Subarachnoid hemorrhage is a collective term for the sudden rupture of intracranial and intravertebral vessels from various causes and the flow of blood into the subarachnoid space. It is not a disease, but a clinical manifestation of a particular disorder. There are two clinical categories: traumatic subarachnoid hemorrhage and spontaneous subarachnoid hemorrhage. Traumatic subarachnoid hemorrhage: It forms mainly due to vascular injury to the intracranial bridging veins and brain surface after trauma, and is often associated with cerebral contusions, subdural hematomas, and intracerebral hematomas. Spontaneous subarachnoid hemorrhage: Any etiology that can cause cerebral hemorrhage can cause this disease. The most common causes are intracranial aneurysms and cerebrovascular malformations. Other causes include atherosclerosis, anomalous vascular network disease of the cerebral base (smog), entrapment aneurysms, vasculitis, thrombosis of the intracranial venous system, blood disorders, intracranial tumors, coagulation disorders, and complications of anticoagulation therapy, but all are rare. The onset of the patient is mostly triggered by emotional excitement, exertion, defecation, and coughing. (A) Relevant anatomical knowledge: The surface of the human brain has three layers of perineurium, which are from the outside to the inside: dura, arachnoid, and soft meninges. The dura mater: consists of two layers of tough and dense collagen fibers, the inner layer of which penetrates deep into the cranial cavity to form a protrusion in the cerebral fissure, i.e. forming the cerebral falx, cerebellar curtain, saddle septum, etc. The main blood supply arteries of the dura are the middle meningeal artery from the maxillary artery (entering the skull by the foramen spinosum), which covers the frontal and parietal lobes of the brain; the anterior meningeal artery, a branch of the anterior sieve artery of the ophthalmic artery, which supplies blood to the anterior part of the dura; the posterior meningeal artery, a meningeal branch of the vertebral and occipital arteries, sometimes originating from the ascending pharyngeal artery, which is distributed in the cerebellar and subcranial dura; the maxillary artery also sends out small branches distributed in the middle fossa of the skull The dura mater at the base of the middle cranial fossa. The nerves of the dura are mainly from the trigeminal nerve, the upper three pairs of cervical nerves and the cervical sympathetic trunk. These nerve fibers form many nerve endings in the dura mater, which are responsive to changes in intracranial pressure, and headaches are related to the sensation of these endings. Arachnoid: thin and transparent, lacking blood vessels and nerves. The cavity between the arachnoid and the soft meninges is called the subarachnoid space, which contains arachnoid trabeculae and is filled with cerebrospinal fluid. In the depressions of the brain surface, the subarachnoid space is enlarged, which forms brain pools. For example, the cricoid pool, the tetraspanic pool, and the lateral fissure pool. Soft meninges: thin and transparent, clinging to the surface of the brain and penetrating deep into the sulci of the brain. The folds formed by the soft meninges protrude into the ventricles of the brain, i.e., forming the choroid plexus, which secretes cerebrospinal fluid. Bridging vein: the “link vein” between the superficial cerebral vein and the venous sinus, is generally free, for example, the upper sagittal sinus, the frontoparietal lateral and medial drainage vein, firstly, penetrates the soft meninges, the subarachnoid space, reaches the subdural, and then walks free for a while, this free section is the bridging vein, from the bridging vein into the upper sagittal or the bridging vein enters the dural venous sinus and then the superior sagittal sinus. (b) Pathophysiology: In subarachnoid hemorrhage, blood flows into the cerebral subarachnoid space and spreads rapidly through the cerebrospinal fluid surrounding the brain and spinal cord, irritating the meninges and causing headache and cervical tonicity and other signs of meningeal irritation. (1) Blood entering the subarachnoid space increases the contents of the cranial cavity and increases the cranial pressure. (2) Hemorrhagic stimulation and harmful substances such as 5-hydroxytryptamine, endothelin and especially oxygen radicals released by red blood cell fragmentation cause cerebral vasospasm, which easily leads to local cerebral tissue ischemia and further decreases cerebral blood flow, aggravating cerebral edema. (3) Hemorrhage can block the midbrain aqueduct, the fourth ventricle and the basal pool, affecting the cerebrospinal fluid circulation, as well as blocking the granular villi pores of the arachnoid membrane. The stimulation of the decomposition products of hemorrhage, especially iron-containing heme and bilirubin, causes arachnoid adhesions and hinders the circulation and absorption of cerebrospinal fluid. As a result, acute traffic hydrocephalus or arachnoid adhesions can occur, causing a rapid rise in intracranial pressure, further reducing cerebral blood flow, aggravating cerebral edema, and even leading to brain herniation formation; (5) leading to the opening of calcium channels, thus destroying intracellular lipid and protein metabolism, and in severe cases leading to neuronal cell death. All of the above can cause patients to reappear with impaired consciousness or limited neurological symptoms after their condition has stabilized and improved. (c) Clinical manifestations: 1. Hemorrhagic symptoms Most of the patients have a rapid onset, with severe and sudden “explosive” headache, and 50% of the patients have nausea, vomiting, pallor, and cold sweat. Transient disorders of consciousness are common, and in severe cases, coma and even brain herniation may occur and lead to death. The causes of coma include: increased intracranial pressure, intracerebral hemorrhage, hemorrhage invading the circumferential pool, diffuse cerebral ischemia, seizures, and decreased cerebral blood flow. 2, neurological deficits One side of the motor nerve palsy is common, and hemiparesis occurs in about 20% before and after hemorrhage, due to lesions or hemorrhage involving the motor area cortical and conduction tracts. 3, epilepsy Hemorrhage stimulates abnormal cortical discharge, which is a risk factor for rebleeding. 4, cerebral vasospasm Appears with temporary limited localization signs, progressive impairment of consciousness, marked signs of meningeal stimulation, and cerebral angiography shows thinning of cerebral vasospasm. 5.Cardiac arrhythmia The mechanism is unclear. (D) Diagnosis: head CT, lumbar puncture. (E) Treatment: 1. Absolute bed rest, reduction of external stimuli, restriction of visitation, prohibition of noise; 2. Close monitoring of vital signs, recording of intake and output, fasting and gastrointestinal decompression in lethargic patients; 3. Oxygenation, ventilation of airway in comatose patients; 4. Early administration of hemostatic agents, control of blood pressure and blood volume, mild dilation, blood pressure dilution and slight elevation of blood pressure to help prevent vasospasm and cerebral salt consumption; 5. seizures; 6. calcium channel blockers —- nimodipine to prevent vasospasm; 7. sedation, antiemetic, analgesic, laxative; 8. hormone therapy, proton pump inhibitors; 9. according to Hunt and Hess classification to formulate the appropriate treatment plan, early clarification of the cause of bleeding, treatment for the cause.