Neurosurgery SAH

  1. Circle of Willis?
    Image Upload 1
  2. Write short note on berry’s aneurysm. [TU 2056]

    Common location of Saccular aneurysms?
    • 1. Carotid system (85-95%) - 3 most common locations:
    • - ACoA (single most common): 30% 
    • - P-comm: 25%
    • - Middle cerebral artery (MCA): 20%

    • 2. Posterior circulation (vertebro-basilar) - 5-15%
    • - basilar artery
    • - vertebral artery

    3. Multiple aneurysms - 20-30%
  3. Etiology of SAH?
    Trauma - most common

    Spontaneous SAH -

    • A. ruptured intracranial aneurysms
    • B. cerebral arteriovenous malformation
    • C. certain vasculitides that involve the CNS
    • D. rarely due to tumor
    • E. cerebral artery dissection
    • F. coagulation disorders:
    • G. Dural Sinus Thrombosis
    • F. Drugs - cocaine,
    • G. Sickle cell anemia
  4. Outcome of SAH?
    • 10-15% of patients die before reaching medical care
    • Mortality is 10% within first few days
    • Overall mortality is - 45% (range: 32-67%)
  5. Risk factors for SAH?
    • Hypertension
    • Oral contraceptives
    • Substance abuse - cigarette, cocaine, alcohol
    • Pregnancy
    • Advancing age
    • During lumbar puncture
  6. Clinical features of SAH?
    • Symptoms
    • 1. Headache
    • - Most common
    • - Severe and sudden in onset, classic description "the worst headache of my life"
    • 2. Vomiting
    • 3. Photophobia
    • 4. Neck pain
    • 5. Syncope
    • 6. Focal cranial nerve deficit causing diplopia, ptopis

    • Signs
    • - Meningismus - nuchal rigidity, Kernig sign, Brudzinski sign
    • - Hypertension
    • - Focal neurologic deficit (e.g. oculomotor palsy, hemiparesis)
    • - Obtundation or coma
    • - Ocular hemorrhage
  7. Types of ocular hemorrhage in SAH?
    • Three types
    • 1. subhyaloid (preretinal) hemorrhage: bright red blood near the optic disc that obscures the underlying retinal vessels. May be associated with a higher mortality rate.
    • 2. (intra)retinal hemorrhage: may surround the fovea
    • 3. hemorrhage within the vitreous humor (Terson syndrome).
  8. Diagnosis of SAH?
    • To diagnose SAH
    • - NCCT Head
    • - Lumbar puncture

    • To identify source
    • - Digital subtraction angiography (DSA)
    • - CT Angiogram (CTA) - gold standard
    • - MRA
  9. Lumbar puncture in SAH?
    • - most sensitive test for SAH
    • - xanthochromia (yellow coloration of CSF supernatant), RBC > 100,000 RBCs/mm3, raised protein, normal glucose
  10. CT finding in SAH?
    • Blood as high density (white) within subarachnoid spaces
    • Hydrocephalus
    • Intracerebral hemorrhage
    • Infarction
  11. Hunt and Hess Scale?
    • 1 - Asymptomatic, mild headache, slight nuchal rigidity
    • 2- Moderate to severe headache, nuchal rigidity, no neurologic deficit other than cranial nerve palsy
    • 3 - Drowsiness, confusion, mild focal neurologic deficit
    • 4 - Stupor, moderate-severe hemiparesis
    • 5 - Coma, decerebrate posturing
  12. World Federation of Neurosurgical Societies (WFNS) grading system?
    • Grade 1: GCS 15, no motor deficit.
    • Grade 2: GCS 13-14 without deficit
    • Grade 3: GCS 13-14 with focal neurological deficit
    • Grade 4: GCS 7-12, with or without deficit.
    • Grade 5: GCS <7, with or without deficit.
  13. The Fisher grading system for SAH?
    • Grade 1: No blood
    • Grade 2: Diffuse or thin layer of blood less than 1 mm thick (interhemispheric, insular, or ambient cisterns)
    • Grade 3: Localized clots and/or layers of blood greater than 1 mm thick in the vertical plane
    • Grade 4: Intracerebral or intraventricular clots with diffuse or absent blood in basal cisterns

    [@Hunt and Hess - Headache, Fischer - Film, WFNS - GCS]
  14. Initial management of SAH?
    • 1. Admit to ICU
    • 2. Vitals and neuro checks every hourly
    • 3. Head end elevation at 30 degree
    • 4. Diet - NPO
    • 5. IV fluids - early aggressive fluid therapy, NS + 20 mEq KCl/L at - 2 ml/kg/hr
    • 6. Medications -
    • - Prophylactic anticonvulsants - controversial, Phenytoin or Levetiracetam can be used
    • - Sedation with propofol
    • - Analgesics - Fentanyl
    • - Dexamethasone - usually given in preoperative phase
    • - Stool softners
    • - Calcium channel blockers - Nimodipine, 60mg 4hrly
    • - Anti-emetics
    • - H2-blockers
    • 7. Oxygenation - 2l via NC
    • 8. HTN: SBP 120-150 mm Hg by cuff is a guideline with unclipped aneurysm
  15. What is Cerebral vasospasm. [TU 2071]
    Cerebral vasospasm is a condition that is most commonly seen following aneurysmal subarachnoid hemorrhage (SAH), but may also follow other intracranial hemorrhages. 

    Definition of vasospasm includes - 

    1. Clinical vasospasm: a delayed ischemic neurologic deficit (DIND) following SAH. Clinically characterized by confusion or decreased level of consciousness sometimes with focal neurologic deficit (speech or motor).

    2. Radiographic vasospasm: Arterial narrowing demonstrated on cerebral angiography, often with slowing of contrast filling.
  16. Clinical features of cerebral vasospasm?
    Findings usually develop gradually, and may progress or fluctuate. May include:

    • 1. Non-localizing findings
    • A. New or increasing headache
    • B. Alterations in level of consciousness
    • C. Disorientation
    • D. Meningismus

    • 2. Focal neurological signs
    • - Cranial nerve palsies
    • - Focal motor deficits.
    • - ACA and MCA syndromes 
    • - Vasospasm incidence is higher in the distribution of the ACA than in that of the MCA
  17. Time course of vasospasm onset?
    • Never before day 3 post-SAH
    • Maximal peak at 6-8 post-SAH (can occur late as day 17)
    • Typical at-risk period is quoted as days 3-14. 
    • Once radiographic cerebral vasospasm is demonstrated, it usually resolves slowly over 3-4 weeks.
  18. Diagnosis of clinical vasospasm?
    • Delayed onset or persisting neuro deficit
    • Deficit appropriate to involved arteries
    • Rule-out other causes of deterioration - rebleeding, hydrocephalus, cerebral edema, seizure, hyponatremia, hypoxia, sepsis
  19. Prevention of vasospasm and delayed cerebral ischemia?
    • 1. Monitoring
    • -  Symptomatic vasospasm and delayed cerebral ischemia are manifested clinically by a decline in neurologic status including the onset of focal neurologic abnormalities
    • - Transcranial Doppler (TCD) sonography is useful for detecting and monitoring vasospasm in SAH. Velocity changes detected by TCD typically precede the clinical sequelae of vasospasm.  

    2. Nimodipine - Nimodipine 60 mg every four hours is administered to all patients with aneurysmal SAH, ideally within four days of SAH

    3. Intravenous fluids -  Euvolemia is the goal of intravenous fluid maintenance, usually with normal saline

    • 4. Hemodynamic augmentation - 
    • Hemodynamic augmentation does not appear useful for the prevention of vasospasm, but may be appropriate in the treatment of symptomatic vasospasm. 
    • - Hyperdynamic therapy, including modest hemodilution, induced hypertension (with pressor agents such as phenylephrine or dopamine), and hypervolemia (so-called "triple-H" therapy), has been used to try to prevent vasospasm

    5. Statins -  it is reasonable to administer statin therapy to patients after SAH to prevent vasospasm

    6. Other investigational approaches - A number of agents are under investigation for the prevention of vasospasm after SAH, including endothelin receptor antagonists, magnesium sulfate, and nicardipine prolonged-release implants.
  20. Complications of SAH and their management?
    1. Re-bleeding - early coiling or surgical clipping

    2. Symptomatic vasospasm
    - Aggressive therapy of vasospasm can only be pursued after the aneurysm has been treated with surgery or intraluminal therapy. Following aneurysmal occlusion, treatment options include:

    • a. Hemodynamic augmentation - Traditionally "triple-H" therapy, instituted in an effort to raise the mean arterial pressure and thereby increase cerebral perfusion. More recently, the focus has shifted toward maintenance of euvolemia using crystalloid or colloid solution, and induced hypertension with vasopressor agents such as phenylephrine, norepinephrine, or dopamine. 
    • b. Balloon angioplasty - mainstay of treatment for symptomatic focal vasospasm of the larger cerebral arteries which is refractory to hemodynamic augmentation
    • c. Intra-arterial administration of vasodilators (nicardipine, nimodipine,Verapamil)  are generally used for diffuse vasospasm involving smaller arterial branches. 

    • 3. Hydrocephalus
    • - treatment with ventricular drainage.
    • - When a ventriculostomy is used, it is recommended to keep ICP in the range of 15-25 mm Hg

    4. Hyponatremia - Hyponatremia following SAH may be due to inappropriate secretion of antidiuretic hormone (SIADH) or rarely, to cerebral salt-wasting. 

    5. Seizures -  treated with AEDs to prevent recurrence

    7. DVT and pulmonary embolism - DVT stockings
  21. Indications of clipping over coiling?
    • 1. Younger age: lower risk of surgery, and lower lifetime risk of recurrence than with coiling
    • 2. Middle cerebral artery (MCA) bifurcation aneurysms
    • 3. Giant aneurysms: > 20 mm diameter, High recanalization rate with coiling
    • 4. Small aneurysm: < 1.5-2 mm diameter, higher incidence of intraprocedural rupture with coiling
    • 5. Wide aneurysm neck
  22. Timing of surgery in SAH?
    • Early surgery -  <48-96 hrs post SAH
    • Late surgery - 10-14 days post SAH

    There is controversy in early vs late surgery.
  23. Difference between SIADH and cerebral salt wasting syndrome?
    Patients with SIADH are euvolemic. While therapy of asymptomatic hyponatremia in SIADH usually consists of water restriction, fluid restriction is not desirable in patients with SAH as it increases the risk of vasospasm-related ischemic injury. Thus, hyponatremia is treated with isotonic saline, or, if necessary, hypertonic saline.

    Cerebral salt-wasting is less common than SIADH in this setting and is characterized by volume depletion, which leads to the release of ADH. It is usually treated with infusions of isotonic saline. Restoration of euvolemia will suppress the release of ADH.
  24. How do we manage SAH?
    SAH is managed by 

    a) Prevention of rebleeding - application of clipping or coiling 

    • b) Prevention of vasospasm - It occurs only after third day. It can cause ischemic brain injury (referred to as "delayed ischemia") and permanent brain damage due to lack of oxygen in parts of the brain. It can be fatal if severe. Delayed ischemia is characterized by new neurological symptoms, and can be confirmed by transcranial doppler or cerebral angiography
    • - Calcium channel blockers - Nimodipine 
    • - Use of intravenous fluids to achieve a state of triple H - Hypertension, Hypervolemia and hemodilution 

    • c) Management of other complications 
    • - Hydrocephalus is managed by lumber puncture, ventricular drainage, 
    • - Management of electrolyte dysbalance, seizure
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Neurosurgery SAH