A 57-year-old man is admitted to the neurosurgical intensive care unit with an acute spontaneous subarachnoid hemorrhage. He initially underwent four-vessel cerebral angiography, which did not demonstrate any evidence of aneurysm or vascular malformation. He now remains in the unit for close monitoring and subsequent studies.

While you are checking on the patient the next morning during rounds, his nurse mentions that he is beginning to experience respiratory distress; his oxygen saturation has dropped to 80%. His vital signs are otherwise stable, and he is neurologically intact. 

You confirm that the patient is a nonsmoker and has no history of chronic lung disease, such as asthma or COPD. The respiratory therapist already placed him on a 50% Ventimask^®; arterial blood gas analysis showed a Pco₂ of 50 mm Hg and a Po₂ of 76 mm Hg with a saturation of 91%. Breath sounds are somewhat decreased bilaterally, with audible crackles. 

As a result, you place him on a 100% nonrebreather mask and order a stat portable chest radiograph, which is shown. What is your impression?

Answer

The radiograph demonstrates diffuse bilateral interstitial and airspace infiltrates consistent with pulmonary edema. Specifically, this patient is likely experiencing neurogenic pulmonary edema.

Though rare, this condition can occur after a neurologic insult, such as a subarachnoid hemorrhage. The exact pathogenesis is unclear, but the current premise is that the increase in intracranial pressure causes a catecholamine surge that then affects the heart and lungs, resulting in this condition.

Obviously, other serious etiologies of a cardiac (acute MI) or pulmonary (acute pulmonary embolus) nature need to be ruled out. Treatment is usually supportive with oxygen, sometimes BiPAP or CPAP therapy, plus diuresis.