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.[1] They vary in size, ranging from 4 to 5 cm in diameter, and may appear hemorrhagic.[2] Coma blisters are usually found in the extremities and trunk.[3] 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.[4] 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. [1]
Diagnosis
[edit]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. [1]
Differential Diagnosis
[edit]Friction Blisters
[edit]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.[5]
Edema Blisters
[edit]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.[6]
Bullous diabeticorum
[edit]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. [7]
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Etiology
[edit]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.[8] Studies also suggested that immune mechanisms play a role in the etiology of these blisters.[1] 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.[10]
Constant pressure forms blisters by causing tissue injury to the vessel walls, thereby interrupting blood and oxygen flow to the tissues.[1] 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.[1]
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.[8] 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 48-72 hours after the start of unconsciousness.[1] Although some lesions may heal on their own, the diagnosis of coma blisters are aided with specific histological characteristics.[1]
Treatment
[edit]Coma blisters typically do not require treatment and usually heal on their own within 1-2 weeks of formation.[13] 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.[14] Wound care of the blisters can also be performed and involve drainage of the blister and the use of hydrocolloid dressings[15], which help to maintain moisture and promote healing[16]. However, topical antibiotics still serve as a option in preventing infections secondary to skin lesions without the need of any specific treatment.[3]
Coma blisters are not contraindications for other medications or therapies, therefore medications should be continued as needed to manage individual's co-morbidities.[1]
References
[edit]- ^ a b c d e f g h i Rocha, Joana; Pereira, Teresa; Ventura, Filipa; Pardal, Fernando; Brito, Celeste (2009). "Coma Blisters". Case Reports in Dermatology. 1 (1): 66–70. doi:10.1159/000249150. ISSN 1662-6567. PMC 2895214. PMID 20652118.
- ^ Agarwal, Abhishek; Bansal, Meghana; Conner, Kelly (2012). "Coma blisters with hypoxemic respiratory failure". Dermatology Online Journal. 18 (3): 10. ISSN 1087-2108. PMID 22483521.
- ^ a b Bosco, Laura; Schena, Donatella; Colato, Chiara; Biban, Paolo; Girolomoni, Giampiero (2013). "Coma blisters in children: case report and review of the literature". Journal of Child Neurology. 28 (12): 1677–1680. doi:10.1177/0883073812464684. ISSN 1708-8283. PMID 23155203.
- ^ "Coma blisters. A key to neurological diagnosis | Neurología (English Edition)". www.elsevier.es. Retrieved 2022-07-26.
- ^ Knapik, J. J.; Reynolds, K. L.; Duplantis, K. L.; Jones, B. H. (1995-09). "Friction blisters. Pathophysiology, prevention and treatment". Sports Medicine (Auckland, N.Z.). 20 (3): 136–147. doi:10.2165/00007256-199520030-00002. ISSN 0112-1642. PMID 8570998.
{{cite journal}}: Check date values in:|date=(help) - ^ Chen, Stella X.; Cohen, Philip R. (2017-10-17). "Edema Bullae Mimicking Disseminated Herpes Zoster". Cureus. 9 (10): e1780. doi:10.7759/cureus.1780. ISSN 2168-8184. PMC 5732012. PMID 29255659.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ Chouk, Chourouk; Litaiem, Noureddine (2022), "Bullosis Diabeticorum", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 30969694, retrieved 2022-07-28
- ^ a b Dinis-Oliveira, Ricardo J. (2019). "Drug Overdose-Induced Coma Blisters: Pathophysiology and Clinical and Forensic Diagnosis". Current Drug Research Reviews. 11 (1): 21–25. doi:10.2174/1874473711666180730102343. ISSN 2589-9783. PMID 30058500.
- ^ Asokan, Neelakandhan; Binesh, Vayappurath Gangadharan; Andrews, Andrews Mekkattukunnel; Jayalakshmi, Pattomthadathil Sankaran (2014). "Bullous Lesions, Sweat Gland Necrosis and Rhabdomyolysis in Alcoholic Coma". Indian Journal of Dermatology. 59: 632. doi:10.4103/0019-5154.143576. ISSN 0019-5154. PMC 4248528. PMID 25484420.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ Ferreli, C; Sulica, Vi; Aste, N; Atzori, L; Pinna, M; Biggio, P (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.
- ^ Arndt, K. A.; Mihm, M. C.; Parrish, J. A. (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. ISSN 0022-202X. PMID 4758735.
- ^ Hollenberg, Steven M. (2011). "Vasoactive drugs in circulatory shock". American Journal of Respiratory and Critical Care Medicine. 183 (7): 847–855. doi:10.1164/rccm.201006-0972CI. ISSN 1535-4970. PMID 21097695.
- ^ Rocha, Joana; Pereira, Teresa; Ventura, Filipa; Pardal, Fernando; Brito, Celeste (2009). "Coma Blisters". Case Reports in Dermatology. 1 (1): 66–70. doi:10.1159/000249150. ISSN 1662-6567. PMC 2895214. PMID 20652118.
{{cite journal}}: CS1 maint: PMC format (link) - ^ Waring, W.S.; Sandilands, E.A. (2007-01-01). "Coma blisters". Clinical Toxicology. 45 (7): 808–809. doi:10.1080/15563650701709189. ISSN 1556-3650.
- ^ "Coma Blister (Comma bullae, drug-induced coma blisters, barbiturate blisters, neurologic blisters)". Dermatology Advisor. 2019-03-13. Retrieved 2022-07-25.
- ^ Bluestein, Daniel; Javaheri, Ashkan (2008-11-15). "Pressure Ulcers: Prevention, Evaluation, and Management". American Family Physician. 78 (10): 1186–1194.