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  • Autopsy and angiography studies have found that about 2% of adults harbor intracranial aneurysms Of the 4 million persons in the United States having aneurysms; the aneurysm will rupture, producing SAH, in 25,000–30,000 cases per year. For patients who arrive alive at hospital, the mortality rate over the next month is about 45%.
  • Of those who survive, more than half are left with major neurologic deficits as a result of the complications of your SAH. If the patient survives but the aneurysm is not obliterated, the rate of rebleeding is about 20% in the first 2 weeks, 30% in the first month, and about 3% per year afterwards
  • Rupture of an aneurysm with clinically significant SAH usually occurs in the 5 th decade of life, more common in women and aneurysms with a diameter of more than 10mm have a 50% risk of bleeding The annual risk of rupture for aneurysms <10 mm in size is 0.1%, and for aneurysms 10 mm in size is 0.5–1%--harrisons
  • EXCLUDING HEAD TRAUMA, the most common cause of SAH is rupture of a saccular aneurysm.
  • According to Robbin’s  Saccular aneurysm- most common type of intracranial aneurysm Other types Atherosclerotic (fusiform; mostly of the basilar artery) Mycotic Traumatic dissecting Mycotic aneurysms are usually located distal to the first bifurcation of major arteries of the circle of Willis. Most result from infected emboli due to bacterial endocarditis causing septic degeneration of arteries and subsequent dilation and rupture. Whether these lesions should be sought and repaired prior to rupture or left to heal spontaneously is controversial.
  • Saccular aneurysms occur at the bifurcations of the large- to medium-sized intracranial arteries It will then rupture is into the SAS in the basal cisterns and into the parenchyma of the adjacent brain As an aneurysm develops, it typically forms a neck with a dome
  • The arterial internal elastic lamina disappears at the base of the neck The media thins, and connective tissue replaces smooth-muscle cells. At the site of rupture (most often the dome) the wall thins, and the tear that allows bleeding is often 0.5 mm long.
  • Other causes include bleeding from a vascular malformation (arteriovenous malformation or dural arterial-venous fistula) and extension into the subarachnoid space from a primary intracerebral hemorrhage
  • Most unruptured intracranial aneurysms are completely asymptomatic . Symptoms are usually due to rupture At the moment of aneurysmal rupture with major SAH, the ICP suddenly rises . sudden transient loss of consciousness that occurs in nearly half of patients. In 10% of cases, aneurysmal bleeding is severe enough to cause loss of consciousness for several days. preceded by a brief moment of excruciating headache , but most patients first complain of headache upon regaining consciousness
  • In 45% of cases, severe headache associated with exertion is the presenting complaint. The patient often calls the headache "the worst headache of my life"; however, the most important characteristic is sudden onset . The headache is usually generalized, often with neck stiffness, and vomiting is common.
  • Although sudden headache in the absence of focal neurologic symptoms is the hallmark of aneurysmal rupture, focal neurologic deficits may occur. Aneurysms can undergo small ruptures and leaks of blood into the subarachnoid space, so-called sentinel bleeds .
  • The initial clinical manifestations of SAH can be graded using the Hunt-Hess or World Federation of Neurosurgical Societies classification schemes (Table 275-3) . For ruptured aneurysms, prognosis for good outcomes falls as the grade increases. For example, it is unusual for a Hunt-Hess grade 1 patient to die if the aneurysm is treated, but the mortality rate for grade 4 and 5 patients may be as high as 80%.
  • Rerupture . The incidence of rerupture of an untreated aneurysm in the first month following SAH is 30%, with the peak in the first 7 days. Rerupture is associated with a 60% mortality rate and poor outcome. Early treatment eliminates this risk
  • Acute hydrocephalus-- can cause stupor and coma and can be mitigated by placement of an external ventricular drain. subacute hydrocephalus--- may develop over a few days or weeks and causes progressive drowsiness or slowed mentation (abulia) with incontinence. Chronic hydrocephalus--- Develop weeks to months Gait difficulty Incontinence Impaired mentation
  • Narrowing of the arteries at the base of the brain following SAH causes symptomatic ischemia and infarction in 30% of patients and is the major cause of delayed morbidity and death. Signs of ischemia appear 4–14 days after the hemorrhage, most often at 7 days. The severity and distribution of vasospasm determine whether infarction will occur.
  • Delayed vasospasm is believed to result from direct effects of clotted blood and its breakdown products on the arteries within the subarachnoid space. In general, the more blood that surrounds the arteries, the greater the chance of symptomatic vasospasm. Spasm of major arteries produces symptoms referable to the appropriate vascular territory (Chap. 370). All of these focal symptoms may present abruptly, fluctuate, or develop over a few days. In most cases, focal spasm is preceded by a decline in mental status.
  • Hyponatremia . Hyponatremia may be profound and can develop quickly in the first 2 weeks following SAH. There is both natriuresis and volume depletion with SAH, so that patients become both hyponatremic and hypovolemic. Both atrial natriuretic peptide and brain natriuretic peptide have a role in producing this "cerebral salt-wasting syndrome." Typically, it clears over the course of 1–2 weeks and, in the setting of SAH, should not be treated with free-water restriction as this may increase the risk of stroke (see below).
  • - The hallmark of aneurysmal rupture is blood in the CSF.
  • More than 95% of cases have enough blood to be visualized on a high-quality noncontrast CT scan obtained within 72 h. The extent and location of subarachnoid blood on noncontrast CT scan help locate the underlying aneurysm, identify the cause of any neurologic deficit, and predict delayed vasospasm.
  • APPEAR AS BRIGHT SIGNAL IN THE FISSURES AND CSF CISTERNS AROUND THE BASE OF THE BRAIN- schwartz
  • APPEAR AS BRIGHT SIGNAL IN THE FISSURES AND CSF CISTERNS AROUND THE BASE OF THE BRAIN- schwartz
  • If the scan fails to establish the diagnosis of SAH and no mass lesion or obstructive hydrocephalus is found, a lumbar puncture should be performed to establish the presence of subarachnoid blood. Lysis of the red blood cells and subsequent conversion of hemoglobin to bilirubin stains the spinal fluid yellow within 6–12 h. This xanthochromic spinal fluid peaks in intensity at 48 h and lasts for 1–4 weeks, depending on the amount of subarachnoid blood. Negative CT and LP essentially rules out SAH-- schwartz Lumbar puncture prior to an imaging procedure is indicated only if a CT scan is not available at the time of the suspected SAH.
  • An LP with xanthochromia and high red blood cell counts (usually 100,000/mL), which do not decrease between tubes 1 and 4, is consistent with SAH.
  • Once the diagnosis of hemorrhage from a ruptured saccular aneurysm is suspected, four-vessel conventional x-ray angiography (both carotids and both vertebrals) is generally performed to localize and define the anatomic details of the aneurysm and to determine if other unruptured aneurysms exist (Fig. 275-8 C ). CT angiography is an alternative method for locating the aneurysm and may be sufficient to plan definitive therapy. ---- Catheter angiography remains the gold standard for assessing the patient's cerebral vasculature, relevant anomalies, and presence, location, and morphology of the cerebral aneurysms- schwartz Conventional x-ray cerebral angiography is the gold standard for identifying and quantifying atherosclerotic stenoses of the cerebral arteries and for identifying and characterizing other pathologies, including aneurysms, vasospasm, intraluminal thrombi, fibromuscular dysplasia, arteriovenous fistula, vasculitis, and collateral channels of blood flow
  • In conventional angiography, the blood vessels are imaged after opacification by contrast medium. In neuroradiology, arteries and veins which supply the brain, skull and spinal cord are examined. After local anaesthesia, the femoral artery is punctured in the groin and under x-ray control, a thin (usual diameter: 1.7 mm) catheter is advanced up into the carotid and/or vertebral arteries. This procedure is painless, but during the injection of contrast medium, the patient experiences a feeling of warmth in the body part supplied by the injected artery. The angiographic images are postprocessed immediately after exposure in a way that bones and other structures of high radiodensity masking the blood vessels are electronically subtracted from the angiograms (digital subtraction angiography). By a rotational technique, three-dimensional images can be computed which are used for planning of endovascular interventions. Being an interventional procedure, conventional angiography of the brain-supplying arteries carries a certain risk of neurologic complications as pareses or disturbances of vision or speech which even in experienced hands and with application of modern equipment and contrast media is in the range of 0.5%. Because of this and due to the rapid improvement of MRT- and CT-based angiographic techniques, indications for diagnostic angiographies are becoming rare. Nowadays, conventional angiography is mainly carried out in the context of an endovascular intervention as embolizations of vascular malformations (aneurysms, angiomas) or recanalization of a stenosed or occluded artery.
  • Early aneurysm repair prevents rerupture and allows the safe application of techniques to improve blood flow An aneurysm can be "clipped" by a neurosurgeon or "coiled" by an endovascular surgeon. Surgical repair involves placing a metal clip across the aneurysm neck, thereby immediately eliminating the risk of rebleeding. This approach requires craniotomy and brain retraction, which is associated with neurologic morbidity. Endovascular techniques involve placing platinum coils, or other embolic material, within the aneurysm via a catheter that is passed from the femoral artery. The aneurysm is packed tightly to enhance thrombosis and over time is walled off from the circulation (Fig. 275-8 D ).
  • . Volume expansion helps prevent hypotension, augments cardiac output, and reduces blood viscosity by reducing the hematocrit. This method is called "triple-H" (hypertension, hemodilution, and hypervolemic) therapy. Nimodipine 60mg PO every 4 hours for 3 weeks for vasospasm - Antifibrinolytic agents are not routinely prescribed but may be considered in patients in whom aneurysm treatment cannot proceed immediately  reduced incidence of aneurysmal rerupture but may also increase the risk of delayed cerebral infarction and deep-vein thrombosis (DVT).
  • Glucocorticoids May help reduce head and neck stiffness due to irritative effects of SAH Short term anticonvulsants For patients with documented seizure Acute hydrocephalus temporary ventricular drainage Chronic hyrdrocephalus ventricular shunting: treatment of choice Intra-arterial vasodilators and percutaneous transluminal angioplasty If symptomatic vasospasm persists despite optimal medical therapy
  • Sah

    1. 1. SUBARACHNOID HEMORRHAGESUBARACHNOID HEMORRHAGE PGI Mae Caridad R. Martinquilla Perpetual Succour Hospital
    2. 2. EPIDEMIOLOGY • 2% of adults harbor intracranial aneurysms • In 4 million persons in US, the aneurysm will rupture, producing SAH in 25,000–30,000 cases per year • Arrive at the hospital- mortality rate over the next month is about 45%
    3. 3. EPIDEMIOLOGY • Of those who survive- >1/2 are left with major neurologic deficits • Aneurysm is not obliterated- rate of rebleeding: – 20% in the first 2 weeks – 30% in the first month – 3% per year afterwards
    4. 4. PREVALENCE • Rupture of an aneurysm with clinically significant SAH – 5th decade – Women – >10mm in diameter 50% risk of bleeding - Robbins and Cotran Pathologic Basis of Diseases
    5. 5. ETIOLOGY Head trauma- the most common cause of SAH Rupture of saccular aneurysm -Harrison’s Principles Internal Medicine
    6. 6. ETIOLOGY Saccular (berry) aneurysm - most common type of intracranial aneurysm - Robbins and Cotran Pathologic Basis of Diseases
    7. 7. ETIOLOGY • 85% of aneurysms occur in the anterior circulation, mostly on the circle of Willis • The three most common locations of aneurysms: 1. Terminal internal carotid artery 2. Middle cerebral artery (MCA) bifurcation 3. Top of the basilar artery -Harrison’s Principles Internal Medicine
    8. 8. PATHOPHYSIOLOGY Saccular (Berry) Aneurysm • Bifurcations of the large- to medium-sized intracranial arteries • Rupture is into the subarachnoid space and into the parenchyma • Forms a neck with a dome -Harrison’s Principles Internal Medicine
    9. 9. PATHOPHYSIOLOGY • arterial internal elastic lamina disappears at the base of the neck • media thins & connective tissue replaces smooth- muscle cells • site of rupture dome -Harrison’s Principles Internal Medicine
    10. 10. ETIOLOGY • Other causes – Bleeding from a vascular malformation – Extension into the subarachnoid space from a primary intracerebral hemorrhage
    11. 11. CLINICAL PRESENTATION • Unruptured – asymptomatic • Ruptured – Transient loss of consciousness/ loss of consciousness for several days – Excruciating headache
    12. 12. CLINICAL MANIFESTATION • Headache – “worst headache of my life” – Sudden onset thunderclap; most important characteristic – Generalized – Often with vomiting and neck stiffness
    13. 13. CLINICAL MANIFESTATION • Sudden headache in the absence of focal neurologic symptoms  hallmark of aneurysmal rupture • Aneurysms can undergo small ruptures and leaks of blood into the subarachnoid spacesentinel bleeds
    14. 14. Fisher Scale (based on CT scan appearance of hemorrhage) Grade 1 No blood detected Grade 2 No layers of blood greater than 1mm Grade 3 Localized clots and/or vertical layers of blood 1mm or greater in thickness Grade 4 Diffuse or no subarachnoid blood, but intracerebral or intraverticular clot present
    15. 15. Delayed Neurologic Deficits 1. Rerupture 2. Hydrocephalus 3. Vasospasm 4. Hyponatremia
    16. 16. Delayed Neurologic Deficits 1. Rerupture – First month following the SAH (30%), peaks in the first 7 days – 60% mortality rate and poor outcome – Early treatment eliminates the risk
    17. 17. Delayed Neurologic Deficits 2. Hydrocephalus – Acute hydrocephalus • Stupor and coma – Subacute hyrocephalus • Progressive drowsiness and abulia with incontinence – Chronic hydrocephalus • Gait difficulty, incontinence and impaired mentation
    18. 18. Delayed Neurologic Deficits 3. Vasospasm – Narrowing of the arteries at the base of the brain after SAH symptomatic ischemia and infarction (30%) – Major cause of delayed morbidity and death – Appear 4-14 days after the hemorrhage, most often at 7 days
    19. 19. Delayed Neurologic Deficits 3. Vasospasm – Effects of clotted blood and its breakdown products  more blood that surrounds the arteries, the greater the chance of symptomatic vasospasm
    20. 20. Delayed Neurologic Deficits 4. Hyponatremia – Develop quickly in the first 2 weeks following SAH – Natriuresis and volume depletion hyponatremic and hypovolemic – “Cerebral salt-wasting syndrome" – Clears over the course of 1–2 weeks
    21. 21. DIFFERENTIAL DIAGNOSIS • Intracerebral hemorrhage • Migraine headache • Brain tumors • Meningitis • Subdural and epidural hematoma
    22. 22. DIFFERENTIAL DIAGNOSIS Intracerebral Hemorrhage • Most common type of Intracranial hemorrhage • Abrupt onset of neurologic deficit – Vomiting – Headache • Putamen- most common site of hypertensive hemorrhage
    23. 23. DIFFERENTIAL DIAGNOSIS Migraine Headache • Second most common cause of headache • 15% of women and 6% of men • Episodic headache associated with certain features such as sensitivity to light, sound, or movement • Nausea and vomiting often accompany the headache
    24. 24. DIFFERENTIAL DIAGNOSIS Brain Tumor • 30% of patients with brain tumors consider headache to be their chief complaint • Classic headache- most evident in the morning and improves during the day • accompanied by nausea or vomiting when ICP increases
    25. 25. DIFFERENTIAL DIAGNOSIS Meningitis • Classic clinical triad of meningitis fever, headache, and nuchal rigidity • Signs of meningeal irritation – Nuchal rigidity ("stiff neck") -pathognomonic sign of meningeal irritation – Kernig's sign – Brudzinski's signs
    26. 26. Epidural hematoma Subdural hematoma Location Between the skull and the dura Between dura and subarachnoid layers Symmetry Usu. unilateral Usu. Bilateral Etiology Rupture of dural veins or middle meningeal artery Rupture of cortical bridging veins Typical injury Direct trauma Direct trauma or shaking Consciousness Impaired-lucid-impaired/ Lucid interval Intact but altered Common associated findings Ipsilateral pupillary dilatation, contralateral hemoparesis Seizures, retinal hemorrhages CT scan Biconcave Cresentic Prognosis Low morbidity, high mortality High morbidity, high mortality Complications Skull fracture, uncal herniation Herniation
    27. 27. DIAGNOSTICS • Blood in the CSF hallmark of aneurysmal rupture • Noncontrast CT scan • Lumbar puncture • Four-vessel conventional x-ray angiography
    28. 28. DIAGNOSTICS Noncontrast CT scan • Rapid, noninvasive, and approx. 95% sensitive Locate the underlying aneurysm Identify the cause of any neurologic deficit Predict delayed vasospasm
    29. 29. DIAGNOSTICS Lumbar puncture • If scan fails to establish SAH and no mass lesion or obstructive hydrocephalus is found • Xanthochromic spinal fluid peaks in intensity at 48 hours and lasts for 1-4 weeks • Negative CT and LP essentially rules out SAH (Schwartz)
    30. 30. DIAGNOSTICS Four-vessel conventional X-ray angiography Localize and define the anatomic details of the aneurysm Determine if other unruptured aneurysms exist • Gold standard
    31. 31. TREATMENT Surgical repair • "clipped" by a neurosurgeon • "coiled" by an endovascular surgeon • Endovascular technique • placing platinum coils, or other embolic material
    32. 32. TREATMENT Medical management • Correction of increased ICP while maintaining adequate cerebral perfusion pressure (60-70mmHg) • Correction of hyponatremia and maintenance of euglycemia and euvolemia • BP management – IV Nicardipine to maintain SBP <150
    33. 33. TREATMENT • “Triple H” therapy – hypertension, hemodilution, and hypervolemic • Nimodipine 60mg PO every 4 hours for 3 weeks for vasospasm • Antifibrinolytic agents
    34. 34. TREATMENT • Glucocorticoids • Short term anticonvulsants • Temporary ventricular drainage and ventricular shunting • Intra-arterial vasodilators and percutaneous transluminal angioplasty
    35. 35. End

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