Are You Confident of the Diagnosis?
What you should be alert for in the history
Be alert for an immoblized patient with bullae formation at pressure sites.
Characteristic findings on physical examination
Characteristic findings include blisters or bullae at sites of pressure (Figure 1). Normal skin develops erythematous patches or plaques about 24 hours after immobilization begins, which then progress into blisters within 48-72 hours. Spontaneous resolution occurs within 1-2 weeks if the patient is mobilized and pressure from site is eliminated.
Expected results of diagnostic studies
Histopathology reveals a subepidermal blister with eccrine gland necrosis (Figure 2).
Friction blisters. Found primarily on the hands and soles. Blisters develop at sites of friction. Histopathology reveals intraepidermal blisters below the granular layer.
Edema blisters. These can appear during an acute exacerbation of chronic edema such as occurs with congestive heart failure, acute aggressive fluid resuscitation, and in the setting of anasarca. Blisters are found at the sites of edema. Histopathology reveals epidermal spongiosis and dermal edema.
Bullous diabeticorum. Acral sites can develop blisters in patients with longstanding diabetes mellitus. Histopathology reveals intraepidermal and subepidermal blisters.
Who is at Risk for Developing this Disease?
Those at risk for coma blister include comatose patients, those with neurologic disease (eg, stroke, spinal cord disease or injury, peripheral nerve disease, encephalitis, or brain tumor, and those suffering prolonged immobilization for various reasons, including drug overdose, hypoglycemia, head trauma, or diabetic ketoacidosis from drug overdose or from postsurgical immobilization.
What is the Cause of the Disease?
Coma blisters are caused by pressure leading to local hypoxia and necrosis. It was once believed to be associated with barbiturate overdose, by way of direct toxic affect on the eccrine glands leading to necrosis. Additional drugs have been implicated as well. Drug overdose remains a frequent predisposing factor for the formation of coma blisters, although coma blisters are no longer believed to be due to the toxic effect of the drug.
Historically, coma blisters were believed to be due to carbon monoxide poisoning. The first coma blisters were reported in 1806 when they were found on soldiers comatose from carbon monoxide poisoning.
Systemic Implications and Complications
There are no systemic Implications associated with coma blisters. Typically, there are no complications since they spontaneously resolve. However, care must be taken to mobilize the patient so they do not develop pressure ulcerations. It is also important to perform good wound care to prevent infection. ]
Treatment focuses on wound care: sterile drainage of bullae, leaving the roof intact to act as a dressing, and hydrocolloid dressings.
Optimal Therapeutic Approach for this Disease
The optimal therapeutic approach includes prompt diagnosis, mobilization and wound care (sterile drainage of bullae, leaving the roof intact to act as a dressing,, and hydrocolloid dressings).
Patient management focuses on prompt diagnosis, mobilization and wound care (sterile drainage of bullae, leaving the roof intact to act as a dressing, and hydrocolloid dressings). When evaluating and treating patients with coma blisters, it is important to rule out unusual cases of bullous disease including bullous amyloidosis, epidermolysis bullosa (ie, Weber-Cockayne subtype), epidermolysis bullosa acquisita, and bullous pemphigoid.
Unusual Clinical Scenarios to Consider in Patient Management
When evaluating and treating patients with coma blisters, it is important to rule out unusual cases of bullous disease including bullous amyloidosis, epidermolysis bullosa (ie, Weber-Cockayne subtype), epidermolysis bullosa acquisita, and bullous pemphigoid.
What is the Evidence?
Arndt , KA, Mihm , MC, Parrish , JA. “Bullae: A cutaneous sign of a variety of neurologic diseases”. J Invest Dermatol . vol. 60. 1973. pp. 312-20. (This article discusses the history of coma blisters and presents seven cases to demonstrate that coma blisters are a result of pressure-induced ischemia and anoxia rather than direct toxic effect from a drug or other endogenous substance.)
Bolognia, J, Mascaro, JM, Bolognia, JL, Jorizzo, JL, Rapini, RP. “Other vesiculobullous diseases”. Dermatology. vol. 1. 2008. pp. 468-9. (This is a section in a textbook chapter for vesicullobullous diseases which comprehensively outlines and discusses coma blisters.)
Rocha , J, Pereira , T, Ventura , F, Pardal , F, Brito , C. ” Coma Blisters”. Case Report Dermatol. vol. 1. 2009. pp. 66-70. (This article reports a case of a young man admitted to the hospital for presumed bacterial meningitis who quickly declined to a comatose state. He developed blisters that were clinically and histologically consistent with coma blisters. He was treated successfully and the blisters resolved with no sequelae after 5 days. This article discusses how his new onset diabetes could lead to a differential diagnosis including bullous diabeticorum.)
Dunn , C, Held , JL, Spitz , J, Silvers , DN, Grossman , ME, Kohn , SR. “Coma blisters: report and review”. Cutis . vol. 46. 1990. pp. 423-26. (This article discusses coma blisters that are commonly seen in the setting of barbiturate overdose but are not due to their direct toxic effect. It explains that the continued use of barbiturates is not contraindicated in this setting. This article also reports a case of coma blisters showing histology characteristically demonstrating eccrine gland necrosis of involved tissue.)
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