Sporadic patients with acute respiratory distress syndrome (ARDS) caused by Mycoplasma pneumoniae have been reported. However, knowledge about the pathophysiology and pharmacological treatment of this condition is insufficient. Moreover, the pulmonary vascular permeability in ARDS related to M. pneumoniae infection has not been reported. We report a case of ARDS caused by Mycoplasma pneumoniae without elevated pulmonary vascular permeability, which was successfully treated using low-dose short-term hydrocortisone, suggesting that pulmonary infiltration in ARDS caused by Mycoplasma pneumoniae does not match the criteria of permeability edema observed in typical ARDS.

The patient was a 74-year-old male. Before lung cancer surgery, during computed tomography (CT)-guided marking, the patient suddenly complained of dyspnea and suffered cardiopulmonary arrest. Cardiopulmonary resuscitation (CPR) was immediately initiated and cardiopulmonary arrest due to air embolism was diagnosed, based on retained air in the left atrium, left ventricle and ascending aorta during CT scan. Since the patient's status progressed to an intractable ventricular fibrillation, we initiated treatment with percutaneous cardiopulmonary support (PCPS) while continuing CPR in the CT laboratory and transferred him to intensive care, where the patient was placed in the Trendelenburg position and given defibrillation shock therapy, which restored spontaneous circulation. Transesophageal echocardiography 4 hours after the onset showed retained air in the ascending aorta and left atrium; emergency thoracotomy was thus performed to remove this air. We confirmed air elimination with transesophageal echocardiography intraoperatively and discontinued PCPS. Thereafter, general status improved and he was discharged without sequelae. We saved the life of a patient experiencing cardiopulmonary arrest due to air embolism, without sequelae, by using PCPS immediately while keeping his head down and removing the air surgically by emergency thoracotomy.

Summary. In this study we evaluated the clinical usefulness of jugular venous -arterial PC0 2 difference (JAPC0 2) as an indicator of cerebral blood flow and metabolism in five patients (male 3; female 2) with brain injury. In the neurointensive care unit under mechanical ventilation, JAPC0 2 , mixed venous -arterial PC0 2 difference (VAPC0 2), and jugular venous hemoglobin oxygen saturation (SjV02) were calculated. JAPC0 2 was maintained at approximately 10mmHg except during brain herniation. JAPC0 2 had an inverse linear relat ionship with SjV02' JAPC0 2 decreased to under 4 mmHg and SjV02increased to over 95mmHg during the brain herniation period in patients who died. JAPC0 2 was greater than VAPC0 2 except during the brain herniation period. JAPC0 2 was a useful monitor of cerebral blood flow and metabolism.