The roles of glucose-6-phosphate dehydrogenase deficiency and ventilation support in outcome of carbon monoxide poisoning.

Sir

Carbon monoxide (CO) is a colorless, odorless, tasteless, and non-irritating gas produced as a byproduct of incomplete combustion and that is easily absorbed through the lungs. The clinical presentation of CO poisoning is so variable.[12]

Central nervous system symptoms are the predominant manifestations of CO poisoning. The most frequently documented complications are persistent or delayed neuropsychiatric sequelae, including dementia, amnestic syndromes, and psychosis. These symptoms may be preceded by a lucid period of 2 to 40 days after the initial exposure.[2-4]

Cardiac toxicity may occur because of myocardial hypoxia or a direct toxic effect of the gas on myocardial mitochondria. Cardiac involvement manifests mainly as ischemic insult, with elevated enzyme levels and ECG changes ranging from ST-segment depression to transmural infarction[56]

Therapy includes normobaric and/or hyperbaric oxygen, besides supportive therapy.[78] We report two cases of severe cardiopulmonary compromise due to unintentional exposure to CO with the same CO serum level, with and without delay neuropsychiatric sequelae. The patient who compromised with delayed neuropsychiatric syndrome (DNS) suffered from G6DP deficiency as underling disease. We considered our finding related to interaction of the G6DP deficiency and CO poisoning, since such cases are rare in the literatures.

We describe CO poisoning in two young boys, while one of them suffered from glucose-6-phosphate dehydrogenase (G6PD) deficiency as an underling disease that affected on outcome.

Two 16- and 19-year-old boys were found with reduced consciousness at about 3:30 AM on November 11, 2009. They had slept in a closed room and used indoor combustion sources (portable fuel-burning). They were found in comatose state. This occurred after they were exposed to CO for an estimated six hours. Younger boy suffered from G6PD deficiency and another had no positive medical history for disease. They had unstable blood pressure and moderate to severe tachycardia accompany with nausea/vomiting.

Arterial blood sample for younger boy showed pH, 7.1; PaCO2, 47.4; PaO2, 60.9 mmHg; HCO3, 11.9; SaO2, 62%; SBE, 19.1; and Hb, 13.1; and for older was pH, 7.22; PaCO2, 33; PaO2, 91.8 mmHg; HCO3, 11.9; SaO2, 84.4%; SBE, 13.1; and Hb, 13.4. Hematologic index were in normal range, but liver function test were impaired and cardiac enzyme were elevated, especially in younger boy. They have similar hemoglobin concentration and HbCO level (22% vs 23%) in arterial blood sample. They had electrocardiographic changes that were indicative of myocardial injury.

Younger patient has shallow and weak spontaneous breathing by facial mask with oxygen flow 5 l/min; so, orotracheal intubation and ventilator support after sedation was done and the other supplied with 100% O2 with noninvasive intermittent positive pressure ventilation because of his upper level of consciousness and intact gag reflex. They were admitted in intensive care unit (ICU).

Brain computed tomography revealed brain edema, especially in younger one who suffered from G6PD deficiency, and the chest X-ray showed mild bilateral pulmonary edema for both of them.

The pulmonary edema was treated with 100% oxygen, with increased positive end-expiratory pressure, and low-dose furosemide and beta blocker prescribed for tachycardia treatment.

Acute respiratory distress syndrome was suspected. Appropriate ventilator mode and FiO2 was set to maintain a PaO2 greater than 100 mm Hg and oxygen saturation greater than 92% accompany with PaCo2 35 mmHg. The cardiopulmonary condition improved progressively, 10 to 12 hours after admission.

Over the next few days, the patient's cardiovascular and respiratory status kept improving. Younger one was weaned from ventilator and extubated successfully on day three. The serum cardiac troponin I level declined, but the neurological findings remained a concern. They were transferred from the ICU to the ward on day four.

The neurological findings were normal in extubation time or discharge at a glance but, after 15 days, the younger one showed various degrees of distractibility, amnesia, and psychometric test abnormalities like impulsiveness and agitation. We followed up these patients for 6 months. We could not find any neuropsychiatric changes in older patient during this period.

The younger one who suffered from G6PD deficiency showed delay neuropsychiatric sequelae and positive finding in MRI, like nonspecific changes in cerebral white matter and basal ganglia, especially in the globus pallidus. However, MRI finding decreased dramatically after 3 months and his psychometric tests improved at fifth month of our follow-up. He could come back to her normal life after 6-month challenge by CO poisoning.

Two young 16- and 19-year-old boys developed cardiopulmonary compromise following CO poisoning. The concentration of CO in the atmosphere is less than 0.001%. A case of CO poisoning was defined as an arterial HbCO greater than or equal to 2% (for nonsmokers) or greater than or equal to 9% (for smokers). Exposure to CO level of 100 ppm produces an HbCO of 16% at equilibration, which is enough to produce clinical symptoms.[2910] Poisoning symptoms usually are seen at HbCO levels of greater than 10% in healthy persons.[1211]

CO intoxication has been properly named “the great imitator” as a comment on the various symptoms which the victim might present.[25] Different people may have a different CO tolerance level due to rate of ventilation, a pre-existing cerebral or cardiovascular disease, cardiac output, anemia and other hematological disorders, barometric pressure, and metabolic rate.[1213] It could be considered in our patients.

Our patients rested in the same room and were exposed to a similar level of CO, but the younger one who suffered from G6PD deficiency had sever presentation, higher cardiac enzyme level, and delay neuropsychiatric sequelae.

CO binds to hemoglobin reversibly with an affinity approximately 210 to 240 times greater than oxygen, thereby reducing the total oxygen-carrying capacity of the hemoglobin. This competitive binding shifts the oxygen-hemoglobin dissociation curve to the left, resulting in the impaired release of oxygen at the tissue level and cellular hypoxia. CO binds to myocardial myoglobin more slowly than it does to hemoglobin, but the bond is stronger and the release slower. Treatment of CO poisoning requires termination of exposure and initiation of therapy with 100% oxygen; hyperbaric oxygen (HBO2) therapy has been recommended for high-risk patients, pregnant women, and children.[14-16] Patients with decreased level of consciousness or ongoing altered mental status are generally deemed to be candidates for HBO2 therapy; the ability of HBO2 therapy to reduce the incidence and severity of neurologic sequelae has been questioned in other studies.[8917] However, we did not have possibility of HBO2 therapy in our center.

The cardiovascular effects of CO include myocardial ischemia, pulmonary edema, arrhythmia, and stunned myocardium syndrome.[6] The possible causes of pulmonary edema include toxic effects of CO on the alveolar membranes and myocardial damage leading to left ventricular failure.[1118] Our cases had pulmonary edema. This clinical presentation is consistent with the known cardiac effects of CO poisoning. Our patients recovered successfully with aggressive cardiopulmonary management, including early intubation and ventilator support. We supposed a prominent effect of ventilation support on CO-poisoned patients with pulmonary edema.

The effects of CO are not confined to the period immediately following exposure. The HbCO concentrations do not always determine the severity of toxic damage at the level of selected organs.[89] Persistent or delayed neurologic effects may be seen. Delayed neurological sequelae may occur in up to 50% of poisoned patients after 2 to 40 days, which may include cognitive dysfunction, memory loss, seizures, personality changes, Parkinsonism, dementia, mutism, blindness, and psychosis, which may occur following apparent recovery from the acute phase of CO intoxication.[911]

In our cases, the younger one recovered with mild neuropsychologic sequelae and the other recovered with good neuropsychologic outcome, despite severe cardiopulmonary compromise.

No clinical findings or laboratory tests reliably predict which patients are at risk of DNS;[49] we consider young patients by hematological disorders, like G6PD deficiency and higher metabolic rate, as high-risk groups for delayed neuropsychiatric sequelae. Although immediate O2 breathing is sometimes an adequate treatment, clinical evaluation of the cardiopulmonary and neurological systems and aggressive treatment like early ventilation support are advisable in these patients. Subsequently, only symptomatic therapy is available for the long-term sequelae of CO poisoning.