P138. Acute onset and reversibility of triphasic waves in the EEG correlating with hypercapnia

Abstract

Triphasic waves are commonly seen in the EEG of patients with encephalopathy. Although typically associated with metabolic encephalopathy or post-hypoxic damage, they are unspecific in respect of the etiology of brain dysfunction. Here, we present a case report of acute-onset triphasic waves induced by hypercapnia. We report on a 27-year-old male with severe sensory and motor neuropathy, tetraparesis, ataxia, dysarthria, and cognitive impairment of yet unknown etiology since the age of 14 years. The patient was referred to our hospital and admitted to the EEG monitoring unit for differential diagnosis of recurrent episodes of loss of consciousness. At time of admission, a borderline oxygen saturation (SatO2) of around 80% was recorded, attributable to his chronic neuromuscular disease. During the first evening after admission, SatO2 repeatedly dropped below 80%. Oxygen insufflation was initiated by the doctor-on-call and the patient’s vigilance was repeatedly tested throughout the night. At a routine check, the patient was found stuporous. Blood gas analysis showed carbon dioxide partial pressure (pCO2) of 85.6 mmHg and oxygen partial pressure (pO2) of 75.6 mmHg. Emergency bag-valve mask ventilation was started, the patient was intubated, and transferred to the intensive care unit. After several days, the patient was extubated without any new-onset neurological deficit. Polysomnography revealed alveolar hypoventilation, and non-invasive assisted bilevel ventilation treatment was initiated before the patient was discharged home. Upon post hoc review, the EEG during the night after admission showed normal sleep patterns which were replaced by triphasic waves just about 10 min before the patient was found to be stuporous. Upon bag-valve-mask ventilation, the triphasic waves disappeared within 2–3 min, and the EEG showed a normal awake state prior to sedation intubation. This case demonstrates that hypercapnia may induce acute-onset triphasic waves in the EEG which are readily reversible within minutes after assisted ventilation. Moreover, this case illustrates the danger of oxygen insufflation in patients with chronic alveolar hypoventilation. We conclude that our patient suffered from chronic alveolar hypoventilation due to severe neuropathy which resulted in chronic moderate hypercapnia, with respiration triggered by hypoxia alone. When receiving oxygen insufflation, hypoxia-induced respiration failed leading to central hypopnea, acute pCO2 increase and stupor.