A young man with no significant past medical history was admitted to the Emergency Department following an assault. His Glasgow Coma Score on arrival was 8 with a motor score of 4 and there was evidence of an external head injury. Pupils were symmetrically reactive. He was intubated to facilitate further management. Both primary and secondary surveys were unremarkable apart from multiple contusions to the face and scalp. Multi-slice CT showed no intrabdominal or intrathoracic injury but significant intracranial pathology with subarachnoid and intraventricular blood and multiple, principally frontal contusions. No associated neuraxial fracture was seen.

Urgent neurosurgical opinion was sought which confirmed no immediate target for surgical intervention. The patient was transferred to the intensive care unit where appropriate monitoring was established including the insertion of a fibreoptic subdural intracranial pressure bolt. Initial intracranial pressure was measured at 18 mmHg. Sedation with propofol and alfentanil infusions was titrated to a RASS score of -3, ventilation adjusted to a PaO2 > 13 kPa and PaCO2 4.5-5.0 kPa as per the Brain Trauma Foundation guidelines and an infusion of noradrenaline started to achieve a cerebral perfusion pressure of 60 mmHg. The patient was nursed 30° head-up and although active cooling was not undertaken, temperature maintained at less 35-37.5°C.

There was initial stability but approximately 24 hours after admission sustained rises in intracranial pressure (ICP) in excess of 25 mmHg were seen, necessitating boluses of sedation, the addition of atracurium by infusion, administration of hypertonic saline, cooling to 35°C and brief periods of hyperventilation to a PaCO2 4.0-4.5 kPa albeit without significant control. Urgent repeat CT brain was undertaken which showed evolution of the contusions with signifiant oedema and loss of both the lateral ventricles and basal cisterns.

On further consultation, neurosurgical colleagues again felt that no immediate surgical option was viable; in particular that attempts to insert and external ventricular drain were unlikely to be successful and that contusionectomy would produce significant disability. The patient was randomised into the RESCUEicp trial and thiopentone infusion started at a rate to produce isoelectrical activity on three lead electroencephalogram.

What are the management options for refractory intracranial hypertension?

Stephen Shepherd

Effective cerebral oxygenation requires an adequate cerebral perfusion pressure which in turn depends upon the ‘resistance’ offered by intracranial or jugular venous pressure (JVP), whichever is the higher. ICP is determined by the relative proportion of soft tissue, blood and CSF within the cranium. In healthy, supine adults normal ICP is 5-15 mmHg, becoming sub-atmospheric on standing (around -10 mmHg).(1)

Sustained elevations in ICP have been shown to adversely affect patient outcomes; intracranial hypertension therefore provides a crucial modifiable risk factor in the management of head-injured patients. The most recent Brain Trauma Foundation guidelines suggest that an ICP of 20-25 mmHg is the threshold at which treatment should be initiated.(2,3) In most cases, relatively conservative methods such as head elevation, sedation and osmotherapy are sufficient.(4) However, in some cases however, ICP remains elevated despite the optimal use of these treatments.Limited treatment modalities exist where no potentially evacuable mass lesions or CSF drainage opportunities exist.

Cooling may be considered for either control of ICP or neuroprotection. The benefit of hypothermia in the latter has been convincingly demonstrated after a transient global brain ischaemia following a cardiac arrest and is recommended in this setting by the European Rescuscitation Council.(5) A recent Cochrane meta-analysis of moderate hypothermia in the setting of traumatic brain injury concluded that there was no beneficial effect of routine hypothermia in TBI.(6) Patients receiving hypothermia were at a greater risk of developing pneumonia and slightly more prone to die. However, hypothermia combined brain-tissue oxygen guided management, may show improved neurological functioning but no survival benefit.(7) The ongoing Eurotherm trial may help to answer this question with more certainty; in this study patients are randomised to a minimum of 48 hours of hypothermia at 32-35 °C with a primary outcome measure of neurological status at 6 month follow-up.(8)

The efficacy of barbiturate coma in lowering ICP was demonstrated over twenty years ago. (1,9) No recent work has established the efficacy of this treatment in refractory intracranial hypertension and barbiturate therapy has become less popular treatment option due to their many potential side effects.(9) An improved survival has been demonstrated retrospectively where barbituate coma was used as a rescue therapy after failure of hyperosmolar treatment.(10) Maintenance of higher cerebral perfusion pressure in this setting was associated with better survival. The RESCUEicp trial comparing rescue barbiturate coma with decompressive craniectomy is currently ongoing.(11)

Various surgical options are available outside of primary management which may limit or prevent secondary insult in traumatic brain injury; indications for these interventions are recognised internationally with recommendations for the appropriate timing of surgery.(12) The role of decompressive craniectomy however, remains controversial. This may be performed prophylactically when removing mass lesions or as a rescue therapy, although as yet no high-quality evidence demonstrates an improved clinical outcome.(1,13) The most recent trial of this therapy demonstrated unfavourable functional outcomes although significant methodological issues existed.(14) These may be addressed by the ongoing RESCUEicp trial are made available.(11) Until then, it appears the role of surgery in the management of brain ischaemia is limited to focal lesions.

---

 

Lessons Learnt

As yet no convincing paradigm exists for the management of refractory hypertension. Ongoing studies may better elucidate the role of pharmcosuppression and surgical decompression but as yet hypothermia appears to offer little benefit on it’s own.

---

 

References

1. Wijayatilake DS, Shepherd SJ, Sherren PB. Updates in the management of intracranial pressure in traumatic brain injury. Current Opinion in Anaesthesiology. 2012 Oct;25(5):540–7.
2.  Metzger J, Eastman A. Year in review 2008: Critical Care-trauma. Crit Care. 2009.
3. Brain Trauma Foundation, American Association of Neurological Surgeons, Congress of Neurological Surgeons. Guidelines for the Management of Severe Traumatic Brainj Injury 3rd Edition. Journal of Neurotrauma. 2007 Apr 26;24:1–116.
4. Dorfman JD, Burns JD, Green DM, DeFusco C, Agarwal S. Decompressive laparotomy for refractory intracranial hypertension after traumatic brain injury. Neurocrit Care. 2011 Dec;15(3):516–8.
5. Deakin CD, Nolan JP, Soar J, Sunde K, Koster RW, Smith GB, et al. European Resuscitation Council Guidelines for Resuscitation 2010 Section 4. Adult advanced life support. Resuscitation. 2010. pages 1305–52.
6. Sydenham E, Roberts I, Alderson P. Hypothermia for traumatic head injury. Cochrane Database Syst Rev. 2009;(2):CD001048.
7. Lee HC, Chuang HC, Cho DY, Cheng KF, Lin PH, Chen CC. Applying Cerebral Hypothermia and Brain Oxygen Monitoring in Treating Severe Traumatic Brain Injury. WNEU. Elsevier Inc; 2010 Dec 1;74(6):654–60.
8. Andrews PJD, Sinclair HL, Battison CG, Polderman KH, Citerio G, Mascia L, et al. European society of intensive care medicine study of therapeutic hypothermia (32-35 °C) for intracranial pressure reduction after traumatic brain injury (the Eurotherm3235Trial). Trials. 2011;12:8.
9. Roberts I SE. Barbiturates for acute traumatic brain injury. Cochrane Database Systemic Review. 2000 Jan 1;2:CD000033.
10. Marshall GT, James RF, Landman MP, OʼNeill PJ, Cotton BA, Hansen EN, et al. Pentobarbital Coma For Refractory Intra-Cranial Hypertension After Severe Traumatic Brain Injury: Mortality Predictions and One-Year Outcomes in 55 Patients. The Journal of Trauma: Injury, Infection, and Critical Care. 2010 Aug;69(2):275–83.
11. Hutchinson PJ, Corteen E, Czosnyka M, Mendelow AD, Menon DK, Mitchell P, et al. Decompressive craniectomy in traumatic brain injury: the randomized multicenter RESCUEicp study (www.RESCUEicp.com). Acta Neurochir. Suppl. 2006;96:17–20.
12. Davella D, Brambilla G, Delfini R. Guidelines for the treatment of adults with … [J Neurosurg Sci. 2000] – PubMed – NCBI. Journal of …. 2000.
13. Eberle BM, Schnüriger B, Inaba K, Gruen JP, Demetriades D, Belzberg H. Decompressive craniectomy: Surgical control of traumatic intracranial hypertension may improve outcome. Injury. Elsevier Ltd; 2010 Sep 1;41(9):894–8.
14. Cooper DJ, Rosenfeld JV, Murray L, Arabi YM, Davies AR, D’Urso P, et al. Decompressive Craniectomy in Diffuse Traumatic Brain Injury. N. Engl. J. Med. 2011 Apr 21;364(16):1493–502.