A 42-year-old male presented with a stroke. He was admitted to a general ward with a right- sided hemiplegia, neglect and speech deficits. He was not thrombolysed.
A day post admission, you are called by your registrar from a MET call because the patient has just become drowsy, although wakes to follow commands.
His CT scan at the time of the MET call is as below.
NB: original college image was removed from this question.
Describe the findings on this image and outline the implications.
It is impossible to guess what the original image was, even approximately. I guess some sort of midline shift and oedema would have been found. That CT above is actually from a case report of some sort of horrific CNS vasculitis (Caneppa-Raggio et al, 2016) which presented as an MCA stroke. The issue of decompressive craniectomy in MMCAS has become the topic of Question 2 from the second paper of 2014, and is discussed at length elsewhere.
Anyway, the findings are:
- Left-sided hypodensity consistent with acute infarction
- Extensive midline shift with effacement of the lateral ventricle
The implications are:
- Brain herniation may be taking place (uncal, subfalcine)
- Hydrocephalus may be taking place due to0 obstruction of flow
- There may be pressure on the ACA, resulting in diminished perfusion of the frontal lobes
What is the expected natural history of this disease in the absence of treatment?
- This is a "malignant" MCA infarct
- The mortality without treatment is ~ 80%
- The patient will develop hydrocephalus or frontal lobe infarction, and will likely progress to brain herniation and possibly brain death
- If death does not occur, one can expect profound ongoing disability.
The neurology team have asked for a surgical opinion regarding decompressive crainectomy.
What is the rationale for craniectomy in this setting?
- MCA infarction has a substantial mortality and morbidity.
- Factors which produce this effect include:
- Large volume of infarcted brain tissue, leading to significantly increased ICP.
- Significant risk for haemorrhagic transformation.
- Significant midline shift, with pressure on medial cerebral structures .
- Temporal herniation, with compression of the posterior cerebral artery.
- Poor perfusion of the contralateral cerebral hemisphere due to raised intracranial pressure.
- Many of these factors are related to the increased intracranial pressure.
- Decompressive craniectomy can decrease intracranial pressure by increasing cranial compliance.
- Ergo, decompressive craniectomy should be able to improve mortality and morbidity from acute MMCAS by vastly improving the perfusion in the penumbra of the stroke shortly after the craniectomy.
The neurology team has referred to this stroke as a "malignant" MCA stroke. What makes it "malignant"? What is the definition of these terms?
From the three belowmentioned European trials, "malignantness" was determined by the presence of the following features:
- MCA territory stroke of >50% on CT
- Perfusion deficit of >66% on CT
- Infarct volume >82 mL within 6 hours of onset (on MRI)
- Infarct volume of >145mL within 14 hours of onset (on MRI)
What is the evidence for decompressive craniectomy in malignant MCA infarction?
- Prospective, multicenter RCT in Germany
- 32 patients were enrolled; then a statistically significant mortality reduction was found, and the study was terminated. The projected sample size was calculated to 188 patients, but the steering committee decided to terminate this trial anyway because of the results of the three other European decompressive craniectomy trials.
- Raw data suggests improved survival for the craniectomy group: 88% vs 47%.
- Prospective, multicenter RCT in France
- After randomization of 38 patients, the data safety monitoring committee recommended stopping the trial because of slow recruitment.
- Absolute reduction of 52.8% in the death rate in the surgery group.
- Survival was 22% in the "conservative management" group, and ~ 75% in the surgery group
- Prospective, multicenter RCT in the Netherlands
- 64 patients were randomised
- Again, survival was better with surgery (absolute risk reduction was 38%)
A pooled analysis of the first three studies, including 93 patient cases, came to a fairly positive conclusion:
"...after decompressive surgery the probability of survival increases from 28% to nearly 80% and the probability of survival with an mRS of ≤3 doubles."
(mRS here being the score of the modified Rankin scale, equating to a disability where one requires some help, some of the time, with some things - but is otherwise able to walk unassisted).
What are the expected outcomes of DC, in terms of NNT?
- NNT for survival is 2
- NNT for severe disability is 6.
- Malignant MCA infarct has a mortality of 70%
- Craniectomy reduces this to 30%, but with residual deficit.
How would you select patients for decompressive craniectomy?
- Age <60 years.
- most survivors in the over-60s group in DESTINY-II had some severe disabilities
- Within 48 hours of symptom onset.
- It seems the benefit of craniectomy was lost after 96 hours; presumably all the salvageable penumbra has died, and mass effect is maximal.
- If there is haemorrhagic transformation, you may need a decompressive craniectomy anyway for clot evacuation
Would you recommend an EVD and ICP monitoring in this patient? Why or why not?
- ICP monitoring has never been shown to improve outcomes from stroke and is currently not one of the recommended options (Torbey et al, 2015)
- There is no good evidence that ICP-targeted therapy improves outcomes from stroke
- An EVD may be required to maintain CSF flow if hydrocephalus has developed
The family have consented to craniectomy. Beyond neurological disability, what complications of craniectomy can they expect?
The complications of decompressive craniectomy are well summarised in an article by Margules and Jallo. I will present them as a list:
- Brain hernation though the opening: This wil result in localised pressure necrosis around the edges, as well as venous "pinching" and congestion of the whole hernated mass. The smaller the craniectomy, the greater the risk of this occurring.
- Delayed paradoxical herneation: This is a weird complication of lumbar puncture in a pre-cranioplasty patient. Essentially, the opening of a lumbar drain allows the CSF to leak freely out of the spinal canal; however because the cranium is open, there is no negative pressure fastening the brainstem into the skull, and it readily herneates through the foramen magnum, killing the patient.
- Subdural hygroma: This is a collection of CSF which forms under the operative site after a craniectomy is finalised. It seems about half of all patients end up with this, to some degree. Most disappear harmlessly; some persist and cause a mass effect.
- Infection: The risk of this is abut 3-7%, with perioperative antibiotics. Bone flap osteomyelitis is more rare, but much more disturbing.
- Bleeding: A non-specific surgical complication.
- Post-traumatic hydrocephalus: In general, people who have decompressive craniectomy tend to develop this about 4 times as often as people who are managed non-surgicaly. However, people who end up needing decompression probably also had a more severe head injury. Potentially, some sort of arachnoid granulation injury could be the aetiological cause of this complication.
- Syndrome of the Trephined, or "Sinking Flap Syndrome": This is a long-term complication, associated with poor cognitive performance, memory loss, irritability, headaches and dizzyness. Nobody actually knows what causes it, but people tend to blame the fact that the brain is exposed to atmospheric pressure, and is thus subject to unusual changes of surface perfusion. These problems tend to resolve after cranioplasty.
- Bone resorption: After you have carefully positioned your bone flap and closed the patient's scalp, you may find to your dismay that within months the flap is gone. Where did it go? It was gobbled up by osteoclasts, as any stray piece of dead bone would be. Synthetic cranioplasty may be the answer to this problem, especially if the flap is in many pieces