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Journal of Pathology and Pathogenic Research (JPPR)

Case Report

Cerebrovascular Accident Coma induced Blisters: Case Report

*Correspondence to: Khadiga Ahmed Ismail*, Laboratory Medicine Department, Faculty of Applied Medical Sciences, Taif University,
Taif, Saudi Arabia, Parasitology Department Faculty of Medicine, Ain-Shams University, Cairo, Egypt,

Article Information

Article Type: Case Report

Received  : September 28, 2018
Accepted  : October 03, 2018
Published : October10, 2018


Coma blisters are lesions that occur as a result of a variety of neurological diseases. They can be seen in cerebrovascular accident coma.We present a case of a comatose patient with bullous skin lesions aftercoma due to bilateral frontal infarction.


Case report:

A 37-year-old Saudi woman with past medical history of diabetes and no drug abuse presented to the emergency department with coma. On admission she was afebrile,her temperature was (37°C) with a Glasgow Coma Scale score of 8 (4/2/2) and no cutaneous lesions. Her blood pressure was 115/74 mm Hg with a heart rate of 87 beats/minute, respiratory rate of 17 breaths/minute, and oxygen saturation of 97%. Toxicological screening was negative. A lumbar puncture was done and the cerebrospinal fluid analysis revealed no signs of bacterial meningitis. Brain CT scan shown bilateral frontal infarction. She was transferred to intensive care unit in a deeply comatose condition, under cefotaxime (2 g i.e. q4h), ampicillin (2 g i.e. q4h), dexamethasone (10 mg i.e. q8h) therapy, and asprin 81 mg.

The patient was hydrated, and serum blood sugar was controlled by insulin. She was treated by methyl prednisolone 1gm i.e. for 3 days.

Two days later, multiple tense blisters with normal-appearing adjacent skin appeared on the patient's upper and lower extremities, and pressure areas (Plate. 1). 

Laboratory Investigations:

As regard her complete blood count showed:

The red blood cell count (RBC) was 5.48 M/µl, hemoglobin of 13 g/dL, andhematocrite of 13.50 %. 

The white blood cell (WBC) count  was elevated (15,03 K/µl),neutrophils count of (12.98 K/µl) (H), the percentage of neutrophils  of 86.40 % (H), lymphocytes count of (1.66 K/µl) (L), the percentage of lymphocytes  of 11% (L), monocytes count of  (0.33 K/µl) (N), the percentage of monocytes of 2.20% (N), eosinophils count of (0 K/µl) (L), the percentage of eosinophils of 0% (L), basophils count of (0.02 K/µl) (N), the percentage of basophils of 0.10% (N).The platelet count was  (315 K/µl) (N).   

As regard her chemistry:

Blood analysis revealed abnormal high serum glucose (425 mg/dl), HbAc1 was 11.84 % (H), hepatic (AST 13 U/l; ALT 11 U/l) and renal dysfunction (creatinine 0.4 mg/dl; urea 15.2 mg/dl), and C-reactive protein (391 mg/l).

As regard coagulation profile:

Partial thromboplastin time (PTT) was 28.20 seconds (N), prothrombin time (PT) was 13.20 seconds (N), and INRwas 0.98% (N).
ANA and others investigations of collagen vascular diseases were within normal. 
HCV, HBV, and HIV antibodies were negative, and serology of syphilis as VDRL and TPHA were also negative.

As regard Culture and sensitivity of fluid of the blisters in the skin:

The culture and sensitivity showed no growth.

As regard urine analysis:

It showed urine sugar was 4++++, acetone of 2++, RBCs o 2++, pus cells, albumin, bilirubin, and casts werenil.  

Plate 1:Multiple tense blisters with normal-appearing adjacent skin and clear fluids appeared on the patient's lower left forearm and hand.

Plate 2:Multiple tense blisters vary in size with normal-appearing adjacent skin and clear fluids appeared on the patient's right extremite.

Histological Findings:

A skin biopsy was performed and revealed an intraepidermal (sub corneal) blister and partially to frankly necrotic epidermis with a mild inflammatory infiltrate in the adjacent dermis (Plate. 2 and 3). There wasvascular dilatation in the papillary dermis as well as eosinophilic infiltration. There were also thrombosis of the vessels in the lower dermis with occlusion of the lumen by fibrinoid eosinophilic thrombi, and red cell extravasation into the surrounding dermis (Plate. 3).There was no eccrine sweat gland necrosis. There was no vasculitis.  

Plate 3:Intraepidermal (sub corneal) blister and partially to frankly necrotic epidermis with a mild inflammatory infiltrate in the adjacent dermis (magnification ×10).

Differential diagnoses to be considered in this case are

1- Coma blisters are characterized by (intraepidermal split, sometimes subepidermal bullae).
2- Friction blistersare characterized by (intraepidermal split without inflammation).
3- Diabetic bullosis (Bullosis diabeticorum) is characterized by dermal-epidermal blistering and re-epithelization process along with a few inflammatory cells within blister space. 
4- Bullous fixed drug reactions are characterized by (Intraepidermal or subepidermal hemorrhagic blister, basal cell vacuolation and lichenoid infiltrate in the superficial dermis).
5- Epidermolysisbullosaacquisita is characterized by (subepidermal bulla and an infiltrate of mixed inflammatory cells in the dermis). 

Plate 4:Intraepidermal (subcorneal) blister and partially to frankly necrotic epidermis with a mild inflammatory infiltrate in the adjacent dermis (magnification ×40).


Looking back at the history of coma blisters, they were firstly described by Dominique Larrey, Napoleon’s surgeon, who noticed these lesions in soldiers who had comatose due to carbon monoxide Intoxication back in 1806. Still the pathogenesis is unclear for coma blisters. In some comatosepatients’ blisters develop within 48 to 72 hours of losing consciousness mostly at pressure sites. Despite of blisters being classically associated with barbiturate overdose, they can occur during a coma because of metabolic disturbances(e.g. hypoglycemia), infections(e.g. viral encephalitis), neurological dysfunction(e.g. cerebrovascular accidents), or other medications(e.g. opioids)[9]. This goes with our case who developed blister after coma due to cerebrovascular accident.

Friction blisters are a skin condition that may occur at sites of combined pressure and friction (such as the hands or feet), and may be enhanced by heat, moisture, or cotton socks [2]. Friction blisters are characterized by vesicles or bullae[3,8]. They result from pressure and shear forces causing delamination at the level of the stratum spinosum [4].

Bullosis diabeticorum is a cutaneous manifestation of diabetes mellitus, mainly observed in the lower extremities in patients with longstanding disease. The etiology is unknown, but an association with neurologic or vascular disturbance[1]. 

Generalized bullous-fixed drug eruption (GBFDE), is a severe form of FDE characterized by widespread blisters and erosions, involving the whole body in addition to lesions typical of FDE. Although GBFDE is believed to have a favorable prognosis, the recent reports suggest it to have a nearly similar mortality rate like Stevens–Johnson syndrome/toxic epidermal necrolysis (SJS/TEN)[5].

The mechanism of FDE involves intraepidermal CD8+ T cells that are present within the lesions and play a role in local tissue destruction. Clinically, resolved FDE lesions continue to harbor a substantial number of effector memory CD8+ T-cells at the dermal-epidermal junction, which allows for recurrence of the lesions in the same location[7].

Epidermolysis bullosa acquisita (EBA) is a chronic mucocutaneous autoimmune skin blistering disease. The pathogenic relevance of autoantibodies targeting type VII collagen (COL7) has been well-documented. Therefore, EBA is a prototypical autoimmune disease with a well-characterized pathogenic relevance of autoantibody binding to the target antigen [6]. 

Plate 5:showed healing of the blisters in the plate 1 after about 10 days with treatment by fusidic acid 2% cream and zinc oxide 15 % cream.


Cerebrovascular Accident Coma induced blisters


We like to thank Dr. Samia Omar Abdul Malek, consultant of Dermatology in King Faisal Medical Complex, Taif, Saudi Arabia, for her valuable assistance. 



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