Decompressive craniectomy for stroke

 

  • Introduction
    • Basics: The role of decompressive craniectomy for stroke is controversial and the postoperative morbidity and mortality is significant. Large ischemic strokes can exert significant mass effect through swelling that normally occurs 24-72 hours from symptom onset in about 10% of patients. Ischemic strokes are not felt to produce clinically significant global elevation in ICPd but causes delayed deterioration through mass effect and progression of ischemic penumbra. Treatment of mass effect is thus the primary goal of surgical management though CSF may be utilized in cerebellar strokes.
      • 10% of ischemic strokes are characterized as malignant space-occupying infarcts
      • Progressive decline in consciousness over 48 hours
      • Transtentorial herniation within 48-92 hours
      • Mortality: 50-78%e
  • Cochrane Reviewa
    • “There is no evidence that surgery to relieve pressure on the brain improves outcome after massive stroke. About four-fifths of strokes are due to blockage of an artery in the brain. When the artery is blocked, part of the brain can be damaged, called a cerebral infarct. If a main artery is blocked the area of brain damage can be large. About 24 to 48 hours after a large infarct the brain can swell, causing a dangerous rise of pressure inside the head. Surgery to remove some of the skull bone over the swollen area of brain can help reduce the pressure and may reduce the risk of death or disability. However, operating on patients who are acutely ill after a stroke can carry significant risks. At present, there is not enough evidence to decide whether surgery does more good than harm. Randomised trials to compare surgery with conservative treatment are in progress.”
    • Note: Literature review from before 2002 and up to this point no randomized controlled trials had been performed. Based on the paucity of data and lack of a recent update no relevant conclusions can be drawn from this Cochrane review.
    • Cochrane review for decompressive craniectomy in traumab: “The authors of the review conclude that there is no evidence to support the routine use of DC to improve mortality and quality of life in brain-injured adults with high ICP. DC may improve survival and neurological outcomes in brain-injured pediatric patients with raised ICP for whom other medical treatments had failed. This one trial involved only a small number of patients and further studies are needed before applying DC as a routine treatment.”
    • Note: The underlying disease process is different but decompression
  • Literature review
    • Class I data- Randomized controlled trials:
      • DECIMALf– Randomized 38 patients, stopped prematurely after “slow recruitment and pooled analysis of 2 other ongoing trials.” Demonstrated statistically significant improvement overall mortality. There was a 52.8% absolute reduction in death after craniotomy (p<0.0001). But the primary end point, a favorable functional outcome defined as a mRS <3, was not achieved to statistical significant. At one year 50% of surgical patients achieved the primary end point as opposed to 22% of the nonsurgical group (p=0.1). The conclusion ignored the lack of statistical significance and stated that both endpoints were obtained.
      • DESTINYg– Randomized 32 patients. Demonstrated a statistically significant reduction in mortality with surgery. 88% survived 30 days with surgery as opposed to 47% without surgery  (p=0.02). Functional outcome differences were not statistically significant. 47% of surgery patients had a mRS <3 versus 27% in nonoperative group (p=0.23). The study failed to demonstrate the primary endpoint and was terminated prematurely. Later analysis demonstrated that 188 patients would to be randomized in order to demonstrate a statistically significant difference in functional outcome. The study’s conclusions fairly state hemicraniectomy reduces mortality but not functional outcome.
      • HAMLETC– Randomized 64 patients. Surgical decompression had no effect on the primary outcome measure (mRS) but did reduce case fatality (ARR 38%).
      • These are three small, European trials that may not reflect a Southern US patient population. Additionally the statistical methods and subgroup analysis used for the joint review of the 3 trials is questionable. Each trial individually only demonstrated a reduction in 30 day mortality but no statistically significant effect was seen in regards to functional outcome.
      • Unanswered questions from these three RCT: What are the long term quality of life outcomes, What are the differences between dominant and non-dominant stroke decompressions, and What is the impact of timing of decompression (ie >48 hours from symptom onset).
    • Systematic reviewh of literature from 1970-2004: 129 patients analyzed
      • Only 7% functionally independent
      • 35% Moderately disabled
      • 58% Severely disabled or died
      • Patients >50- 80% died
  • Initial Diagnostic assessment
    • Neurological exam
      • GCS
      • NIHSS
      • CN and Motor exam
    • Imaging
      • CT Head wo contrast
      • MRI
  • Initial medical management
    • Central venous and arterial line
    • Hypertonic saline- either 3% or 1.5%
      • Goal Na >140
    • Mannitol: 25gq6h hold for CVP<6
  • Neurosurgical consultation
    • Neurosurgical consultation is to be made prior to discussion with family regarding the possibility of operative intervention. The discussion of any potential operation is to be performed only by the neurosurgical team.
    • Operative decisions are at the discretion of the individual attending on call
  • Consultation criteria
    • Age 18-60
    • GCS >8
    • Signs of infarction on CT of >50% of R MCA territory or infarct volume >145cm3 on DWI
    • Cerebellar stroke
  • Exclusion criteria
    • Age greater than 60
    • Large dominant infarction- ie >50% L MCA infarct
    • Significant medical comorbidities
    • Known coagulopathy or systemic bleeding disorder
    • Poor neurologic exam
      • GCS <8
      • Fixed dilated pupils
    • Presentation >2 days from stroke onset
  • Operative timing
    • There are NO indications for EMERGENT decompressive craniectomy for MCA strokes.
    • Emergent decompressive craniectomy will be considered in cerebellar stroke
  • Post-operative follow-up
    • Patient is to remain on the neurology service
    • POD #1 Head CT
  • References
    • Morley NCD, Berge E, Cruz-Flores S, Whittle IR. Surgical decompression for cerebral oedema in acute ischaemic stroke. Cochrane Database of Systematic Reviews 2002, Issue 3. Art. No.: CD003435. DOI: 10.1002/14651858.CD003435
    • Sahuquillo J. Decompressive craniectomy for the treatment of refractory high intracranial pressure in traumatic brain injury. Cochrane Database of Systematic Reviews 2006, Issue 1. Art. No.: CD003983. DOI: 10.1002/14651858.CD003983.pub2
    • Hofmeijer, J et al. “Surgical decompression for space-occupying cerebral infarction HAMLET: a multicentre,  open, randomized trial. Lancet Neurology Vol 8, Issue 4: April 2009
    • Frank JI ; Large hemispheric infarction, deterioration, and intracranial pressure. – Neurology – 01-JUL-1995; 45(7): 1286-90
    • Gupta, R. Connolly, S. Hemicraniectomy for Massive MCA Territory Infarction. A Systemic Review. Stroke 2004;35;539-543; originally published online Jan 5, 2004;
    • Vahedi, K. et al DECIMAL Trial. Stroke 2007; 38;2506-2517
    • Juttler, E. et al. DESTINY Trial. Stroke 2007;38,2518-2525
    • Gupta, R. et al. Hemicranietomy for massive MCA territory infarction. Stroke 2004;35;539-543
Joseph MillerDecompressive craniectomy for stroke

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