erythrocytes , and dilated blood vessels in the dermis [ figures 4 and 5 ] .
there was necrosis of sweat glands with denudation of secretory epithelial lining cells [ figure 6 ] .
spongiosis , intraepidermal vesiculation , and focal dermal lymphocytic infiltrate around eccrine sweat gland and duct .
h and e , 400 necrosed eccrine sweat gland with denuded secretory epithelial lining cells .
h and e , 400 provisional diagnosis was bullous lesions related to coma , alcoholic liver disease , and acute renal failure ( arf ) due to rhabdomyolysis .
he was treated with parenteral fluids , injections of ceftriaxone , and metronidazole ; other supportive measures and four cycles of hemodialysis .
this patient had a sudden onset of hemorrhagic blisters progressing to erosions and necrotic ulcers , strikingly on the areas in contact with the floor in comatose state .
the skin lesions were not considered to be associated with sepsis as the bullae were hemorrhagic , neither flaccid nor pustular ; nikolsky 's sign was negative and the bullous fluid did not grow bacteria on culture . histopathological examination confirmed the diagnosis of sweat gland necrosis in our patient .
presence of dark coloured urine and elevated cpk levels in the context of arf suggested the possibility of rhabdomyolysis .
bullous lesions have been reported in patients with carbon monoxide poisoning as early as in 1865 , while such lesions have been associated with barbiturate poisoning from 1950 . both of the previously reported cases of sweat gland necrosis associated with alcoholic coma had bullous lesions on pressure points .
one of them also had biochemical evidence of muscle damage as in our patient . however , our case is unique in that rhabdomyolysis complicated by arf was a prominent clinical presentation .
vesiculobullous lesions seen in unconscious patients are believed to be due to a combined effect of generalized or localized hypoxia or drug toxicity coupled with trauma and friction .
inflammation is usually minimal or absent in the adjacent dermis . in severe cases , sweat ducts , and the pilosebaceous units
this case highlights the need for greater awareness about this relatively uncommon cause of bullous disease on the skin .
when one encounters a case of sudden appearance of bullous lesions in a comatose patient , history of ingestion of drugs or toxins including alcohol should be sought for .
a skin biopsy showing spongiosis , intraepidermal as well as subepidermal vesicles and necrosis of eccrine sweat glands will confirm the diagnosis .
these patients should be evaluated for associated rhabdomyolysis and other life - threatening complications such as arf .
while evaluating comatose patients with bullous skin lesions , history of excessive consumption of alcohol should be sought for .
a 42-year - old male developed hemorrhagic bullae and erosions while in alcohol induced coma . 
 the lesions were limited to areas of the body in prolonged contact with the ground in the comatose state . 
 he developed rhabdomyolysis , progressing to acute renal failure ( arf ) . 
 histopathological examination of the skin showed spongiosis , intraepidermal vesicles , and necrosis of eccrine sweat glands with denudation of secretory epithelial lining cells . with supportive 
 treatment and hemodialysis , the patient recovered in 3 weeks time . 
 this is the first reported case of bullous lesions and sweat gland necrosis occurring in alcohol - induced coma complicated by rhabdomyolysis and arf .