Carbon monoxide poisoning: a clinical case report

This case report on carbon monoxide (CO) poisoning in a young couple brings forth several important clinical considerations and insights into the diagnosis, management, and long-term implications of this potentially fatal condition.

Clinical assessment and diagnosis

The diagnostic challenge in CO poisoning is underscored in these cases. The triad of symptoms consistent with CO poisoning, a history of exposure, and elevated carboxyhemoglobin (COHb) levels is crucial for diagnosis [6]. The diversity in clinical presentations observed in these cases exemplifies the hallmark variability of carbon monoxide (CO) poisoning. The male patient exhibited severe symptoms, including unconsciousness, which contrasted sharply with the female patient’s cardiovascular manifestations, notably Takotsubo cardiomyopathy (TTC). This variability highlights the critical need for a broad differential diagnosis and a heightened index of suspicion for CO poisoning, particularly in ambiguous cases, when patients present with non-specific, multisystem symptoms, or when multiple individuals from the same environment develop similar clinical features [7].Factors influencing severity and symptoms of CO poisoning include CO concentration and duration of exposure; pre-existing conditions that might impact oxygen carrying capacity (e.g., chronic lung disease); age; smoking; and pregnancy. CO binds more readily to fetal hemoglobin than to adult hemoglobin, potentially leading to fetal distress, low birth weight, or even miscarriage [8].Importance of Arterial Blood Gas and COHb Testing:

Given that no single symptom is pathognomonic for CO poisoning, arterial blood gas analysis and measurement of COHb levels are indispensable for diagnosis. The clinical diagnosis of acute CO poisoning should be confirmed by demonstrating an elevated carboxyhemoglobin level. COHb levels of more than 3–4% in nonsmokers and 10% in smokers are considered outside the expected physiological range [7].

Other tests which help determine need for admission and further follow up, also help determine spectrum of treatment lactate, creatine phosphokinase, troponin, and ECG [8, 9].

Takotsubo cardiomyopathy

Myocardial injury in CO poisoning results from both tissue hypoxia and cellular-level damage [10]. Research indicates that younger patients, with fewer cardiac risk factors, are more likely to develop global hypokinesis of the left ventricle, which typically improves with treatment. In contrast, older patients, who have a higher prevalence of cardiac risk factors, often reveal underlying coronary artery disease due to CO poisoning’s disruption of the balance between oxygen supply and demand [10, 11]. Since such pathology, including Takotsubo cardiomyopathy (TTC), often resolves spontaneously, it may be prudent to monitor asymptomatic or mildly symptomatic patients with adequate organ perfusion, allowing the natural healing process to occur [12].

CO poisoning in pregnancy

The management of CO poisoning in pregnancy, as seen in the female patient, presents unique challenges. The increased affinity of CO for fetal hemoglobin and slower clearance in the fetus necessitates prompt and effective treatment [13]. Eichorn described a case that showed a COHb measurement of 61% at fetal autopsy, although the mother had a measurement of 7% after just an hour of O2 treatment [14]. If HBO therapy is planned for the patient, the therapy duration should be longer for pregnant women than for non-pregnant women due to the slower dissociation of carboxyhemoglobin in the fetus [15]. Although this patient had a COHb level of 9.6%, the fetus was exhibiting tachycardia, suggesting fetal distress. However, there is no guarantee that HBO would have changed our patient’s fetal outcome. This case raises awareness about the risks to both the mother and the fetus, and the need for careful monitoring and management, including considerations for hyperbaric oxygen therapy (HBO).

Hyperbaric oxygen therapy

The role of HBO in the treatment of CO poisoning is emphasized in the male patient’s case. HBO therapy is recommended for severe cases and specific scenarios like pregnancy, prolonged exposure, and high COHb levels (> 25%) [16]. While effective in reducing COHb levels it is believed to reduce mortality and neurological sequelae [17,18,19]. However, HBO therapy comes with potential complications such as lung damage, ear barotrauma, vision changes, hydrothorax, and may also cause seizures [20].

Disposition

Recommendations for disposition are presented in Table 1.

Table 1 Recommendations for disposition [8, 9]Long-term effects and delayed neuropsychological sequelae

CO poisoning can manifest long-term effects despite receiving treatment. Both patients exhibited long-term cognitive and psychological effects post-CO poisoning, highlighting the potential for delayed neuropsychological sequelae (DNS).

DNS can occur after CO poisoning, typically developing within weeks after an initial complete clinical recovery from acute poisoning. The reported incidence varies widely, ranging from 3 to 40%, due to the absence of established diagnostic criteria [21]. The most frequently described sequelae encompass a broad spectrum of neurological deficits, cognitive impairments, and affective disorders. DNS typically resolve gradually over the first few months but can be permanent in about 25% of cases [21].

HBO therapy has been utilized to prevent DNS, although there is limited evidence proving its effectiveness in improving patient outcomes in this area. Buckley et al. examined seven randomized trials to assess the efficacy of HBO compared to normobaric oxygen for preventing neurologic sequelae in patients with acute carbon monoxide poisoning [22]. Existing randomized trials did not establish whether the administration of HBO to patients with carbon monoxide poisoning reduces the incidence of adverse neurologic outcomes [22].

Preventive measures

The report also emphasizes the importance of preventive measures against CO poisoning. According to available data, accidental CO poisoning in the US conservatively costs society over $1.3 billion, encompassing direct hospital expenses and lost earnings [23]. While data for Lithuania is limited, the consistent number of patients with this poisoning suggests that the issue persists.

One effective solution is the installation of CO sensors in houses. Although no extensive studies have been published to examine the effectiveness of CO alarms in preventing CO exposure, a comparable example is smoke alarms: homes with working smoke alarms have an 88% lower risk of fire-related injury or death [23]. A British cost-benefit analysis estimated CO alarms to be 75% effective [23]. Public education, especially for vulnerable groups like pregnant women, also plays a crucial role in prevention [24].

Limitations and future research

Our case report has its limitations. The limitations in this case, including the patients’ refusal for further evaluation and the lack of definitive answers regarding the optimal HBO therapy for pregnant patients, highlight the need for more research. Furthermore, there is a lack of large-scale studies on the prevention of CO poisoning. These areas highlight the need for more comprehensive research on the long-term cognitive effects of CO poisoning.

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