Subarachnoid Hemorrhage
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Subarachnoid Hemorrhage Dr.B.Ga n g a d h a r
Subarachnoid Hemorrhage Excluding head trauma, the most common cause of SAH is rupture of a saccular aneurysm. Other causes include bleeding from a vascular malformation (AV malformation or dural AV fistula) and primary intracerebral hemorrhage extension into the SA space. Idiopathic SAHs are localized to the perimesencephalic cisterns and o are benign o they probably have a venous or capillary source, and o angiography is unrevealing.
Saccular ("Berry") Aneurysm
2% of adults harbor intracranial aneurysms
The aneurysm will rupture, producing SAH, in 25,000–30,000 cases per year in USA.
Unruptured, asymptomatic aneurysms are much less dangerous than a recently ruptured aneurysm.
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%.
Saccular ("Berry") Aneurysm
90 to 95 percent of SAs lie on the anterior part of COW.
The most common sites are (1) the proximal portions of the ACoA, (2) at the origin of the PCoA from the stem of the IC, (3) at the first major bifurcation of the MCA, and (4) at the bifurcation of the IC into MCA & ACA.
Saccular ("Berry") Aneurysm
Giant aneurysms( >2.5 cm) -5% of cases. o Most common locations are the terminal internal carotid artery, MCA bifurcation, and top of the basilar artery. o Their risk of rupture is ~6% in 1ST year after identification and may remain high indefinitely. o They often cause symptoms by compressing the adjacent brain or cranial nerves.
Mycotic aneurysms – o usually located distal to the 1ST bifurcation of major arteries of COW. o Most result from infected emboli due to bacterial endocarditis causing septic degeneration of arteries and subsequent dilatation and rupture.
Pathophysiology Saccular aneurysms occur at the bifurcations of the large to medium-sized intracranial arteries; Rupture is into the subarachnoid space in the basal cisterns and often 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. Aneurysm size and site are important in predicting risk of rupture. o Those >7 mm in diameter and those at the top of BA and at the origin of PCoA are at greater risk of rupture.
Clinical Manifestations Ø Most unruptured intracranial aneurysms - asymptomatic
Ø Symptoms are usually due to rupture and resultant SAH, although some present with mass effect on cranial nerves or brain parenchyma.
Ø At the moment of aneurysmalrupture with major SAH, the ICP suddenly rises. This may account for the sudden transient LOC that occurs in nearly half of patients.
Ø Sudden LOC may be preceded by a brief moment of excruciating headache, but most patients first complain of headache upon regaining consciousness. Ø
Clinical Manifestations § In 10% of cases, aneurysmal bleeding is severe enough to cause loss of consciousness for several days. § § 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“
The most important characteristic is sudden onset
The headache is usually generalized, often with neck stiffness, and vomiting is common. focal neurologic deficits may occur.
Clinical Manifestations
ACA or MCA bifurcation aneurysms may rupture and form a hematoma large enough to produce mass effect. The common deficits that result include hemiparesis, aphasia, and abulia.
Occasionally, prodromal symptoms suggest the location of a progressively enlarging unruptured aneurysm.
A 3RD cranial nerve palsy may occur with an expanding aneurysm at the junction of the PCoA and the ICA.
A 6th nerve palsy may indicate an aneurysm in the cavernous sinus, and
visual field defects can occur with an expanding supraclinoid carotid or anterior cerebral artery aneurysm
Clinical Manifestations
Occipital and posterior cervical pain may signal a PICA or AICA aneurysm.
Pain in or behind the eye and in the low temple can occur with an expanding MCA aneurysm.
Aneurysms can undergo small ruptures and leaks of blood into the subarachnoid space, so-called sentinel bleeds.
Sudden unexplained headache at any location should raise suspicion of SAH and be investigated, because a major hemorrhage may be imminent
Grading Scales for SAH
Hunt-Hess Scale
o 1
Mild headache, normal mental status, no cranial nerve or motor findings
o 2
Severe headache, normal mental status, may have cranial nerve deficit
o 3
Somnolent, confused, may have cranial nerve or mild motor deficit
o 4 Stupor, moderate to severe motor deficit, may have intermittent reflex posturing
World Federation of Neurosurgical Societies (WFNS) Scale
o 1
Glasgow Coma Scalea (GCS) score 15, no motor deficits
o 2
GCS 13–14, no motor deficits
o 3
GCS 13–14, with motor deficits
o 4
GCS 7–12, with or without motor deficits
o 5 o
GCS 3–6, with or without motor deficits
Delayed Neurologic Deficits 4 major causes of delayed neurologic deficits: ü rerupture, ü hydrocephalus, ü vasospasm, and ü Hyponatremia
v Rerupture
The incidence of rerupture of an untreated aneurysm in the 1st month following SAH is ~30%, with the peak in the first 7 days. Rerupture is associated with a 60% mortality and poor outcome. Early treatment eliminates this risk
Delayed Neurologic Deficits v Hydrocephalus
Acute hydrocephalus can cause stupor and coma Subacute hydrocephalus may develop over a few days or weeks and causes progressive drowsiness or slowed mentation (abulia) with incontinence. Hydrocephalus is differentiated from cerebral vasospasm with a CT scan, CT angiogram, transcranial Doppler (TCD) ultrasound, or conventional x-ray angiography. Hydrocephalus may clear spontaneously or require temporary ventricular drainage. Chronic hydrocephalus may develop weeks to months after SAH and manifest as gait difficulty, incontinence, or impaired mentation
Delayed Neurologic Deficits v Vasospasm
Narrowing of the arteries at the base of the brain following SAH causes symptomatic ischemia and infarction in ~30% of patients 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.
Delayed Neurologic Deficits
Vasospasm can be detected reliably with conventional x-ray angiography( invasive ,expensive and carries the risk of stroke).
TCD ultrasound on a daily or every-other-day basis, vasospasm can be reliably detected.
CT angiography is another method that can detect vasospasm.
Severe cerebral edema in patients with infarction from vasospasm may increase the ICP enough to reduce cerebral perfusion pressure.
Delayed Neurologic Deficits v 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 ANP and BNP have a role in producing this "cerebral saltwasting 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
Laboratory Evaluation and Imaging
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. 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. Lumbar puncture prior to an imaging procedure is indicated only if a CT scan is not available at the time of the suspected SAH. spinal fluid stained to yellow within 6–12 h, peaks in intensity at 48 h and lasts for 1–4 weeks, depending on the amount of subarachnoid blood. Sr .electrolytes- daily or twice daily ECG
IMAGING FINDINGS
General Features • Best diagnostic clue: Hyperdense CSF on NECT • Location: Interhemispheric SAH suggests ACoA aneurysm, sylvian correlates with MCA CT Findings • NECT: 95% positive in first 24 h, < 50% by 1 week • CTA: Multislice CTA 90-95% + for aneurysm > 2 mm MR Findings • T1WI: "Dirty" CSF (isointense to brain) • T2WI: Hyperintense CSF • FLAIR: Hyperintense (not pathognomonic for SAH) • T2* GRE: Hypointense hemosiderin deposition in 70-75% of patients with prior SAH • DWI: May show multifocal restrictions • MRA: 85-95% sensitive
IMAGING FINDINGS
Angiographic Findings • Conventional o Negative in 15-20% of aSAHi , repeat positive < 5% o Considered "gold standard“
Imaging Recommendations • Best imaging tool: NECT + multi slice CTA • Protocol advice: Thin slices, low pitch, arterial phase only
Anterior communicating artery aneurysm rupture
SAH due to rupture of a basilar artery aneurysm
Axial TlWI MR
Axial FLAIR MR
IMAGING FINDINGS
DIFFERENTIAL DIAGNOSIS Nonaneurysmal SAH • Occult trauma, dissection • Perimesencephalic nonaneurysmal SAH • Vascular malformation, neoplasm (e.g., ependymoma) "PseudoSAH" • Low density brain (e.g., with diffuse cerebral edema) • High density CSF (e.g., following intrathecal contrast) NonSAH causes of high CSF signal on FLAIR • Meningitis (inflammatory, neoplastic ) • High oxygen tension or gadolinium in CSF
NONANEURYSMAL PERIMESENCEPHALIC SAH
Clinically benign entity with SAH confined to perimesencephalic , prepontine cisterns No identifiable source demonstrated at angiography
IMAGING FINDINGS General Features • Best diagnostic clue: Hyperdense prepontine, perimesencephalic CSF • Location: "Pretruncal" (anterior to pons, around midbrain) • CTA/MRA/DSA o Angiography negative in 90-95% of pnSAH o 5-10% prevalence of vertebrobasilar aneurysm in pnSAH
NONANEURYSMAL PERIMESENCEPHALIC SAH CT Findings • NECT o High attenuation anterior to midbrain, in ambient cisterns o No extension into distal sylvian, interhemispheric fissures • CTA: Posterior circulation aneurysm in 5-10%
MR Findings • T1WI: "Dirty" CSF (iso-, not hypo intense) • T2WI: Acute pnSAH -hyperintense (difficult to see) • FLAIR: Hyperintense CSF in/around pons, midbrain • T2* GRE: Hypointense
NONANEURYSMAL PERIMESENCEPHALIC SAH Angiographic Findings • Conventional o Considered "gold standard" o Saccular or blister-like aneurysm identified as cause of pnSAH in 5-10% o Vasospasm, hydrocephalus rare « < aSAH) Imaging Recommendations • Best imaging tool: NECT scan = best screening for pnSAH • Protocol advice: If NECT scan positive, CTA +/- DSA DIFFERENTIAL DIAGNOSIS Aneurysmal SAH (aSAH) Traumatic SAH (tSAH) Meningitis Artifact
Axial graphic shows classic pnSAH. Hemorrhage is confined to the interpeduncular fossa and ambient (perimensencephalic) cisterns (arrows). Source is usually venous.
NONANEURYSMAL PERIMESENCEPHALIC SAH Axial TlWI MR shows "dirty" CSF in angio-negative pnSAH
Axial NECT
SUPERFICIAL SIDEROSIS
Recurrent SAH causes hemosiderin deposition on surface of brain, brain stem & cranial nerve leptomeninges. IMAGING FINDINGS General Features • Best diagnostic clue: Contours of brain & cranial nerves outlined by hypointense rim on T2 or T2* GRE MRimages • Location: Cerebral hemispheres, cerebellum, brainstem, cranial nerves & spinal cord may all be affected • Size: Linear low signal along CNS surfaces varies in thickness but usually <2 mm CT Findings • NECT o Cerebral & cerebellar atrophy
SUPERFICIAL SIDEROSIS
o Especially marked in posterior fossa • Cerebellar sulci often disproportionately large o Slightly hyperdense rim over brain surface CECT: No enhancement typical
MR Findings • T1WI: Hyperintense signal may be seen on CNS surfaces • T2WI o High-resolution, thin section T2 MR of CPA-lAC • Cranial nerves 7 & 8 appear darker & thicker than normal • Adjacent cerebellar structures & brain stem show low signal surfaces • Less easily seen than on T2* GRE images
SUPERFICIAL SIDEROSIS
FLAIR: Dark border on local surface of brain , brain stem, cerebellum & cranial nerves
T2* GRE o Most sensitive to hemosiderin deposition on CNS surfaces MR findings do not correlate with severity of disease Imaging Recommendations Best imaging tool o Brain MR • Once diagnosis of superficial siderosis is made, search for cause of recurrent SAH must commence • Whole brain MR with contrast & MRA first • Total spine MR second if brain negative for underlying lesion
S UP ERFICIAL S ID EROS IS
Axial graphic shows darker brown hemosiderin staining on all surfaces of the brain, meninges and cranial nerves.
S UP ERFICIAL S ID EROS IS
Axial T2* GRE MR reveals superficial siderosis as dark hemosiderin staining in folia of cerebellum (arrows). In addition, the 7th & 8th cranial nerves in the CPA-lAC are black (open arrows)
S UP ERFICIAL S ID EROS IS
Axial T2* GRE MR in patient with ataxia and bilateral SNHL shows intense hemosiderin staining of the surface of the cerebellum as hypointense, blooming stripes (arrows).
S UP ERFICIAL S ID EROS IS
Coronal T2* GRE MR in patient with superficial siderosis shows low signal along all dural and cerebellar surfaces in the posterior fossa (arrows).
S UP ERFICIAL S ID EROS IS
Axial T2WI MR reveals juvenile pilocytic astrocytoma (arrow) causing chronic SAH yielding superficial siderosis of adjacent brain surfaces
SUPERFICIAL SIDEROSIS
DIFFERENTIAL DIAGNOSIS MR sequence artifact Brain surface vessels Neurocutaneous melanosis Meningioangiomatosis (MA)
SACCULAR ANEURYSM IMAGING FINDINGS Ruptured SAs have high density blood in basal cisterns, sulci Multi-slice CTA positive in 95% of patients with aSAH 50% have "flow void" on T1WI Typically hypointense on T2WI Best imaging tool: NECT for aSAH + multislice CTA DIFFERENTIAL DIAGNOSIS Vessel loop Infundibulum < 3 mm, conical, small PCoA arises directly from apex Pseudoaneurysm -Often arises distal to COW "Flow void" mimic on MR -Aerated anterior clinoid or supraorbital cell Short T1 on MRA- Lipoma Pituitary gland (contrast-enhanced MRA)
Saccular aneurysm at the ICA bifurcation.
Axial T2WI MR "flow void" adjacent to COW
DSA of the right ICA
DDx: Saccular Intracranial Aneurysm
Treatment
The medical management of SAH focuses on protecting the airway, managing BP before and after aneurysm treatment, preventing rebleeding prior to treatment, managing vasospasm, treating hydrocephalus, treating hyponatremia, and preventing pulmonary embolus.
Treatment Intracranial hypertension Pts who are stuporous should undergo emergent ventriculostomy to measure ICP and to treat high ICP in order to prevent cerebral ischemia. Medical therapies- mild hyperventilation, mannitol , and sedation High ICP refractory to treatment is a poor prognostic sign Care is required to maintain adequate cerebral perfusion pressure while avoiding excessive elevation of arterial pressure. If the patient is alert, it is reasonable to lower the BP to normal using nicardipine, labetolol, or esmolol. If the patient has a depressed level of consciousness, ICP should be measured and the cerebral perfusion pressure targeted to 60–70 mmHg
Treatment Preventing Rebleeding Bed rest in a quiet room and Stool softeners to prevent straining. If headache or neck pain is severe, mild sedation and analgesia are prescribed. Extreme sedation is avoided because it can obscure changes in neurologic status. Adequate hydration is necessary to avoid a decrease in blood volume predisposing to brain ischemia Phenytoin is often given as prophylactic therapy since a seizure may promote rebleeding.
Treatment
Glucocorticoids may help reduce the head and neck ache caused by the irritativeeffect of the subarachnoid blood. Their routine use is not recommended.
Antifibrinolytic agents are not routinely prescribed but may be considered in patients in whom aneurysm treatment cannot proceed immediately. They are associated with a reduced incidence of aneurysmal rerupture but may also increase the risk of delayed cerebral infarction and DVT
Vasospasm
Nimodipine (60 mg PO every 4 h) improves outcome, perhaps by preventing ischemic injury rather than reducing the risk of vasospasm.
Symptomatic cerebral vasospasm -also treated by increasing CPP by raising MAP through plasma volume expansion and the judicious use of IV vasopressor agents, usually phenylephrine or norepinephrine.
Volume expansion helps prevent hypotension, augments cardiac output, and reduces blood viscosity by reducing the hematocrit. This method is called "triple-H" therapy(hypertension, hemodilution, and hypervolemic).
Vasospasm
Intraarterial vasodilators and PTA are considered If symptomatic vasospasm persists despite optimal medical therapy Vasodilatation by direct angioplasty appears to be permanent, allowing triple-H therapy to be tapered sooner Intraarterial papaverine (neurotoxic ) should be reserved for refractory cases Free-water restriction is contraindicated in patients with SAH at risk for vasospasm because hypovolemia and hypotension may occur and precipitate cerebral ischemia
Treatment Acute hydrocephalus can cause stupor or coma. It may clear spontaneously or require temporary ventricular drainage. When chronic hydrocephalus develops, ventricular shunting is the treatment of choice.
Hyponatremia parenteral fluids containing normal saline. Frequently, oral salt supplementation coupled with normal saline will mitigate hyponatremia, but often patients also require hypertonic saline. Care must be taken not to correct serum sodium too quickly
Treatment Prevention of pulmonary embolism
pneumatic compression stockings.
Unfractionated heparin S/C for DVT prophylaxis can be initiated immediately following endovascular treatment and within days following craniotomy and surgical clipping.
Systemic anticoagulation with heparin is contraindicated in patients with ruptured and untreated aneurysms. It is a relative contraindication following craniotomy.
Following craniotomy, use of IVC filters is preferred to prevent further pulmonary emboli, while systemic anticoagulation with heparin is preferred following successful endovascular treatment.
Early aneurysm repair
Prevents rerupture and allows the safe application of techniques to improve blood flow (e.g., induced hypertension and hypervolemia) should symptomatic vasospasm develop. 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.
Refernces: Harrison's principles of internal medicine,17th e Diagnostic imaging: Brain by Anne 0. Osborn Adams & Victors' Principles of Neurology, 8th Edition
THANK YOU
Subarachnoid Hemorrhage Excluding head trauma, the most common cause of SAH is rupture of a saccular aneurysm. Other causes include bleeding from a vascular malformation (AV malformation or dural AV fistula) and primary intracerebral hemorrhage extension into the SA space. Idiopathic SAHs are localized to the perimesencephalic cisterns and o are benign o they probably have a venous or capillary source, and o angiography is unrevealing.
Saccular ("Berry") Aneurysm
2% of adults harbor intracranial aneurysms
The aneurysm will rupture, producing SAH, in 25,000–30,000 cases per year in USA.
Unruptured, asymptomatic aneurysms are much less dangerous than a recently ruptured aneurysm.
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%.
Saccular ("Berry") Aneurysm
90 to 95 percent of SAs lie on the anterior part of COW.
The most common sites are (1) the proximal portions of the ACoA, (2) at the origin of the PCoA from the stem of the IC, (3) at the first major bifurcation of the MCA, and (4) at the bifurcation of the IC into MCA & ACA.
Saccular ("Berry") Aneurysm
Giant aneurysms( >2.5 cm) -5% of cases. o Most common locations are the terminal internal carotid artery, MCA bifurcation, and top of the basilar artery. o Their risk of rupture is ~6% in 1ST year after identification and may remain high indefinitely. o They often cause symptoms by compressing the adjacent brain or cranial nerves.
Mycotic aneurysms – o usually located distal to the 1ST bifurcation of major arteries of COW. o Most result from infected emboli due to bacterial endocarditis causing septic degeneration of arteries and subsequent dilatation and rupture.
Pathophysiology Saccular aneurysms occur at the bifurcations of the large to medium-sized intracranial arteries; Rupture is into the subarachnoid space in the basal cisterns and often 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. Aneurysm size and site are important in predicting risk of rupture. o Those >7 mm in diameter and those at the top of BA and at the origin of PCoA are at greater risk of rupture.
Clinical Manifestations Ø Most unruptured intracranial aneurysms - asymptomatic
Ø Symptoms are usually due to rupture and resultant SAH, although some present with mass effect on cranial nerves or brain parenchyma.
Ø At the moment of aneurysmalrupture with major SAH, the ICP suddenly rises. This may account for the sudden transient LOC that occurs in nearly half of patients.
Ø Sudden LOC may be preceded by a brief moment of excruciating headache, but most patients first complain of headache upon regaining consciousness. Ø
Clinical Manifestations § In 10% of cases, aneurysmal bleeding is severe enough to cause loss of consciousness for several days. § § 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“
The most important characteristic is sudden onset
The headache is usually generalized, often with neck stiffness, and vomiting is common. focal neurologic deficits may occur.
Clinical Manifestations
ACA or MCA bifurcation aneurysms may rupture and form a hematoma large enough to produce mass effect. The common deficits that result include hemiparesis, aphasia, and abulia.
Occasionally, prodromal symptoms suggest the location of a progressively enlarging unruptured aneurysm.
A 3RD cranial nerve palsy may occur with an expanding aneurysm at the junction of the PCoA and the ICA.
A 6th nerve palsy may indicate an aneurysm in the cavernous sinus, and
visual field defects can occur with an expanding supraclinoid carotid or anterior cerebral artery aneurysm
Clinical Manifestations
Occipital and posterior cervical pain may signal a PICA or AICA aneurysm.
Pain in or behind the eye and in the low temple can occur with an expanding MCA aneurysm.
Aneurysms can undergo small ruptures and leaks of blood into the subarachnoid space, so-called sentinel bleeds.
Sudden unexplained headache at any location should raise suspicion of SAH and be investigated, because a major hemorrhage may be imminent
Grading Scales for SAH
Hunt-Hess Scale
o 1
Mild headache, normal mental status, no cranial nerve or motor findings
o 2
Severe headache, normal mental status, may have cranial nerve deficit
o 3
Somnolent, confused, may have cranial nerve or mild motor deficit
o 4 Stupor, moderate to severe motor deficit, may have intermittent reflex posturing
World Federation of Neurosurgical Societies (WFNS) Scale
o 1
Glasgow Coma Scalea (GCS) score 15, no motor deficits
o 2
GCS 13–14, no motor deficits
o 3
GCS 13–14, with motor deficits
o 4
GCS 7–12, with or without motor deficits
o 5 o
GCS 3–6, with or without motor deficits
Delayed Neurologic Deficits 4 major causes of delayed neurologic deficits: ü rerupture, ü hydrocephalus, ü vasospasm, and ü Hyponatremia
v Rerupture
The incidence of rerupture of an untreated aneurysm in the 1st month following SAH is ~30%, with the peak in the first 7 days. Rerupture is associated with a 60% mortality and poor outcome. Early treatment eliminates this risk
Delayed Neurologic Deficits v Hydrocephalus
Acute hydrocephalus can cause stupor and coma Subacute hydrocephalus may develop over a few days or weeks and causes progressive drowsiness or slowed mentation (abulia) with incontinence. Hydrocephalus is differentiated from cerebral vasospasm with a CT scan, CT angiogram, transcranial Doppler (TCD) ultrasound, or conventional x-ray angiography. Hydrocephalus may clear spontaneously or require temporary ventricular drainage. Chronic hydrocephalus may develop weeks to months after SAH and manifest as gait difficulty, incontinence, or impaired mentation
Delayed Neurologic Deficits v Vasospasm
Narrowing of the arteries at the base of the brain following SAH causes symptomatic ischemia and infarction in ~30% of patients 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.
Delayed Neurologic Deficits
Vasospasm can be detected reliably with conventional x-ray angiography( invasive ,expensive and carries the risk of stroke).
TCD ultrasound on a daily or every-other-day basis, vasospasm can be reliably detected.
CT angiography is another method that can detect vasospasm.
Severe cerebral edema in patients with infarction from vasospasm may increase the ICP enough to reduce cerebral perfusion pressure.
Delayed Neurologic Deficits v 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 ANP and BNP have a role in producing this "cerebral saltwasting 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
Laboratory Evaluation and Imaging
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. 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. Lumbar puncture prior to an imaging procedure is indicated only if a CT scan is not available at the time of the suspected SAH. spinal fluid stained to yellow within 6–12 h, peaks in intensity at 48 h and lasts for 1–4 weeks, depending on the amount of subarachnoid blood. Sr .electrolytes- daily or twice daily ECG
IMAGING FINDINGS
General Features • Best diagnostic clue: Hyperdense CSF on NECT • Location: Interhemispheric SAH suggests ACoA aneurysm, sylvian correlates with MCA CT Findings • NECT: 95% positive in first 24 h, < 50% by 1 week • CTA: Multislice CTA 90-95% + for aneurysm > 2 mm MR Findings • T1WI: "Dirty" CSF (isointense to brain) • T2WI: Hyperintense CSF • FLAIR: Hyperintense (not pathognomonic for SAH) • T2* GRE: Hypointense hemosiderin deposition in 70-75% of patients with prior SAH • DWI: May show multifocal restrictions • MRA: 85-95% sensitive
IMAGING FINDINGS
Angiographic Findings • Conventional o Negative in 15-20% of aSAHi , repeat positive < 5% o Considered "gold standard“
Imaging Recommendations • Best imaging tool: NECT + multi slice CTA • Protocol advice: Thin slices, low pitch, arterial phase only
Anterior communicating artery aneurysm rupture
SAH due to rupture of a basilar artery aneurysm
Axial TlWI MR
Axial FLAIR MR
IMAGING FINDINGS
DIFFERENTIAL DIAGNOSIS Nonaneurysmal SAH • Occult trauma, dissection • Perimesencephalic nonaneurysmal SAH • Vascular malformation, neoplasm (e.g., ependymoma) "PseudoSAH" • Low density brain (e.g., with diffuse cerebral edema) • High density CSF (e.g., following intrathecal contrast) NonSAH causes of high CSF signal on FLAIR • Meningitis (inflammatory, neoplastic ) • High oxygen tension or gadolinium in CSF
NONANEURYSMAL PERIMESENCEPHALIC SAH
Clinically benign entity with SAH confined to perimesencephalic , prepontine cisterns No identifiable source demonstrated at angiography
IMAGING FINDINGS General Features • Best diagnostic clue: Hyperdense prepontine, perimesencephalic CSF • Location: "Pretruncal" (anterior to pons, around midbrain) • CTA/MRA/DSA o Angiography negative in 90-95% of pnSAH o 5-10% prevalence of vertebrobasilar aneurysm in pnSAH
NONANEURYSMAL PERIMESENCEPHALIC SAH CT Findings • NECT o High attenuation anterior to midbrain, in ambient cisterns o No extension into distal sylvian, interhemispheric fissures • CTA: Posterior circulation aneurysm in 5-10%
MR Findings • T1WI: "Dirty" CSF (iso-, not hypo intense) • T2WI: Acute pnSAH -hyperintense (difficult to see) • FLAIR: Hyperintense CSF in/around pons, midbrain • T2* GRE: Hypointense
NONANEURYSMAL PERIMESENCEPHALIC SAH Angiographic Findings • Conventional o Considered "gold standard" o Saccular or blister-like aneurysm identified as cause of pnSAH in 5-10% o Vasospasm, hydrocephalus rare « < aSAH) Imaging Recommendations • Best imaging tool: NECT scan = best screening for pnSAH • Protocol advice: If NECT scan positive, CTA +/- DSA DIFFERENTIAL DIAGNOSIS Aneurysmal SAH (aSAH) Traumatic SAH (tSAH) Meningitis Artifact
Axial graphic shows classic pnSAH. Hemorrhage is confined to the interpeduncular fossa and ambient (perimensencephalic) cisterns (arrows). Source is usually venous.
NONANEURYSMAL PERIMESENCEPHALIC SAH Axial TlWI MR shows "dirty" CSF in angio-negative pnSAH
Axial NECT
SUPERFICIAL SIDEROSIS
Recurrent SAH causes hemosiderin deposition on surface of brain, brain stem & cranial nerve leptomeninges. IMAGING FINDINGS General Features • Best diagnostic clue: Contours of brain & cranial nerves outlined by hypointense rim on T2 or T2* GRE MRimages • Location: Cerebral hemispheres, cerebellum, brainstem, cranial nerves & spinal cord may all be affected • Size: Linear low signal along CNS surfaces varies in thickness but usually <2 mm CT Findings • NECT o Cerebral & cerebellar atrophy
SUPERFICIAL SIDEROSIS
o Especially marked in posterior fossa • Cerebellar sulci often disproportionately large o Slightly hyperdense rim over brain surface CECT: No enhancement typical
MR Findings • T1WI: Hyperintense signal may be seen on CNS surfaces • T2WI o High-resolution, thin section T2 MR of CPA-lAC • Cranial nerves 7 & 8 appear darker & thicker than normal • Adjacent cerebellar structures & brain stem show low signal surfaces • Less easily seen than on T2* GRE images
SUPERFICIAL SIDEROSIS
FLAIR: Dark border on local surface of brain , brain stem, cerebellum & cranial nerves
T2* GRE o Most sensitive to hemosiderin deposition on CNS surfaces MR findings do not correlate with severity of disease Imaging Recommendations Best imaging tool o Brain MR • Once diagnosis of superficial siderosis is made, search for cause of recurrent SAH must commence • Whole brain MR with contrast & MRA first • Total spine MR second if brain negative for underlying lesion
S UP ERFICIAL S ID EROS IS
Axial graphic shows darker brown hemosiderin staining on all surfaces of the brain, meninges and cranial nerves.
S UP ERFICIAL S ID EROS IS
Axial T2* GRE MR reveals superficial siderosis as dark hemosiderin staining in folia of cerebellum (arrows). In addition, the 7th & 8th cranial nerves in the CPA-lAC are black (open arrows)
S UP ERFICIAL S ID EROS IS
Axial T2* GRE MR in patient with ataxia and bilateral SNHL shows intense hemosiderin staining of the surface of the cerebellum as hypointense, blooming stripes (arrows).
S UP ERFICIAL S ID EROS IS
Coronal T2* GRE MR in patient with superficial siderosis shows low signal along all dural and cerebellar surfaces in the posterior fossa (arrows).
S UP ERFICIAL S ID EROS IS
Axial T2WI MR reveals juvenile pilocytic astrocytoma (arrow) causing chronic SAH yielding superficial siderosis of adjacent brain surfaces
SUPERFICIAL SIDEROSIS
DIFFERENTIAL DIAGNOSIS MR sequence artifact Brain surface vessels Neurocutaneous melanosis Meningioangiomatosis (MA)
SACCULAR ANEURYSM IMAGING FINDINGS Ruptured SAs have high density blood in basal cisterns, sulci Multi-slice CTA positive in 95% of patients with aSAH 50% have "flow void" on T1WI Typically hypointense on T2WI Best imaging tool: NECT for aSAH + multislice CTA DIFFERENTIAL DIAGNOSIS Vessel loop Infundibulum < 3 mm, conical, small PCoA arises directly from apex Pseudoaneurysm -Often arises distal to COW "Flow void" mimic on MR -Aerated anterior clinoid or supraorbital cell Short T1 on MRA- Lipoma Pituitary gland (contrast-enhanced MRA)
Saccular aneurysm at the ICA bifurcation.
Axial T2WI MR "flow void" adjacent to COW
DSA of the right ICA
DDx: Saccular Intracranial Aneurysm
Treatment
The medical management of SAH focuses on protecting the airway, managing BP before and after aneurysm treatment, preventing rebleeding prior to treatment, managing vasospasm, treating hydrocephalus, treating hyponatremia, and preventing pulmonary embolus.
Treatment Intracranial hypertension Pts who are stuporous should undergo emergent ventriculostomy to measure ICP and to treat high ICP in order to prevent cerebral ischemia. Medical therapies- mild hyperventilation, mannitol , and sedation High ICP refractory to treatment is a poor prognostic sign Care is required to maintain adequate cerebral perfusion pressure while avoiding excessive elevation of arterial pressure. If the patient is alert, it is reasonable to lower the BP to normal using nicardipine, labetolol, or esmolol. If the patient has a depressed level of consciousness, ICP should be measured and the cerebral perfusion pressure targeted to 60–70 mmHg
Treatment Preventing Rebleeding Bed rest in a quiet room and Stool softeners to prevent straining. If headache or neck pain is severe, mild sedation and analgesia are prescribed. Extreme sedation is avoided because it can obscure changes in neurologic status. Adequate hydration is necessary to avoid a decrease in blood volume predisposing to brain ischemia Phenytoin is often given as prophylactic therapy since a seizure may promote rebleeding.
Treatment
Glucocorticoids may help reduce the head and neck ache caused by the irritativeeffect of the subarachnoid blood. Their routine use is not recommended.
Antifibrinolytic agents are not routinely prescribed but may be considered in patients in whom aneurysm treatment cannot proceed immediately. They are associated with a reduced incidence of aneurysmal rerupture but may also increase the risk of delayed cerebral infarction and DVT
Vasospasm
Nimodipine (60 mg PO every 4 h) improves outcome, perhaps by preventing ischemic injury rather than reducing the risk of vasospasm.
Symptomatic cerebral vasospasm -also treated by increasing CPP by raising MAP through plasma volume expansion and the judicious use of IV vasopressor agents, usually phenylephrine or norepinephrine.
Volume expansion helps prevent hypotension, augments cardiac output, and reduces blood viscosity by reducing the hematocrit. This method is called "triple-H" therapy(hypertension, hemodilution, and hypervolemic).
Vasospasm
Intraarterial vasodilators and PTA are considered If symptomatic vasospasm persists despite optimal medical therapy Vasodilatation by direct angioplasty appears to be permanent, allowing triple-H therapy to be tapered sooner Intraarterial papaverine (neurotoxic ) should be reserved for refractory cases Free-water restriction is contraindicated in patients with SAH at risk for vasospasm because hypovolemia and hypotension may occur and precipitate cerebral ischemia
Treatment Acute hydrocephalus can cause stupor or coma. It may clear spontaneously or require temporary ventricular drainage. When chronic hydrocephalus develops, ventricular shunting is the treatment of choice.
Hyponatremia parenteral fluids containing normal saline. Frequently, oral salt supplementation coupled with normal saline will mitigate hyponatremia, but often patients also require hypertonic saline. Care must be taken not to correct serum sodium too quickly
Treatment Prevention of pulmonary embolism
pneumatic compression stockings.
Unfractionated heparin S/C for DVT prophylaxis can be initiated immediately following endovascular treatment and within days following craniotomy and surgical clipping.
Systemic anticoagulation with heparin is contraindicated in patients with ruptured and untreated aneurysms. It is a relative contraindication following craniotomy.
Following craniotomy, use of IVC filters is preferred to prevent further pulmonary emboli, while systemic anticoagulation with heparin is preferred following successful endovascular treatment.
Early aneurysm repair
Prevents rerupture and allows the safe application of techniques to improve blood flow (e.g., induced hypertension and hypervolemia) should symptomatic vasospasm develop. 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.
Refernces: Harrison's principles of internal medicine,17th e Diagnostic imaging: Brain by Anne 0. Osborn Adams & Victors' Principles of Neurology, 8th Edition
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