Transcription
A sub-recorded hemorrhage is a type of stroke that causes bleeding around the brain—subarachnoid hemorrhage. The bleeding happens in a part of the head called the subarachnoid space. This is the area between the arachnoid and pia mater, which is the meninges of the brain, a layer that protects the actual brain. Normally, you have cerebral spinal fluid floating around the subarachnoid space, but with a subarachnoid hemorrhage, you see blood occupying this area.
Most spontaneous subarachnoid hemorrhages are caused by ruptured sacular aneurysms. If the saccular aneurysm is large enough, it actually weakens the walls of the blood vessel, causing rupture and hemorrhage. Other types of aneurysms can also include fusiform aneurysm and mycotic aneurysms secondary to infectious organisms. Other causes of subarachnoid hemorrhage aside from an aneurysm include occult trauma, arteriovenous malformations or fistula, vasculidities, intracranial arterial dissection, amyloid angiopathy, bleeding diathesis, and illicit drug use, especially the use of sympathomimetics such as cocaine and amphetamines. We will focus on the most common cause of subarachnoid hemorrhage, which is from an aneurysm, but all the pathophysiology that follows can be related back to any of the causes.
Now, specifically for the aneurysm, the risk of an aneurysmal rupture includes the size of the aneurysm, how quickly it grows, and the site of where the aneurysm is. So, for example, posterior circulation aneurysms involving the vertebral basilar artery or the posterior communicating arteries have the highest rates of rupture. Physical exertion is a risk, as are hypertension, smoking, alcohol, and the use of sympathomimetics. When an aneurysm ruptures, bleeding occurs in the subarachnoid space, causing subarachnoid hemorrhage. Note that with a ruptured aneurysm, there can also be a concurrent intracerebral hemorrhage, as well as an intraventricular hemorrhage—bleeding within the ventricles of the brain.
The classic clinical presentation is a sudden onset, severe headache—the worst headache ever. Some people also describe it as a blow to the back of the head. They may also describe what's called a sentinel headache, which is a severe headache preceding the actual rupturing of the aneurysm. Patients may also have neck stiffness, vomit, and have an altered level of consciousness or loss of consciousness. Examination findings include hypertension, meningismus (neck stiffness), and photophobia. Terson syndrome, which is where if you look at the back of the eye you can see multiple vitreous hemorrhages, may also be present. They may have signs of raised intracranial pressure and/or any new neurological deficit; for example, a third nerve palsy is associated with a posterior communicating artery aneurysm.
Subarachnoid hemorrhage is a medical emergency because it can cause death in the first 24 hours. Re-bleeding from the site of the aneurysmal rupture can occur; this occurs in up to 15 percent of people and is associated with high mortality. Re-bleeding is characterized by any new neurological deficit. Subarachnoid hemorrhage can lead to hydrocephalus, which can be an early or late complication occurring in about a quarter of the patients. What happens here is that you have an obstruction of the cerebral spinal fluid flow because of the blood products in the subarachnoid space. As a result, there is reduced cerebral spinal fluid absorption at the arachnoid granulation. Cerebral spinal fluid accumulates within the subarachnoid space, leading to what is known as hydrocephalus.
Other immediate complications include intracerebral hemorrhage, and depending on the hemorrhage volume, this can lead to a significant increase in intracranial pressure. An increase in intracranial pressure means the pressure is elevated inside the cranium—the skull, the head. When the pressure inside your skull and around your brain increases, you can imagine it would cause a lot more complications. An increase in intracranial pressure leads to early brain injury due to reduced cerebral blood flow—reduced blood flow to the brain—and this will cause what's called transient global cerebral ischemia. To appreciate the mechanism behind this, you need to appreciate that normally blood vessels supplying the brain are patent and allow oxygenation of tissues easily. With subarachnoid hemorrhage, there are pathological changes as a response to the injury, bleeding, and inflammation. This includes vasoconstriction, microthrombus formation, endothelial damage of the surrounding cells, apoptosis of the cells, and cerebral edema from extravasation—the movement of fluid from the blood vessel out to the brain tissue. All in all, what happens is that you get reduced blood flow as a response, leading to early brain injury. Over time, an increase in intracranial pressure causes death due to reduced cerebral blood flow and acute cardiopulmonary changes.
Another common complication of subarachnoid hemorrhage is vasospasm, which occurs 3 to 14 days after the injury. Vasospasm is where the blood vessels in the brain spasm, causing altered neurological status. Every time this happens, vasospasm is thought to be a result of lysis of subarachnoid blood and damage to endothelial cells, causing reduced nitric oxide production and increased endothelin production, causing the vasoconstriction that we see. Vasospasm, in turn, can cause delayed cerebral ischemia and infarction. Delayed cerebral ischemia occurs in approximately 30 percent of patients with aneurysmal subarachnoid hemorrhage. The definition of delayed cerebral ischemia requires the occurrence of a focal neurological impairment or a decrease of at least two points of the Glasgow Coma Scale that lasts for at least one hour. Delayed cerebral ischemia may result in cerebral infarction and thus contributing to possible death with increased mortality. Delayed cerebral ischemia is really similar to early brain injury; however, it's a later event.
Hyponatremia is another complication and develops in up to 30 percent of patients with subarachnoid hemorrhage and is probably mediated by hypothalamic injury. The water retention that leads to hyponatremia may result from either the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) or from cerebral salt wasting. In SIADH, excess ADH is produced, which will target the kidneys and cause inappropriate retention of water, causing hyponatremia. During sub-recular hemorrhage, you have an increased sympathetic response, which can lead to cardiopulmonary complications including neurogenic pulmonary edema and cardiac arrhythmias. The body's response to the central sympathetic overdrive is to produce natriuretic peptides such as brain natriuretic peptide (BNP). BNP causes natriuresis—essentially peeing out salt from the body. This is one of the potential causes of hyponatremia termed cerebral salt wasting.
Other complications of subarachnoid hemorrhage include seizures (about 15%), anemia, hyperglycemia (which is associated with poor outcomes), fevers (it's important to differentiate between infective and non-infective causes of fever), and finally, hypothalamic pituitary dysfunction.
Investigations for someone who has a subarachnoid hemorrhage suspected is a CT brain non-contrast, best within 12 hours, and this will show blood collecting in the subarachnoid space. Lumbar puncture can also be performed if the CT brain is not definitive. Lumbar puncture will show increased pressure and xanthochromia, which is the presence of bilirubin in the cerebrospinal fluid secondary to the breakdown of the red blood cells, resulting in the yellow discoloration.
Treatment of a subarachnoid hemorrhage: It's important to maintain oxygen between 94 to 98%. If the GCS is low, intubation is necessary. Treat the hypertension; aim for a blood pressure less than 140 millimeters of mercury of systolic pressure. Anything over 150 systolic blood pressure is associated with re-bleeding; important to avoid hypertension as this may lead to cerebral ischemia. Analgesia and antimetics can be used. Anti-epileptic medications may also be used. Correct any coagulopathy, so vitamin K and prothrombin complex concentrate for Warfarin. Calcium channel blockers such as nimodipine are important to prevent secondary vasospasm. Mannitol intravenously is used if there is evidence of raised intracranial pressure. Finally, and most importantly, neurosurgical review should be done early to secure aneurysmal bleeding through coiling or clipping. If coiling is unavailable, treat the complications of subarachnoid hemorrhage such as hydrocephalus, either through an external or internal shunt, or if a shunt is unable to be performed right away, intravenous Mannitol can be used.
In summary, subarachnoid hemorrhage is bleeding within the subarachnoid space; the most common cause is a circular aneurysmal rupture.