Managing Moderate and Severe Head Injuries

Traumatic Brain Injury (TBI) is a leading cause of death and disability. It is most commonly graded using the Glasgow Coma Scale (GCS), assessed following the initial resuscitation and within 48 hours of injury. Severe is typically defined by a GCS score <9, while 9-12 represents moderate and 13-15 represents mild. [1][2]

The Goal

A principal focus of management for moderate to severe TBI is to limit secondary brain injury which the brain is especially vulnerable to in the first 24 hours. [3]

Initial Evaluation and Treatment

For prehospital management, preventing secondary brain injury is done through treating hypotension and hypoxia. Hypoxia is managed by intubation if airway concerns arise and there are trained personnel whilst hypotension is managed by adequate fluid resuscitation.

When arriving in the Emergency Department, treatment and diagnostic assessment are performed according to the Advanced Trauma Life Support (ATLS) including airway maintenance, breathing, circulation with bleeding control, disability assessment and exposure and environmental control. Important considerations in TBI include intubation if a patient has a GCS score <9 and is unable to protect their own airway, neurologic examination, and evaluation and management of increased intracranial pressure (see below).

A non contrast CT scan is performed as quickly as possible and can detect skull fractures, intracranial hematomas, and cerebral oedema. Skull base or vertebral fractures increase the risk of a blunt cerebrovascular injury which can lead to stroke. When suspected, CT angiography is performed to assess the carotid and vertebral arteries to rule such an injury out.

To prevent further bleeding, antifibrinolytic therapy in the form of tranexamic acid within 3 hours of injury is often done for patients who present with a moderate TBI (GCS 9-12) or milder injuries where intracranial bleeding is suspected.

Surgical Treatment

The decision to operate is based upon neurological status (often defined by the GCS) and findings on neuroimaging. Particular indications include:

• Epidural haematoma larger than 30mL regardless of patient’s GCS [4]
• Acute subdural haematomas >10mm or associated with >5mm midline shift regardless of GCS [5]
• Intracerebral haemorrhage in the posterior fossa when there is evidence of significant mass effect [6]
• Open skull fractures depressed greater than the thickness of the cranium or where there is dural penetration [7]
• Refractory intracranial hypertension

Managing raised intracranial pressure

Impending cerebral herniation is an emergency and patients are continuously assessed for significant pupillary asymmetry, unilateral or bilateral fixed and dilated pupils, decorticate or decerebrate posturing [insert diagram], respiratory depression, and the “Cushing triad” of hypertension, bradycardia, and irregular respiration.

When impending herniation due to elevated ICP is suspected, management measures include:

• intubation (if patients have not already been)
• head of bed (HOB) elevation and optimising venous drainage by keeping neck neutral
• brief hyperventilation to lower the CO2 in the blood [8]
• ventriculostomy and ICP monitoring (link EVD Brainbook article)
• cerebrospinal fluid drainage [9]
• sedation and analgesia [10]
• use of osmotic agents such as mannitol and hypertonic saline [11]

If the above medical measures fail, treatment options include decompressive craniectomy to give the brain room to swell, barbiturate coma, and induced hypothermia. [12] [13]

Further Management

Further management often occurs in the intensive care unit and focuses on areas including:

• Haemodynamic management with fluids and medications affecting blood pressure to ensure an adequate cerebral perfusion pressure
• Ventilation, as often traumatic brain injury patients are too sedated to maintain their own airway [14]
• Anti-seizure mediations and electroencephalography (EEG) monitoring as patients with TBI are at increased risk
• Venous thromboembolism prophylaxis as patients with TBI are at increased risk
• Management of coagulopathy as approximately one-third of patients with severe TBI demonstrate a coagulopathy increasing the risk of the bleed worsening. [15]
• Glucose control as both high and low glucose levels are associated with worse outcomes [16]
• Temperature management to avoid fever as it worsens intracranial pressure control
• Paroxysmal sympathetic hyperactivity management which occurs in approximately 10 percent of patients with severe TBI
• Nutritional support

Outcomes

Studies have suggested that patients with severe TBI have approximately a 30 percent risk of death. [17] Multiple studies indicate, however, that significant proportions (30 to 65 percent) of patients with severe TBI will regain an independence, and that functional recovery following severe TBI can occur very slowly, extending beyond even 6 to 12 months. [18, 19, 20]

References

1. Foulkes MA, Eisenberg HM, Jane JA, et al. The Traumatic Coma Data Bank: design, methods, and baseline characteristics. J Neurosurg 1991; 75:S8.
2. Kay T, Harrington DE, Adams R, et al. Definition of mild traumatic brain injury. J Head Trauma Rehabil 1993; 8:86.
3. Brain Trauma Foundation, American Association of Neurological Surgeons, Congress of Neurological Surgeons, et al. Guidelines for the management of severe traumatic brain injury. I. Blood pressure and oxygenation. J Neurotrauma 2007; 24 Suppl 1:S7.
4. Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of acute epidural hematomas. Neurosurgery 2006; 58:S7.
5. Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of acute subdural hematomas. Neurosurgery 2006; 58:S16.
6. Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of posterior fossa mass lesions. Neurosurgery 2006; 58:S47.
7. Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of depressed cranial fractures. Neurosurgery 2006; 58:S56.
8. Cadena R, Shoykhet M, Ratcliff JJ. Emergency Neurological Life Support: Intracranial Hypertension and Herniation. Neurocrit Care 2017; 27:82.
9. Carney N, Totten AM, O’Reilly C, et al. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery 2017; 80:6.
10. Devlin JW, Skrobik Y, Gélinas C, et al. Clinical Practice Guidelines for the Prevention and Management of Pain, Agitation/Sedation, Delirium, Immobility, and Sleep Disruption in Adult Patients in the ICU. Crit Care Med 2018; 46:e825.
11. Hinson HE, Stein D, Sheth KN. Hypertonic saline and mannitol therapy in critical care neurology. J Intensive Care Med 2013; 28:3.
12. Roberts I, Sydenham E. Barbiturates for acute traumatic brain injury. Cochrane Database Syst Rev 2012; 12:CD000033.
13. Sadaka F, Veremakis C. Therapeutic hypothermia for the management of intracranial hypertension in severe traumatic brain injury: a systematic review. Brain Inj 2012; 26:899.
14. Vandromme MJ, Melton SM, Griffin R, et al. Intubation patterns and outcomes in patients with computed tomography-verified traumatic brain injury. J Trauma 2011; 71:1615.
15. de Oliveira Manoel AL, Neto AC, Veigas PV, Rizoli S. Traumatic brain injury associated coagulopathy. Neurocrit Care 2015; 22:34.
16. Jeremitsky E, Omert LA, Dunham CM, et al. The impact of hyperglycemia on patients with severe brain injury. J Trauma 2005; 58:47.
17. McMillan TM, Teasdale GM, Weir CJ, Stewart E. Death after head injury: the 13 year outcome of a case control study. J Neurol Neurosurg Psychiatry 2011; 82:931.
18. Andelic N, Hammergren N, Bautz-Holter E, et al. Functional outcome and health-related quality of life 10 years after moderate-to-severe traumatic brain injury. Acta Neurol Scand 2009; 120:16.
19. Hoofien D, Gilboa A, Vakil E, Donovick PJ. Traumatic brain injury (TBI) 10-20 years later: a comprehensive outcome study of psychiatric symptomatology, cognitive abilities and psychosocial functioning. Brain Inj 2001; 15:189.
20. Katz DI, Polyak M, Coughlan D, et al. Natural history of recovery from brain injury after prolonged disorders of consciousness: outcome of patients admitted to inpatient rehabilitation with 1-4 year follow-up. Prog Brain Res 2009; 177:73.