spontaneous_subarachnoid_hemorrhage

Spontaneous subarachnoid hemorrhage

hypertension

oral contraceptives

substance abuse

cigarette smoking

following cocaine abuse

alcohol consumption: controversial

diurnal variations in blood pressure

pregnancy and parturition

slight increased risk during lumbar puncture and/or cerebral angiography in patient with cerebral aneurysm

slight increased risk with advancing age

conditions with an increased incidence of cerebral aneurysms


An adverse lipid profile seems to elevate SAH risk similar to its effect in other cardiovascular diseases, especially in men. Whether SAH incidence diminishes with increasing statin use remains to be studied 1).


Some case reports on the association of the COVID-19 infection and occurrence of spontaneous subarachnoid hemorrhage (SAH) have been reported 2).

The extent and nature of impairment in autoregulation accurately predicts neurologic complications on an individual patient level, and suggests potentially differential impairments in underlying physiologic mechanisms. A better understanding of these can lead to targeted interventions to mitigate neurologic morbidity 3).

see Subarachnoid hemorrhage clinical features


Differential diagnosis of severe, acute, paroxysmal headache (25% will have SAH):

subarachhnoid hemorrhage. AKA “warning headache” or sentinel H/A

benign “thunderclap headaches” (BTH) or crash migraine“, severe global headaches of abrupt onset that reach maximal intensity in < 1 minute, accompanied by vomiting in e 50%. They may recur, and are presumably a form of vascular headache, some may have transient focal symptoms. There are no clinical criteria that can reliably differentiate these from SAH. There is no suharachnoid blood on CT and LP, which should probably be performed on at least the first presentation to R/O SAH. Earlier recommendations to angiogram these individuals have since been tempered by experience.

reversible cerebral vasoconstrictive syndrome (RCVS) (AKA benign cerebral angiopathy or vasculitis) severe H/A with paroxysmal onset, ± neurological deicit.

Küchler et al., retrospectively reviewed 87 sSAH patients with WFNS (World Federation of Neurosurgical Societies) grade III-IV, who received tracheostomy. Decannulation events and the time from tracheostomy to decannulation were recorded in a 200-days follow-up. Variables analyzed were: age, sex, WFNS grade, Fisher grade, the presence of intracerebral or intraventricular hematoma, acute hydrocephalus, aneurysm location, aneurysm obliteration (surgical vs. endovascular), treatment related complications, decompressive craniectomy, symptomatic cerebral vasospasm, vasospasm-related infarction and timing of tracheostomy. Further risk factors analyzed were preexisting chronic lung disease and pneumonia. Functional outcome was assessed by the modified Rankin Scale (mRS).

The rate of successful decannulation was 84% after a median of 47 days. A higher WFNS grade and pneumonia were associated with both a prolonged time to decannulation (TTD) and decannulation failure (DF). Older age (> 60 years) and necessity for decompressive craniectomy were only associated with prolonged TTD. Outcome analysis revealed that patients with DF show a significantly (p < 0.01) higher rate of unfavorable outcome (mRS 3-6).

Successful decannulation is possible in the majority of sSAH patients and particularly, in all patients with WFNS grade III. WFNS grading, age, the necessity for decompressive craniectomy and pneumonia are significantly associated with the TTD. WFNS grade and pneumonia are significantly associated with DF. The mean cannulation time of sSAH patients is shorter in relation to stroke patients 4).


1)
Lindbohm J, Korja M, Jousilahti P, Salomaa V, Kaprio J. Adverse lipid profile elevates risk for subarachnoid hemorrhage: A prospective population-based cohort study. Atherosclerosis. 2018 May 5;274:112-119. doi: 10.1016/j.atherosclerosis.2018.05.011. [Epub ahead of print] PubMed PMID: 29772479.
2)
Batcik OE, Kanat A, Cankay TU, Ozturk G, Kazancıoglu L, Kazdal H, Gundogdu H, Ozdemir B, Bahceci I, Kostakoglu U, Batcik S, Gundogdu O, Sevilgen G. COVID-19 infection produces subarachnoid hemorrhage; acting now to understand its cause: A short communication. Clin Neurol Neurosurg. 2021 Jan 19;202:106495. doi: 10.1016/j.clineuro.2021.106495. Epub ahead of print. PMID: 33493886.
3)
Santos GA, Petersen N, Zamani AA, Du R, LaRose S, Monk A, Sorond FA, Tan CO. Pathophysiologic differences in cerebral autoregulation after subarachnoid hemorrhage. Neurology. 2016 Apr 22. pii: 10.1212/WNL.0000000000002696. [Epub ahead of print] PubMed PMID: 27164675.
4)
Küchler J, Wojak JF, Smith E, Brocke J, Abusamha A, Tronnier VM, Ditz C. Management of tracheostomized patients after poor grade subarachnoid hemorrhage: Disease related and pulmonary risk factors for failed and delayed decannulation. Clin Neurol Neurosurg. 2019 Jul 8;184:105419. doi: 10.1016/j.clineuro.2019.105419. [Epub ahead of print] PubMed PMID: 31306892.
  • spontaneous_subarachnoid_hemorrhage.txt
  • Last modified: 2023/01/23 10:04
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