Letter to the Editor: Sudden death following cranioplasty: autoregulatory failure?

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TO THE EDITOR: I read with interest the recent article by Sviri in which three patients died due to massive uncontrolled cerebral swelling following an uneventful cranioplasty (Sviri GE: Massive cerebral swelling immediately after cranioplasty, a fatal and unpredictable complication: report of 4 cases. J Neurosurg 123:1188–1193, November 2015).11 There are two points upon which I would like to comment. The first is a minor correction. In Table 1 it states that the outcome in two patients in the 2011 publication was not reported. This is incorrect. The publication was entitled “Sudden death following cranioplasty: a

TO THE EDITOR: I read with interest the recent article by Sviri in which three patients died due to massive uncontrolled cerebral swelling following an uneventful cranioplasty (Sviri GE: Massive cerebral swelling immediately after cranioplasty, a fatal and unpredictable complication: report of 4 cases. J Neurosurg 123:1188–1193, November 2015).11 There are two points upon which I would like to comment. The first is a minor correction. In Table 1 it states that the outcome in two patients in the 2011 publication was not reported. This is incorrect. The publication was entitled “Sudden death following cranioplasty: a complication of decompressive craniectomy for head injury” and in the last line of the introduction it is stated, “Each patient failed to recover despite immediate return to theatre for removal of the bone flap.”6 I only point this out to highlight that the incidence may be higher than previously appreciated, and although I agree it may be a rare occurrence, it may be that it is just underreported. Indeed, a recent publication listed death following bone flap replacement on the outcome algorithm for patients who have had a decompressive craniectomy following ischemic stroke.7

The second point is regarding the possible pathophysiology. I agree that this is yet to be determined, but I would suggest that it may relate to the severity of the brain injury and failure of autoregulation.

Autoregulation Following Traumatic Brain Injury

A number of studies have demonstrated that autoregulation can be impaired in patients who have sustained a traumatic brain injury (TBI), and this can occur over a variable time course.5,9,10 When cerebrovascular pressure reactivity is impaired, cerebral blood volume, and therefore intracranial pressure, will increase or decrease passively (in the same direction) in response to changes in intracranial pressure. It is this loss of autoregulation that reduces the ability of the brain to control adequate blood flow in the presence of hypo- or hypertensive episodes.2,3,12 This increased vulnerability of the injured brain to secondary hemodynamic impairments has increased our awareness of maintaining a perfusion pressure in TBI, and targeted perfusion pressure therapy has gained wide acceptance.1

A number of studies have demonstrated that impaired autoregulation is correlated with poor outcome and an increased mortality rate, and they have also shown that the pressure reactivity index (PRx) is one of the most important predictors.4,7,9,12 It has also been demonstrated that loss of autoregulation can evolve over the first 24 hours. It is at its lowest after 36–48 hours postinjury and thereafter slowly recovers.5,12 While there are limited data on long-term time course of autoregulation recovery, it would appear to remain impaired in a small number of severely injured patients.5,12 Based on these studies, it could be postulated that certain patients who survive a serious TBI by undergoing a decompressive craniectomy may do so not only with poor neurological function but also with residual impairment in cerebral autoregulation.

Current Literature

Most patients in whom this complication has occurred have sustained either a severe TBI of an extensive ischemic stroke. While it was not demonstrated preoperatively that these patients had impaired autoregulation, it would be difficult to attribute the massive and uncontrolled cerebral swelling to any other mechanism. Notwithstanding this assumption, the question remains as to how the clinical management of these patients may have been altered.

At our institutions we have had no further episodes of sudden death following cranioplasty, and this may due to a heightened awareness of this problem. There is now close attention to seizure prophylaxis and, in certain cases, preoperative electroencephalography is performed in order to detect subclinical seizure activity. There is also close attention to avoiding hypertension in the immediate postoperative period, and while we still use suction drains, we do not place them on high suction in order to prevent significant pressure differentials. Currently we do not perform any type of preoperative autoregulatory assessment, but this may be an interesting avenue of future research. If it is established that autoregulation is impaired, it may be necessary to consider a period of postoperative sedation and ventilation whereby the intracranial pressure and blood pressure are closely monitored in much the same way that patients are managed following removal of large arteriovenous malformations.8

Future Directions

There appears little doubt that the use of decompressive craniectomy will become increasingly common for patients with neurological emergencies. If this is the case, then there may be a significant number of patients who survive not only with poor neurological function but also with some degree of cerebral autoregulatory impairment. It may be that these patients need to be identified preoperatively so that measures may be put in place to prevent this complication occurring following cranioplasty.

References

  • 1

    Brain Trauma Foundation: AANS/CNS Joint Section on Neurotrauma and Critical Care: Guidelines for the management of severe traumatic brain injury. I Blood pressure and oxygenation. J Neurotrauma 24:Suppl 1S7S132007

  • 2

    Czosnyka MGuazzo EWhitehouse HSmielewski PCzosnyka ZKirkpatrick P: Significance of intracranial pressure waveform analysis after head injury. Acta Neurochir (Wien) 138:5315411996

  • 3

    Czosnyka MSmielewski PKirkpatrick PLaing RJMenon DPickard JD: Continuous assessment of the cerebral vasomotor reactivity in head injury. Neurosurgery 41:11191997

  • 4

    Czosnyka MSmielewski PPiechnik SSteiner LAPickard JD: Cerebral autoregulation following head injury. J Neurosurg 95:7567632001

  • 5

    Hlatky RFuruya YValadka ABGonzalez JChacko AMizutani Y: Dynamic autoregulatory response after severe head injury. J Neurosurg 97:105410612002

  • 6

    Honeybul S: Sudden death following cranioplasty: a complication of decompressive craniectomy for head injury. Br J Neurosurg 25:3433452011

  • 7

    Kelly AGHolloway RG: Health state preferences and decision-making after malignant middle cerebral artery infarctions. Neurology 75:6826872010

  • 8

    Morgan MKSekhon LHFinfer SGrinnell V: Delayed neurological deterioration following resection of arteriovenous malformations of the brain. J Neurosurg 90:6957011999

  • 9

    Overgaard JTweed WA: Cerebral circulation after head injury. 1. Cerebral blood flow and its regulation after closed head injury with emphasis on clinical correlations. J Neurosurg 41:5315411974

  • 10

    Panerai RBKerins VFan LYeoman PMHope TEvans DH: Association between dynamic cerebral autoregulation and mortality in severe head injury. Br J Neurosurg 18:4714792004

  • 11

    Sviri GE: Massive cerebral swelling immediately after cranioplasty, a fatal and unpredictable complication: report of 4 cases. J Neurosurg 123:118811932015

  • 12

    Sviri GEAaslid RDouville CMMoore ANewell DW: Time course for autoregulation recovery following severe traumatic brain injury. J Neurosurg 111:6957002009

Disclosures

The author reports no conflict of interest.

Response

I would like to thank Dr. Honeybul for his letter to the editor.

I cannot state that the occurrence of this phenomenon of fatal massive brain edema after cranioplasty is related to the severity of the initial brain injury. All my patients actually recovered quite well from the initial injury and were ambulatory; some were independent at the time of cranioplasty.1 Definitely there are autoregulation impairments after head injury that are related to the severity of the initial injury, but the fact that, at the time of the cranioplasty surgery, all of the 4 reported patients recovered quite well from the initial injury indicates that the initial injury was not as severe as might be expected and was probably more focal than diffuse. These patients usually show a fast recovery of autoregulation and definitely should have intact autoregulation reactivity at the time of the cranioplasty surgery several months or more after the initial injury.

The massive fatal brain edema may have been related to some autoregulation impairments and may have been associated with reduction in the cerebral perfusion pressure as the edema was global and resembled an acute severe hypoxic injury. The trigger can be vasomotor impairments initiated by the elimination of the atmospheric pressure, which leads to a significant reduction in the cerebral perfusion pressure and increased resistance to blood flow.

References

1

Sviri GEAaslid RDouville CMMoore ANewell DW: Time course for autoregulation recovery following severe traumatic brain injury. J Neurosurg 111:6957002009

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Article Information

INCLUDE WHEN CITING Published online January 22, 2016; DOI: 10.3171/2015.7.JNS151538.

© AANS, except where prohibited by US copyright law.

Headings

References

1

Brain Trauma Foundation: AANS/CNS Joint Section on Neurotrauma and Critical Care: Guidelines for the management of severe traumatic brain injury. I Blood pressure and oxygenation. J Neurotrauma 24:Suppl 1S7S132007

2

Czosnyka MGuazzo EWhitehouse HSmielewski PCzosnyka ZKirkpatrick P: Significance of intracranial pressure waveform analysis after head injury. Acta Neurochir (Wien) 138:5315411996

3

Czosnyka MSmielewski PKirkpatrick PLaing RJMenon DPickard JD: Continuous assessment of the cerebral vasomotor reactivity in head injury. Neurosurgery 41:11191997

4

Czosnyka MSmielewski PPiechnik SSteiner LAPickard JD: Cerebral autoregulation following head injury. J Neurosurg 95:7567632001

5

Hlatky RFuruya YValadka ABGonzalez JChacko AMizutani Y: Dynamic autoregulatory response after severe head injury. J Neurosurg 97:105410612002

6

Honeybul S: Sudden death following cranioplasty: a complication of decompressive craniectomy for head injury. Br J Neurosurg 25:3433452011

7

Kelly AGHolloway RG: Health state preferences and decision-making after malignant middle cerebral artery infarctions. Neurology 75:6826872010

8

Morgan MKSekhon LHFinfer SGrinnell V: Delayed neurological deterioration following resection of arteriovenous malformations of the brain. J Neurosurg 90:6957011999

9

Overgaard JTweed WA: Cerebral circulation after head injury. 1. Cerebral blood flow and its regulation after closed head injury with emphasis on clinical correlations. J Neurosurg 41:5315411974

10

Panerai RBKerins VFan LYeoman PMHope TEvans DH: Association between dynamic cerebral autoregulation and mortality in severe head injury. Br J Neurosurg 18:4714792004

11

Sviri GE: Massive cerebral swelling immediately after cranioplasty, a fatal and unpredictable complication: report of 4 cases. J Neurosurg 123:118811932015

12

Sviri GEAaslid RDouville CMMoore ANewell DW: Time course for autoregulation recovery following severe traumatic brain injury. J Neurosurg 111:6957002009

1

Sviri GEAaslid RDouville CMMoore ANewell DW: Time course for autoregulation recovery following severe traumatic brain injury. J Neurosurg 111:6957002009

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