When defects in the cerebral blood vessel walls cause blood to extravasate into the subarachnoid space, it is called subarachnoid hemorrhage. Brain trauma is often a triggering factor, and intracranial vascular malformations are the primary cause of primary subarachnoid hemorrhage. Other causes such as aneurysm, blood disorders, hypertension, intracranial tumors, deficiencies in vitamin K or C, and liver disease can also lead to subarachnoid hemorrhage.

bubble_chart Diagnosis

(I) Clinical Manifestations The onset is acute, with intracranial hypertension and meningeal irritation as the main manifestations. A large amount of blood entering the subarachnoid space can cause a sudden increase in intracranial pressure, even leading to tentorial herniation. Older children may complain of severe headache, often accompanied by frequent vomiting. Further progression of the condition may result in unconsciousness and convulsions. In young infants, convulsions may sometimes be the first symptom. High fever may also occur occasionally. Physical examination may reveal significant neck stiffness, with positive Kernig's and Brudzinski's signs. In infants with an unclosed fontanelle, increased fontanelle tension may be observed. (II) Laboratory Examination

1. Bloody cerebrospinal fluid (CSF) is an important basis for diagnosing this condition, but it must be differentiated from traumatic bleeding during lumbar puncture. For example, if the CSF collected in three consecutive tubes is uniformly bloody without clotting, and the supernatant turns yellow, it suggests bleeding prior to the lumbar puncture. If the CSF color gradually lightens across the three tubes and the supernatant turns yellow, it indicates bleeding caused by the lumbar puncture. Shortly after hemorrhage, the ratio of white blood cells to red blood cells in the CSF approximates that of peripheral blood, followed by an increase in lymphocytes and protein content.
2. CT Examination Within the first week of hemorrhage, CT scans may show increased density in the cerebral sulci and cisterns. In cases of massive subarachnoid hemorrhage, a cast-like appearance of the blood-filled cisterns may be observed. The high-density shadows gradually disappear after 1–2 weeks. After the acute phase subsides, cerebral angiography or MRI should be performed to assess for conditions such as cerebrovascular malformations or intracranial aneurysms.

bubble_chart Treatment Measures

﹝Treatment﹞

(1) Hemostatic medication: Mainly use antifibrinolytic agents, such as 6-aminocaproic acid, administered intravenously once or twice daily, with 1–2 g dissolved in 50–100 ml of glucose or 0.9% saline. Alternatively, p-aminomethylbenzoic acid can be used, with 100 mg added to glucose solution or 0.9% saline for slow intravenous drip. The purpose of these drugs is not to stop bleeding but to prevent rebleeding. For delayed-onset intracranial hemorrhage caused by vitamin K deficiency, vitamin K1 can be administered intramuscularly or intravenously at 10 mg per dose. (2) Reducing intracranial pressure: Dehydrating agents such as mannitol and dexamethasone can be used, but the dosage should not be excessive. For mannitol, 0.25 g/kg per dose is recommended to avoid excessive changes in intracranial pressure, which may lead to rebleeding. (3) Sedation and anticonvulsant therapy: Drugs such as phenobarbital or diazepam (Valium) may be selected. (4) Surgical treatment: If combined with intraventricular hemorrhage or intracerebral hematoma, ventricular drainage or surgical intervention should be considered. (5) Treating the underlying disease: Such as leukemia, hypertension, or liver disease.