Isolated unilateral brachial plexus injury following carbon monoxide intoxication: a case report

Abstract

Background

CO is an odorless, colorless gas that often still undetectable until exposure results in coma or death. Carbon monoxide (CO) intoxication is a common fatal poisoning worldwide. The toxic effects of CO lead to tissue hypoxia and produce systemic and neurological complications. Besides, some severe neurological manifestations and delayed sequelae may occur after CO intoxication. However, peripheral neuropathy following CO poisoning is relatively rare that usually occurs in young people. Beforehand, only one case reported unilateralplexopathy following CO poisoning, which combined with rhabdomyolysis and cognitive dysfunction.

Case presentation

A 31-year-old young man slept in his private car with closed doors and windows. His wife discovered him in about 7 hours when he was in an unconscious state. He was diagnosed with acute carbon monoxide poisoning. After about 12 hours in a coma, he returned to an alert state without conscious disorder. However, he woke up with left upper arm weakness associated with limitation of movement of the left upper limb. The electrophysiological conclusion was left incomplete total brachial plexopathy.

Conclusion

Ischemia of spinal cordcaused by CO intoxication may be a key mechanism in this case. Hyperbaric oxygen therapy as soon as possible is necessary to prevent peripheral neuropathy after acute CO intoxication. Besides, persisting in rehabilitation training might be important to treat peripheral neuropathy after acute CO intoxication.

Background

Carbon monoxide (CO) intoxication is the most common fatal poisoning all over the world. Symptoms of carbon monoxide poisoning can vary from a mild headache to critical illness. It can affect multiple organs including brain, heart, lung, kidney, skeletal muscle and peripheral nerve. Most complications have been widely described. However, few studies have reported peripheral neuropathy and electrophysiological features[1]. We present a case of isolated unilateral brachial plexopathy following CO poisoning.

Case Presentation

A 31-year-old young man slept in his private car with closed doors and windows at about 11 o’clock in 11th of February 2022. His wife discovered him in about 7 hours when he was in an unconscious state. He was admitted to the hospital and diagnosed with acute carbon monoxide poisoning. His blood test showed elevated carbon monoxide hemoglobin (16.2%), normal glucose, hepatic function and complete blood count tests. On brain magnetic resonance imaging (MRI), punctate slightly hyperintense signal at the bilateral basal ganglia was detected. After about 12 hours in a coma, he returned to an alert state without conscious disorder. However, he woke up with left upper arm weakness associated with limitation of movement of the left upper limb. Neurological examination showed the left arm paralysis (Manual muscle tests revealed 1 medical research council (MRC) grade), distal vibratory, thermic and algic hypoesthesia, disappeared deep tendinous reflect in left upper arm. Ultrasonic examination showed that the left median and left radial nerves were swollen in the forearm and upper arm. A motor nerve conduction study showed a normal motor conduction velocity (MCV) for left ulnar, median, and radial nerves, and a decreased amplitude of compound muscle action potentials (CMAP) for left axillary and musculocutaneous nerves. Besides, sensory conduction velocity (SCV) for left median nerve and ulnar nerves are in the normal range (Table 1). Needle electromyography revealed abnormal spontaneous activities including positive sharp wave and fibrillation potential in left deltoid, left biceps brachii, and left triceps brachii (Table 2). The electrophysiological interpretation was left brachial plexopathy involve upper and middle branches(severe upper branches abnormalities and moderate middle branches abnormalities). The patient underwent rehabilitation training and about 80 sessions of hyperbaric oxygen therapy. He readmitted to hospital due to check-up 70 days after CO intoxication. The limitation of movement in his left upper limb is slightly improved(Manual muscle tests revealed 3 medical research council (MRC) grade). There was existed sensation to pinprick and light touch in the left upper limb. In addition, the patient remained no other sequelae. We found marked atrophy of left deltoid and biceps (Fig. 1). Compared to admission, the re-examination of the cerebral magnetic resonance imaging (MRI) showed no significant change. The sense nerve conduction study showed a decreased nerve conduction velocity and amplitude for left radial nerves (Table 3). Motor nerve conduction was normal except for the left axillary and musculocutaneous motor amplitude which were highly decreased (Table 4). The electrophysiological conclusion for this admission was left incomplete total brachial plexopathy involved axillary, musculocutaneous and radial nerves. It seems that the patient’s relevant examination results did not change much compared with the first. However, we did a total spine magnetic resonance imaging (MRI) for the man. Long strip T2 high signal was shown in the left part of the cervical medulla at the level of the 4/5 intervertebral space (Fig. 2). During this hospitalization, the man continue to receive rehabilitation training and hyperbaric oxygen therapy.

Fib, fibrillation potential; PSW, positive sharp wave; ADM, abductor digiti minimi; Abd, abductor.

Discussion

Carbon monoxide (CO) has the toxic effects of tissue hypoxia and produces various systemic complications. CO poisoning has previously been related to central nervous system, cardiovascular system, respiratory system, hematological system, metabolic and endocrinological system, musculoskeletal system and changes in perception of the visual and auditory systems, especially the cardiovascular system and central nervous system such as amnesia, encephalopathy, dysarthria, parkinsonism and peripheral neuropathy. Among them, little has been reported regarding peripheral neuropathies.

To our knowledge, there was a large-scale clinical study about neuropathy after CO poisoning. Among 2759 patients with acute CO poisoning examined clinically between 1976 and 1982, peripheral neuropathy was diagnosed in 23 subjects( 11 men and 12 women, mean age was 29.3) by electrophysiological detection. Of all patients, 14 subjects had sensory symptoms, 8 subjects had mixed symptoms and only one had isolated motor symptoms. All are involve in the lower extremity except 2 subjects. The study also show that peripheral neuropathy after CO poisoning commonly affected young people and all recovered within 3–6 months[2]. Rahmani et al reported a 42-year-old man with reversible bilateral brachial plexus injury after acute CO poisoning, who had good prognosis after hyperbaric oxygen therapy[3]. Gi-Young Park et al reported unilateral brachial plexopathy with impaired cognitive function after CO intoxication. Electrophysiological interpretation was left incomplete total brachial plexopathy with axonal involvement. The 45-year-old patient had poor prognosis with no significant change of left upper extremity weakness and impaired cognitive function when 11 months after CO intoxication[4]. Other articles have also reported peripheral neuropathy after

CO intoxication: Sciatic neuropathy and rhabdomyolysis, motor and sensory peripheral neuropathy, unilateral diaphragmatic paralysis.

The precise pathogenesis of peripheral neuropathy following CO intoxication remains in doubt. However, 4 possible mechanisms may be responsible for this: hypoxia due to CO and subsequently ischemia, nerve compression, cytotoxic effect of CO and petechial hemorrhages. CO causes hypoxia through the formation of COHb and binding to heme-containing proteins, particularly cytochrome c oxidase and myoglobin. In addition, CO binds to platelet heme protein, causing the release of NO. Increased NO produces peroxynitrite (ONOO), which impairs mitochondrial function and worsens tissue hypoxia[5]. The central nervous system are most vulnerable to the effects of ischaemia and hypoxia. The thoracic spinal cord was feed by the radiculomedullary arteries, which originate from a few intercostal arteries (from the subclavian artery and aorta), compromise of blood flow from these arteries potentially creates a great risk of ischemia because of poor collateralization in the thoracic vascular region. Besides, The watershed effect is common in the vascular system of the spinal cord. It occurs when 2 streams of blood flowing in opposite directions meet. The watershed effect is at its maximum in the midthoracic area because the distance between radicular arteries is the greatest[6]. In the case, we found that Long strip T2 high signal was shown in the left part of the cervical medulla at the level of the 4/5 intervertebral space. Abnormal signal intensity of the left cervical spinal cord is present at MRI at a level suggestive of a correlation with the clinical symptoms and signs. At that level there is also a disk protrusion. However, it is clear that this lumbar disk protrusion did not compress the spinal cord of patient, so it was not sufficient to cause brachial plexus injury. The patient’s wife found him lying in the driver's seat with his head tilted to the left. It is possible that it is a spondilogenic compression myelopathy (ischemic pathomechanism?) possibly related to the position of the unconscious patient in the car. So we suspect that the ischemia of spinal cord caused by CO intoxication may be a key mechanism of left brachial plexopathy. Besides, nerve compression and cytotoxic effect of CO should also be considered. The young man in our case experienced isolated unilateral brachial plexus injury following acute CO poisoning with incomplete improvement after nearly 3 months, which is the second case on unilateral brachial plexopathy following CO intoxication in literature so far. Ischemia of spinal cord caused by CO may be the main mechanism about unilateral brachial plexopathy. Therefore, correct hypoxia caused by CO (hyperbaric oxygen and normobaric 100% oxygen) as soon as possible is necessary to prevent peripheral neuropathy after acute CO intoxication. In addition, persisting in rehabilitation training might be important to treat peripheral neuropathy after acute CO intoxication.

Declarations

Competing interests The authors declare no competing interests.

Ethical approval and consent to participate The Institutional Review Board at Chongqing General Hospital approved this case report. 

Consent for publication Written informed consent for publication of this case report was obtained from the patient.

Availability of data and materials The datasets used or analysed during the current study are available from the corresponding author on reasonable request.

Funding   This work was supported by the Construction Project of Capacity Improvement Plan for Chongqing Municipal Health Commission affiliated unit (2019NLTS001)-ZS03174, operating grant to Chongqing Key Laboratory of Neurodegenerative Diseases (1000013), Chongqing Talent Project (2000062), Overseas Students entrepreneurial fund (2000079), and Plan for High-level Talent Introduction (2000055).

Author Contributions Shu, Liu: Data Curation, Writing - Original Draft, Visualization. Hou-chao Sun: Writing - Review & Editing. Xu Yang: Writing - Review & Editing. Zhi-you Cai: Writing - Review & Editing.

Acknowledgements This work was supported by the Construction Project of Capacity Improvement Plan for Chongqing Municipal Health Commission affiliated unit (2019NLTS001)-ZS03174, operating grant to Chongqing Key Laboratory of Neurodegenerative Diseases (1000013), Chongqing Talent Project (2000062), Overseas Students entrepreneurial fund (2000079), and Plan for High-level Talent Introduction (2000055).

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