Hyperbaric oxygen therapy for carbon monoxide ...

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CASE REPORT

Hyperbaric oxygen therapy for carbon monoxide poisoning Verda Tuna, Kesıcı Sevgi1, Selma Ozkan, Gulgun Elif Akcali, Ebubekir Esen2, Ozkan Orhan Departments of Anesthesiology and Reanimation, Ministry of Health, Kanuni Training and Reseach Hospital, Trabzon, 1 Faculty of Medicine, University of Giresun, Giresun, 2Ministry of Health, Vakfikebir State Hospital, Trabzon, Turkey

A B S T R A C T Carbon monoxide poisoning is a life-threatening poisoning. In this case report neurological ﬁndings developed in carbon monoxide poisoning and the importance of multidisciplinary approach are discussed. The patient, 16-year-old male, was found unconscious following a 1-hour exposure to gas water heater poisoning and brought to our hospital after being intubated at the scene of the accident. After treatment for bicarbonate deﬁcit, hepatamine infusion was started and hyperbaric oxygen treatment was performed. The patient was connected to mechanical ventilator in our department. The treatment were performed for cerebral edema. And hyperbaric oxygen treatment continued for 12 days. The patient was disconnected from the ventilator on the 36th day of the follow-up. Medical history and clinical examination are very important in the diagnosis of carbon monoxide poisoning. The patient should be followed up with laboratory examinations and imaging methods such as magnetic resonance imaging in order not to overlook neurological sequelae or any organ injury. Additionally hyperbaric oxygen treatment performed in acute period and goal-directed therapy decrease mortality and morbidity. Keywords: Carbon monoxide poisoning, hyperbaric oxygen, oxygen therapy

INTRODUCTION Carbon monoxide (CO) is a colorless, odorless, tasteless, non-irritating, but significantly toxic gas. [1] CO is one of the leading causes of accidental poisonings.[2] CO poisoning is a life-threatening poisoning.[3] In this case report neurological findings developed in CO poisoning, its treatment and the importance of multidisciplinary approach are discussed.

CASE REPORT A 16-year-old male child was admitted with a history of having been found unconscious in the bathroom by his mother. The patient was found following exposure Access this article online Quick Response Code: Website: www.cjhr.org DOI: 10.4103/2348-3334.134279

to leakage from a gas water heater for about 60 minutes. The patient’s mother phoned to The Medical Emergency Team immediately and they arrived about 10 minutes to the home. There was no evidence of associated tonic-clonic movements, tongue bite, vomiting, or trauma. The patient was brought to our hospital after being intubated at the scene of the accident by The Medical Emergency Team. Pupils were normal size and well reacting to light and systemic examination was normal. The patient was connected to mechanical ventilator in our intensive care unit. Glasgow Coma Scale score was 8; eye opening-to pain: 2, verbal response-incomprehensible sounds: 2, motor responsewithdraws from pain: 4. Arterial blood gas analysis was; pH: 7.1, PC02: 56 mmHg, P02:93 mmHg, COHb: 34.2%, HCO3 :10.6 mmol/L, Base Excess: -14 mmol/L with fiO2: 100%. The other laboratory values were; Aspartat Aminotranspherase (AST): 199 U/L, Alanine Aminotranspherase (ALT): 86 U/L. After treatment for bicarbonate deficit, hepatamine infusion, and other supportive treatment were started. Following that hyperbaric oxygen (HBO) treatment was performed in the pressure chamber for 90 minutes twice a day.

Corresponding Author: Dr. Sevgi Kesici, Department of Anesthesiology and Reanimation, Faculty of Medicine, University of Giresun, Giresun, Turkey. E-mail: [email protected]

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CHRISMED Journal of Health and Research /Vol 1/Issue 2/Apr-Jun 2014


Tuna, et al.: Carbon monoxide poisoning

In the third day of the follow-up, MR imaging of brain revealed areas of altered signal intensity in bilateral globus pallidi and cerebral edema. The globus pallidal lesions were bilaterally symmetrical, hyperintense on T2 images [Figure 1]. Symmetrical hyperintense lesions in bilateral globus pallidus was seen in the MRI of patient. Fundus examination was normal, bilateral Babinski was positive and deep tendon reflexes increased. 1 gr kg-1 mannitol, 0.15 mg kg-1 dexamethasone, 1 mg kg-1 furosemide and 3% NaCl infusion were performed for cerebral edema. HBO treatment continued for 12 days. The patient was disconnected from the ventilator on the 36th day of the follow-up. His COHb level was less than 4% and the other laboratory examinations (Arterial blood gas analysis, AST, ALT, etc.) and hemodynamic parameters were normal. When he discharged from the hospital on the 40th day of the follow-up, he had neurological sequelae. Neuropsychiatric controls of the patient with memory loss, learning disability, and mutism have continued.

DISCUSSION AND CONCLUSION The sources of CO poisoning could be house fires, gas water heaters, faulty furnaces, wood burning stoves and motor vehicle exhaust, etc.[2] Spectrum of CO poisoning symptoms may be wide and variable, most common symptoms are mild headache, nausea, malaise, dizziness, syncope, altered mental state, and loss of consciousness.[1] Normal COHb levels are less than 5%. Serious toxicity is associated with levels above 25%, and risk of fatality at 70%.[2] This patient exposed to intense CO gas, so his COHb level was 34.2% and he was found unconscious. Serious symptoms, such as syncope, occurred more often in patients having

increased COHb levels, but normal COHb levels could not be used to rule out CO poisoning.[4] Various systemic and neurological complications (50-70%) may arise related to tissue hypoxia developed in CO poisoning.[3] Necrosis, bilateral white matter in globus pallidus in T2-weighted sections and hyperintensities in periventricular regions can be seen in MRI in cases where neurological findings developed.[5] Cerebral edema may occur early and presages poor outcome i.e. death or severe permanent damage.[6] CO toxicity occurs by competitive binding of CO to the hemoglobin heme groups with a resulting increase in the affinity of the remaining for oxygen, shifting the oxygen-hemoglobin dissociation curve to the left.[7] A “rebound effect” with delayed return of symptoms may be due to late release of CO from myoglobin with subsequent binding to hemoglobin.[8] The pathophysiology of CO poisoning is complex and involves direct toxicity at the cellular level.[9] HBO therapy for the treatment of CO poisoning was first discussed by Haldane in the 1890s and was first used in the 1960s.[10] The consensus has still not been reached for or against HBO’s use.[2] HBO treatment can decrease central nervous system injuries, mortality and neuropsychiatric findings. [11] Several animal studies show that treatment with HBO is effective in reducing CO-associated brain injury and suggests that HBO acts possibly by inhibiting cellular processes such as oxidative injury and brain lipid peroxidation. HBO inhalation can hasten disassociation of CO from hemoglobin to occur at rate greater than that achievable by breathing pure oxygen at sea-level pressure and is better than normobaric oxygen.[1] The patient was found unconscious, so HBO treatment was performed to him. Indications for HBO therapy in CO poisoning is given in Table 1.[12] HBO treatment has provided an improvement in the early and late effects of CO poisoning and improvement is more effective when performed in acute phase.[1] In our case report, HBO treatment was Table 1: Indications for HBO therapy in CO poisoning Comatose patients Any period of unconsciousness Any abnormal score on the Carbon monoxide neuropsychological screening battery Patients with COHb levels >40% Cardiovascular involvement (chest pain, ECG changes arrhythmias) History of ischaemic heart disease and COHb levels >15% Pregnant patients with COHb levels >15% Patients who do not respond to 100% oxygen after 4 to 6 h Patients with recurrent symptoms up to three weeks after exposure

Figure 1: Symmetrical hyperintense lesions in bilateral globus pallidus seen on the MRI of patient

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HBO: Hyperbaric oxygen, CO: Carbon monoxide, ECG: Electrocardiography, COHb: Carboxyhemoglobin



Tuna, et al.: Carbon monoxide poisoning

performed to the patient in acute phase. The patient continued to have some degree of neurological sequelae despite the treatment given, but less than before. In conclusion, medical history and clinical examination are very important in the diagnosis of CO poisoning. The patient should be followed up with laboratory examinations and imaging methods such as MRI in order not to overlook neurological sequelae or any organ injury. Additionally HBO treatment performed in acute period and goal directed therapy decrease mortality and morbidity.

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