Predictors for Delayed Encephalopathy Following Acute Carbon Monoxide Poisoning

Kaoru Kudo; Kotaro Otsuka; Junko Yagi; Katsumi Sanjo; Noritaka Koizumi; Atsuhiko Koeda; Miki Yokota Umetsu; Yasuhito Yoshioka; Ayumi Mizugai; Toshinari Mita; Yu Shiga; Fumito Koizumi; Hikaru Nakamura; Akio Sakai

Disclosures

BMC Emerg Med. 2014;14(3) 

In This Article

Background

Carbon monoxide (CO) poisoning has been a preferred method of suicide due to its high success rate of approximately 30%,[1] its simplicity, and the minimal external injury involved. According to the 2011 "White Paper on Suicide (Jisatsu Taisaku Hakusho)" compiled by the Japanese Cabinet Office, "briquettes or similar materials" were the second most used means of suicide used by men (2,137 persons, 10.2%), next only to "hanging" (14,354 persons, 68.5%), with their use spread across a wide range of age groups from those in their twenties to those in their sixties.[2]

In general, CO poisoning occurs due to such causes as inhalation of exhaust gas from automobiles, or incomplete combustion of charcoal, briquettes, fuel gas or oil in a closed place, or in such settings as a fire. Its pathology consists mainly of dysfunction of various organs due to tissue hypoxia. Since hypoxia is reversible, early removal of CO is essential and high levels of oxygen should be administered wherever possible during transportation, examination and treatment. Means to administer high concentrations of oxygen include normobaric oxygen (NBO) and hyperbaric oxygen (HBO) therapies. Previous studies comparing the two therapies have reported that HBO therapy is effective as a treatment to reduce the incidence of DNS and reduce its severity in cases of acute CO poisoning.[3–6] Other studies, however, have disputed that finding, so there is still worldwide controversy regarding the effectiveness of HBO therapy.[7] In addition, various studies worldwide have cited different criteria for administering HBO therapy during acute CO poisoning due to the ambiguity of indices of the clinical severity of acute CO poisoning. Criteria for administering HBO therapy have yet to be standardized. Moreover, a patient transfer from a medical facility with no HBO chamber to a facility with an HBO chamber has to be considered.[8]

CO poisoning is generally classified as acute CO poisoning or chronic CO poisoning depending on the duration of CO exposure. CO poisoning is categorized into different forms based on the clinical manifestations resulting from CO exposure over time. With acute CO poisoning, the patient recovers without sequelae, but with delayed CO poisoning or intermittent CO poisoning the patient can be left with neurologic sequelae.

Delayed CO poisoning refers to impaired consciousness that develops at the time of poisoning and that persists without improving. This form of poisoning causes brain cells to be deprived of oxygen and can lead to sequelae such as amnestic syndrome, loss of initiative, affective incontinence, and parkinsonism.[9] Intermittent CO poisoning is pathology where, after a certain asymptomatic period (from several days to four weeks; an average of two weeks) following recovery from acute-phase symptoms, neuropsychiatric symptoms develop rapidly, such as amnesia, disorientation, loss of mathematical ability, slowness of movement, urinary incontinence, apathy, anxiety or emotional lability. These symptoms may lead to Apallic syndrome in some cases and/or to death in worst cases.[5] Intermittent CO poisoning is thought to develop as a result of the progression of focal demyelination of the cerebral white matter and subsequent neuronal death. Intermittent CO poisoning has been reported to occur in 2.8% of acute CO poisoning cases and 11.8% of those who were hospitalized.[10] These two types of CO poisoning are sometimes referred to collectively as "delayed neuropsychiatric sequelae (DNS)."

Iwate Medical University Hospital ("Hospital") has an HBO chamber, and its emergency department accepts more than 10 cases of attempted suicide with CO poisoning annually. The Hospital sometimes accepts CO poisoning cases in a very acute phase from neighboring medical institutions with no HBO chamber. Virtually all of these cases have been hospitalized after admission and have received treatment including HBO therapy, with some developing DNS and remaining having been hospitalized for prolonged periods.

While it is necessary to predict the potential development of DNS at the initial stage following admission to the emergency department, no correlation has been found between CO-Hb level in the blood and clinical severity.[11] It has also been found impossible to predict prognosis from EEG findings obtained at the initial stage.[12] Based on the fact that DNS is caused by demyelinating changes in the cerebral white matter, some researchers have pointed out the need to measure myelin basic protein (MBP) levels in the cerebrospinal fluid (CSF) soon after injury,[13] as well as to assess nerve fibers in the white matter by diffusion tensor imaging[14] or 1H-magnetic resonance spectroscopy.[15] However, since head MRI depicts all the various histological changes, it may not be possible to accurately tell the progress of the condition in the cerebral white matter.[16] In addition, there have been cases who developed DNS despite having subnormal MBP levels in the CSF two weeks immediately following injury.[17] A recent study examined development of cognitive sequelae and genetic factors 6 weeks after CO poisoning. The study found that the apolipoprotein (APOE) epsilon4 allele was not associated with development of cognitive sequelae.[18] Taken together, at present no reliable means to predict DNS have been established, making prediction during the acute phase difficult.

However, if the development of DNS can be predicted during the acute phase, it would help making decisions on treatment strategy, by such means as identifying cases to which HBO therapy should be actively administered and setting an appropriate period of hospital treatment. In the present study, we studied cases of attempted suicide with acute CO poisoning admitted to our emergency department, and reviewed and analyzed these cases with the intention of identifying risk factors for developing DNS and characterizing the clinical course after the development of DNS.

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