Minnaganti Divya, Gampala Arjun R, Khanna Yash P, Haury Emily
Internal Medicine, University of Missouri Kansas City School of Medicine, Kansas City, USA.
Internal Medicine and Pediatrics, University of Missouri Kansas City School of Medicine, Kansas City, USA.
Cureus. 2024 Apr 20;16(4):e58646. doi: 10.7759/cureus.58646. eCollection 2024 Apr.
Coma blisters, or coma bullae, are lesions often seen in the setting of impaired consciousness. Most commonly associated with drug-induced comas, coma bullae have been repeatedly linked to central nervous system (CNS) depressing agents, such as opiates. These lesions are believed to develop due to a complex multifactorial process involving external pressure on the skin, which leads to hypoxia and eventual death of eccrine sweat glands. In addition, the vasoactive and inflammatory properties of CNS depressing agents may play a role in this process. Come bullae usually develop on pressure points 48-72 hours after the onset of impaired consciousness and are self-limiting. We present the case of a 68-year-old male who was brought to the emergency department after being found unresponsive on the street. The urine drug screen was positive for cocaine and fentanyl. The initial examination showed several large, non-tender bullae on his scalp that continued to expand over two days. He subsequently developed similar lesions on his thighs, right shoulder, and knuckles. Dermatology was consulted and clinically diagnosed the patient with coma bullae, likely attributed to his altered consciousness and opiate use. Notably, more violaceous bullae were found on the bilateral lower extremities, with dermatology suspecting additional vasculitic features related to concurrent opiate and cocaine use. Skin biopsy and aspiration were deferred to avoid the risk of infection, and the patient was discharged per dermatology's recommendations for no immediate intervention. He continued to follow with wound care for the next six months, with most of the bullae healing. However, eschars developed over the scalp and left lower extremity, requiring debridement by general surgery. This case report underscores a unique manifestation of coma bullae. Unlike typical presentations localized to pressure-dependent areas and appearing after two to three days of unconsciousness, our patient exhibited blisters in atypical sites with associated vasculitic features. Moreover, the development of eschars over time may be linked to ongoing vasoactive drug use, reperfusion injury, and social determinants of health. This case highlights the complex and multifactorial nature of coma bullae, emphasizing the challenges in wound care and management despite their expected self-resolution.
昏迷水疱,或称昏迷大疱,是意识障碍情况下常见的病变。昏迷水疱最常与药物性昏迷相关,反复与中枢神经系统(CNS)抑制药物有关,如阿片类药物。据信这些病变是由于一个复杂的多因素过程而形成的,该过程涉及皮肤外部压力,导致汗腺缺氧并最终死亡。此外,中枢神经系统抑制药物的血管活性和炎症特性可能在这一过程中起作用。昏迷水疱通常在意识障碍发作后48 - 72小时出现在受压部位,且具有自限性。我们报告一例68岁男性病例,该患者在街上被发现无反应后被送往急诊科。尿液药物筛查显示可卡因和芬太尼呈阳性。初步检查发现其头皮上有几个大的、无压痛的水疱,在两天内持续扩大。随后他的大腿、右肩和指关节也出现了类似病变。咨询皮肤科后,临床诊断该患者为昏迷水疱,可能归因于其意识改变和阿片类药物使用。值得注意的是,双侧下肢发现了更多紫红色水疱,皮肤科怀疑与同时使用阿片类药物和可卡因有关的额外血管炎特征。为避免感染风险,未进行皮肤活检和抽吸,患者按照皮肤科的建议出院,无需立即干预。在接下来的六个月里,他继续接受伤口护理,大部分水疱愈合。然而,头皮和左下肢出现了焦痂,需要普通外科进行清创。本病例报告强调了昏迷水疱的一种独特表现。与典型表现局限于受压部位且在昏迷两到三天后出现不同,我们的患者在非典型部位出现水疱并伴有血管炎特征。此外,随着时间推移焦痂的形成可能与持续使用血管活性药物、再灌注损伤以及健康的社会决定因素有关。本病例突出了昏迷水疱的复杂多因素性质,强调了尽管其预期会自行消退,但在伤口护理和管理方面仍存在挑战。