Subarachnoid hemorrhage ( SAH ) is bleeding into the subarachnoid space - the area between the arachnoid membrane and the pia mater surrounding the brain. Symptoms may include severe headaches, rapid attacks, vomiting, decreased level of consciousness, fever, and sometimes seizures. Neck stiffness or neck pain is also relatively common. About a quarter of people experience small bleeding with obvious symptoms occurring within a month more bloody.
SAH may occur as a result of a head injury or spontaneously, usually from a ruptured cerebral aneurysm. Risk factors for spontaneous cases include high blood pressure, smoking, family history, alcoholism, and cocaine use. Generally, the diagnosis can be determined by a CT scan of the head if done within six hours. Sometimes a lumbar puncture is also required. After confirmation, further tests are usually performed to determine the underlying cause.
Treatment is with rapid neurosurgery or radiologically guided intervention. Drugs such as labetalol may be needed to lower blood pressure until improvement can occur. Efforts to treat fever are also recommended. Nimodipine, a calcium channel blocker, is often used to prevent vasospasm. Regular use of drugs to prevent further seizures is an unclear benefit. Almost half of people with SAH because underlying aneurysms die within 30 days and about a third of those who survive have ongoing problems. 10-15 percent die before reaching the hospital.
Spontaneous SAH occurs in about one per 10,000 people per year. Women are more often affected than men. While it is becoming more common with age, about 50% of people are present under 55 years of age. It is a form of stroke and consists of about 5 percent of all strokes. Surgery for aneurysms was introduced in the 1930s. Since the 1990s many aneurysms have been treated with a less invasive procedure called "coiling", which is done through large blood vessels.
Video Subarachnoid hemorrhage
Signs and symptoms
The classic symptoms of subarachnoid hemorrhage are thunderclap headaches (headaches described as "kicked in the head", or "worst ever", develop for a few seconds to minutes). These headaches often pulsate toward the nape (the back of the head). About one-third of people do not have symptoms apart from typical headaches, and about one in ten people seeking medical treatment with these symptoms are then diagnosed with subarakhnoid hemorrhage. Vomiting may be present, and 1 in 14 experience seizures. Confusion, decreased level of consciousness or coma may exist, such as neck stiffness and other signs of meningism.
Neck stiffness usually presents six hours after the initial onset of SAH. The isolated dilation of the pupil and the disappearance of the light pupil reflex may reflect brain herniation as a result of increased intracranial pressure (pressure inside the skull). Intraocular bleeding (bleeding into the eyeball) may occur in response to pressure: subhyaloid hemorrhage (bleeding below the hyaloid membrane, enveloping the eye's vitreous body) and vitreous bleeding may be seen on the funduscopy. This is known as Terson's syndrome (occurring in 3-13 percent of cases) and is more common in more severe SAHs.
Oculomotor nerve disorders (exposed eyes looking down and out and inability to lift eyelids on the same side) or palsy (movement loss) may indicate bleeding from the posterior communicative artery. Seizures are more common when bleeding comes from aneurysms; If not difficult to predict the site and the origin of bleeding from the symptoms. SAH in a person known to have seizures is often a diagnosis of cerebral arteriovenous malformations.
The combination of intracerebral hemorrhage and increased intracranial pressure (if any) leads to "sympathetic waves", ie over-activation of the sympathetic system. This is thought to occur through two mechanisms, a direct effect on the medulla that leads to decreased sympathetic nervous system activation and local release of inflammatory mediators circulating into the peripheral circulation in which they activate the sympathetic system. As a result of a sympathetic spike there is a sudden increase in blood pressure; mediated by increased ventricular contractility and increased vasoconstriction leading to increased systemic vascular resistance. The consequences of this sympathetic wave can be sudden, severe, and often life-threatening. High plasma adrenaline concentrations may also cause cardiac arrhythmias (irregularities in heart rate and rhythm), electrocardiographic changes (in 27 percent of cases) and heart attacks (in 3 percent of cases) can occur rapidly after onset of bleeding. A further consequence of this process is neurogenic pulmonary edema in which the process of increasing pressure in the pulmonary circulation causes leakage of fluid from the pulmonary capillaries into the air space, alveoli, lungs.
Subarachnoid haemorrhage may also occur in people who have head injury. Symptoms may include headache, decreased level of consciousness and hemiparesis (weakness of one side of the body). SAH often occurs in traumatic brain injury, and it leads to a poor prognosis when associated with a decreased level of consciousness.
While thunderclap headache is a typical symptom of subarachnoid hemorrhage, fewer than 10% of those who have symptoms are associated with SAH in the investigation. A number of other causes may need to be considered.
Maps Subarachnoid hemorrhage
Cause
Most SAH cases are caused by trauma. In 85 percent of spontaneous SAH cases, the cause is a rupture of cerebral aneurysm - a weakness in the wall of one of the arteries in the enlarged brain. They tend to be in the circle of Willis and its branches. While most SAH cases are due to bleeding from small aneurysms, larger (less common) aneurysms are more likely to break out. Aspirin also appears to increase the risk.
In 15-20 percent of cases of spontaneous SAH, no aneurysm is detected in the first angiogram. About half of this is associated with non-aneurysmal perimesencephalic bleeding, where the blood is confined to the subarachnoid space around the midbrain (ie mesencephalon). In this case, the origin of blood is uncertain. The rest is due to other disorders affecting the blood vessels (such as arteriovenous malformations of the brain), vascular disorders in the spinal cord, and bleeding to various tumors. Abuse of cocaine and sickle cell anemia (usually in children) and, rarely, anticoagulant therapy, problems with blood clots and pituitary apoplection can also cause SAH. Vertebral artery dissection, usually caused by trauma, may cause subarakhnoid hemorrhage if surgery involves a portion of a vessel within the skull.
Subarachnoid blood can be detected on CT scans as many as 60 percent of people with traumatic brain injury. Traumatic SAH (tSAH) usually occurs near the site of a skull fracture or intracerebral contusions. It usually occurs in the setting of other forms of traumatic brain injury and has been associated with a worse prognosis. It is not clear, however, if this is a direct result of SAH or whether the presence of subarachnoid blood is just an indicator of the severity of head injury and prognosis determined by other related mechanisms.
Pathophysiology
Cerebral vasospasm is one of the complications caused by subarachnoid hemorrhage. It usually occurs from the third day after the aneurysm, and peaks from day 5 to day 7. There are several mechanisms proposed for this complication. Blood products released from subarachnoid hemorrhages stimulate the tyrosine kinase pathway that causes the release of calcium ions from intracellular storage, resulting in smooth muscle contraction of the cerebral artery. Oxyhaemoglobin in cerebrospinal fluid (CSF) causes vasoconstriction by increasing free radicals, endothelin-1, prostaglandins and reducing levels of nitric oxide and prostacyclin. In addition, impaired autonomic nervous systems that supply the cerebral arteries are also thought to cause vasospasm.
Diagnosis
Because only 10 percent of people treated in the emergency department with thunderclap headaches have SAH, other possible causes are usually considered concurrent, such as meningitis, migraine, and cerebral venous sinus thrombosis. Intracerebral hemorrhage, in which bleeding occurs within the brain itself, is twice as common as SAH and is often misdiagnosed as the last. It is not uncommon for SAHs initially misdiagnosed as migraine or tension headaches, which can cause delays in obtaining CT scans. In a 2004 study, this occurred in 12 percent of all cases and was more likely in people who had smaller bleeding and no disturbance in their mental status. Delay in diagnosis leads to poor results. In some people, the headache disappears on its own, and no other symptoms are present. This type of headache is referred to as "sentinel headache", as it is thought to be the result of a small leak ("warning leak") of the aneurysm. Sentinel headaches still require investigation with CT scans and lumbar punctures, as further bleeding can occur within the next three weeks.
The first step to evaluating a person with subarachnoid haemorrhage is to get a medical history and perform a physical exam. Diagnosis can not, however, be made on a clinical basis only and in general medical imaging and possible lumbar puncture is required to confirm or exclude bleeding.
Imaging
The modalities of choice are computed tomography (CT scan) without contrast, from the brain. It has high sensitivity and will correctly identify more than 95 percent of cases - especially on the first day after the onset of bleeding. Magnetic resonance imaging (MRI) may be more sensitive than CT after a few days. Within six hours of onset of CT symptoms it took 98.7% of cases.
Lumbar puncture
Lumbar puncture, in which cerebrospinal fluid (CSF) is removed from the spinal canal subarachnoid space using a hypodermic needle, shows evidence of bleeding in 3 percent of people found in normal CT; The lumbar puncture is therefore considered mandatory to the person suspected of SAH if the imagery is negative. At least three CSF tubes are collected. If an increase in the number of red blood cells is present equally in all the bottles, this indicates subarakhnoid hemorrhage. If the number of cells decreases per bottle, it is more likely due to damage to small blood vessels during the procedure (known as "traumatic faucet"). Although there is no official cutoff for red blood cells in CSF, no recorded cases occur less than "several hundred cells" per high-powered field.
CSF samples were also examined for xanthochromia - yellow appearance of centrifugation fluid. This can be determined by spectrophotometry (measuring the absorption of certain wavelengths of light) or visual examination. It is not clear which method is superior. Xanthochromia remains a reliable way to detect SAH a few days after the onset of headaches. A interval of at least 12 hours between onset of headache and lumbar puncture is required, since it takes several hours for hemoglobin from red blood cells to be metabolized to bilirubin.
Angiography
After subarachnoid hemorrhage is confirmed, its origin needs to be determined. If the bleeding may be from an aneurysm (as determined by the appearance of CT scan), the choice is between cerebral angiography (radiocontrast injection via catheter to cerebral artery) and CT angiography (visualizing blood vessels with radiocontrast on CT scan) to identify aneurysms. Catheter angiography also offers the possibility of rolling up aneurysms (see below).
ECG
Electrocardiographic changes are relatively common in subarachnoid hemorrhage, occurring in 40-70 percent of cases. They may include QT prolongation, Q waves, cardiac dysrhythmias, and ST elevations that resemble a heart attack.
Classification
There are several assessment scales available for SAH. The Glasgow Coma scale is used extensively to assess awareness. Three special scores are used to evaluate SAHs; in each, higher numbers are associated with poor results. This scale has been derived with the retrospective matching characteristics of people with their results.
The first severity scale was described by Hunt and Hess in 1968:
Fisher Grade classifies the appearance of subarachnoid hemorrhage on CT scans.
This scale has been modified by Claassen and colleagues, which reflect the risk of additives of SAH size and accompanying intraventricular bleeding (0 - none; 1 - minimal SAH w/o IVH; 2 - SAH minimal with IVH; 3 - thick SAH without IVH ; 4 - thick SAH with IVH);
The World Federation of Neurosurgeons (WFNS) classification uses the Glasgow coma score (GCS) and focal neurological deficits to measure the severity of symptoms.
A comprehensive classification scheme has been suggested by Ogilvy and Carter to predict outcomes and measure therapies. The system consists of five classes and sets a point for the presence or absence of each of the five factors: age over 50 years; Hunt and Hess grade 4 or 5; Fisher Scale 3 or 4; aneurysm size more than 10 mm; and posterior circulation aneurysm 25 mm or more.
Filtering and prevention
Screening for aneurysms is not done at the population level; because they are relatively rare, it will not be cost effective. If a person has two or more first-degree relatives who experience subarachnoid haemorrhage aneurysms, screening may be helpful.
The dominant autosomal polycystic kidney disease (ADPKD), a hereditary renal condition, is known to be associated with cerebral aneurysm in 8 percent of cases, but most such aneurysms are small and therefore unlikely to rupture. As a result, screening is only recommended in families with ADPKD in which one family member experiences an aneurysm rupture.
Aneurysm can be accidentally detected on brain imaging; this presents a puzzle, as all treatments for cerebral aneurysms are associated with potential complications. International Studies of Uninterrupted Intracranial Aneurysms (ISUIA) provide prognostic data both in people who previously had subarachnoid hemorrhage and people who experienced aneurysms were detected by other means. Those who previously had a SAH were more likely to bleed from other aneurysms. Conversely, those who have never bleed and have a small aneurysm (smaller than 10 mm) are highly unlikely to have a SAH and are likely to sustain damage from attempts to repair this aneurysm. On the basis of ISUIA and other studies, it is now recommended that people be considered for preventative treatment only if they have a reasonable life expectancy and have a highly ruptured aneurysm. At the same time, there is only limited evidence that endovascular treatment of an undiagnosed aneurysm is really useful.
Treatment
Management involves common steps to stabilize people while also using special investigations and treatments. These include the prevention of recurrent bleeding by eliminating sources of bleeding, prevention of a phenomenon known as vasospasm, and the prevention and treatment of complications.
Stabilizing people is the first priority. Those with depressed levels of consciousness may need to be intubated and mechanically ventilated. Blood pressure, pulse rate, respiratory rate, and Glasgow Coma Scale are frequently monitored. Once the diagnosis is confirmed, admission to the intensive care unit may be preferred, especially since 15 percent may experience further bleeding shortly after admission. Nutrition is an early priority, with oral or nasogastric feeding being preferred over the parenteral route. In general, pain control is limited to less sedating agents such as codeine, because sedation can have an impact on mental status and thus interferes with the ability to monitor awareness levels. Deep venous thrombosis is prevented by compression stockings, intermittent pneumatic compression of the calf, or both. Bladder catheters are usually included to monitor fluid balance. Benzodiazepines may be given to help relieve distress. An antiemetic drug should be given to an awake person.
People with poor clinical value at admission, acute neurologic impairment, or ventricular progressive enlargement of CT scan, are generally, indicative for the placement of external ventricular ducts by a neurosurgeon. External ventricular channels can be inserted at the bedside or in the operating room. In both cases, strict aseptic techniques must be maintained during insertion. In people with subarachnoid hemorrhage aneurysm, EVD is used to elevate cerebrospinal fluid, blood, and blood byproducts that increase intracranial pressure and may increase the risk of cerebral vasospasm.
Prevent re-bleeding
Attempts to maintain a person's systolic blood pressure below somewhere between 140 and 160 mmHg are generally recommended. Medications to achieve this may include labetalol or nicardipine.
People who have CT scans show a large hematoma, depressed consciousness, or focal neurological signs may benefit from surgical removal of the urgent blood or occlusion of the site of bleeding. The rest is stabilized more widely and undergo a transfemoral angiogram or CT angiogram later. It's hard to predict who will go down, but it can happen anytime and bring a bleak prognosis. After the first 24 hours have passed, the risk of re-bleeding remains about 40 percent over the next four weeks, suggesting that the intervention should be aimed at reducing this risk as soon as possible. Some predictors of recurrent bleeding are high systolic blood pressure, presence of hematoma in the brain or ventricle, poor Hunt-Hess class (III-IV), posterior circulation aneurysm, and aneurysm size & gt; 10 mm.
If a cerebral aneurysm is identified in angiography, two steps are available to reduce the risk of further bleeding from the same aneurysm: clipping and scrolling. Clipping requires a craniotomy (opening of the skull) to find an aneurysm, followed by placement of clips around the aneurysm of the neck. Coiling is done through a large vein (endovascular): the catheter is inserted into the femoral artery in the groin and progresses through the aorta to the artery (both the carotid artery and the two vertebral arteries) supplying the brain. When an aneurysm has been found, platinum coils are deployed causing a blood clot to form in the aneurysm, obliterating it. Decisions about treatment are usually done by a multidisciplinary team of neurosurgeon, neurologist, and often other health professionals.
In general, the decision between clipping and rolling is made on the basis of the location of the aneurysm, its size and the condition of the person. Aneurysms of the central cerebral artery and associated vessels are difficult to achieve with angiography and tend to agree to cut. Those from the basilar artery and the posterior cerebral artery are difficult to achieve surgery and are more accessible for endovascular management. This approach is based on common experience, and the only direct randomized controlled trial comparing different modalities is performed on relatively good people with small aneurysms (less than 10 mm) of the anterior cerebral artery and the anterior communicative artery (together "circulation anterior "), which is about 20 percent of all people with aneurysmal SAH. These trials, International Subarachnoid Aneurysm Trial (ISAT), show that in this group the chances of death or dependent on others for daily life activities are reduced (7.4 percent absolute risk reduction, 23.5 percent relative risk reduction) if endovascular coiling is used as opposed to surgery. The major disadvantage of the circle is the possibility that the aneurysm will recur; This risk is very small in the surgical approach. At ISAT, 8.3 percent require further treatment in the long run. Therefore, people who have been overthrown are usually followed up for years later with angiography or other measures to ensure an anonymous recurrence is identified early on. Other experiments also found higher rates of recurrence requiring further treatment.
Vasospasm
Vasospasm, in which the blood vessels narrow and thus restrict blood flow, is a serious complication of SAH. This can cause ischemic brain injury (referred to as "delayed ischemia") and permanent brain damage due to lack of oxygen in the brain. This can be fatal if it is severe. Delayed ischemia is characterized by new neurological symptoms, and can be confirmed by transcranial doppler or cerebral angiography. About one-third of people treated with subarachnoid hemorrhage will have ischemic delay, and half of them have permanent damage as a result. It is possible to screen for the development of vasospasm with transcranial Doppler every 24-48 hours. Blood flow rate of more than 120 centimeters per second indicates the presence of vasospasm.
The use of calcium channel blockers, considered to prevent vascular seizures by preventing calcium from entering smooth muscle cells, has been proposed for prevention. Nimodipine calcium channel blockers when taken boost yield if given between the fourth and twenty-first days after bleeding, even if it does not reduce the amount of vasospasm detected in the angiography. This is the only FDA-approved drug to treat cerebral vasospasm. In subarachnoid traumatic bleeding , nimodipine does not affect long-term outcomes, and is not recommended. Other calcium channel inhibitors and magnesium sulfate have been studied, but are not currently recommended; there is no evidence to suggest a benefit if nimodipine is administered intravenously.
Some older studies have suggested that statin therapy may reduce vasospasm, but subsequent meta-analyzes including further trials show no benefit in vasospasm or outcome. While corticosteroids with mineralocorticoid activity may help prevent vasospasm its use does not seem to alter the outcome.
The so-called "triple H" protocol is often used as a measure to treat vasospasm when causing symptoms; this is the use of intravenous fluids to achieve hypertension (hypertension), hypervolemia (excess fluid in the circulation), and hemodilution (mild dilution of the blood). The evidence for this approach can not be inferred; no randomized controlled trials were performed to demonstrate its effect.
If delayed ischemic symptoms do not improve with medical treatment, angiography may be attempted to identify vasospasm sites and administer vasodilator drugs (drugs that loosen blood vessel walls) directly into the arteries. Angioplasty (opening a restricted area with a balloon) can also be done.
Other complications
Hydrocephalus (cerebrospinal fluid flow obstruction) may complicate the SAH both in the short and long term. This is detected on a CT scan, where there is a lateral ventricle enlargement. If the level of consciousness decreases, excess fluid drainage is performed by therapeutic lumbar puncture, extraventricular drain (a temporary device inserted into one of the ventricles), or occasionally permanent shortcuts. Relief of hydrocephalus can cause a remarkable increase in one's condition. Fluctuations in blood pressure and electrolyte imbalance, as well as pneumonia and cardiac decompensation occur in about half of people admitted to hospital with SAH and can worsen prognosis. Seizures occur during hospital stay in about one third of cases.
Many believe that the person may benefit from prevention with antiepileptic drugs. Although this is widely practiced, it is controversial and not based on good evidence. In some studies, the use of these drugs is associated with a poor prognosis; although it is unclear whether this is possible because the drugs themselves actually cause harm, or because they are used more often in people with a worse prognosis. There is a possibility of stomach bleeding due to stress ulcers.
Prognosis
Short-term results
SAH is often associated with poor results. The mortality rate for SAHs is between 40 and 50 percent, but the tendency for survival increases. Of those who stay in the hospital, more than a quarter have significant restrictions on their lifestyle, and less than a fifth have no residual symptoms. The delay in the diagnosis of a minor SAH (incorrectly assuming a sudden headache for a migraine) contributes to poor outcomes. Factors found in acceptance associated with poorer outcomes include worse neurologic levels; systolic hypertension; previous diagnosis of heart attack or SAH; liver disease; more blood and aneurysms are greater on early CT scans; location of the aneurysm in the posterior circulation; and a higher age. Factors that lead to a poorer prognosis during hospital stay include delayed ischemia due to vasospasm, intracerebral hematoma development, or intraventricular hemorrhage (bleeding to the ventricle of the brain) and fever on day eight.
The so-called "subarachnoid angiogram-negative hemorrhage", SAH which shows no aneurysm with four-vessel angiography, carries a better prognosis than SAH with aneurysms; However, it is still associated with ischemic risk, rebleeding, and hydrocephalus. Perimeencephalic SAD (bleeding around the mesencephalon in the brain), however, has a very low rate of re-bleeding or delayed ischaemia, and the prognosis of this subtype is excellent.
The prognosis of head trauma is thought to be affected in part by the location and amount of subarachnoid hemorrhage. It is difficult to isolate the effects of SAH from other aspects of traumatic brain injury; it is not known whether the presence of subarachnoid blood actually worsens the prognosis or whether it is just a sign that significant trauma has occurred. People with moderate and severe traumatic brain injury who have SAH when admitted to the hospital have as many as two death risks as those who do not. They also have a higher risk of severe disability and a sedentary vegetative state, and traumatic SAH has been correlated with other markers of poor outcomes such as posttraumatic epilepsy, hydrocephalus, and longer stay in the intensive care unit. However, more than 90 percent of people with traumatic subarachnoid hemorrhage and Glasgow Coma Score above 12 have good results.
There is also simple evidence that genetic factors influence the prognosis in SAH. For example, having two copies of ApoE4 (a variant of a gene encoding apolipoprotein E that also plays a role in Alzheimer's disease) appears to increase the risk for delayed ischemia and worse outcomes. The occurrence of hyperglycemia (high blood sugar) after one episode of SAH confers the risk of higher adverse outcomes.
Long-term results
Neurocognitive symptoms, such as fatigue, mood disorders, and other related symptoms are frequent residual symptoms. Even in those who have made good neurological recovery, anxiety, depression, posttraumatic stress disorder, and cognitive impairment are common; 46 percent of people who experience subarachnoid hemorrhage have cognitive impairments that affect their quality of life. Over 60 percent report frequent headaches. Subarachnoid haemorrhage aneurysms can cause damage to the hypothalamus and pituitary gland, two areas of the brain that play a central role in hormonal regulation and production. More than a quarter of people with SAHs previously developed hypopituitarism (deficiency in one or more of the hypothalamus-pituitary hormones such as growth hormone, luteinizing hormone, or follicle stimulating hormone).
Epidemiology
According to a review of 51 studies from 21 countries, the average incidence of subarakhnoid hemorrhage is 9.1 per 100,000 per year. Studies from Japan and Finland show higher rates in these countries (22.7 and 19.7 respectively), for reasons not fully understood. South and Central America, by contrast, has an average rate of 4.2 per 100,000.
Although the group of people at risk for SAH is younger than the stroke-prone population, the risk continues to increase with age. Young people are much less likely than middle-age people (risk ratio 0.1, or 10 percent) to have subarakhnoid hemorrhage. The risk continues to increase with age and 60 percent higher in elderly (more than 85) compared to those between 45 and 55 years of age. The risk of SAH is about 25 percent higher in women over 55 compared with men of the same age, possibly reflecting hormonal changes resulting from menopause, such as decreased estrogen levels.
Genetics may play a role in a person's disposition to SAHs; the risk increases three to five times in the first-degree relatives of people who experience subarakhnoid hemorrhage. However, lifestyle factors are more important in determining overall risk. Risk factors for smoking, hypertension (high blood pressure), and excessive alcohol consumption. Having smoking in the past poses a double risk of SAH compared with those who never smoked. Some protective significance is uncertain given by caucasian ethnicity, hormone replacement therapy, and diabetes mellitus. There is a possibility of an inverse relationship between total serum cholesterol and non-traumatic SAH risk, although confirmation of this association is hindered by a lack of research. About 4 percent of aneurysm bleeds occur after sexual intercourse and 10 percent of people with SAH bend or lift heavy objects at the beginning of their symptoms.
Overall, about 1 percent of all people have one or more brain aneurysms. Most of these, however, are small and unlikely to break.
History
While the clinical picture of subarachnoid hemorrhage may have been recognized by Hippocrates, the presence of cerebral aneurysms and the fact that they could be ruptured was not established until the 18th century. The related symptoms were described in more detail in 1886 by Edinburgh physician Dr. Byrom Bramwell. In 1924, London neurologist Sir Charles P. Symonds (1890-1978) gave a full account of all the major symptoms of subarachnoid hemorrhage, and he coined the term "spontaneous subarakhnoid hemorrhage". Symonds also describes the use of lumbar puncture and xanthochromia in diagnosis.
The first surgical intervention was performed by Norman Dott, who was a student of Harvey Cushing who later worked in Edinburgh. He introduced aneurysm packing in the 1930s, and was the earliest pioneer in the use of an angiogram. American neurosurgeon Dr. Walter Dandy, who worked in Baltimore, was the first to introduce a clip in 1938. Microsurgery was applied to aneurysm treatment in 1972 to further improve results. The 1980s saw the introduction of triple H therapy as a treatment for delayed ischemia due to vasospasm, and trials with nimodipine in an attempt to prevent these complications. In 1983, Russian neurosurgeon Zubkov and colleagues reported the first use of transluminal balloon angioplasty for vasospasm after an aneurysm SAH. Italian neurosurgeon Dr. Guido Guglielmi introduced his endovascular coil treatment in 1991.
References
External links
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