· Burning charcoal produces carbon monoxide, an odorless, tasteless, and colorless gas.
· Charcoal, when burnt in an enclosed space, can cause carbon monoxide poisoning.
· The most common clinical manifestations of CO poisoning are headache, dizziness, vomiting, nausea, confusion, impaired judgment, chest pain, and weakness.
· CO poisoning may be accidental or intentional. Approximately 5,000 people die in the United States per year due to CO toxicity.
· Here is a case of intentional CO poisoning.
A 41-year-old male was brought to the emergency department after being found unconscious. The patient had attempted suicide by burning charcoal in a closed room.
In the emergency room, the patient had a poor Glasgow Coma Scale (GCS) warranting intubation.
On the 6th day, the patient was transferred to another hospital after successful extubation.
On examination, the patient had a normal Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MOCA) score. There were no neurological deficits.
Computerized Tomography (CT scan) of the brain was performed after 2 days of hospital transfer (8 days after initial presentation). After another 2 days (10th day of presentation), a brain Magnetic Resonance Imaging (MRI) was performed.
The patient showed symptoms of depression, so he was referred to a psychiatrist, where the initial neuropsychological assessment showed mild deficits in learning, memory, and verbal fluency.
Approximately 2 weeks later (3 weeks after the presentation), the patient became less communicative, less active with daily life, and started having difficulties in mobilization; therefore, further evaluation was warranted.
The patient had a magnetic gait and truncal rigidity. Magnetic walking is the gait abnormality in which the affected individual cannot lift feet off the ground; therefore, the mobility decreases, and the falls increase.
A repeat MRI brain was done:
C- Interval decrease in swelling with residual cystic encephalomalacia in both globus pallidus;
D- Interval areas of restricted diffusion in both superior frontal subcortical white matter/anterior corona radiata indicating ongoing neuronal white matter injury.
Pharmacological Treatment:
The patient was treated with madopar (an antiparkinsonian drug: levodopa benserazide) and fluoxetine (SSRI: antidepressant).
Rehabilitation:
Subsequently, the patient underwent rehabilitation, and 6 months later, the patient improved substantially with mild residual lower limb hypertonicity. He was able to perform his daily activities of life independently.
One year later:
A year later, his neuropsychological assessment revealed:
- Slowed processing speed
- Impaired visuospatial construction
- Reduced mental flexibility
- Reduced attention.
The patient was diagnosed with mild cognitive impairment secondary to carbon monoxide poisoning.
Carbon Monoxide Poisoning:
Carbon Monoxide (CO) poisoning can cause early and late complications, as seen in this patient. Patients who present with loss of consciousness are at a higher risk of delayed neuropsychiatric symptoms. He had presented in an unconscious state requiring intubation. Later on, he developed the late complications of CO toxicity, i.e., the delayed neurological complications including cognitive impairment, parkinsonism, gait disturbances, and mutism.
Although the patient showed substantial recovery, there was residual mild cognitive impairment.
References:
Lo CP, Chen SY, Lee KW, Hsueh CJ, Huang GS, et al. (2007) Brain injury after acute carbon monoxide poisoning: early and late complications. AJR Am J Roentgenol 189: 205-211.
Lim EW, Pang YH, Ratnagopal P (2017) Interval Form of Carbon Monoxide Intoxication. Clin Med Img Lib 3:062. doi.org/10.23937/2474-3682/1510062
Weaver LK. Clinical practice. Carbon monoxide poisoning. N Engl J Med 2009; 360: 1217-1225.
