I. Diagnosis and auxiliary examinations
(1)CT examination
SAH should be suspected in patients with sudden headache, nausea, vomiting, and positive meningeal irritation, and SAH should be considered when the patient complains of “the worst headache in his life”. The CT rate of SAH is more than 90%, especially the basal, lateral and longitudinal fissure pools around the brainstem. If the bleeding is minimal or several days after the bleeding, CT may be negative. At this point, the finding of subarachnoid hemorrhage or CSF yellowing by lumbar puncture suggests a recent hemorrhage.
(2) Cerebrospinal fluid examination
When it is not possible to determine whether the bleeding is SAH or misperforation by traditional methods, a spectrophotometric examination of cerebrospinal fluid must be performed.
(3) To determine the site of aneurysm using the hemoconcentration area on CT.
(①Hemorrhage in the interpeduncular pool and the circumferential pool, generally without aneurysm.
(ii) Asymmetric hemorrhage in the suprasellar pool suggests aneurysm in the internal carotid artery system.
③Lateral fissure hemorrhage suggests middle cerebral artery aneurysm.
④Hemorrhage at the base of the frontal interhemispheric fissure suggests an aneurysm of the anterior communicating artery.
(4) Cerebral angiography to clarify the cause
Cerebral angiography is the “gold standard” to confirm the diagnosis of aneurysm, which is usually selected within three days or three weeks after the onset of the disease.
General treatment
Recommended: general treatment within hours of subarachnoid hemorrhage
Anti-vascular spasm treatment
Cerebral vasospasm is a delayed constriction of large vessels at the base of the skull after SAH, often manifested on angiography or cerebral blood flow as reduced perfusion in the distal region of the involved vessels. There is a typical transient course of angiographic vasospasm – starting 3-5 days after hemorrhage, narrowing to maximal 5-14 days, and gradually recovering after 2-4 weeks. In about half of cases vasospasm manifests as a delayed neurological deficit that resolves or progresses to cerebral infarction. 15-20% of patients have a stroke or die from vasospasm after standard treatment.
Recommendation: Apply nimodipine early to reduce the severe neurological deficits associated with SAH.
Nimodipine may reduce severe neurological deficits associated with SAH. Patients in good clinical condition (Hunt & Hess classification I, II, III) should be administered as early as possible (10 mg to 20 mg, 1 mg/h IV for 14 days), the period most likely to result in neurological deficits due to vasospasm. Recent studies have shown that nimodipine also reduces mortality and disability in patients with grades IV and V. At these doses, some patients experience hypotension, which may be slowed or reduced. There are no other effective therapeutic agents specifically for SAH after retrospective studies.
Antifibrinolytic therapy
The most commonly used antifibrinolytic agent is 6-aminocaproic acid, usually 24 g/day for 3 days, followed by 8 g/day for 3 weeks or until surgery (level of evidence I-V, level A recommendation). However, it is important to focus on the fact that antifibrinolytic therapy may be complicated by cerebral ischemia, and a concomitant calcium antagonist is required.
V. Cerebrospinal fluid replacement
Patients with SAH presenting with acute hydrocephalus and severe headache may consider lumbar puncture to release cerebrospinal fluid, slowly releasing 10-20 ml of fluid each time, twice a week, which can reduce intracranial pressure and alleviate headache. However, it is necessary to pay attention to the risk of inducing brain herniation, intracranial infection and rebleeding.
VI. Surgical treatment
Recommendation: Patients with good clinical condition (Hunt&Hess grading I, II, III) should be operated as early as possible (preferably within 3 days or 3 weeks after the onset of the disease).
The site of the aneurysm, the aneurysm causing bleeding, and the patient’s clinical classification need to be clarified. Patients whose aneurysm is operable and who have no medical disease affecting the operation and who are in good clinical condition (Hunt & Hess classification I, II, III) should be operated as soon as possible (preferably within 24 hours of admission). For cases not suitable for surgery, endovascular treatment can be considered. patients with hydrocephalus of Hunt&Hess classification grade IV and V require emergency ventricular drainage. Patients with intracerebral hematoma grade IV and V should have surgical removal of the hematoma and emergency clamping of the aneurysm to save their lives. The prognosis will be worse for such patients with surgical treatment of the source of hemorrhage. In case of severe vasospasm with infarction, surgery should be postponed.
VII. Complications of subarachnoid hemorrhage and their management
(I) Hydrocephalus Recommendations.
(1) Acute (obstructive) hydrocephalus (enlargement of the ventricles within 72 hours) complicates about 20% of cases after SAH. Ventricular drainage is recommended, despite increased rebleeding and infection (level IV-V evidence, level C recommendation). Disposition.
①observation for 24 hours ;
② Cerebrospinal fluid replacement;
(iii) Ventricular drainage.
(2) Chronic (traffic) hydrocephalus often occurs after SAH. Temporary or permanent cerebrospinal fluid drainage is recommended for symptomatic patients (level IV-V evidence, level C recommendation). ventricular enlargement often occurs after SAH, and the etiology is usually intraventricular hemorrhage leading to obstructive hydrocephalus; acute hydrocephalus from SAH occurs more often in patients with severe clinical symptoms. The diagnosis relies on imaging, and many patients are asymptomatic, with only a subset of cases requiring shunts to improve clinical status. Ventricular drainage is generally recommended for patients with acute hydrocephalus and reduced level of consciousness after SAH; about 50-80% of such cases have varying degrees of improvement after drainage.
(ii) Rehemorrhage
Reduce the factors that may cause rebleeding. The patient needs to be bedridden to reduce stimulation. Use pain medication to control pain. Use tranquilizers. Regular use of stool softeners and laxatives. The aim of these measures is to avoid elevated blood pressure that could cause rebleeding due to increased intracranial pressure. If possible, surgery is the best way to prevent rebleeding.
(iii) Hyponatremia
Recommendations.
(1) Treatment of hyponatremia after SAH should include intravascular infusion of isotonic fluids (evidence III-IV, level C recommendation).
(2) Monitor central venous pressure, pulmonary capillary wedge pressure, fluid balance, and body weight in patients with recent SAH to assess volume status. A trend toward decreased volume should be corrected with fluid replacement (Level III-IV evidence, Level C recommendation).
(3) Avoid hypotonic fluids as they can lead to hyponatremia; do not treat hyponatremia by fluid restriction (Level IV-V evidence, Level C recommendation).
The incidence of hyponatremia after SAH has been reported in the literature to be 10-34%. It usually occurs several days after bleeding and often parallels the timing of vasospasm. Hyponatremia is more commonly seen in patients with clinically significant hydrocephalus and is an independent risk factor for poor prognosis. Fluid restriction for hyponatremia increases delayed ischemic neurological deficits. Hyponatremia is usually slightly insufficient to produce symptoms.