I. What is subarachnoid hemorrhage?
Subarachnoid hemorrhage (SAH) is a collective term for the sudden rupture of cerebral blood vessels caused by various reasons and the flow of blood into the subarachnoid space, which can be divided into spontaneous (accounting for about 15% of cerebrovascular accidents, mostly seen in 30-70 years old) and traumatic subarachnoid hemorrhage.
Why does subarachnoid hemorrhage occur?
1. The most common causes are intracranial aneurysm and cerebral (spinal cord) vascular malformation, which together account for about 70% of subarachnoid hemorrhage.
Other causes include hypertensive atherosclerosis, smog, hematologic disease, arterial occlusion, intracranial tumor stroke hemorrhage, and mixed causes.
3. Other rare causes include leptospirosis, subacute endocarditis, fibromuscular dysplasia, Ehlers-Danlos syndrome, aortic arch stenosis, polycystic kidney and Amphtamine arteritis, etc. Oral contraceptives and drug abuse can also cause.
Third, will there be an aura before going out of school? How to prevent and what conditions suggest that subarachnoid hemorrhage may occur?
1. The triad of subarachnoid hemorrhage is headache and vomiting, meningeal irritation and bloody cerebrospinal fluid.
Aura symptoms prior to subarachnoid hemorrhage (especially prior to aneurysm rupture) may include headache, drowsiness, ocular motility disorders (motoneuropathy), trigeminal nerve distribution pain, and back of neck pain.
The typical presentation of subarachnoid hemorrhage is a sudden, severe headache of indeterminate nature (the worst headache ever) with or without transient loss of consciousness, nausea and vomiting, neurological dysfunction (including cerebral nerve palsy), and neck stiffness.
4. Symptoms at the time of hemorrhage may include severe headache, photophobia, nausea and vomiting, pallor, generalized cold sweat, vertigo, collar and back pain or lower limb pain, half of them have mental symptoms such as agitation, confusion, disorientation, etc., with transient disorders of consciousness being the most common. 20%~30 combined with hydrocephalus, meningeal irritation signs may appear 1~2 days after hemorrhage.
5. Neurological impairment is common with one side of the arterial nerve palsy, mostly suggesting ipsilateral internal carotid-posterior communicating artery aneurysm or posterior cerebral artery aneurysm; 20% may have hemiparesis.
6. Epilepsy is common after MCA aneurysm surgery.
The signs of cerebral vasospasm are most common in the first week after the onset of disease, and may include transient limited localization signs, progressive impairment of consciousness, obvious signs of meningeal irritation and cerebral angiography showing vasospastic thinning.
About half of the patients with subarachnoid hemorrhage have electrocardiographic changes.
Intracranial murmurs may be present in 9.1%.
10. Some patients may have hypothermia for several days.
How can we diagnose subarachnoid hemorrhage?
1. CT head examination is feasible in patients with the above clinical manifestations and suspected subarachnoid hemorrhage, lumbar puncture can be performed cautiously if CT is negative and cranial pressure is not too high, DSA can clarify the etiology, MRA and CTA are feasible if DSA cannot be performed, TCD can also be used as a means of diagnosis and monitoring.
2. CT shows increased density in the cerebral sulcus and brain pool, intracerebral (ventricular) hematoma, hydrocephalus, cerebral infarction and edema, and enhanced CT can show AVM, cavernous hemangioma and brain tumor.
3. MRI is difficult to detect subarachnoid hemorrhage within 24-48 hours of onset, but can help to exclude AVM, cavernous angioma and brain tumor.
4. MRA can be used to screen for carotid stenosis, intracranial vascular malformations and aneurysms.
5. Cerebral angiography is the gold standard for the diagnosis of cerebral aneurysm and helps to clarify the cause of subarachnoid hemorrhage. Bilateral internal carotid arteries, bilateral vertebral arteries and spinal arteriogram are routinely performed when necessary.
6. Lumbar puncture is suitable for those with negative CT, typical clinical manifestations, and expected less high cranial pressure can be cautiously performed, and uniform light blood cerebrospinal fluid can be seen.
7. TCD is a convenient, noninvasive test to detect blood flow velocity in the proximal segment of ICA, MCA, ACA, VA, and BA; in general, blood flow velocity higher than 120 cm/s is considered moderate vasospasm, and higher than 200 cm/s is considered severe vasospasm.
V. How to treat subarachnoid hemorrhage?
1. In the acute stage of hemorrhage, the patient should be absolutely bedridden, closely monitor vital signs, apply hemostatic agents, analgesics and sedatives, and keep the bowels open.
2. Apply mannitol dehydration treatment for those with increased intracranial pressure, and dexamethasone can be given to reduce cerebral edema, and extraventricular drainage is feasible for those with combined intraventricular hemorrhage or hydrocephalus.
3. If the patient’s condition allows, cerebral angiography should be performed as soon as possible to clarify the cause of bleeding and provide early treatment, such as aneurysm clamping, aneurysm intervention embolization, cerebrovascular malformation resection, etc.
4. Maintain electrolyte balance, paying special attention to low blood sodium.
5. Anti-fibrinolytic drugs can reduce the rate of rebleeding, but increase the incidence of cerebral infarction.
6. Prevention of epilepsy recommends prophylactic application of antiepileptic drugs early in the hemorrhage, but long-term antiepileptic treatment is recommended only for patients who have had epilepsy, hematoma, infarction and middle cerebral aneurysm.
7. Treatment of cerebral vasospasm ① “3H” treatment, i.e. hypervolemia, hypertension and hemodilution treatment, is the main protocol for the treatment of cerebral underperfusion and cerebral ischemia after vasospasm, but it can also cause cerebral edema, myocardial ischemia, hyponatremia and the risk of rupture of other aneurysms in multiple aneurysms ② Calcium channel blockers mainly The main effect is to inhibit the entry of calcium ions into vascular smooth muscle cells, inhibit the release of vasoactive substances from platelets and endothelial cells, improve microcirculation, and promote the establishment of collateral circulation; the main adverse effect is hypotension ③ Fasudil hydrochloride (Elidel) mainly acts to inhibit myosin phosphorylation in the final stage of smooth muscle contraction, causing vasodilation, thus preventing and relieving cerebral vasospasm, improving cerebral blood flow and brain tissue utilization of The main adverse effects are intracranial hemorrhage, gastrointestinal hemorrhage, hypotension and anemia.4 Intracerebroventricular fibrinolysis and intracerebroventricular injection of recombinant tissue fibrinogen activator can dissolve fibrin clumps and reduce the incidence of asymptomatic and symptomatic vasospasm.5 Other agents such as endothelin antagonists, endothelium-dependent relaxation mechanisms and intracerebroventricular slow release systems are still in the experimental stage. stage.
What is the prognosis for subarachnoid hemorrhage?
Approximately 70% to 80% of subarachnoid hemorrhages are surgical in nature and require surgical intervention as soon as possible after the cause is identified. The overall prognosis for subarachnoid hemorrhage is poor, with an overall mortality rate of 25% and a disability rate for survivors approaching 50%.