Subarachnoid Hemorrhage

SUB-ARACHNOID HAEMORRHAGE  Subarachnoid hemorrhage (SAH) refers to extravasation of blood into the subarachnoid space between the pial and arachnoid membranes.

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It comprises half of spontaneous atraumatic intracranial hemorrhages, the other half consist of bleeding that occurs within the brain parenchyma. NB the most common cause of SAH is head trauma. However, the familiar medical use of the term SAH refers to nontraumatic (or spontaneous) hemorrhage, which usually occurs in the setting of a ruptured cerebral aneurysm or arteriovenous malformation (AVM). Its devastating condition with high morbidity and mortality

Etiology  Rupture of “berry,” or saccular, aneurysms of the basal vessels of the brain comprises 77% of nontraumatic SAH cases  Aneurysms mostly arise from the terminal portion of the internal carotid artery (ICA) and from the major branches of the anterior portion of the circle of Willis. Pathophysiology  Congenital and acquired factors are thought to play a role in occurrence of aneurysm.

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Aneurysms usually occur at the branching sites on the large cerebral arteries of the circle of Willis. The early precursors of aneurysms are small outpouchings through defects in the media of the arteries. These defects are thought to expand as a result of hydrostatic pressure from pulsatile blood flow and blood turbulence, which is greatest at the arterial bifurcations. A mature aneurysm has a paucity of media, replaced by connective tissue, and has diminished or absent elastic lamina. The rate of rupture is directly related to the size of the aneurysm. Aneurysms with a diameter of 5 mm or less have a 2% risk of rupture, whereas 40% of those 6-10 mm have already ruptured upon diagnosis. Brain injury from cerebral aneurysm formation can occur in the absence of rupture via compressive forces that cause injury to local tissues and/or compromise of distal blood supply (mass effect). When an aneurysm ruptures, blood extravasates under arterial pressure into the subarachnoid space and quickly spreads through the cerebrospinal fluid (CSF) around the brain and spinal cord. Blood released under high pressure may directly cause damage to local tissues. Blood extravasation causes a global increase in intracranial pressure (ICP). Meningeal irritation occurs. Congenital defects in the muscle and elastic tissue of the arterial media in the vessels. These defects lead to microaneurysmal dilatation. Aneurysms are acquired lesions related to hemodynamic stress on the arterial walls at bifurcation points and bends. AVMs are the second most identifiable cause of SAH, accounting for 10% of cases of SAH LOC often is transient; however some patients are comatose for several days, depending on the location of the aneurysm and the amount of bleeding. Seizures during the acute phase

Risk factors for aneurismal SAH: 1.Hypertension - Fibromuscular dysplasia, polycystic kidney disease, and aortic coarctation

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2.Increased blood flow - Cerebral arteriovenous malformation (AVM); persistent carotid-basilar anastomosis; ligated, aplastic, or hypoplastic contralateral vessel 3.Blood vessel disorders – Atherosclerosis ,Systemic lupus erythematosus (SLE), Moyamoya disease, and granulomatous angiitis 4.Genetic - Marfan syndrome, Ehlers-Danlos syndrome, OslerWeber-Rendu syndrome, pseudoxanthoma elasticum, and Klippel-Trenaunay-Weber syndrome 5.Congenital - Persistent fetal circulation and hypoplastic/absent arterial circulation 6.Metastatic tumors to cerebral arteries - Atrial myxoma, choriocarcinoma, and undifferentiated carcinoma 7.Infectious - Bacterial, fungal 8.Use of oral contraceptives ,Hormone replacement therapy, 9.Hypercholesterolemia and alcohol consumption may contribute to HTN or atherosclerosis. Saccular or berry aneurysms are specific to the intracranial arteries because their walls lack an external elastic lamina and contain a very thin adventitia—factors that may predispose to the formation of aneurysms. An additional feature is that they lie unsupported in the subarachnoid space. Mortality/Morbidity: As many as 60% of patients die in the first 30 days as the result of SAH. Sex: The incidence of SAH is slightly higher in women than in men. Age: The mean age for SAH is 50 years. Clinical presentation History The signs and symptoms of SAH range from subtle prodromal events, which often are misdiagnosed, to the classic presentation of catastrophic headache. A) Sentinel, or "warning," leaks that produce minor blood leakage Sentinel leaks produce sudden focal or generalized head pain that may be severe. In addition to headaches, sentinel leaks may produce nausea, vomiting, photophobia, malaise, or, less commonly, neck pain. Signs of raised ICP don’t occur B)Aneurysmal rapture SAH The classic symptoms and signs of aneurysmal rupture into the subarachnoid space comprise one of the most pathognomonic presentations in all of clinical medicine 1.A sudden onset of very severe headache, often described as the “worst headache of my life” 2.Nausea and/or vomiting 3. Symptoms of meningeal irritation, including nuchal rigidity and pain, back pain, and bilateral leg pain (but may take several hours to manifest). 4. Photophobia and visual changes are common. 5. A sudden loss of consciousness (LOC) occurs at the ictus in as many as 45% of patients as ICP exceeds cerebral perfusion pressure c)Mass effect Expanding aneurysm or hemorrhage, characteristic features based upon aneurysm location. 1.Posterior communicating artery/internal carotid artery - Focal, progressive retro-orbital headaches and oculomotor nerve palsy 2.Middle cerebral artery - Contralateral face or hand paresis, aphasia (left side), contralateral visual neglect (right side)

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3.Anterior communicating artery - Bilateral leg paresis and bilateral Babinski sign 4.Basilar artery apex - Vertical gaze, paresis, and coma 5.Intracranial vertebral artery/posterior inferior cerebellar artery - Vertigo, components of lateral medullary syndrome. Physical Examination 1.Focal neurologic signs hemiparesis, aphasia, hemineglect, cranial nerve palsies, and memory loss 2. Ophthalmologic examination may reveal subhyaloid retinal hemorrhages and papilledema. 3. Blood pressure elevation is observed in about .BP often becomes labile as ICP increases. Bradycardia may occur 4. Temperature elevation, secondary to chemical meningitis. Hunt and Hess grading system of SAH Grade 1 - Asymptomatic or mild headache Grade 2 - Moderate-to-severe headache, nuchal rigidity, and no neurological deficit other than possible cranial nerve palsy Grade 3 - Mild alteration in mental status (confusion, lethargy), mild focal neurological deficit Grade 4 - Stupor and/or hemi paresis Grade 5 - Comatose and/or decerebrate MANAGEMENT Indications for surgical management have been described recently and include the following:

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For patients with a mild- or intermediate-grade SAH (Hunt and Hess 1-3), surgical treatment (Surgical clipping) is strongly recommended because the risks of SAH complications greatly exceed the risk of surgical complications For patients with a poor grade of SAH (Hunt and Hess grades 4-5) The overall outcome is poor, with or without surgical intervention. Patients with a higher grade of SAH or poor medical status that do not qualify for early surgery may be candidates for delayed surgery or endovascular obliteration of the aneurysm. Other indications of surgey     

Large and giant aneurysm Wide-necked aneurysms Vessels emanating from the aneurysm dome Mass effect or hematoma associated with the aneurysm Recurrent aneurysm after coil embolization

Indications for endovascular treatment Endovascular treatment with the Guglielmi detachable coil system  Patients with poor clinical grade  Patients who are medically unstable  In situations where aneurysm location imparts an increased surgical risk, such as cavernous sinus and many basilar tip aneurysms  Small-neck aneurysms in the posterior fossa  Patients with early vasospasm  Cases where the aneurysm lacks a defined surgical neck (although these are also difficult to "coil")  Patients with multiple aneurysms in different arterial territories if surgical risk is high Location of aneurysm rupture Approximately 85% of saccular aneurysms occur in the anterior circulation. The most common sites of rupture are as follows: -The internal carotid artery, including the posterior communicating junction (41%)

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-The anterior communicating artery/anterior cerebral artery (34%) -The middle cerebral artery (20%) -The vertebral-basilar arteries (4%) -Other arteries (1%) Lab Studies: 1.CBC count - For evaluation of possible infection or hematologic abnormality 2.Prothrombin time (PT) and activated partial thromboplastin time (aPTT) - For evaluation of possible coagulopathy 3.Serum electrolytes - To establish a baseline for detection of future complications 4.Blood type and screen - In case intraoperative transfusion is required or in the setting of massive hemorrhage 5.Cardiac enzymes - For evaluation of possible myocardial ischemia 6.Arterial blood gas (ABG) - Assessment is necessary in cases with pulmonary compromise Imaging Studies: 1. CT scan: the location of the hemorrhage and the mass effects of the hemorrhage on the ventricles. 2. LP If diagnosis not clear, do lumbar puncture after funduscopy to rule out raised ICP. D-dimer assay: can be used to discriminate SAH from traumatic LP. After 24 hours, CSF samples may demonstrate a polymorphonuclear and mononuclear polycytosis secondary to chemical meningitis caused by the degradation products of subarachnoid blood. 3. Cerebral angiography can provide the following important surgical information in the setting of SAH: a) Cerebrovascular anatomy b) Aneurysm location and source of bleeding c) Aneurysm size and shape, as well as orientation of the aneurysm dome and neck d) Relation of the aneurysm to the parent artery and perforating arteries e) Presence of multiple or mirror aneurysms (identically placed aneurysms in both the left and right circulations) Other Tests 1. Transcranial Doppler studies are useful in the detection and monitoring of arterial vasospasm. 2. Chest radiograph: All patients with SAH should have a baseline chest radiograph to serve as a reference point for evaluation of possible pulmonary complications. 3, Evaluation of ventricular wall motion via echocardiogram may be necessary in cases with suspected myocardial ischemia. 4.ECG- Nonspecific ST and T wave changes Decreased PR intervals, Increased QRS intervals, Increased QT intervals,Presence of U waves Medical Management  The initial management of patients with SAH is directed at patient stabilization.  Assess the level of consciousness and airway, as well as breathing and circulation (ABCs).  Endotracheal intubation should be performed for patients presenting with coma, depressed level of consciousness, inability to protect their airway, or increased ICP.  Intravenous (IV) access should be obtained, including central and arterial lines.  A short-acting benzodiazepine, such as midazolam, should be administered prior to all procedures Hypertension control

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The traditional treatment of ruptured cerebral aneurysms included strict blood pressure control, with fluid restriction and antihypertensive therapy. The current recommendations advocate the use of antihypertensive agents when the mean arterial pressure (MAP) exceeds 130 mm Hg. Intravenous beta-blockers, which have a relatively short half-life, can be titrated easily and do not increase ICP. Beta-blockers are the agents of choice in patients without contraindications. Most clinicians avoid the use of nitrates, such as nitroprusside or nitroglycerin, which elevate ICP. Hydralazine and calcium channel blockers have a fast onset and lead to relatively less increase in ICP than do nitrates. Angiotensin-converting enzyme inhibitors have a relatively slow onset and are not first-line agents in the setting of acute SAH.

Increased ICP 1. Patients with signs of increased ICP or herniation should be intubated and hyperventilated. Minute ventilation should be titrated to achieve a PCO2 of 30-35 mm Hg. Avoid excessive hyperventilation, which may potentiate vasospasm and ischemia. 2. Osmotic agents (eg, mannitol), which can decrease ICP dramatically (50% after 30 min postadministration) Loop diuretics (eg, furosemide) also can decrease ICP 3.The use of IV steroids (eg, Decadron) is controversial Additional medical management is directed to prevent and treat the following common complications of SAH:

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Rebleeding Vasospasm Hydrocephalus Hyponatremia Seizures Pulmonary complications Cardiac complications

Rebleeding Is the most dreaded early complication of SAH. The greatest risk of rebleeding occurs within the first 24 hours of rupture. The overall mortality rate from rebleeding is reported to be as high as 78%. Measures to prevent rebleeding include the following: 1.Bedrest in a quiet room 2. Analgesia, preferably with a short-acting and reversible agent such as fentanyl: Pain is associated with a transient elevation in blood pressure and increased risk of rebleeding. 3.Sedation (used with caution to avoid distorting subsequent neurologic evaluation) with a short-acting benzodiazepine such as midazolam 4.Stool softeners 5.Antifibrinolytics have been shown to reduce the occurrence of rebleeding. However, outcome likely does not improve because of a concurrent increase in the incidence of cerebral ischemia 2.Cerebral vasospasm The delayed narrowing of the large capacitance vessels at the base of the brain, is a leading cause of morbidity and mortality in survivors of nontraumatic SAH. -Vasospasm is reported to occur in as many as 70% of patients .Most commonly, this occurs 4-14 days after the hemorrhage.

-Vasospasm can lead to impaired cerebral auto regulation and may progress to cerebral ischemia and infarction. Measures used for prevention of vasospasm include the following: 1.Maintenance of normovolemia, normothermia, and normal oxygenation are paramount to vasospasm prophylaxis. Volume status should be monitored closely, with avoidance of volume contraction, which can predispose to vasospasm. 2.Prophylaxis with oral nimodipine: -Calcium channel blockers have been shown to reduce the incidence of ischemic neurological deficits, and nimodipine has been shown to improve overall outcome within 3 months of aneurysmal SAH. -Nimodipine may prevent the ischemic complications of vasospasm by the neuroprotective effect of blockading the influx of calcium into damaged neurons. -Should be used cautiously to avoid the deleterious effects of hypotension. If vasospasm becomes symptomatic use of hypertensive, hypervolemic, and hemodilutional (HHH) therapy. There is demonstrated improved cerebral blood flow and resolution of the ischemic effects of vasospasm with this therapy. Initiation of HHH therapy requires placement of a pulmonary artery catheter in order to guide volume expansion and inotropic or vasopressor therapy. This therapy should be reserved for patients with aneurysms secured by surgical clipping or endovascular techniques in order to reduce the risk of rebleeding. Hypervolemia may be achieved by using packed erythrocytes, isotonic crystalloid, and colloid and albumin infusions in conjunction with vasopressin injection. Corticosteroids may be of some benefit; however, such treatment remains controversial. The hematocrit should be maintained at 30-35% via hemodilution or transfusion in order to optimize blood viscosity and oxygen delivery. Aggressive hypertensive therapy with inotropes and vasopressors (eg, dobutamine) can be initiated, if warranted Hydrocephalus Acute type Occurs within the first 24 hours after hemorrhage. This condition can precipitate life-threatening brainstem compression and occlusion of blood vessels. Hydrocephalus presents as a relatively abrupt mental status change, including lethargy, stupor, or coma. CT scan differentiates hydrocephalus from rebleeding. Treatment for acute hydrocephalus includes external ventricular drainage, depending on the severity of clinical neurologic dysfunction or CT scan findings. Chronic hydrocephalus usually the communicating type Hyponatremia Elevated levels of atrial natriuretic factor (ANF) and syndrome of inappropriate secretion of antidiuretic hormone (SIADH) have been implicated in recent studies of post-SAH hyponatremia. Use of slightly hypertonic sodium chloride (1.5% sodium chloride) at rates above maintenance requirements usually is efficacious for SAH-induced hyponatremia. Avoid fluid restriction in patients with SAH. Seizures Agents used for seizure prophylaxis include the following: Phenytoin, the agent of choice, can achieve rapid therapeutic concentrations when loaded intravenously, and it does not cause alterations in consciousness. Phenobarbital produces a sedative effect, which may mask the neurological evaluation; phenobarbital is used less frequently than phenytoin. Acute pulmonary edema and hypoxia

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Are almost universal in severe SAH. Neutrogenic in origin and unrelated to HHH therapy; however, the latter is associated with an increased risk of fluid overload. Treatment of acute pulmonary edema may include the use of gentle diuresis, dobutamine, and positive end-expiratory pressure (PEEP). Cardiac dysfunction occurs in a significant number of people with SAH. Neurogenic sympathetic hyperactivity, as well as increased levels of systemic catecholamines, has been implicated in SAH-associated cardiac dysfunction. Arrhythmias occur in as many as 90% of patients and most commonly include the following -Premature ventricular complexes (PVCs) -Bradyarrhythmias -Supraventricular tachycardia -Arrhythmias are most prevalent in the first 48 hours following SAH. Only a small percentage of arrhythmias (usually those associated with hypokalemia) are life threatening

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