East Asian Arch Psychiatry 2022;32:43-4 | https://doi.org/10.12809/eaap2054

CASE REPORT

Refractory Psychosis After Carbon Monoxide Poisoning: a Case Report
WM Metekiya, AT Gebreselassie, TA Amare, DZ Wondafrash

CKW Wong, Department of Psychiatry, Kowloon Hospital
MM Kwan, Department of Psychiatry, Kowloon Hospital
WK Lam, Department of Psychiatry, Kowloon Hospital

Address for correspondence: Dr CKW Wong, Department of Psychiatry, Kowloon Hospital. Email: wkw711@ha.org.hk

Submitted: 15 June 2020; Accepted: 23 July 2021


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Abstract

We report a case of refractory psychosis after carbon monoxide poisoning in a 65-year-old woman who attempted suicide by charcoal burning in 2018. On discharge from hospital, she was bedbound, tube- fed, and had limited verbal output. In early 2019, she was able to resume oral feeding and her physical condition improved. However, she started to have paranoid ideas and auditory hallucinations. She was diagnosed as having organic brain syndrome and was prescribed with quetiapine 300 mg every night. Because of the poor clinical response, quetiapine was switched to olanzapine 20 mg every night and augmented with amisulpride and valproate sodium. However, she remained distressed, psychotic, and suicidal. She was then prescribed with clozapine 300 mg every night. Her symptoms improved despite residual auditory hallucinations remained, but she was less distressed about them.

Key words: Carbon monoxide poisoning; Psychotic disorders

Introduction

Carbon monoxide (CO) is an odourless, colourless, tasteless molecule. The toxicity of CO is attributable to its high affinity toward haemoglobins (250 times higher than that for oxygen), causing hypoxic damage to organs. The blood level of CO is reflected by level of carboxyhaemoglobin (COHb). COHb concentration of >10% may result in initial signs of CO poisoning including fatigue, headache, and nausea, and subsequently respiratory failure, renal failure, rhabdomyolysis, and severe acidosis. COHb concentration of >51% may result in seizure, coma with or without tachycardia or arrhythmia, and death. The death rate of CO poisoning is 1% to 3%. Long-term neurocognitive sequelae, including impaired memory and cognitive dysfunction, are observed in 15% to 40% of CO poisoning survivors. These sequelae are evident by 6 weeks and can improve over time. However, 6 years after CO poisoning, 19% and 37% of patients remain to have cognitive deficits and neurologic deficits, respectively.1

We report a case of refractory psychosis after CO poisoning in a 65-year-old woman who attempted suicide by charcoal burning in 2018. Magnetic resonance imaging showed bilateral symmetric T2 hyperintense signals in the globi pallidi and cerebral peduncles with additional diffuse involvement of bilateral cerebral white matter and corticospinal tracts. She later presented with delayed neuropsychiatric manifestation of CO poisoning including refractory psychosis. Neuropsychiatric symptoms were highly predictive for globus pallidus necrosis, with an odds ratio of 8.0.2

Case presentation

In April 2018, a 65-year-old woman was admitted to the accident and emergency department after a suicide attempt by charcoal burning. Since 1999, she had recurrent depressive disorder. She had tried many antidepressants including amitriptyline, dothiepin, sertraline, mirtazapine, duloxetine, and milnacipran, with lithium augmentation. Since 2016, her mood had deteriorated significantly resulting in psychiatric admission for suicidal ideation, but computed tomography of the brain showed no abnormality.

After oxygen treatment, her COHb level was mildly elevated. She stayed in the medical ward for 2 days with some physical improvement. She was transferred to the psychiatric ward for further treatment. Three weeks later, she started to have limb rigidity and reduced verbal response. Lorazepam was added but little improvement was seen. She was transferred back to the medical department for examination. Magnetic resonance imaging of the brain showed bilateral symmetric T2 hyperintense signals in the globi pallidi and cerebral peduncles with additional diffuse involvement of bilateral cerebral white matter with or without corticospinal tracts. The findings were compatible with recent CO poisoning. The neurologist concluded that she had delayed neuropsychiatric manifestation of CO poisoning. After a course of rehabilitation, she was discharged to an old age home in September 2018. She was bedbound, receiving Ryles tube feeding, and had limited verbal output on discharge from the hospital.

In early 2019, her physical condition improved. She was able to resume oral feeding. However, she started to hear non-existing female voices scolding her and telling her to commit suicide. She saw shadows wandering around at night. She had persecutory ideas of the staff beating her, scolding her, and covering her head with cloth. In August 2019, she attempted suicide by self-strangulation with a phone wire and was sent to the accident and emergency department and subsequently admitted to the psychiatric ward.

She was diagnosed as having organic brain syndrome. She was previously taking quetiapine for her mood disorder, and thus quetiapine alone was resumed and titrated up to 300 mg every night. She continued to have persistent paranoid ideas and auditory hallucinations. She attempted suicide again by self-suffocation. Quetiapine was switched to olanzapine because of the poor clinical response.Olanzapine dosage was increased to 20 mg every night and augmented with amisulpride and valproate sodium. However, she remained distressed and was actively psychotic and suicidal. Because of her resistant symptoms, she was prescribed clozapine 300 mg every night, and her symptoms improved. She had residual auditory hallucinations but was less distressed about them. She was able to control herself from responding to the auditory hallucinations manifesting as voices.

Discussion

Sublethal CO poisoning can cause severe neuropsychiatric complications. Medical treatment using oxygen or hyperbaric oxygen usually focuses on immediate symptoms, which may not be effective for preventing the delayed neuropsychiatric sequelae including impaired memory, cognitive dysfunction, depression, anxiety, motor deficit, and parkinsonism features.

Our patient received oxygen therapy, and the COHb level was mildly elevated. Her physical symptoms resolved quickly. However, significant motor symptoms of CO poisoning occurred 3 weeks later, with evident damages in globi pallidi, cerebral peduncles, and cerebral white matter.

The anterior and medial pallidum are supplied by ends of small branches of the middle and anterior cerebral artery, leading to a ‘triple watershed’ region that is poorly vascularised and vulnerable to hypoxic-ischaemic injury.

Our patient showed a slow but progressive improvement after rehabilitation. A lucid interval of 2 to 4 weeks was common, which has been reported in a similar case report of CO poisoning in Hong Kong.4 Almost 1 year after CO poisoning, she had psychotic symptoms of paranoid delusion and auditory hallucination and was diagnosed as having ‘organic psychosis’. The symptoms were so severe and distressing that necessitated the use of clozapine. Significant size and shape differences in caudate and globus pallidus were found between schizophrenic patients and normal controls; these provide anatomical evidence of associations between globus pallidus and psychosis.5

The onset and clinical presentation of CO poisoning vary. In addition to managing the immediate complication of CO poisoning, physicians should be aware of the possibility of delayed complications, despite a sublethal CO exposure or a low level of COHb. All patients should have baseline and follow-up neuropsychological assessment targeting to maintain residual cognitive function. Most impairments are chronic and significant; further studies for effective treatment of cognitive impairment (eg, anticholinesterase inhibitors) after CO poisoning are warranted.

Contributors

All authors designed the study, acquired the data, analysed the data, drafted the manuscript, and critically revised the manuscript for important intellectual content. All authors had full access to the data, contributed to the study, approved the final version for publication, and take responsibility for its accuracy and integrity.

Conflicts of interest

All authors have disclosed no conflicts of interest.

Funding/support

This study received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

Data Availability

All data generated or analysed during the present study are available from the corresponding author on reasonable request.

Ethics approval

The patients were treated in accordance with the tenets of the Declaration of Helsinki. The patients provided written informed consent for all treatments and procedures and for publication.

References

  1. Rose JJ, Wang L, Xu Q, et al. Carbon monoxide poisoning: pathogenesis, management, and future directions of therapy. Am J Respir Crit Care Med 2017;195:596-606. Crossref
  2. Ku CH, Huang WH, Hsu CW, et al. Incidence rate and predictors of globus pallidus necrosis after charcoal burning suicide. Int J Environ Res Public Health 2019;16:4426. Crossref
  3. Hashim NA, Shuib N, Mohamed S, Ling LS, Nor KM. Delayed neuropsychiatric sequelae of carbon monoxide poisoning: a case report. J Clin Health Sci 2016;1:64-8. Crossref
  4. Lam SP, Fong SY, Kwok A, Wong T, Wing YK. Delayed neuropsychiatric impairment after carbon monoxide poisoning from burning charcoal. Hong Kong Med J 2004;10:428-31.
  5. Womer FY, Wang L, Alpert KI, et al. Basal ganglia and thalamic morphology in schizophrenia and bipolar disorder. Psychiatry Res 2014;223:75-83. Crossref
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