The ICU outreach team

Abstract

A 76-YEAR-OLD WOMAN with long-standing chronic obstructive pulmonary disease (COPD) was admitted to the medical floor of the hospital after 1 week of progressively worsening dyspnea, productive cough, and intermittent fever. Her past medical history was significant for myasthenia gravis. Ten years previously she had a thymectomy, and now infrequently requires pyridostigmine. She required admission to the hospital on 2 previous occasions for exacerbations of COPD, but did not require admission to the intensive care unit (ICU). Her only medications included ipratropium bromide and salbutamol puffers (taken twice daily), pyridostigmine as needed, and acetaminophen. At the time of presentation her pulse was 108 beats per minute, her respiratory rate was 24 per minute, and her blood pressure was 136/78 mm Hg. She was observed to be using accessory muscles of respiration. Pulse oximetry revealed her oxygen saturation to be only 78% while breathing room air, but this improved to 92% with a 50% admixture of supplemental oxygen. Her jugular venous pressure was not elevated and her heart sounds were normal. Auscultation of her chest revealed bilateral expiratory wheezes. Laboratory investigations showed a mild leukocytosis (white blood cells, 10.2 10/L), a normocytic anemia (hemoglobin, 98 g/L), and normal platelet count. Her creatinine level was 78 mol/L and her electrolyte levels were normal. Arterial blood gas analysis was consistent with an acuteon-chronic respiratory acidosis (pH 7.25, PCO2 78 mm Hg, bicarbonate 33, PO2 68 mm Hg). She was admitted to the hospital and started on treatment with frequent bronchodilators and empiric antibiotics (cefuroxime and erythromycin). Supplemental oxygen was provided, with instructions to keep her oxygen saturation above 91%. The next morning she was found somnolent and difficult to rouse. Her breaths were shallow and her respiratory rate was 24 per minute. Hear rate was 114 per minute and blood pressure was 142/78 mm Hg. The concentration of the delivered oxygen mixture was increased to 70%. Repeat arterial blood gas analysis revealed a worsening of her respiratory acidosis (pH 7.19, PCO2 102 mm Hg, bicarbonate 36, PO2 136 mm Hg). A few hours later the patient was found obtunded, and she could not be roused with deep stimulation. Her systolic blood pressure measured by palpation was 100 mm Hg and her pulse was 120 beats per minute. A code blue was called, and the patient was intubated by the cardiac arrest team. She was transferred to the ICU where mechanical ventilation was initiated. She was started on systemic steroids and pyridostigmine, and the previously instituted therapies were continued. On her third day in the unit she was extubated, but was kept in the ICU for a total of 5 days because of concern regarding her respiratory status. At the time of her transfer to the floor her PCO2 was 56 mm Hg, and she was requiring 30% supplemental oxygen. Two days later it was noted that her PCO2 had increased to 72 mm Hg, and she was brought back to the ICU. Therapy with noninvasive positive pressure ventilation was initiated, and her PCO2 decreased to 64 mm Hg over the next 2 days. She was returned to the floor and was well enough to be discharged home 1 week later. This case raises several important questions regarding the process of care. Was the respiratory arrest on the floor preventable? Should the patient have received closer monitoring when initially admitted to the hospital? Could her ICU readmission have been prevented? Intensive Care Medicine has been described tra-