Nonaneurysmal Subarachnoid Hemorrhage: A Review of Clinical Course and Outcome in Two Hemorrhage Patterns

Linda L. Herrmann; Joseph M. Zabramski


J Neurosci Nurs. 2007;39(6):135-142. 

In This Article

Case Study 2

LD, a 59-year-old Caucasian female, presented to the ED reporting a sudden onset of "the worst headache of my life." Her past medical history was significant for congestive heart failure, peripheral vascular disease, and coronary artery disease. Medications upon admission included clopidogrel and 81 mg of aspirin. Her admission GCS score was 10. A CT scan demonstrated extensive SAH in the basilar cisterns and Sylvian fissures bilaterally, as well as evidence of acute hydrocephalus (Fig 3, Fig 4). A CT angiogram performed at the same time showed no evidence of aneurysm.

LD was admitted to the intensive care unit, where she was intubated; an EVD was immediately placed to manage acute hydrocephalus. A CT scan after placement confirmed good position of the catheter in the right lateral ventricle. A nicardipine drip was ordered and titrated to achieve a goal SBP of less than 140 mm Hg. A subsequent four-vessel cerebral angiogram was negative for aneurysm or arterial venous malformation.

LD remained stable over the next several days with a GCS score of 10T. An MRI scan of the brain and cervical spine and an MR angiogram were performed. These studies revealed no evidence of vascular malformation or tumor to explain the SAH. The initial plan was to repeat her cerebral angiogram on the 10th postbleed day.

On her fourth postbleed day, LD developed increased pulmonary congestion, and a pulmonary artery catheter was placed. At that point, target hemodynamic parameters were to maintain SBP at 120–140 mm Hg and a wedge pressure of no greater than 8 mm Hg. LD was able to maintain these parameters without medication.

On her fifth postbleed day, LD was found to be less responsive and was not following commands. A cerebral angiogram showed mild bilateral middle cerebral artery (MCA) vasospasm. No other vascular abnormality was noted. Because of the vasospasm, her SBP parameters were raised to 140–200 mm Hg, and a phenylephrine drip was ordered to maintain these parameters. The goal for the pulmonary wedge pressure was increased to no greater than 10 mmHg, and 5% human albumin was ordered to maintain this wedge parameter.

During the next several days, LD became more alert, and her pulmonary status improved. On her 11th postbleed day, a follow-up cerebral angiogram demonstrated resolution of the vasospasm and no evidence of vascular malformation or aneurysm. Her phenylephrine drip and pulmonary artery catheter were discontinued 3 days later. She was alert and following commands with a GCS score of 11T. She was extubated on the 12th day after her hemorrhage.

Her EVD was weaned, and no evidence of hydrocephalus was seen on serial CT scans. Her neurological examination remained stable, with only mild short-term memory deficits. A repeat CT scan of her brain, performed the day before her transfer to acute neurological rehabilitation, showed resolution of her subarachnoid blood and no evidence of hydrocephalus.

LD was evaluated in the outpatient clinic 6 weeks after her SAH. She had returned home and participated in outpatient physical, occupational, and speech therapies. Her 6-week follow-up CT scan of the brain showed no evidence of delayed hydrocephalus. She was given permission to resume her usual doses of clopidogrel and daily aspirin. LD had made an excellent recovery, with only occasional mild short-term memory deficits and decreased endurance. The extent of SAH in this patient may have been related to her being on double antiplatelet therapy; nevertheless, a four-vessel cerebral angiogram was planned for her 6-month follow-up visit.