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SAH (Subarachnoid Haemorrhage)

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SAH

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SAH (Subarachnoid Haemorrhage)

  1. 1. SUBARACHNOID HAEMORRHAGE DR JIGAR R PADALIA
  2. 2.  Bleeding into the subarachnoid space (space between pia & arachnoid layers) where blood vessels lie & CSF flows
  3. 3. RELEVANT ANATOMY  Arachnoid comes from the Greek "arachne" meaning spiderweb + "eidos" meaning resemblance = spider-web-like.  Subarachnoid space is the interval between the arachnoid membrane and pia mater.  It is occupied by a spongy tissue consisting of trabeculae and intercommunicating channels in which the CSF is contained.  The subarachnoid space extends from the basal cisterns surrounding the brainstem superiorly to S2 level inferiorly.  Subarachnoid space is the location of the interface between the vascular tissue and CSF.
  4. 4. SAH Etiology –Non Traumatic  Aneurysmal Rupture : 80-85%  Non aneurysmal perimesencephalic haemorrhage : 10%  AVM/ Fistula  Intracranial vessel dissection  Venous Sinus thrombosis  Vasculitis  Coagulopathy  Drug & Toxins (cocaine abuse, amphetamine, MAO inhibitor, alcohol, CO, nicotine, quinine, snake venom)  Hypertensive crisis
  5. 5. PATHOPHYSIOLOGY  Blood extravasates under pressure into the subarachnoid space and quickly spreads through the CSF around the brain & spinal cord  Blood released under high pressure – direct damage to local tissues  Blood extravasation - ↑ ICP  Meningeal irritation occurs
  6. 6. Aneurysm  Focal out pouching from the arterial wall
  7. 7. Incidence and prevalence of aSAH  12-15% die before hospital admission  Incidence increases with age  Typical average age of onset in adults ≥ 50 years  Higher incidence of aSAH in women
  8. 8. Risk Factors for and Prevention of aSAH  Behavioral risk factors - hypertension, smoking, alcohol, and use of sympathomimetic drugs (cocaine)  Female sex  Presence of an un-ruptured cerebral aneurysm  H/o previous aSAH  Familial aneurysms and family h/o aSAH  Genetic syndromes - ADPKD & type IV Ehlers-Danlos  Aneurysm size >7 mm - risk factor for rupture  There does not appear to be an increased risk of aSAH in pregnancy, delivery, and puerperium
  9. 9. Risk Factors for and Prevention of aSAH - recommendations  Treatment of high blood pressure with antihypertensive medication is recommended to prevent ischemic stroke, intracerebral hemorrhage, and cardiac, renal, and other end-organ injury (Class I; Level of Evidence A).  Hypertension should be treated, and such treatment may reduce the risk of aSAH (Class I; Level of Evidence B).  Tobacco use and alcohol misuse should be avoided to reduce the risk of aSAH (Class I; Level of Evidence B).  After any aneurysm repair, immediate cerebrovascular imaging is generally recommended to identify remnants or recurrence of the aneurysm that may require treatment (Class I; Level of Evidence B) (New recommendation)
  10. 10. Natural History and Outcome of aSAH  Mortality rates - 8% to 67%  The severity of clinical presentation is the strongest prognostic indicator in aSAH (Hunt & Hess scale OR WFNS Scale)  Rebleeding is another major predictor of poor outcome  Other factors predictive of poor prognosis include  Older age  Preexisting severe medical illness  Global cerebral edema on CT scan  IVH & ICH  Symptomatic vasospasm, delayed cerebral infarction  Hyperglycemia, fever, anemia  Systemic complications - pneumonia and sepsis
  11. 11. Natural History and Outcome of aSAH: Recommendations  The initial clinical severity of aSAH should be determined rapidly by use of simple validated scales (eg, Hunt and Hess, World Federation of Neurological Surgeons), because it is the most useful indicator of outcome after aSAH (Class I; Level of Evidence B).  The risk of early aneurysm rebleeding is high, and rebleeding is associated with very poor outcomes. Therefore, urgent evaluation and treatment of patients with suspected aSAH is recommended (Class I; Level of Evidence B).
  12. 12. CLINICAL PRESENTATION  Headache  97% of patients  Thunderclap headache  Warning/Sentinel headache - in 10-43% of aSAH  Minor leaks are not a feature of AVM  Reduced consciousness  Meningism  Vomiting/nausea  Neck stiffness  Photophobia/visual changes  Seizures – 20%
  13. 13.  Meningeal irritation  >75% of cases of aSAH  May take several (6-24 hrs) hours to develop  Coma - Raised ICP, ICH, HCP, seizures or low CBF  Focal neurologic abnormalities - (25%)  Ocular hemorrhages (20-40%)  Temperature elevation  Secondary to chemical meningitis from subarachnoid blood products  Common after the 4th day following bleeding
  14. 14.  Hypertension - 50% of patients.  BP often becomes labile as ICP increases  Tachycardia often is present for several days after SAH  The most common diagnostic error - failure to obtain NCCT Head
  15. 15. What causes symptoms & signs?  Blood leaking from the aneurysm  Headache  Meningism  Local pressure effects of the aneurysm  Associated ICH
  16. 16. Local pressure effects of the aneurysm  ACom  Visual symptoms due to optic chiasma compression  Positive babinski  Bilateral lower limb paresis  MCA  Contralateral hand & face paresis  Contralateral visual neglect  Aphasia (dominant side)  ICA/PCom  CN III signs
  17. 17. Associated ICH  The aneurysm usually lies within the subarachnoid cisterns  It can become adherent to adjacent brain due to adhesions (e.g. from a previous leak)  The bleed therefore can also extend into the brain  MCA = hemiparesis & aphasia (if dominant)  Acom = mutism  AVM is more likely to cause ICH as they usually lie somewhat in brain parenchyma
  18. 18. Findings Likely location of aneurysm Mental status change Any Meningismus • Seen in 60% of pts of aSAH • Takes 3-12hrs to develop Any Third nerve palsy • 90% of pts with 3rd nerve palsy due to aneurysm(compared to other causes of 3rd nerve palsy) have anisocoria >2mm Posterior communicating artery Sixth nerve palsy • Presents 3-14 days after aSAH • A/W higher clot burden • Gradually resolves Any (due to ↑ICP) Bilateral weakness in legs or abulia Anterior communicating artery Nystagmus, ataxia or dizziness Posterior circulation Hemiparesis with aphasia or neglect Middle cerebral artery Subhyaloid haemorrhage (Terson syndrome) • Seen in 10% of aSAH • A/W worse clinical grades on presentation and poorer outcome Any
  19. 19. SAH GRADING Hunt and Hess Scale  Grade 1 - Asymptomatic or mild headache  Grade 2 - Moderate-to-severe headache, nuchal rigidity, and 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 rigidity
  20. 20. SAH GRADING WFNS scale  Grade 0 – Intact aneurysm  Grade 1 - GCS of 15, major focal deficit absent  Grade 2 - GCS of 13-14, major focal deficit absent  Grade 3 - GCS of 13-14, major focal deficit present  Grade 4 - GCS of 7-12, major focal deficit absent/present  Grade 5 - GCS of 3-6, major focal deficit absent/present * Major focal deficit – aphasia/hemiparesis/hemiplegia
  21. 21. SAH GRADING Fischer scale (based on CT scan)  Group 1 - No blood detected  Group 2 - Diffuse deposition of subarachnoid blood and no layers of blood greater than 1 mm  Group 3 - Localized clots and/or vertical layers of blood 1 mm or greater in thickness  Group 4 - Diffuse or no subarachnoid blood, but intracerebral or intraventricular clots are present
  22. 22. SAH GRADING  The Hunt & Hess and the WFNS grade  Correlate with patient outcome  Fischer classification  Predict the likelihood of symptomatic cerebral vasospasm  Admission H&H Gr 1 and 2 - 20% mortality  Major cause is rebleed (international cooperative aneurysm study)
  23. 23. WORK UP  CBC  PT INR & aPTT  Serum Electrolytes  BGRh  Cardiac Enzymes  ABG
  24. 24. CT SCAN  NCCT – cornerstone of diagnosis  Most sensitive imaging study in SAH  The sensitivity of CT in the first 3 days after aSAH remains very high (close to 100%)  After 5 to 7 days, the rate of negative CT increases sharply  CT scan head-positive in up to - 95-100% in 12-24 hours - 80% in 3 days - 70% in 5 days - 50% at1 week - 30% at 2 weeks
  25. 25. CT SCAN  The location of blood correlates with the location of the aneurysm in 70% of cases  In general, blood localized to the basal cisterns, the sylvian fissure, or the intrahemispheric fissure indicates rupture of a saccular aneurysm.  Blood found lying over the convexities or within the superficial parenchyma of the brain often is indicative of AVM or mycotic aneurysm rupture.
  26. 26.  Anterior inter-hemispheric fissure bleed, frontal lobe – ACom Rupture
  27. 27.  Sylvian fissure bleed – ICA/MCA/PCom aneurysm
  28. 28.  IVH (3 & 4th ventricular) - PICA/ VA aneurysm rupture
  29. 29.  CT falsely negative  Small hemorrhages  Severe anemia  CT also helpful to rule out HCP  CECT head may reveal AVM
  30. 30. CT Scan  Intraventricular Hemorrhage (IVH)  Hydrocephalus  Intracerebral hematoma (ICH)  Brain edema  Infarction caused by vasospasm
  31. 31. Lumbar puncture (LP) Positive in  100% in 12 hrs to 2 weeks  >70% after 3 weeks  40% after 4 weeks
  32. 32. LUMBAR PUNCTURE  CT scan performed before LP to exclude  Significant intracranial Mass effect  Obstructive HCP or obvious  Intracranial hematoma  LP should not be performed if the CT scan demonstrates an SAH  because of the (small) risk of further intracranial bleeding associated with a drop in ICP.  Findings often are negative within 2 hours of the ictus & is most sensitive 12 hours after the bleed.  SAH can be distinguished from traumatic LP.
  33. 33.  Xanthochromia – because of bilirubin in CSF  100% present 12 hours after the bleed  Remains for approximately 2 weeks.  3 weeks after the bleed in 70%  4 weeks in 40% of patients  Better appreciated by spectrophotometry.  RBC count usually > 1,00000/cumm  Higher protein level d/t blood break down product.
  34. 34.  When blood enters the CSF (e.g. from SAH or during LP) the red cells are broken down & oxyhaemoglobin is released  Oxyhaemoglobin conversion to bilirubin  Takes 12 hrs  Enzyme found in the brain.  Blood which entered the CSF during the LP would not encounter the enzyme & could not produce bilirubin
  35. 35. Supernatant xanthochromia
  36. 36. CEREBRAL ANGIOGRAPHY (DSA)  Gold standard for evaluation of cerebral aneurysm (80-85% sensitivity)  Useful in cases of diagnostic uncertainty (after CT and LP)  Can provide surgical information in the setting of SAH:  Cerebrovascular anatomy  Aneurysm location & source of bleeding  Aneurysm size/shape/orientation of dome and neck  Relation to the parent/perforating arteries  Presence of multiple or mirror aneurysms  If cerebral angiography findings are negative (10-20%) a repeat test should be performed after 10-21 days  May be useful to evaluate for possible cerebral vasospasm
  37. 37. DSA
  38. 38. DSA
  39. 39. CT ANGIOGRAPHY  Non invasive  Routinely performed  Sensitivity and specificity comparable to DSA  Beneficial in very unstable patients who cannot undergo angiography  Detect aneurysms larger than 3 mm  sensitivity 95% and Specificity 83%  Anatomic detail especially relation to near by bony structure.
  40. 40. CT Angiogram
  41. 41. MRI  MRI is not sensitive for SAH within the first 48 hours.  Useful tool to diagnose cerebral / spinal AVMs causing SAH  MRI can be used to evaluate the degree of intramural thrombus in giant aneurysms.
  42. 42. MR Angiography  The role of MRA in the detection of SAH currently is under investigation.  Risk/benefit ratio still favors conventional angiography  Can detect aneurysms >3 mm with 86% sensitivity and is useful for monitoring the status of small, unruptured aneurysms  False +ve in approx. 16%  Can be used to evaluate the degree of intramural thrombus in giant aneurysms  Useful as a screening test in high risk patients including 1st degree relative of patients with IC aneurysm
  43. 43. MR Angiography  Takes ½ to 1 hour  Detects aneurysms >3 to 5 mm  MRI detects thrombosed aneurysms  Screening modality
  44. 44. TCD :  Detection and monitoring of arterial vasospasm ECG :  Changes attributed to ischemia/infarction  ↑ catecholamines.  Myocardial ischemia/infarction is present in 20% of SAH cases Chest radiograph:  Baseline chest radiograph to serve as a reference point Echocardiogram:  Evaluation of ventricular wall motion may be necessary in cases with suspected myocardial ischemia
  45. 45. Clinical Manifestations and Diagnosis of aSAH -Recommendations  aSAH is a medical emergency that is frequently misdiagnosed. A high level of suspicion for aSAH should exist in patients with acute onset of severe headache (Class I; Level of Evidence B).  Acute diagnostic workup should include noncontrast head CT, which, if nondiagnostic, should be followed by lumbar puncture (Class I; Level of Evidence B).  DSA with 3D rotational angiography is indicated for detection of aneurysm in patients with aSAH and for planning treatment (to determine whether an aneurysm is amenable to coiling or to expedite microsurgery) (Class I; Level of Evidence B). (New recommendation)
  46. 46. Critical Care Management of Patients Following aSAH 1. Medical measures to prevent rebleeding 2. Seizure and prophylactic anticonvulsant use 3. Cardiopulmonary complications 4. Management of hydrocephalus 5. Monitoring intravascular volume status 6. Managing intravascular volume status 7. Glucose management 8. Management of pyrexia 9. DVT prophylaxis 10. Statins 11. Magnesium 12. Delayed neurological deterioration(DND), Vasospasm and delayed cerebral ischaemia(DCI) 13. Hemodynamic monitoring of DCI 14. Anemia and transfusion 15. Management of hyponatremia 16. Endocrine function
  47. 47. MANAGEMENT  Initial management of patients with SAH is stabilization. Assess the level of consciousness, airway, breathing and circulation (ABCs).  Endotracheal intubation should be performed for patients presenting with coma/depressed consciousness/inability to protect airway/ increased ICP.  Vascular access should be obtained, including central and arterial lines.  Monitoring  Cardiac monitoring  Pulse oximetry  BP monitoring (arterial BP monitoring is indicated in high-grade SAH)  End-tidal carbon dioxide.  Urine output measurement via placement of a Foley’s catheter.
  48. 48. Patients with signs of increased ICP  Intubated and hyperventilated to achieve a PCO2 of 30-35 mm Hg.  Avoid excessive hyperventilation - may potentiate vasospasm and ischemia.  Osmotic agents (mannitol) - decrease ICP dramatically (50% after 30 min post administration).  Loop diuretics also can decrease ICP.  IV steroids - controversial.
  49. 49. STANDARD ADMITTING ORDERS :  Admission in ICU with monitored bed  Vital parameter and neurological status check 1 hrly  Bed rest with head end elevated by 30 degrees  Nursing : strict I-O charting / daily weights / DVT pumps at LL / urinary catheterization/ NG tube  IVF : Aggressive fluid therapy to head off cerebral salt wasting.  Oral Nimodipine 60mg q4h for 21 days  Stool softeners
  50. 50.  Anti Convulsants - Phenytoin is the usual agent used.  Mild sedation (propofol/midazolam/lorazepam)  Analgesic : fentanyl ( lower ICP and doesn’t cause histamine release unlike morphine )  Steroid : effect on brain edema is controversial, usually given prior to craniotomy
  51. 51.  Oxygenation :  Non intubated - Oxygen support to maintain SPo2>92  Intubated - Normocarbia & Po2 > 100 mm Hg  Monitoring of CVP  For unsecured aneurysm , gentle volume expansion with slight hemodilution and mild elevation of BP may help reducing effects of vasospasm and cerebral salt wasting
  52. 52. REBLEEDING  Most disastrous and disabling  Mortality rate – up to 70%  Incidence  First 24 hrs- 4-6 %  1-2 %/day for 2 weeks (cumulative 20%)  30% rebleed by 30 days  50% rebleed by 6 months  There after 3% per year  Risk increases with higher H/H grade
  53. 53. Measures to prevent rebleeding  Early aneurysm repair should be undertaken, when possible and reasonable  Blood pressure control  Modest elevations of blood pressure (Mean BP <110mmhg) does not require therapy
  54. 54. Seizures  Early - 6% to 18%  Delayed - 3% to 7%  Risk factors  MCA aneurysm  Thickness of SAH  ICH  Re-bleeding  Infarction  Poor neurological grade  History of hypertension  Routine use of anticonvulsants is not recommended  If prophylactic anticonvulsants are used – use for shorter duration 3-7 days
  55. 55. CARDIAC PROBLEMS  SAH may be a/w cardiac arrhythmias and ECG changes in over 60% cases; may be indistinguishable from acute MI  Possible mechanism : hypothalamic ischemia causes ↑sympathetic tone with resultant catecholamine surge  Stunned myocardium : reversible post ischemic myocardial dysfunction  Hypotension usually does not occur since reduced CO is offset by increased SVR.
  56. 56. Cardiac Complications  Hypertension (27%)  Hypotension (18%)  Life-threatening arrhythmia (8%)  Myocardial ischemia (6%)  Successful resuscitation from cardiac arrest (4%)  Troponin I elevation (20%- 68%)  Regional wall motion abnormalities (26%) ECG Changes  ST segment changes (15%– 67%)  T-wave changes (12%– 92%)  Prominent U waves (4%– 52%)  QT prolongation (11%–66%)  Conduction abnormalities (7.5%)  Sinus bradycardia (16%)  Sinus tachycardia (8.5%)
  57. 57. Neurogenic stunned myocardium  Most severe form of cardiac injury  Transient lactic acidosis  Cardiogenic shock  Pulmonary edema  Widespread T-wave inversions  Prolonged QT interval  Reversible left ventricular wall motion abnormalities
  58. 58. Pulmonary complications  Chest Infection  Neurogenic pulmonary edema
  59. 59. Neurogenic pulmonary edema  Symptomatic pulmonary edema occurs in about 20% of SAH patients  Detectable oxygenation abnormalities occur in 80%  Potential mechanisms:  Hyper-sympathetic state  Cardiogenic pulmonary edema  Neurogenic pulmonary edema
  60. 60.  Radiographic pulmonary edema - 23% of SAH patients  A minority of cases are associated with documented LV dysfunction or iatrogenic volume overload  Neurogenic pulmonary edema appears to be a consequence of the constriction of pulmonary venous sphincters
  61. 61. Conditions associated with neurogenic pulmonary edema  Common:  SAH  Status epilepticus  Severe head trauma  ICH  Rare:  Brainstem infections  Medullary tumors  Multiple sclerosis  Spinal cord infarction  ↑ICP from a variety of causes
  62. 62. Mechanisms of neurogenic pulmonary edema  Hydrostatic:  CNS disorder → hyper-sympathetic state → ↑ afterload → diastolic dysfunction → hydrostatic pulmonary edema  Neurogenic:  Contraction of postcapillary venular sphincters raises PCWP without raising left atrial pressure  Structural:  Fracture of pulmonary capillary endothelium
  63. 63. Managing neurogenic pulmonary edema  Supplemental oxygen and CPAP or PEEP  Place pulmonary artery catheter and, if there is coexisting cardiogenic edema, lower the wedge pressure to ~ 18 mmHg  Echocardiography may be useful to determine whether cardiac dysfunction is also present  NPE usually resolves in a few days
  64. 64. Monitoring Intravascular Volume Status  Monitoring of volume status may be beneficial  Vigilant fluid balance management should be the foundation for monitoring intravascular volume status.  Central venous lines should not be placed solely to obtain CVP measures and fluid management based solely on CVP measurements is not recommended.  Routine use of PAC is not recommended
  65. 65. Managing Intravascular Volume Status  Target euvolemia  Avoid prophylactic hypervolemia  There is evidence for harm from aggressive administration of fluid aimed at achieving hypervolemia (high quality evidence; strong recommendation).  Isotonic crystalloid is the preferred agent for volume replacement (moderate quality evidence; weak recommendation).  In patients with a persistent negative fluid balance, use of fludrocortisone or hydrocortisone may be considered (moderate quality evidence; weak recommendation).
  66. 66. Glucose management  Hypoglycemia (serum glucose <80 mg/dl) should be avoided (High quality evidence-strong recommendation).  Serum glucose should be maintained below 200 mg/dl (Moderate quality evidence-strong recommendation).
  67. 67. Management of Pyrexia  Temperature should be monitored frequently; infectious causes of fever should always be sought and treated (High quality evidence—strong recommendation).  While the efficacy of most antipyretic agents (acetaminophen, ibuprofen) is low, they should be used as the first line of therapy (Moderate quality evidence—strong recommendation).  Surface cooling or intravascular devices are more effective and should be employed when antipyretics fail in cases where fever control is highly desirable (High quality evidence—strong recommendation).  Patients should be monitored and treated for shivering (High quality evidence-strong recommendation).
  68. 68. Deep Venous Thrombosis Prophylaxis  Measures to prevent DVT should be employed in all SAH patients (high quality evidence - strong recommendation).  Sequential compression devices, should be routinely used in all patients (high quality evidence – strong recommendation).  UFH for prophylaxis could be started 24 h after surgery (moderate quality evidence - strong recommendation).  UFH and LMWH should be withheld 24 h before and after intracranial procedures (moderate quality evidence - strong recommendation).
  69. 69. Magnesium  Inducing hypermagnesemia is not recommended pending the conclusion of current randomized trials (moderate quality evidence, strong recommendation).  Hypomagnesemia should be avoided (Moderate quality evidence, strong recommendation).
  70. 70. VASOSPASM  Delayed ischemic neurologic deficit  Onset on the 3rd day  Peak 6_8 days  Resolves by 3 weeks
  71. 71.  CLINICAL VASOSPASM  Delayed ischemic neurological deficit (DIND) : a delayed focal ischemic neurologic deficit following SAH, clinically characterized by confusion/deceased level of consciousness with FND (speech/motor)  RADIOGRAPHIC VASOSPASM (angiographic vasospasm)  Arterial narrowing demonstrated on cerebral angiography (Slow Contrast filling)  SYMPTOMATIC VASOSPASM  When DIND corresponds to a region of vasospasm seen on angiogram
  72. 72.  Clinical finding of cerebral vasospasm – usually develop gradually, may progress and fluctuate  Non localizing findings  New or increasing headache  Alteration of level of consciousness  Disorientation  Meningismus  Focal neurological sign  Cranial nerve palsy  Focal neurological deficit  ACA syndrome (MC)  MCA syndrome
  73. 73.  ACA syndrome  Frontal lobe findings predominate ( abulia, grasp/suck reflex, urinary incontinence, drowsiness, slowness, delayed response, confusion ).  B/L ACA infract are usually d/t vasospasm after AComA aneurysm rupture  MCA syndrome  Hemiparesis, monoparesis, aphasia, ideomotor apraxia
  74. 74. SEVERITY :  Cerebral vasospasm is the most significant cause of morbidity and mortality in patients surviving SAH  Ranges from mild reversible dysfunction to severe permanent deficit secondary to ischemic infarction (7%) and may be fatal (7%)  Earlier onset Cerebral vasospasm is a/w greater deficit
  75. 75. TIME COURSE OF VASOSPASM  Onset is almost never before day 3 post SAH.  Max frequency on day 6-8 post SAH.  Clinical Cerebral vasospasm usually resolves by day 12 post SAH but radiological Cerebral vasospasm is demonstrated , it usually resolves slowly over 3-4 weeks time.  Onset is usually insidious but in 10% may have abrupt and severe deterioration.
  76. 76. Diagnosis of Cerebral vasospasm  Clinical Criteria  Delayed onset of persistent neuro deficit  Onset 4-20 days post SAH  Deficit appropriate to involved arteries  R/O other causes of deterioration  Rebleeding  HCP  Cerebral edema  Seizure  Metabolic disturbances  Hypoxia  Sepsis
  77. 77. Trans Cranial Doppler ( TCD )  May precede clinical symptoms by 24-48 hrs Mean MCA velocity MCA : ICA (Lindegaard Ratio) Interpretation < 120 cm/sec < 3 Normal 120- 200 cm/sec 3 -6 Mild vasospasm > 200 cm/sec > 6 Severe vasospasm
  78. 78.  Cerebral IA-DSA : vasospasm appear as concentric narrowing which can be focal/segmental/diffuse.  Mild (<25%)  Moderate (25-50%)  Severe (>50%)  MRA / CTA : may be useful, not a practical alternative to DSA  EEG : decline in percent of Alpha activity - called relative alpha  predicted onset of vasospasm earlier then TCD  MRI : DWI & PWI may detect early ischemia  Xenon CT : insensitive to detect focal blood flow changes  PET / SPECT : non-quantitative and takes longer time
  79. 79. STRATEGIES FOR VASOSPASM PREVENTION Strategies Mechanism Avoidance of hypovolemia/ hypotension/ antihypertensive/ antifibrinolytics / raised ICP Prevent ischemia Subarachnoid clot removal or lysis with fibrinolytic agents Prevent vasospasm CCB or other potential calcium based neuro-protectant Prevent ischemic damage 21- aminosteroid & other antioxidant, lipid peroxidation inhibitor, free radical scavenger Prevent ischemic damage (?) Intra-thecal slow release vasodilator Prevent vasospasm (experimental ) Endothelin inhibitor and antagonist Prevent vasospasm (experimental )
  80. 80. STRATEGIES FOR VASOSPASM REVERSAL Strategies Mechanism Hypervolemia, hemodilution and hypertension Reverses ischemia Intra-arterial papaverine administration Reverses vasospasm Percutaneous transluminal balloon angioplasty (PTBA) Reverses vasospasm Intraventricular nitroprusside Reverses vasospasm (experimental) Intra aortic balloon counterpulsation (for concomitant heart failure ) Reverses vasospasm along With PTBA
  81. 81. VASOSPASM MANAGEMENT PROTOCOL – POST INTERVENTION Condition Management No vasospasm • Clinically intact • Normal TCD 1. Hemodynamics : normotension, SBP>120mmHg 2. IVF : NS 200 ml/hr Subclinical vasospasm • High TCD (> 200 cm/sec) • Radiographic vasospasm • Clinically intact 1. Monitors : PA/CVC catheter, Arterial line 2. ECG, cardiac echo, cardiac enzymes to assess LVEF 3. Monitor for S/S of a/e of 3-H therapy (chest pain , pulmonary rhonchi, ECG changes ) 4. Hemodynamics : maintain SBP 160-220 mm Hg (may add DA/NorAd/Dobutamine), maintain PCWP 12-14 mmHg 5. Hematocrit : to maintain < 33% 6. Fluid : - monitor I/O and ser. Na IVF = NS + plasma 200-250 ml/hr, 0.45% NS if Na>150 meq/L DDAVP if UO > 200 ml / hr X 4 hrs Clinical vasospasm • DIND • High TCD (> 200 cm/sec) • Radiographic vasospasm 1. Increase SBP 200-220 mm Hg 2. Increase PCWP to 18-21 mm Hg (CXR- to r/o pulmonary edema) / CVP 8-12 cm H2O 3. Refractory case : angioplasty , IA verapamil
  82. 82. TRIPLE “H” THERAPY HYPERTENSION 1. Dopamine : start at 2.5 mcg/kg/min and titrate up to 15-20 mcg/kg/min 2. Dobutamine : start at 5 mcg/min titrate to 20 mcg/kg/min 3. Phenylephrine : start at 5 mcg/min titrate up to 10 mcg/kg 4. Norepinephrine : start at 1-2 mcg/min & then increase by 10 mcg/min HYPERVOLEMIA 1. IVF : NS @ 200 -250 ml / hr 2. Albumin / plasma 3. DDAVP : antidiuretic , 2-4 mcg SQ q D in divided Doses HEMODILUTION 1. Target hematocrit : < 33% 2. Blood transfusion for Hct < 25%
  83. 83. Complications of hyperdynamic therapy  Intra cranial  Cerebral edema  Raised ICP  Hemorrhagic infarction in the area of ischemia  Extra cranial  Pulmonary edema (17%)  Cardiac failure  Dilutional hyponatremia (3%)  MI (2%)  Complication related to catheter  Catheter related sepsis (13%)  Subclavian vein thrombosis (1.3%)  Pneumothorax (1%)  Hemothorax
  84. 84.  Oral nimodipine (60 mg every 4 h) should be administered after SAH for a period of 21 days (High quality evidence – strong recommendation).  TCD may be used for monitoring and detection of large artery vasospasm with variable sensitivity. (Moderate quality Evidence - strong recommendation).  DSA is the gold standard for detection of large artery vasospasm (High quality evidence - strong recommendation).
  85. 85. ANTI-HYPERTENSIVE  To maintain SBP 120-150 mm Hg for unclipped aneurysm  The current recommendations advocate the use of antihypertensive agents when MAP > 130 mmHg  Intravenous beta-blockers – Agents of choice  Hydralazine and CCB’s - fast onset and lead to relatively less increase in ICP  ACE inhibitors - slow onset and are not first-line agents
  86. 86. Calcium channel blockers  Nimodipine 60 mg PO/NG q4h, initiated within 96hrs of aSAH.  BRANT : British aneurysm nimodipine trial shown 22% vs. 33% incidence of cerebral infarction in compared to placebo.  Side effects are – systemic hypotension / renal failure / pulmonary edema.
  87. 87. Anemia and Transfusion  Transfusion criteria for general medical patients should not be applied to decisions in SAH patients.  Patients should receive packed RBC transfusions to maintain hemoglobin concentration above 8–10 g/dl (moderate quality evidence, strong recommendation).
  88. 88. HYPONATREMIA  10-30%  Hypovolemia and hyponatremia as result of natriuresis / diuresis.  MC cause is SIADH & CSWS (↑ANP/BNP/C-peptide).  Hyponatremia may mimic or a/w DIND.  Risk factors : H/O DM, CHF, cirrhosis, adrenal insufficiency, use of NSAID/narcotic/thiazide.  Treatment : correction of hypovolemia & anemia / salt replacement (oral/IV) fludrocortisone may be tried.
  89. 89. Cerebral salt wasting syndrome SIADH ECF volume ↓ ↑ Hematocrit ↑ Normal Albumin conc. ↑ Normal BUN Normal / ↑ ↓ BUN/Creat ratio ↑ ↓ Potassium Normal / ↑ Normal Uric acid Normal / ↓ ↓ Urine Na+ ↑↑ ↑ Treatment Normal saline Fluid restriction
  90. 90. HYDROCEPHALUS ACUTE HCP  Incidence 15-20% after initial CT  30-60% has no impairment of consciousness.  3% develop delayed HCP within 1 week.  Possible mechanism : CSF outflow obstruction by blood at aqueduct / 4th ventricular outlet / subarachnoid space and/or at arachnoid granulation.
  91. 91. Treatment of acute HCP :  Patients in poor grade SAH with large ventricles may be symptomatic from HCP and considered for ventriculostomy, which causes improvement in 80% cases.  ICP recommended to keep in the range of 15-25 mm Hg. After securing the aneurysm ICP should be maintained in the range of 5-10 mm Hg.
  92. 92. Chronic HCP  Reported range is 8-45%.  Chronic HCP is due to pia-arachnoid adhesions or permanent impairment of arachnoid granulations.  Acute HCP does not inevitably lead to chronic HCP.  50% need permanent CSF diversion.
  93. 93. Angiogram-negative SAH  15 to 20%  65 % are prepontine or perimesencephalic  Causes  Vasospasm  Hypoperfusion  Poor angiographic technique  Thrombosis  Repeat angiography  Undetected aneurysms found in an additional 2–5% of cases at 2–4 weeks
  94. 94. Perimesencephalic bleed  Younger  Non-hypertensive  Better grade  More in males  Excellent prognosis  Re-bleeding is rare  Delayed ischemic deficit very few
  95. 95. Perimesencephalic SAH (pmSAH)  10% of patients of SAH  2/3rd patients of angiographic negative SAH  Benign course  Venous bleed  Better clinical grade on presentation  Excellent prognosis  Blood confined to midbrain cisterns with no evidence of ICH or IVH  Rebleeding is rare  Delayed ischaemic neurological deficit(DIND) in very few cases
  96. 96. DEFINITIVE TREATMENT  Microsurgical Clipping OR Endovascular coiling - early as feasible  Complete obliteration of the aneurysm should be achieved whenever possible  Multidisciplinary decision based on characteristics of the patient and the aneurysm
  97. 97. Coiling  Endovascular technique done in angiography by interventional radiologists under GA  May be best if small necked aneurysm  Used in particularly sensitive areas e.g. basilar tip  Must be able to access the aneurysm (e.g. any stenosis or tortuous vessels)  Like dome:neck ratio to be 2:1 or greater Clipping  Craniotomy & careful dissection using microscope to reach aneurysm & clip usually at neck  May be performed after failed clipping  If aneurysm can’t be reached by the endovascular root
  98. 98. Coiling
  99. 99. DACA Aneurysm Coiling
  100. 100. Coiling or Clipping  For patients with ruptured aneurysms judged to be technically amenable to both endovascular coiling and neurosurgical clipping, endovascular coiling should be considered
  101. 101. Clipping preferred  Patients presenting with large ICH and MCA aneurysm  Aneurysm characteristics  Wide neck  Blebs  Geometrically complex with incorporation of branch artery  Partially thrombosed  Giant  Inability to navigate delivery system  Patients preference
  102. 102. Coiling preferred  In elderly  In poor-grade  Aneurysms of basilar artery
  103. 103. CTA Spot Sign
  104. 104. SAH: Differential Diagnosis  Aneurysmal  Non-aneurysmal  Pseudo-SAH  Reversible cerebral vasoconstriction syndrome (RCVS)
  105. 105. Reversible Cerebral Vasoconstriction Syndrome (RCVS)  Reversible, multifocal cerebral vasoconstrictions  Clinical thunderclap headache +/- neurodeficit  NCCT often negative: 20% with small cortical SAH  Vasculitic pattern on CTA, MRA and DSA  Segmental arterial constriction  Interval DSA may show rapid improvement with vasodilator Rx
  106. 106. Pseudo-SAH Increased density in basal cisterns, frequently related to cardiopulmonary arrest • Hypodense brain (severe edema): cisternal effacement, distension +/-thrombosis of vessels
  107. 107. Pseudo SAH  Intrathecal contrast  Meningitis  Polycythemia  Falx cerebri  Tentorium cerebelli  Streak artifact – bone from skull base  Motion artifact
  108. 108. Sudden onset severe headache ABCs History – ask about anticoagulants Routine bloods & coag & group & screen IV access Non-sedating analgesia & hold any anticoagulants ExaminationKeep fastingInvestigations CT brain non- contrast Blood on CT = SAH Is there any other pathology on CT? Where is the aneurysm? CT COW +/- cerbral angiogram For angiogram & coiling if suitable For craniotomy & clipping if not suitable for coiling Meanwhile chart nimodipne, fluids, anti- seizure medication Monitor GCS for any changes from admission examination Ensure pre-op ready – consent, G&S, check bloods, fasting

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