An Autopsy Case of Acute Carbon Monoxide Poisoning After a Long-Term Vegetative State

Abstract

A 23-year-old woman was rescued from an accidental fire in a state of cardiopulmonary arrest. Based on the diagnosis of carbon monoxide (CO) poisoning, she received hyperbaric oxygen therapy and survived in a vegetative state. After 1 and a half years, she died without recovering from the vegetative state. At autopsy, the brain was observed to be moderately softened with a severely atrophied appearance and ventricular enlargement. In addition, a characteristic damage of hypoxic-ischemic leukoencephalopathy was also observed clearly in both the bilateral globus pallidus and cerebral white matter, which are typical findings of past acute CO poisoning. A long-term vegetative state causes the brain to soften and liquefy because of reactive gliosis and autolytic change. The cause of death becomes difficult to diagnose only from the autopsy findings in general. This case is rare in that the past acute CO poisoning could be diagnosed from the remaining typical cerebral findings even after a long-term vegetative state.

Breaking and building the wall: the biology of the blood-brain barrier in health and disease

“…Hypoxia accompanies disorders like stroke, carbon monoxide poisoning, and cardiac arrest. Interestingly, carbon monoxide poisoning causes selective damage to the globus pallidus and cerebral white matter, indicating that certain brain areas are more vulnerable [89]. Also, high altitude is known to cause vaso-genic cerebral oedema [90]; however, the pathogenic mechanisms leading to oedema remain elusive.…”

Structural brain injury in patients with disorders of consciousness: A voxel-based morphometry study

“…We examined five aspects, namely: (1) structural brain injury associated with DOC; (2) the effect of time spent in DOC on brain grey and white matter integrity; (3) aetiology-based differences in structural brain injury; (4) differences between VS/UWS and MCS; (5) differences between patients in MCS-and MCS+. Given the results from previous studies, widespread structural brain injury was expected in patients with DOC [20][21][22][23][24]27,38], which might become more severe with increasing time spent in DOC [31,34,[39][40][41]. Patients with DOC with a traumatic aetiology, as compared to those with a non-traumatic aetiology, might have more focal injury centred on regions that are especially susceptible to acceleration, deceleration, and rotational forces often experienced in trauma and near rough skull edges.…”

Gambaran Kasus Kematian akibat Keracunan Karbon Monoksida

“…Pada laporan toksikologi kasus oleh Galante et al 15 didapatkan kadar COHb pada korban laki-laki ialah 62% sedangkan untuk korban perempuan sebesar 55%. Penelitian Sato et al 16 menyatakan dalam laporan kasus yang mengalami keracunan CO akut dengan kadar COHb pada korban sebesar 30,8%, tetapi pada hasil otopsi tidak ditemukan kadar COHb dalam darah.…”

“…Berdasarkan paparan hasil penelitian-penelitian dapat dinyatakan bahwa keracunan CO akan menunjukkan kadar COHb dalam darah, namun berdasarkan penelitian Sato et al 16 dari hasil otopsi tidak ditemukan kadar COHb dalam darah. Hal ini kemungkinan disebabkan oleh korban yang memasuki keadaan koma sehingga rumah sakit tetap mengurus dan mengawasi kondisi korban sampai korban meninggal dunia satu setengah tahun kemudian yang menyebabkan gambaran COHb tidak muncul karena kemungkinan korban telah pulih dari keracunan CO akut tersebut.…”

“…Jejak asap hitam pada saluran pernapasan atau mukosa esofageal juga ditemukan pada korban terbakar. Sato et al 16 mendapatkan hasil otopsi yang tidak menunjukkan warna merah terang (cherry red) pada permukaan kulit, otot, dan organ dalam. Otak pasien melunak karena edema tetapi tidak ditemukan pewarnaan apapun.…”