Non-traumatic subarachnoid hemorrhage, also known as spontaneous subarachnoid hemorrhage, occurs when blood leaks from the normal intracranial vessels into the space between the soft meninges and the arachnoid on the surface of the brain. s-SAH is a very serious neurological condition, and although mortality rates have begun to decline with advances in treatment, about 10-15% of patients still die pre-hospital.
Epidemiological characteristics
The incidence of s-SAH increases with age, reaching a peak at around 50 years of age. Approximately 80% occur at the age of 45-60 years, and the global incidence of s-SAH has a range of 2-49/100,000, with a higher incidence in women than in men (female:male=3:2).
The most common cause of s-SAH is aneurysm rupture. Ruptured round or saccular aneurysms of the skull base vessels account for 77% of s-SAH. Intracranial arteriovenous malformations are considered to be the second leading cause of SAH, accounting for approximately 10%. Some secondary causes are: bacterial aneurysms, fibromuscular dysplasia, hematological disorders, smog, infections, tumors, trauma (intracarotid aneurysms due to skull fractures), amyloid angiopathy (especially in the elderly), and vasculitis.
Risk factors for SAH
Although a number of risk factors are thought to contribute to s-SAH, there is little clear evidence. Smoking and heavy alcohol consumption are both considered to be high risk factors for s-SAH. There are data from studies showing no definite link between hypertension and s-SAH.
The chance of rupture of aneurysm, the most common disease in s-SAH, is closely related to the size of the aneurysm. Aneurysms ≤5 mm in diameter have only a 2% chance of rupture, whereas aneurysms between 6 and 10 mm in diameter already have a 40% chance of rupture at the time of presentation. Although hypertension is considered a high risk factor for aneurysm formation, it is controversial whether it causes aneurysm rupture. For intracranial arteriovenous malformations, there are no clear studies showing that AVMs <62.5 px in diameter have a higher chance of rupture than large AVMs >125 px in diameter.
Clinical manifestations: The signs and symptoms of s-SAH can be either minor prodromal symptoms that are often misdiagnosed or typical symptoms of severe headache.
(1) Prodromal symptoms: mainly warning headache, often due to blood leakage before aneurysm rupture, occupying effect caused by aneurysm enlargement or embolism caused by embolus dislodgement within the aneurysm can also appear as prodromal symptoms. It has been reported that 30-50% of aneurysms resulting in SAH have a small amount of blood leakage prior to aneurysm rupture. The pre-rupture leakage can cause more severe focal or global headache.
(2) Acute presentation: Sudden severe headache, often described as “the most severe headache I have ever experienced in my life”, nausea with/ or vomiting, brain irritation including stiff neck and back pain, bilateral lower extremity pain, and sudden loss of consciousness due to intracranial pressure exceeding cerebral perfusion pressure in about 45% of patients. On examination, there may be fever, elevated blood pressure, focal neurological signs (including mild hemiparesis, aphasia, hemianesthesia, cranial nerve palsy, and memory loss) and ophthalmologic examination with fundus hemorrhage and optic papilledema.
Diagnosis
The diagnosis of s-SAH depends on the combination of clinical manifestations and CT examinations. The detection rate of CT decreases with time of onset, and the accuracy of CT diagnosis of s-SAH is 92%. the accuracy of CT imaging in the early stage of SAH to predict the location of aneurysm is about 70%. In general, blood appears in the basal pool, lateral fissure or longitudinal fissure pool of the brain mostly for rupture of cystic aneurysm. Hemorrhage in the convex surface of the brain and in the surface cortex of the brain is mostly rupture of intracranial arteriovenous malformation (AVM) or bacterial aneurysm.
Cerebral angiography is the gold standard for the diagnosis of s-SAH, CTA and MRA can provide a better diagnosis with some patients, and MRA has a high value for the diagnosis of AVM. As far as the results of various clinical studies are concerned, CTA/MRA cannot yet completely replace invasive cerebral angiography. No positive findings on cerebral angiography (10%-20%) should be followed by cerebral angiography in 3-4 weeks. Negative angiograms may be due to secondary hemorrhage from the aneurysm leading to intra-aneurysmal thrombosis without visualization, and peripheral hemorrhage in the midbrain should also be taken into account.
Treatment
Symptomatic management: The first step for patients with SAH is to keep their vital signs stable, assess their level of consciousness, and ensure airway patency, breathing and circulation (ABCs). General medical treatment includes quiet bed rest, appropriate lowering of intracranial pressure, regulation of blood pressure (<130 mmhg), analgesia, sedation, antiemetic and control of psychiatric symptoms, anti-convulsions, correction of hyponatremia, application of drugs for prevention and control of rebleeding, prevention and control of cerebrovascular spasm and cerebrospinal fluid replacement therapy. Control of blood pressure and appropriate lowering of cranial pressure are aimed at reducing the risk of re-rupture and bleeding of the aneurysm.
Etiological treatment: The indications for surgical treatment of s-SAH are based on the clinical classification, and other factors such as the patient’s general condition, the size and location of the aneurysm, the possibility of surgical treatment of the aneurysm, and the possibility of thrombosis must also be considered. patients with Hunt-Hess classification I-III have indications for surgical treatment, because the complications of s-SAH are more harmful to the patient than those of surgery. The risk of complications of s-SAH is greater than the risk of surgical complications. Other conditions requiring surgical treatment include large or massive aneurysms, wide basilar aneurysms, aneurysms with angiogenesis at the apex of the aneurysm, aneurysms that cause an occupying effect or form a hematoma, and aneurysms that recur after spring-ring embolization. The main procedure is aneurysm clamping, others include aneurysm isolation, and the wrap or envelope approach may be the only treatment for aneurysms that are clotted or pyknotic.
In recent years, an increasing number of physicians have adopted interventional treatment (spring-ring embolization) as an alternative to open aneurysm clamping, with better results. Molina explored which treatment was better in The Lancet and found that patients treated with intervention had a higher survival rate than those with open clamping. Although the rebleeding rate was not high in either group, it was relatively higher in the interventional group. However, there are still many different opinions on which treatment method is better. Interventional treatment is better than cranial clamping in the following cases: patients with high clinical grading, patients with unstable disease, patients with high risk of cranial clamping where the aneurysm is located, such as aneurysms in the cavernous sinus and apical basilar artery, narrow neck aneurysms in the posterior cranial fossa, patients with early vasospasm, aneurysms with an obscure neck (balloon or stent-assisted spring-ring embolization), and multiple aneurysms in different vessels.
Prevention and treatment of complications
Common complications of s-SAH include: rebleeding, vasospasm and hydrocephalus. Other complications include: hyponatremia, seizures, pulmonary complications and cardiac complications.
Rehemorrhage is the most serious complication of s-SAH. The incidence of rebleeding within the first 24 hours of aneurysm rupture is 41%. The cumulative incidence of rebleeding within two weeks is 19%, and the mortality rate after rebleeding is as high as 78%.
Measures to prevent rebleeding include.
(1) quiet bed rest.
(2) analgesia.
(3) use of short-acting benzodiazepine sedatives.
(4) antifibrinolytic drugs. Early diagnosis and treatment is the key to prevent rebleeding!
CVS occurs in 70% of patients with s-SAH and 30% of patients will develop symptoms. CVS usually occurs 4-14 days after bleeding. s-SAH leads to impaired self-regulation of the cerebral vasculature, which further leads to cerebral ischemia or cerebral infarction. Usually the distal end of the internal carotid artery and the proximal end of the anterior and middle cerebral arteries are prone to spasm. risk factors for CVS include: large amount of SAH, severe clinical symptoms, female, youth, and smoking. Spasm of different intracranial vessels leads to different associated symptoms, but all present with a typical decrease in consciousness or focal neurological symptoms. Cerebral vasospasm may be caused by rebleeding and requires CT review to rule out rebleeding. Cerebral angiography with a lumen less than 50% of normal confirms the diagnosis of CVS, which can also be diagnosed with a non-invasive transcranial Doppler examination.
The main measure to prevent CVS is the prophylactic application of calcium channel blockers. Nimotope can prevent cerebral ischemic attacks caused by cerebral vasospasm by blocking the flow of calcium into the damaged nerves. Attention should be paid to the corresponding complications due to hypotension caused by calcium channel blockers and antihypertensive drugs. In addition, it is important to maintain normal blood volume, normal body temperature, and normal blood oxygenation in patients with CVS. Blood volume should be monitored to avoid its hypotension inducing CVS. triple H therapy of hypertension, hypervolemia and hemodilution is recommended after the onset of CVS. Transcatheter balloon angioplasty may be attempted in cases where conventional therapy fails.
Hydrocephalus has an incidence of about 20% in the acute phase of SAH, mainly obstructive hydrocephalus, which mostly occurs within 24 hours after hemorrhage. CT can differentiate hydrocephalus from rebleeding. External ventricular drainage is easy and effective, but too rapid a drainage results in too rapid a drop in intracranial pressure and a risk of rebleeding, which should be controlled to a height of about 200 mmH2o. 10-15% of patients with SAH have delayed or chronic hydrocephalus due to arachnoid granular scar formation or altered cerebrospinal fluid reabsorption, which occurs 10 days or more after SAH and manifests as urinary incontinence, unsteady gait, or cognitive Decreased cognition. Symptomatic hydrocephalus can be treated with temporary lumbar pool drainage or ventriculo-abdominal drainage.
Follow-up and prognosis
Patients with SAH should be followed up with imaging, including CTA, MRA, and cerebral angiography, for residual lesions and recurrence after surgery or intervention, if their condition permits.
Despite great advances in medical and surgical techniques, the mortality rate of SAH due to aneurysm rupture is around 50% per year. Survival rates are inversely proportional to the grading of SAH, with Hunt-Hess grade I having a survival rate of 70%, grade II 60%, grade III 50%, grade IV 20%, and grade V 10%. Approximately 25% of surviving patients have lifelong neurological symptoms. The majority of surviving patients had transient or long-term cognitive impairment. The amount of bleeding, age at onset, general physical condition and complications determine patient morbidity and mortality.