Abstract
In 1985, van Gijn et al 1 were the first to report the existence of a variant of subarachnoid hemorrhage (SAH) characterized by negative angiography and focal bleeding in the prepontine cistern, referred to as nonaneurysmal perimesencephalic subarachnoid hemorrhage (PMSAH). Early prospective series revealed that patients with PMSAH had superior clinical outcomes when compared with aneurysmal or classic bleeding patterns on computed tomography (CT) that were also angiographically unremarkable, including reduced rebleeding and neurologic deficits. 2 , 3 These findings prompted the need for developing a diagnostic paradigm for angiographically occult patients with SAH, especially in those patients with classic SAH patterns on CT with no evidence of aneurysm rupture.
Key words
subarachnoid hemorrhage – angiographically negative hemorrhage – perimesencephalic hemorrhage – nonaneurysmal hemorrhage – catheter-based angiography7 Nonaneurysmal Subarachnoid Hemorrhage
7.1 Goals
Evaluate the natural history of patients with nonaneurysmal subarachnoid hemorrhages (SAHs).
Explore the basis for the evaluation and management of patients with nonaneurysmal SAHs.
Understand the results of repeated testing for nonaneurysmal SAHs.
7.2 Case Example
7.2.1 History of Present Illness
A 65-year-old female with a history of coronary artery disease status postbypass graft, hypertension, hyperlipidemia, and diabetes mellitus presented to the emergency department with sudden onset 10/10 bitemporal and occipital headache with altered mental status, confusion, nausea, vomiting, photophobia, and weakness. Her blood pressure was 229/89 on admission, and she was started on a nicardipine drip and intravenous labetalol. She was well oriented and responsive but appeared distressed. Noncontrast computed tomography (CT) head demonstrated spontaneous SAH of unknown origin, and the patient was transferred to the Neurological Interventional Care Unit.
Past medical history: Angina pectoris; coronary artery disease status post bypass graft; diabetes mellitus; high cholesterol; hypertension; migraine headache.
Past surgical history: Cardiac catheterization (x2); cardiac ablation of ventricular tachycardia and premature ventricular contraction; coronary artery bypass graft; vascular surgery.
Allergies: Phenergan; Levaquin (rash); Penicillins (rash); Per-cocet (anxiety).
Medications: Acetaminophen; ascorbic acid, calcium carbonate-vitamin D; clobetasol; desoximetasone; fexofenadine; fish oil; furosemide; detemir; lispro; levothyroxine; lisinopril; multivitamin; nitroglycerin; nystatin-hydrocortisone-zinc oxide; rosuvas-tatin; tramadol.
Family history: Mother—diabetes; father—stroke age 62, lung cancer age 72; brother—myocardial infarction age 60, history of drug abuse; brother—myocardial infarction age unknown, history of drug abuse.
Social history: Married; works as a bookkeeper; former smoker 20 pack-years, quit date January 1,1970; rare alcohol consumption.
Physical examination: Pulse 89, temperature 36.2 °C, respiratory rate 12, Sp02 98%, blood pressure 229/89.
Glasgow Coma Scale (GCS) of 15, Hunt and Hess grade 1. Cranial nerves were intact, no pronator drift, 5/5 strength, and sensation intact to light touch in all extremities. Imaging studies: See Fig. 7.1.
7.2.2 Treatment Plan
Given the continued need for monitoring and the appearance of early hydrocephalus on the CT scan, a right frontal ventriculostomy catheter was placed, and the patient was transferred to the Neurosurgical Intensive Care Unit. A six-vessel diagnostic cerebral angiogram the following morning was negative for any source of the diffuse SAH.
7.2.3 Hospital Course
The patient was admitted to the Neurointensive Care Unit. The patient received serial transcranial Doppler studies and repeat angiography was performed 1 week later, which did not show clear pathology explaining the SAH. The external ventricular drain (EVD) was discontinued during the course of her hospitalization, and the patient was discharged to an acute rehabilitation facility. A follow-up computed tomography angiography (CTA) head performed after 6 weeks was negative for any significant vascular pathology.
7.3 Case Summary
What is the time course for the treatment of nonaneurysmal SAH?
Care for nonaneurysmal SAH (NASAH) is generally the same as aneurysmal SAH (ASAH), in that both are treated as an acute emergency. Neurologic decompensation occurs in up to 35% of patients within 24 hours of symptom onset. 4 In addition, patients presenting in a hypertensive state often require blood pressure control.
The amount of subarachnoid blood present, neurologic status on admission, and volume and blood pressure status are predictors of delayed cerebral ischemia (DCI). 5 Nimodipine is administered to minimize the complications secondary to cerebral vasospasm. While it is the standard of care for patients with ASAH, there are no formal studies showing benefit of nimodipine in perimesencephalic subarachnoid hemorrhage (PMSAH) or NASAH.
Some studies suggest that the reduced incidence of vasospasm in this cohort argues against nimodipine use. 6 Triple H therapy is another method used to address vasospasm. Triple H therapy represents induced hypertension, hypervolemia, and hemodilution therapy. Cardiac complications, such as transient left ventricular dysfunction (TLVD) in SAH, are also contributing factors to DCI. 7 While vasospasm is the most critical side effect of SAH to address, hyponatremia, deep venous thrombosis (DVT), hyperglycemia, anemia, and fever are other medical complications that may arise.
How do different hemorrhage patterns impact treatment and patient outcomes?
The specific bleeding pattern is useful in guiding clinical decision making and predicting overall prognosis in patients who present with SAH. PMSAH pattern is characterized by blood restricted to the prepontine or interpeduncular cistern with limited extension into the Sylvian fissure. 8 PMSAH are angiographically negative with an unclear etiology. Other bleeding patterns include convex, intraventricular, or inter-hemispheric, although less is known with respect to clinical course and outcomes in this cohort of patients without a defined source of the hemorrhage. 9
Patients with NASAH should continue to have their symptomatic needs met as they would in the setting of an ASAH.
Once an aneurysmal source is definitively ruled out with repeat angiography, minor treatment modifications can be implemented. For instance, some studies suggest the discontinuation of nimodipine in angiographically negative SAH given both the reduced incidence and clinical significance of vasospasm in this population. 10 , 11 The timeline for the reinstatement of anticoagulation in patients following a nonaneurysmal SAH continues to remain unclear. It is well known that patients previously on antiplatelet or anticoagulant therapy who present with SAH often fare worse than patients not on these medications. 12 Considering the reduced rebleed rate in NASAH when compared to ASAH, the argument for resuming anticoagulation earlier in these patients has been proposed. However, continuing anticoagulation therapy within the first few days of hemorrhage incurs re-bleeding in patients with NASAH similar to those with ASAH. 13 Therefore, both hemorrhage patterns should be treated the same in this respect. Generally, nonaneurysmal SAHs are regarded as “benign” variants of spontaneous SAH with a better prognosis, lower risk of vasospasm, and reduced hospital stay. 6 , 14
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