Coma blister

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A coma blister, or coma bullae, is a skin lesion or blister that typically arises due to pressure in an individual with impaired consciousness. They vary in size, ranging from 4 to 5 centimeters in diameter, and may appear hemorrhagic or blood filled. [1] Coma blisters are usually found in the extremities and trunk. [2] These types of blisters have been associated with the overdose of central nervous system (CNS) depressants especially barbiturates, but also tricyclic antidepressants, hypnotics, benzodiazepines, opiates, antipsychotics, and alcohol. [3] 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 comatose individual's skin from being immobilized. [1] Coma blisters have been frequently found on individuals who have overdosed on drugs, but have also been found on individuals with chronic kidney failure, hypercalcemia, diabetic ketoacidosis, and a variety of neurologic conditions. [4] Coma blisters are more frequent in adults and less common among children as demonstrated by the few cases published in literature. [2]

Contents

Etiology

The development of coma blisters derives from various causes in the setting of neurologic disease and other conditions, with crucial factors being inadequate amounts of oxygen at the tissue level and external pressure. [5] Examples of neurological disorders that are associated with coma blisters include cranioencephalic trauma, cerebrovascular disease, and meningoencephalitis. [6] Metabolic disorders such as diabetic ketoacidosis, hyperkalemia, and hypoglycemia are also associated with blister formation. [6] Drug overdose-induced comas are 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. [5] [7] Recent studies also suggested that immune mechanisms play a role in the etiology of these blisters, specifically in the drug induced comas. [5] IgG, IgA, and C3 with fibrin are seen with direct immunoflourence staining. [8] 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. [9] However, it is still possible to see coma blisters in non-comatose individuals with granulomatosis with polyangiitis or long immobilization. [10] [6]

Constant pressure forms blisters by causing tissue injury to the vessel walls, thereby interrupting blood and oxygen flow to the tissues. [5] This constant pressure is often caused by a reflex mechanism to counteract the low arterial blood pressure exacerbated by vasoactive drugs or shock. [11] 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. [5] As a result of pressure, coma blisters most commonly develop on pressure points such as the ankles, heels, knees, elbows, fingers, and toes. [6]

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. [7] 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. [12]

Blisters occur specifically at vasoactive pressure sites between 48 and 72 hours after the start of unconsciousness. [5] Although some lesions may heal on their own, the diagnosis of coma blisters are aided with specific histological characteristics. [5]

Diagnosis

Coma blisters usually develop on pressure point sites within a few days on individuals who have been immobilized die to external events. Barbiturate overdose is the most frequent predisposing event, but coma 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 from drug overdose-induced coma blisters. Necrosis on sweat glands and ducts usually occur in coma blisters, but its absence does not exclude the diagnosis. [5] In children, diagnosis may be dependent on careful clinicopathological correlation to omit other blistering diseases. [2]

Differential diagnosis

Friction blisters

Friction blisters are only found in areas that undergo repetitive friction. This type of blister is caused by frictional forces in which the epidermal cells are separated mechanically at the level of the stratum spinosum. Hydrostatic pressure causes the area of the separation to fill with fluid, a bullae that is characteristic for blisters. [13]

Edema blisters

Edema Blisters form at the sites of swelling from acute volume overload, also as known as edema. Edema can occur for 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. [14]

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. [15]

Epidermolysis bullosa

Epidermolysis bullosa (EB) is a genetic disease that causes the skin to be extremely fragile and individuals with the disease are prone to blisters, even with minimal friction and trauma. There are thirty subtypes of epidermolysis bullosa which are arranged into four major categories: EB simplex (EBS), dystrophic EB (DEB), kindler EV, and junctional EB (JEB). There is currently no cure for epidermolysis bullosa and treatment is based on bandaging, wound management, and pain management. [16]

Bullous pemphigoid

Bullous pemphigoid is an autoimmune bullous disease that mainly affects older individuals. Individuals typically present with itchy rashes that transform into fluid filled bullous lesions on the skin. Although these blisters usually appear on the arms, legs, and trunk of the body, they can also be found in the mouth as sores. The most common treatment options for blisters caused by bullous pemphigoid are topical and systemic corticosteroids, which help to relive itching and heal the blistering skin. [17]

Treatment and management

Coma blisters typically do not require treatment and will usually heal on their own within one to two weeks of formation. [5] Early identification and management of coma blisters is important and involves treating any underlying conditions that may have led to the formation of the blisters, and decreasing the risk of subsequent infections. [18]

Before starting any treatment, it is important to rule out other cases of potential bullous diseases, such as epidermolysis bullosa, bullous pemphigoid, bullous amyloidosis, and epidermolysis bullosa acquisita, since bullous lesions of the skin are characteristic in these conditions. [19] It is also important to differentiate coma blisters from other types of dermatologic lesions, such as friction blisters and edema blisters, as their characteristics may also be similar to coma blisters. [20] If treatment is needed, a possible option is topical antibiotics, which can be used to prevent infections of the blisters. [18]

Management and wound care can also be performed and involve sterile drainage of the blister, positioning the individual away from their wound to relieve any pressure on the site, and preventing the formation of pressure ulcerations. When draining the blisters, leaving the roof of the blister undamaged can allow the roof to act as an additional layer of dressing for the wound and the use of hydrocolloid dressings can also help to maintain moisture and promote healing. [21] Some individuals may experience visible scarring in the area after the blisters have healed, but this is non-concerning. [2]

Coma blisters are not seen as contraindications for other medications or therapies, therefore medications should be continued as needed to manage other co-morbidities even in the presence of coma blisters. [5]

See also

Related Research Articles

<span class="mw-page-title-main">Blister</span> Small pocket of fluid within the upper layers of the skin

A blister is a small pocket of body fluid within the upper layers of the skin, usually caused by forceful rubbing (friction), burning, touching poison ivy, freezing, chemical exposure or infection. Most blisters are filled with a clear fluid, either serum or plasma. However, blisters can be filled with blood or with pus.

<span class="mw-page-title-main">Epidermolysis bullosa</span> Rare medical conditions that result in easy blistering of the skin and mucous membranes

Epidermolysis bullosa (EB) is a group of rare medical conditions that result in easy blistering of the skin and mucous membranes. Blisters occur with minor trauma or friction and are painful. Its severity can range from mild to fatal. Inherited EB is a rare disease with a prevalence in the United States of 8.2 per million live births. Those with mild cases may not develop symptoms until they start to crawl or walk. Complications may include esophageal narrowing, squamous cell skin cancer, and the need for amputations.

<span class="mw-page-title-main">Hemidesmosome</span>

Hemidesmosomes are very small stud-like structures found in keratinocytes of the epidermis of skin that attach to the extracellular matrix. They are similar in form to desmosomes when visualized by electron microscopy, however, desmosomes attach to adjacent cells. Hemidesmosomes are also comparable to focal adhesions, as they both attach cells to the extracellular matrix. Instead of desmogleins and desmocollins in the extracellular space, hemidesmosomes utilize integrins. Hemidesmosomes are found in epithelial cells connecting the basal epithelial cells to the lamina lucida, which is part of the basal lamina. Hemidesmosomes are also involved in signaling pathways, such as keratinocyte migration or carcinoma cell intrusion.

<span class="mw-page-title-main">Pemphigus</span> Blistering autoimmune diseases

Pemphigus is a rare group of blistering autoimmune diseases that affect the skin and mucous membranes. The name is derived from the Greek root pemphix, meaning "blister".

<span class="mw-page-title-main">Bullous pemphigoid</span> Autoimmune disease of skin and connective tissue characterized by large blisters

Bullous pemphigoid is an autoimmune pruritic skin disease that typically occurs in people aged over 60, that may involve the formation of blisters (bullae) in the space between the epidermal and dermal skin layers. It is classified as a type II hypersensitivity reaction, which involves formation of anti-hemidesmosome antibodies, causing a loss of keratinocytes to basement membrane adhesion.

<span class="mw-page-title-main">Epidermolysis bullosa simplex</span> Medical condition

Epidermolysis bullosa simplex (EBS) is a disorder resulting from mutations in the genes encoding keratin 5 or keratin 14.

<span class="mw-page-title-main">Pemphigoid</span> Autoimmune blistering diseases

Pemphigoid is a group of rare autoimmune blistering diseases of the skin, and mucous membranes. As its name indicates, pemphigoid is similar in general appearance to pemphigus, but, unlike pemphigus, pemphigoid does not feature acantholysis, a loss of connections between skin cells.

<span class="mw-page-title-main">Kindler syndrome</span> Medical condition

Kindler syndrome is a rare congenital disease of the skin caused by a mutation in the KIND1 gene.

<span class="mw-page-title-main">Collagen, type XVII, alpha 1</span> Mammalian protein found in humans

Collagen XVII, previously called BP180, is a transmembrane protein which plays a critical role in maintaining the linkage between the intracellular and the extracellular structural elements involved in epidermal adhesion, identified by Diaz and colleagues in 1990.

<span class="mw-page-title-main">Genodermatosis</span> Medical condition

Genodermatosis is a hereditary skin disease with three inherited modes including single gene inheritance, multiple gene inheritance and chromosome inheritance. There are many different types of genodermatosis, the prevalence of genodermatosis ranges from 1 per 6000 people to 1 per 500,000 people. Genodermatosis has influence on the texture, color and structure of skin cuticle and connective tissue, specific lesion site and clinical manifestations on the body vary depending on the type. In the spite of the variety and complexity of genodermatosis, there are still some common methods that can help people diagnose. After diagnosis, different types of genodermatosis require different levels of therapy including interventions, nursing interventions and treatments. Among that, research of therapy for some new, complex and rare types are still in the developing stage. The impact of genodermatosis not only can be seen in body but also can be seen in all aspects of patients' life, including but not limited to psychological, family life, economic conditions and social activities. Accordingly, the patients need treatment, support and help in these areas.

<span class="mw-page-title-main">Dermatitis herpetiformis</span> Chronic autoimmune disorder leading to blistering skin

Dermatitis herpetiformis (DH) is a chronic autoimmune blistering skin condition, characterised by intensely itchy blisters filled with a watery fluid. DH is a cutaneous manifestation of coeliac disease, although the exact causal mechanism is not known. DH is neither related to nor caused by herpes virus; the name means that it is a skin inflammation having an appearance similar to herpes.

Epidermolysis bullosa acquisita, also known as acquired epidermolysis bullosa, is a longterm autoimmune blistering skin disease. It generally presents with fragile skin that blisters and becomes red with or without trauma. Marked scarring is left with thin skin, milia and nail changes. It typically begins around age 50.

Paraneoplastic pemphigus (PNP) is an autoimmune disorder stemming from an underlying tumor. It is hypothesized that antigens associated with the tumor trigger an immune response resulting in blistering of the skin and mucous membranes.

<span class="mw-page-title-main">Linear IgA bullous dermatosis</span> Medical condition

Linear IgA bullous dermatosis is a rare immune-mediated blistering skin disease frequently associated with medication exposure, especially vancomycin, with men and women being equally affected. It was first described by Tadeusz Chorzelski in 1979 and may be divided into two types:

Junctional epidermolysis bullosa is a skin condition characterized by blister formation within the lamina lucida of the basement membrane zone.

Transient bullous dermolysis of the newborn (TBDN) is a skin condition that presents in newborns. It is characterized by blister formation secondary to even mild trauma.

<span class="mw-page-title-main">Vesiculobullous disease</span> Medical condition

A vesiculobullous disease is a type of mucocutaneous disease characterized by vesicles and bullae. Both vesicles and bullae are fluid-filled lesions, and they are distinguished by size. In the case of vesiculobullous diseases which are also immune disorders, the term immunobullous is sometimes used. Examples of vesiculobullous diseases include:

Mucous membrane pemphigoid is a rare chronic autoimmune subepithelial blistering disease characterized by erosive lesions of the mucous membranes and skin. It is one of the pemphigoid diseases that can result in scarring.

References

  1. 1 2 Agarwal A, Bansal M, Conner K (March 2012). "Coma blisters with hypoxemic respiratory failure". Dermatology Online Journal. 18 (3): 10. doi:10.5070/D35175b1pg. PMID   22483521.
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  3. ↑ "Coma blisters. A key to neurological diagnosis". Neurología (English Edition). Elsevier. Retrieved 2022-07-26.
  4. ↑ Piede J, Wallace E (January 2011). "Coma bullae: associations beyond medications". Mayo Clinic Proceedings. 86 (1): e5. doi:10.4065/mcp.2010.0364. PMC   3012639 . PMID   21193646.
  5. 1 2 3 4 5 6 7 8 9 10 Rocha J, Pereira T, Ventura F, Pardal F, Brito C (October 2009). "Coma Blisters". Case Reports in Dermatology. 1 (1): 66–70. doi:10.1159/000249150. PMC   2895214 . PMID   20652118.
  6. 1 2 3 4 Vázquez-Osorio I, Gonzalvo-Rodríguez P, Rodríguez-Díaz E (2017). "Coma Blisters after an Overdose of Central Nervous System Depressants". Actas Dermo-Sifiliograficas. 108 (1): 81–83. doi: 10.1016/j.adengl.2016.11.015 . PMID   27737761.
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  8. ↑ Reilly GD, Harrington CI (December 1983). "Positive immunofluorescence in bullous lesions in drug-induced coma". The British Journal of Dermatology. 109 (6): 720. doi:10.1111/j.1365-2133.1983.tb00554.x. PMID   6360197. S2CID   32953723.
  9. ↑ Asokan N, Binesh VG, Andrews AM, Jayalakshmi PS (November 2014). "Bullous lesions, sweat gland necrosis and rhabdomyolysis in alcoholic coma". Indian Journal of Dermatology. 59 (6): 632. doi: 10.4103/0019-5154.143576 . PMC   4248528 . PMID   25484420.
  10. ↑ Ferreli C, Sulica VI, Aste N, Atzori L, Pinna M, Biggio P (July 2003). "Drug-induced sweat gland necrosis in a non-comatose patient: a case presentation". Journal of the European Academy of Dermatology and Venereology. 17 (4): 443–445. doi:10.1046/j.1468-3083.2003.00695.x. PMID   12834457. S2CID   45514949.
  11. ↑ Arndt KA, Mihm MC, Parrish JA (May 1973). "Bullae: a cutaneous sign of a variety of neurologic diseases". The Journal of Investigative Dermatology. 60 (5): 312–320. doi: 10.1111/1523-1747.ep12723147 . PMID   4758735.
  12. ↑ Hollenberg SM (April 2011). "Vasoactive drugs in circulatory shock". American Journal of Respiratory and Critical Care Medicine. 183 (7): 847–855. doi:10.1164/rccm.201006-0972CI. PMID   21097695.
  13. ↑ Knapik JJ, Reynolds KL, Duplantis KL, Jones BH (September 1995). "Friction blisters. Pathophysiology, prevention and treatment". Sports Medicine. 20 (3): 136–147. doi:10.2165/00007256-199520030-00002. PMID   8570998. S2CID   40287087.
  14. ↑ Chen SX, Cohen PR (October 2017). "Edema Bullae Mimicking Disseminated Herpes Zoster". Cureus. 9 (10): e1780. doi: 10.7759/cureus.1780 . PMC   5732012 . PMID   29255659.
  15. ↑ Chouk C, Litaiem N (2022). "Bullosis Diabeticorum". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID   30969694 . Retrieved 2022-07-28.
  16. ↑ Bardhan A, Bruckner-Tuderman L, Chapple IL, Fine JD, Harper N, Has C, et al. (September 2020). "Epidermolysis bullosa". Nature Reviews. Disease Primers. 6 (1): 78. doi:10.1038/s41572-020-0210-0. PMID   32973163. S2CID   221861310.
  17. ↑ Miyamoto D, Santi CG, Aoki V, Maruta CW (2019-05-09). "Bullous pemphigoid". Anais Brasileiros de Dermatologia. 94 (2): 133–146. doi:10.1590/abd1806-4841.20199007. PMC   6486083 . PMID   31090818.
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  19. ↑ Northover JM, Pickard JD, Murray-Lyon IM, Presbury DG, Haskell R, Keith DA (June 1972). "Bullous lesions of the skin and mucous membranes in primary amyloidosis". Postgraduate Medical Journal. 48 (560): 351–353. doi:10.1136/pgmj.48.560.351. PMC   2495229 . PMID   5049254.
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  21. ↑ Bluestein D, Javaheri A (November 2008). "Pressure ulcers: prevention, evaluation, and management". American Family Physician. 78 (10): 1186–1194. PMID   19035067.
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