|Year : 2021 | Volume
| Issue : 2 | Page : 64-67
Carbon monoxide poisoning with reversible cardiomyopathy: A case of accidental exposure in the foothills of Himalayas
Mayank Agarwal, Ravi Kant, Arnav Kalra, Dheeraj
Department of Internal Medicine, All India Institute of Medical Sciences, Rishikesh 249203, Uttarakhand, India
|Date of Submission||26-Jun-2021|
|Date of Acceptance||23-Sep-2021|
|Date of Web Publication||28-Feb-2022|
Department of Internal Medicine, All India Institute of Medical Sciences, Rishikesh 249203, Uttarakhand.
Source of Support: None, Conflict of Interest: None
Carbon monoxide (CO) can cause intoxication without the victim being aware of it. Its exposure is common in Northern India but is infrequently reported because the clinical features are non-specific. In CO poisoning, myocardial injury is a significant predictor of mortality. We present a case of a middle-aged male, found unconscious inside a closed room on a winter morning. Upon presentation, the patient was drowsy with hypotension. CO oximetry showed carboxyhemoglobin (CO-Hb) of 28.6% and brain imaging, suggestive of hypodensities in bilateral globus pallidus. The patient was managed with high flow oxygen following which his sensorium improved gradually but hypotension persisted with echocardiography showing global left ventricular dysfunction. A session of hyperbaric oxygen therapy was given after which he improved hemodynamically with resolution of cardiac dysfunction over the next 3 days. We highlight the importance of early diagnosis of cardiomyopathy as CO-induced cardiomyopathy may be reversed if timely intervention is done.
Keywords: Carbon monoxide, cardiomyopathy, globus pallidus hypodensity
|How to cite this article:|
Agarwal M, Kant R, Kalra A, Dheeraj &. Carbon monoxide poisoning with reversible cardiomyopathy: A case of accidental exposure in the foothills of Himalayas. J Cardio Diabetes Metab Disord 2021;1:64-7
|How to cite this URL:|
Agarwal M, Kant R, Kalra A, Dheeraj &. Carbon monoxide poisoning with reversible cardiomyopathy: A case of accidental exposure in the foothills of Himalayas. J Cardio Diabetes Metab Disord [serial online] 2021 [cited 2022 Jun 28];1:64-7. Available from: http://www.cardiodiabetic.org/text.asp?2021/1/2/64/338608
| Key Messages:|| |
Carbon monoxide (CO) can cause intoxication without the victim being aware of it. In CO poisoning, myocardial injury is a significant predictor of mortality. Patients with suspected CO poisoning presenting with hypotension should be evaluated for left ventricular dysfunction. Oxygen therapy remains the treatment of choice as cardiac dysfunction in the early stages can be reversed.
| Introduction|| |
Carbon monoxide (CO) is a colorless, odorless gas produced by incomplete combustion of organic compounds. Domestic exposure is common in rural India, especially due to the widespread use of biomass fuels., CO poisoning is common in winters, but is infrequently reported as clinical features are non-specific. Mild exposures may cause headache and dizziness, whereas severe intoxication usually results in loss of consciousness or even death. A high index of suspicion with history of exposure to CO in a closed environment is suggestive of the diagnosis.
In CO poisoning, myocardial injury is a significant predictor of mortality, but CO-induced myocardial dysfunction has been infrequently reported in literature. It is important to identify cardiac dysfunction in the early stages of presentation as cardiomyopathy may be reversed if timely intervention is done. We present a case of CO poisoning highlighting the importance of early diagnosis and treatment to prevent cardiovascular complications.
| Case History|| |
A middle-aged male priest, residing in a hilly town of Northern India, was found unconscious in a closed room on a winter morning by his neighbors. The room was full of coal fumes from a heater kept near his bed. The patient was fine the previous night. There was no history of fever, seizures, headache, or loss of consciousness in the past. No history of substance abuse was present. The patient’s past medical and drug history was unremarkable. He was brought to the Emergency Department approximately 4 h later by his neighbors.
Upon presentation, he was confused and drowsy with a Glasgow Coma Scale (GCS) of 10/15 (E2V3M5), his pulse rate was 110/min, BP was 80/60 mmHg, and axillary temperature was 98.2 F. Pulse oximeter showed oxygen saturation of 88% at room air. His lips were cherry red and pupils bilaterally equal and reactive. Other examination findings were normal. The arterial blood gas analysis showed respiratory acidosis with pH 7.3, pCO2 48, pO2 88, and HCO3 24. CO oximetry showed carboxyhemoglobin (CO-Hb) of 28.6% (normal 0.1–2%). Other investigations showed a normal hemogram, serum electrolytes, and blood sugar, elevated liver enzymes, and raised serum creatinine [Table 1]. Electrocardiography was normal with no ST-T changes.
A non-contrast computed tomography head was done [Figure 1]. 2D-echocardiography was done in the emergency which was suggestive of global left ventricular (LV) dysfunction with an ejection fraction of 40% [Figure 2]. CK-MB and troponin I were elevated (73 IU/L and 1.5 ng/mL, respectively). Based on pointers in history, clinical presentation, and investigations, the patient was diagnosed with CO poisoning and cardiomyopathy.
|Figure 1: Non-contrast computed tomography (NCCT) brain showing symmetrical hypodensities in bilateral globus pallidus (arrows)|
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|Figure 2: Parasternal long-axis view (PLAX) showing (A) diastolic filling phase and (B) systolic phase with global LV hypokinesia|
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The patient was managed with oxygen at 15 L/min via a non-rebreather face mask. After 3–4 h his sensorium improved, became alert, and started following commands. His CO-Hb became 8.6%; however, hypotension persisted requiring vasopressor support. A session of hyperbaric oxygen (HBO) therapy at 2.5 atmospheric pressure in HBO chamber available at our facility was given.
Over the next 3 days, the patient showed complete clinical recovery. His GCS was 15/15 with no residual deficit. Blood pressure improved with no inotropic requirement. CK-MB showed considerable decline (33 IU/L). Interestingly, 2D-echocardiography showed a significant improvement in LV systolic function and wall hypokinesia with normalization after 72 h. The patient was discharged 24 h later in stable condition. A follow-up echocardiography and neurological assessment was done 2 months later which was normal.
| Discussion|| |
CO poisoning-induced cardiomyopathy is a rare manifestation. In a study by Aslan et al., out of 83 patients with CO poisoning, only 7.2% had cardiac dysfunction. In a retrospective study by Jung et al., the incidence of CO-induced cardiomyopathy was only 3.0% in the CO-poisoned population and the pattern of cardiomyopathy was predominantly Takotsubo cardiomyopathy (63.2%), whereas Satran et al.’s study showed that the majority of the patients had regional wall motion abnormality. These findings contrasted with our case in which the ECHO showed global LV dysfunction.
The mechanism of cardiomyopathy is poorly understood, but it is mainly hypothesized to be myocardial stunning caused by hypoxia. Hypoxia involves direct myocardial effects in which CO binds to intracellular myoglobin and impairs oxygen supply to the mitochondria. This subsequently impairs oxidative phosphorylation leading to decreased myocardial contractility. Studies have demonstrated that myocardial injury can lead to poor outcomes due to increased risk of arrhythmia and coronary artery disease. However, these acute effects are transient and reversible as seen in a prospective observational study by Yong et al., in which it was observed that out of 32 patients with CO poisoning who developed global LV dysfunction and received timely oxygen therapy, 81.8% of them exhibited normalization of cardiac function within 72 h. In the same study, they found that ischemic changes in the ECG were present in only 18.6% of the cases. Akdemir et al., reported a case of CO poisoning who developed atrial fibrillation with rapid ventricular response which spontaneously returned to normal sinus rhythm after a 3-h treatment with oxygen.
Oxygen therapy remains the treatment of choice. The half-life of CO-Hb is about mean 5 h (range: 2–7 h) when a patient breathes room air. With 100% normobaric oxygen, the half-life is approximately 90 min. Hyperbaric oxygen at 2–3 atmospheric pressure decreases the half-life of CO-Hb to about 23 min. Whether HBO is needed in such cases remains debatable with some trials showing beneficial effects whereas others have not. Most of the studies have revealed no clear-cut indication for HBO. Our patient although was initially managed with high flow oxygen, his cardiac functions improved drastically only after hyperbaric oxygen therapy. Thus, the exact indications and role of HBO need to be further evaluated in patients with CO poisoning and cardiomyopathy as it is not available at every facility.
The authors are grateful to all the members of the Department of Internal Medicine, AIIMS, Rishikesh for their cooperation.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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