User:Ucsfrdu/Coma blister

A coma blister, or coma bullae, is a skin lesion or blister that arises typically due to pressure in an individual with impaired consciousness. They vary in size, ranging from 4 to 5 cm in diameter, and may appear hemorrhagic. Coma blisters are usually found in the extremities and trunk. These types of blisters in the past have been associated with the overdose of central nervous system (CNS) depressants especially barbiturates, but also tricyclic antidepressants, hypnotics, opiates, antipsychotics, and alcohol. However, studies have found that coma blisters are not caused by the toxicity of these drugs, but due to hypoxia and external pressure on the individual’s skin from immobilization of unconsciousness.

Diagnosis
Coma blisters usually develop on pressure point sites within a few days on individuals who have been immobilized from external events. Barbiturate overdose is the most frequent predisposing event, but comatose or any other condition that renders an individual unconscious can lead to the formation of coma blisters. These blisters resolve on their own within one to two weeks and its diagnosis can be further characterized by histological evidence such as subepidermal bullae, focal necrosis of epidermis, dermis, subcutaneous tissue and all epidermal appendages. For non-drug induced coma blisters, the absence of inflammation along with the presence of thrombosis in dermal wall vessels are the two most significant differences. Necrosis on sweat glands and ducts usually occur in coma blisters, but its absence does not exclude the diagnosis.

Friction Blisters
Friction blisters are only found in areas that undergo repetitive friction. These types of blisters is caused by frictional forces in which the epidermal cells are separated mechanically at level of the stratum spinosum. Hydrostatic pressure causes the area of the separation to fill with fluid, a bullae that is characteristic for blisters.

Edema Blisters
Edema Blisters form at the sites of swelling from acute volume overload, also as known as edema. Edema can occur from various reasons that may include renal or heart failure. Histopathology may show subepidermal edema and a negative immunofluorescence staining may be performed to differentiate acute edema blisters from other bullous diseases.

Bullous diabeticorum
Bullous diabeticorum occurs in individuals with diabetes mellitus. Since the majority of diabetic individuals with bullous diabeticorum have nephropathy and neuropathy, it is suggested that  the premature aging of local subbasement membrane zone connective-tissue may lead to these types of blisters.

Etiology
The development of coma blisters derives from various causes in the setting of neurologic disease, with crucial factors being inadequate amounts of oxygen at the tissue level and external pressure. Drug overdose-induced comas are upon one of the most frequent predisposing factors of coma blister formation, where studies have reported the development of coma blisters in 4% of barbiturate overdose. Studies also suggested that immune mechanisms play a role in the etiology of these blisters. Despite there being multiple causes of unconscious states, a common reoccurrence and feature of coma blisters include the death of body tissue or necrosis in the eccrine sweat glands. However, it is still possible to see coma blisters in non-comatose individuals.

Constant pressure forms blisters by causing tissue injury to the vessel walls, thereby interrupting blood and oxygen flow to the tissues. This constant pressure is often caused by a reflex mechanism to counteract the low arterial blood pressure exacerbated by vasoactive drugs or shock. A lack of oxygen to local tissue leads to the formation of necrotic bulla and the deterioration of the eccrine sweat glands, where metabolically active cells are present.

Administration of antidepressants, antipsychotics, barbiturates, benzodiazepines, ethanol, or opioids are often connected to drug overdose-induced comas because of their vasoactive properties and possible toxicity on eccrine sweat glands. Due to the over usage of vasoactive drugs, more pressure is applied to the arterial walls, thereby increasing the risk of tissue damage, loss of oxygen to local tissue, and blister formation.

Blisters occur specifically at vasoactive pressure sites between 48-72 hours after the start of unconsciousness. Although some lesions may heal on their own, the diagnosis of coma blisters are aided with specific histological characteristics.

Treatment
Coma blisters typically do not require treatment and usually heal on their own within 1-2 weeks of formation. Early identification and management of coma blisters is important and involve lowering any risks of infections from the lesions and treating any underlying conditions that may have led to the formation of the blisters. Wound care of the blisters can also be performed and involve drainage of the blister and the use of hydrocolloid dressings, which help to maintain moisture and promote healing. However, topical antibiotics still serve as a option in preventing infections secondary to skin lesions without the need of any specific treatment.

Coma blisters are not contraindications for other medications or therapies, therefore medications should be continued as needed to manage individual's co-morbidities.