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Sub arachanoid heamorrhage
- 2. Background Etiology of SAH Risk factors of SAH Diagnostic investigations Management of SAH in ED Disposition Complication of SAH
- 3. A 60 year old male k/c/o HTN presented to the emergency department complaining of a sudden, acute onset headache “worst headache of my life “ that radiated into his neck. Symptoms began three hours prior to presentation and were associated with nausea and vomiting.
- 7. Subarachnoid hemorrhage (SAH) is a pathologic condition that exists when blood enters the subarachnoid space
- 8. SAH traumatic Non traumatic Aneurismal 85% Non aneurismal 15% perimesencephalic hemorrhage 50% Other disorders
- 9. CATEGORY CAUSES TRAUMA CLOSED, PENETRATING, ELECTRIC,ETC… VASCULAR ANEURYSMS, ATHEROSCLEROSIS, AVM, VASCULITIDES IDIOPATHIC BENIGN PERIMESENCEPHAIC SUBARACHNOID HEMORRHAGE BLOOD DYSCRASIAS LEUKEMIAS, HEMOPHILIAS, THROMBOCYTOPENIAS INFECTIONS DENGUE, LEPTOSPIROSIS, BACTERIAL MENINGITIS TOXINS AMPHETAMINES, COCAINE, NICOTINE, ANTICOAGULANTS NEOPLASMS GLIOMAS, MENINGIOMAS, HEMANGIOBLASTOMA, ETC
- 10. Incidence about 9-10/100,000/yr Higher in Japan (3 times) and Finland Mean age of onset 51 years (6th decade) Facts and figures Men predominate until age 40, then more women (55%); some studies – 3:2 ratio 30 % rupture during sleep?? About 50 % of patients with an aneurysm have warning prior to SAH (6-20 days).
- 11. Average case fatality rate for SAH was 51 % Population-based study in England with essentially complete case ascertainment 24 hour mortality: 25% 7 days: 37% 30 days: 45% Pobereskin JNNP 2001;70:340-3
- 12. Hypertension Cigarette smoking Oral contraceptives Alcohol consumption Diurnal variations in blood pressure Pregnancy and parturition Slight increased risk with advancing age Following cocaine abuse
- 13. Headache: Features: Sudden and severe "worst headache of my life“ Associated Symptoms: brief loss of consciousness (coma is unusual) 57% nausea or vomiting 77% meningismus 35%?? Seizure <10% poor prognostic indicator
- 14. CT Scan : Within 6-12 hr sensitivity 100% (Perry JJ ,et al, 2011) CT sensitivity progressively declines over time to about 58% at day five. Lumbar Puncture: LP is mandatory if strong suspicion of SAH despite negative CT Negative CT and LP effectively eliminate the diagnosis of SAH Follow-up LP unnecessary , If CT scan preformed within 6 hr. Findings: elevated opening pressure and an elevated RBC count in all tubes, Xanthochromia
- 16. MRI: Less sensitive than CT scan in diagnosing acute SAH FLAIR and T2 have a high sensitivity in patients with a sub-acute presentation of SAH
- 18. If there is a large amount of SAH particularly in the basal cisterns, sulci & fissures the physician should consider a ruptured aneurysm
- 19. Traumatic SAH occurs most commonly over the cerebral convexities or adjacent to otherwise injured brain (i.e. adjacent to a cerebral contusion)
- 20. Angiography: To determine the etiology of hemorrhage DSA MRA /CTA CTA/MRA Conventional angiography •noninvasive tests •screening and pre-surgical planning •identify aneurysms 3 to 5 mm or larger •Less resolution than conventional Angiography •Less sensitive -Better resolution -High sensitivity in detecting aneurysm -invasive
- 21. GRADE SIGNS/SYMPTOMS SURVIVAL 1 Asymptomatic/Minimal headache or neck stiffness 70% 2 Severe headache, stiff neck, no neurologic deficit except cranial nerve palsy 60% 3 Drowsy/ minimal neurological deficit 50% 4 Stuporous with hemeparesis 20% 5 Comatose with decereberate posturing/response 10% HUNT AND HESS IN 1968
- 22. WORLD FEDERATION OF NEUROSURGEONS (WFNS) GRADE GCS NEURODEFICIT 1 15 ABSENT 2 13-14 ABSENT 3 13-14 PRESENT 4 7-12 ABSENT/PRESENT 5 <7 ABSENT/PRESENT
- 23. GRADE CT APPEARANCE 1 No blood detected 2 Diffuse deposition or thin layer with all vertical layers (in interhemispheric fissure, insular cistern, ambient cistern) less than 1 mm thick 3 Localized clot and/or vertical layers 1 mm or more in thickness 4 Intracerebral or intraventricular clot with diffuse or no subarachnoid blood FISHERS CLAASSENS MODIFICATION GRADE CT APPEARANCE 0 No SAH or IVH 1 Minimal SAH and no IVH 2 Minimal SAH with bilateral IVH 3 Thick SAH (completely filling one or more cistern or fissure) without bilateral IVH 4 Thick SAH (completely filling one or more cistern or fissure) with bilateral IVH
- 24. ABC Triage and transport patients with ALC or an abnormal neurologic examination to the closest medical center with a CT scan and neurosurgical backup.
- 25. ABC Intubation. Acute medical care: Control BP (decrease risk of Rebleeding): sBP<160 or mean arterial BP <110 Use Labetalol, nicardipine DVT prophylaxis : pneumatic compression stockings. unfractionated heparin 5000 units TID can be added. IV fluid analgesia kept at bed rest
- 26. Nimodipine {CCB} (60mg PO or NGT every 6hr) reduce incidence and severity of Vasospasm. Antifibrinolytic agents (eg, tranexamic acid) Reduce risk of re-bleeding Antiepileptic drug therapy and steroids: controversial Statins: unknown mechanism but advisable
- 27. ICU bed Neurosurgeon & neuroradiologist consultation: for surgical clipping or endovascular coiling Nonaneurysmal SAH generally has a more benign course, so angiographic intervention is not typically undertaken in these cases.
- 28. Re-bleeding: 8 to 23 % highest in the first 24 hours Manifestation : acute deterioration of neurologic status accompanied by appearance of new hemorrhage on CT scan Aneurismal Rx is best way to prevent re-bleeding. Vasospasm and Delayed cerebral Ischemia: 40 to 60 % Late presentation: >3 days Manifestation: neurologic deterioration in LOCor new focal neurologic deficits
- 29. Hydrocephalus: 15% of pt with SAH 75% of pt resolve spontaneously Seizure Hyponatremia Cardiac abnormalities: ECG changes: ST segment depression, QT interval prolongation, deep symmetric T wave inversions, and prominent U waves Left ventricular dysfunction Elevated trop I level Elevated BNP
- 30. http://ezproxy.squ.edu.om:2983/contents/clinical-manifestations-and- diagnosis-of-aneurysmal-subarachnoid-hemorrhage? source=search_result&search=subarachnoid+hemorrha ge&selectedTitle=1~150 http://ezproxy.squ.edu.om:2983/contents/treatment-of-aneurysmal-subarachnoid- hemorrhage?source=see_link&anchor=H259178626 http://www.bmj.com/content/343/bmj.d4277 http://stroke.ahajournals.org/content/40/3/994.full#sec-9 http://emedicine.medscape.com/article/794076- overview#aw2aab6b4 http://www.medscape.com/viewarticle/803838_3
Editor's Notes
- -the dura mater is attached to the skull, or to the bones of the vertebral canal in the spinal cord -arachnoid is attached to the dura mater -pia mater is attached to the central nervous system tissue
- -Most SAHs are caused by ruptured saccular aneurysms>> event with mortality rates that approach 50 percent, perimesencephalic hemorrhage -Mortality rates due to SAH appear to be decreasing over time in Western populations [1-4]. Improvements in rates of smoking, treatment of hypertension, and management of SAH are plausible but unproven reasons for the reduction in mortality. Improved diagnostic accuracy over time, including exclusion of SAH mimics, as well as therapeutic advances may also be playing a role -perimesencephalic hemorrhage, in which the blood is limited to the subarachnoid spaces around the midbrain (i.e. mesencephalon). In these, the origin of the blood is uncertain
- -Cocaine-related SAH occurs in younger patients and has an outcome similar to that in other SAH patients.44 Diabetes does not appear to be a risk factor for SAH. -
- -Meningismus and often lower back pain may not develop until several hours after the bleed since it is caused by the breakdown of blood products within the CSF, which lead to an aseptic meningitis.
- -The sensitivity of head CT for detecting SAH is highest in the first 6 to 12 hours after SAH (nearly 100 percent) and then progressively declines over time to about 58 percent at day five -Some studies and experts suggest that the sensitivity of CT when performed within six hours of the onset of symptoms is sufficiently sensitive (100 percent) to make a follow up LP unnecessary *comment on follow up with LP: here are important caveats that suggest that this approach may not be generally applicable. One is that such studies are performed in centers where CT scans are generally interpreted by expert reviewers. Another is that the sensitivity of CT may be reduced, when symptoms are atypical, such as isolated neck pain. The sensitivity of head CT is also reduced with more minor bleeds; in one study, for example, a minor SAH was not diagnosed by CT scan in 55 percent of patients; lumbar puncture was positive in all cases ============================ Xanthochromia : -represents hemoglobin degradation products. -unexplained xanthochromic supernatant in CSF is highly suggestive of SAH. -The presence of xanthochromia indicates that blood has been in the CSF for at least two hours; therefore if the CSF is analyzed quickly after a traumatic LP, there will not be xanthochromia. -Xanthochromia can last for two weeks or more However, if LP is performed within two hours after the onset of SAH, xanthochromia may similarly be absent; the absence of xanthochromia cannot be used as evidence of a traumatic tap if an LP is performed in a SAH of less than two hours duration. For a LP performed several hours after the ictus, a finding of erythrocytosis without xanthochromia is unlikely to be SAH [38]. [39,40].
- -CT scan :cornerstone of SAH diagnosis is the noncontrast head CT scan -The sensitivity of head CT for detecting SAH is highest in the first 6 to 12 hours after SAH (nearly 100 percent) and then progressively declines over time to about 58 percent at day five
- The grading system proposed by Hunt and Hess (table 1) and that of the World Federation of Neurological Surgeons (WFNS) (table 3) are among the most widely used
- The WFNS system incorporates the Glasgow Coma scale (table 4) combined with the presence of motor deficit.
- -The Fisher grade is an index of vasospasm risk based upon a CT-defined hemorrhage pattern - Claassen grading system is a similar index of the risk of delayed cerebral ischemia due to vasospasm
- -ensure and maintain an adequate ABC
- Intubate to: To protects them from aspiration to hyperventilate patients with signs of herniation. ndications for endotracheal intubation include a GCS ≤8 (table 1), elevated ICP, poor oxygenation or hypoventilation, hemodynamic instability and requirement for heavy sedation or paralysis. Thiopental and etomidate are the optimal induction agents in subarachnoid hemorrhage (SAH) during an intubation ETOMIDATE used for induction in hypertensive or normotensive pt Thiopental use in HTN pt only: because of its propensity to drop systolic blood pressure (SBP), which is the leading cause of secondary brain injury Precautions: Avoid excessive Hyperventilation target PaCO2 30-35 Excessive hyperventilation may be harmful to areas of vasospasm. Avoid excessive sedation: increase ICP and makes serial neurologic exams more difficult In case of increase ICP: – raise head of stretcher 20o if patient hemodynamically stable – intubate and hyperventilate (100% O2) to a pCO2 of 30-35 mmHg mannitol, which reduces ICP 50% in 30 minutes, peaks after 90 minutes, and lasts 4 hours furosemide, also decrease ICP without increasing serum osmolality ntravenous steroid therapy to control brain edema is controversial and debated
- -the 2012 American Stroke Association guidelines state that when definitive treatment of the aneurysm is unavoidably delayed and there are no other contraindications to treatment, short term therapy (<72 hours) with tranexamic acid or aminocaproic acid is reasonable [7]. -Many experts believe that seizure prophylaxis in the setting of an unsecured aneurysm is reasonable, given the relatively low risk associated with AED administration versus the potential deleterious effects of seizures on an already dysautoregulated brain [4,46]. However, evidence from a large case series suggests that AED exposure to phenytoin may be associated with worse neurologic and cognitive outcome after SAH [47]. Therefore, the use of AEDs for seizure prophylaxis after SAH should probably be minimized whenever possible; and phenytoin is generally avoided. -Guidelines from the American Stroke Society and other expert opinion state that despite lack of conclusive evidence of benefit, it is reasonable to administer statin therapy to patients after SAH to prevent vasospasm
- -Clipping requires a craniotomy (opening of the skull) to locate the aneurysm, followed by the placement of clips around the neck of the aneurysm. Coiling is performed through the large blood vessels (endovascularly): a catheter is inserted into the femoral artery in the groin and advanced through the aorta to the arteries (both carotid arteries and both vertebral arteries) that supply the brain Cerebral perfusion pressure (CPP) equals the mean arterial pressure (MAP) minus the ICP. Intravenous fluid administration should target euvolemia and normal electrolyte balanc
- Vasospasm: Vasospasm causes symptomatic ischemia and infarction in approximately 20 to 30 percent of patients with aneurysmal SAH severity of symptoms depends upon the artery affected and the degree of collateral circulation Fisher (table 5) and Claassen (table 6) are often used to predict the likelihood of vasospasm and cerebral ischemia. Other factors: Hyperglycemia Age <51 High grad of severity Hydrocephalus: Hydrocephalus after SAH is thought to be caused by obstruction of cerebrospinal fluid (CSF) flow by blood products or adhesions, or by a reduction of CSF absorption at the arachnoid granulations
- -hyponatremia is due to increased secretion of antidiuretic hormone, which may result from either the syndrome of inappropriate ADH secretion -Myocardial injury is most likely the result of a centrally mediated release of catecholamines within the myocardium due to hypoperfusion of the posterior hypothalamus.