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Global Translational Medicine                                     Complication of carbon monoxide poisoning



            nausea, difficulty in concentration, confusion, shortness   of the mid-apical segments of the left ventricle with a
            of breath, visual changes, chest pain, loss of consciousness,   slightly reduced global systolic function (EF 50%); these
            abdominal pain, and muscle cramping. Severe CO poisoning   findings were compatible with the diagnosis of Takotsubo
            can cause skin lesions (cherry-red erythema, vesicles, bullae,   cardiomyopathy (Figure 1B). After the initial stabilization,
            and cutaneous necrosis); these lesions are often misdiagnosed   the patient was transferred to the geriatric department, and
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            as burns.  Takotsubo cardiomyopathy is a form of non-ischemic   a week later, troponin I, CPK, lactate, and cardiac kinetics
            cardiomyopathy, characterized by transient regional systolic   normalized (Figure 1C). The submammary cherry-red skin
            dysfunction of the left ventricle mimicking acute myocardial   lesion partially healed (Figure 1D), and a skin biopsy was
            infarction but with only minimal release of cardiac enzymes.   not performed due to a lack of consent. The myocardial
            The term “Takotsubo” means octopus trap in Japanese, as the   perfusion imaging test (SPECT) result (Figure  1E) was
            shape resembles the systolic apical ballooning appearance of   negative for myocardial ischemia.
            the left ventricle. 4
                                                               3. Discussion
            2. Case presentation
                                                               Takotsubo cardiomyopathy is a syndrome characterized by
            An 83-year-old female patient, diagnosed with Alzheimer’s   transient left ventricular dysfunction (hypokinesia, akinesia,
            dementia and Type 2 diabetes mellitus, was transported to   or dyskinesia), usually presenting as apical ballooning or
            the emergency department by ambulance due to impaired   midventricular, basal, or focal wall motion abnormalities
            consciousness. Her caregiver reportedly discovered the   that extend beyond a single epicardial vessel territory. New
            patient unconscious, sitting in the wheelchair with vomit on   ECG abnormalities (ST-segment elevation or depression,
            her clothes, in the morning. The heating in the apartment   T-wave inversion,  and rate-related [or corrected]  QT
            was powered by liquefied petroleum gas. On admission   interval [QTc] prolongation) and mild increases in
            to the emergency department, the reported vital signs of   troponin levels are common. Takotsubo usually affects
            the patient were as follows: blood pressure, 110/67 mmHg;   postmenopausal women with ischemic-like chest pain and
            body temperature, 36°C; heart rate, 90 beats/min; and   is strongly correlated with physical and emotional stress.
            respiratory  rate,  22  breaths/min.  Physical  examination   Although most patients present with a complete recovery,
            revealed mild dyspnea, warm and dry skin with a cherry-  mortality  is higher than previously thought.  According
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            red lesion in the submammary area, rhythmic heart   to a 2016 study by Sung et al., 30% of patients affected by
            action, a normal vesicular murmur over the entire lung   CO intoxication report myocardial damage; 25.6% of these
            area, and a Glasgow Coma Scale score of 8 (E2-V2-M4).   patients had normal echocardiography; 51.2% presented
            The electrocardiogram (ECG) revealed sinus rhythm at 90   with global changes in left ventricular kinetics; and 23.2%
            bpm, with normal ST segment and T waves. Additionally,   had Takotsubo-like cardiomyopathy.  The abnormalities of
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            the arterial blood gas analysis in ambient air was as follows:   Takotsubo CO-related cardiomyopathy are thought to be
            pH 7.32; pCO 31 mmHg; pO 60 mmHg; HCO 16 mmol/L;   caused by an increase in catecholamines and consequent
                                  2: 
                                                3: 
                      2: 
            COHb: 23.8%; and lactate: 10.5 mmol/L. Laboratory test   myocardial stunning.  This condition is usually transient
                                                                                7
            results were as follows: creatinine: 1.12  mg/dL; creatine   and is managed with supportive care, but some patients
            phosphokinase (CPK): 2352 U/L; myoglobin: 1141 ng/mL;   require intensive care due to acute complications such as
            and troponin I: 3276 ng/L. A head computed tomography   cardiogenic shock or acute heart failure; in patients with
            revealed  age-compatible  brain  atrophy.  Following  the   severe left ventricular systolic dysfunction, the risk of left
            diagnosis of CO poisoning, the patient was admitted to the   ventricular thrombosis and systemic embolization should be
            emergency medicine ward. Subsequently, the patient was   considered. Rhabdomyolysis is characterized by an elevation
            administered O  via continuous positive airway pressure   in CPK due to the damage to striated muscle fibers and the
                         2
            (CPAP), with a FiO of 50% and a positive pressure of 7.5 cm   consequent release of intracellular muscular constituents
                           2
            H O. Large volumes of crystalloids were administered to   into  the  blood  circulation.  This  complication  is  reported
             2
            prevent renal damage due to rhabdomyolysis, and low-  in approximately 30% of patients with CO intoxication;
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            molecular-weight heparin (LMWH) was administered for   among non-traumatic causes of rhabdomyolysis, CO
            antithrombotic prophylaxis. Hyperbaric O  therapy was   intoxication represents 3.2% of the total number of cases.
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                                               2
            deemed unnecessary by the poison control center. The   In  CO  poisoning,  muscle  compression,  caused  by  the
            CPAP rapidly reduced COHb levels (1.6% after 4 h and   patient’s own weight, increases the pressure within the
            0.3% after 5 h). On the following day, we found changes   muscle compartment, causing edema and ischemia. If this
            in the ECG, specifically the appearance of negative T   condition persists, COHb production increases and the
            waves in the precordial leads (V1–V6) (Figure 1A). The   O  supply further decreases, leading to necrosis of muscle
                                                                2
            bedside echocardiogram showed akinesia and dilatation   fibers and rhabdomyolysis.  Numerous CO-related skin
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            Volume 3 Issue 1 (2024)                         2                        https://doi.org/10.36922/gtm.1718
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