Head Injury (Surgical Aspects)

Summary

• Head injury accounts for 3–4% of emergency department attendances, with an annual incidence of around 1500 per 100,000 population in the UK, and remains the leading cause of death and disability from childhood to early middle age [1].
• Traumatic brain injury (TBI) comprises a primary injury sustained at the moment of impact, which is not medically modifiable, and a secondary injury developing over subsequent hours to days, which is the principal target of medical and surgical management [1][2].
• Head injury is the most common cause of death after reaching the emergency room alive [3].
• Roughly 75% of head injuries are mild, 15% moderate and 10% severe, and up to half of all trauma deaths under the age of 45 are due to a head injury, with sequelae common in survivors [4].

Definition

• Head injury severity is classified by the post-resuscitation Glasgow Coma Scale (GCS): minor (GCS 15, no loss of consciousness), mild (GCS 14–15 with loss of consciousness), moderate (GCS 9–13), and severe (GCS 3–8) [1].
• The GCS motor score is the best predictor of neurological outcome [1][3].
• Sabiston and Oxford both use the three-band version, mild TBI at GCS 13–15, moderate at 9–12 and severe at 3–8 [4][6].

Sabiston makes the point that this classification is increasingly recognised as inadequate. The term traumatic brain injury encompasses a heterogeneous group of diseases with distinct means of primary prevention, targets for treatment, and trajectories of recovery, and there is growing awareness of the need to classify TBI beyond mild, moderate and severe by incorporating neuroimaging detail, TBI-specific biomarkers such as GFAP and UCH-L1, and disease modifiers including social determinants of health [6]. The chapter also notes that TBI and criminal offences are bidirectionally linked, with a high prevalence of self-reported TBI history in the incarcerated population, and that TBI overlapping with intimate partner violence has disproportionately worse outcomes than other forms of intimate partner violence [6].

Pathophysiology

• Cerebral perfusion pressure (CPP) equals mean arterial pressure (MAP) minus intracranial pressure (ICP); normal cerebral blood flow of about 55 mL/min per 100 g of brain tissue is preserved across a MAP range of 50–150 mmHg through cerebral autoregulation, which can be disrupted after trauma [1].
• The Monro–Kellie doctrine holds that the cranium is a rigid box containing a nearly incompressible brain; expanding mass lesions are initially compensated by exclusion of venous blood and CSF, but further expansion produces an exponential rise in ICP [1].
• Uncontrolled ICP rise causes herniation syndromes: subfalcine, where the cingulate gyrus passes under the falx; uncal, where the temporal lobe passes over the tentorium compressing CN III; and central or tonsillar herniation compressing the brainstem, producing Cushing's triad of hypertension, bradycardia and irregular respiration as a late sign of impending herniation, or "coning" [1][3].
• Sabiston expresses the same doctrine as the reason mass lesions matter surgically: any increase in intracranial blood displaces brain and CSF within the fixed space of the skull, and the building pressure ultimately seeks an exodus by pushing the brain downward through the foramen magnum or across the tentorium or falx [6].

The three primary injuries

Sabiston divides primary brain injury into three components, which can occur in isolation or in any combination [6].

Fractures of the cranial vault and skull base are classified as open versus closed by violation of the overlying skin and soft tissue, depressed versus non-depressed, and linear versus comminuted. Skull base fractures should always prompt assessment for associated cranial nerve injuries, cerebrovascular injuries and CSF fistulas because of the close anatomical relationships, and they frequently accompany intracranial haemorrhage because disruption of the bone commonly disrupts the underlying meningeal arteries or dural venous sinuses [6].

• Intracranial haemorrhage is subdivided by compartment: epidural haemorrhage between dura and skull, typically from a meningeal artery tear; subdural haemorrhage between dura and arachnoid, from injury to the bridging veins running between the brain and the dural venous sinuses; subarachnoid haemorrhage into the spinal fluid spaces around the cortical vessels; and intraparenchymal or intracerebral haemorrhage, sometimes by a coup–contrecoup mechanism [6].
• Small intraparenchymal bleeds are also called contusions, and Sabiston's caution about them is that although initially underwhelming on imaging and physical examination, contusions can blossom and become life threatening within hours to days, earning them the label "talk and die" [6].
• Intraventricular haemorrhage is seen but rarely in isolation, because the blood must originate somewhere [6].
• Epidural and subdural collections occupy the space outside the brain and are therefore both the most likely to place external pressure on it and cause herniation, and the most amenable to urgent surgical decompression [6].
• Traumatic subarachnoid haemorrhage must be distinguished early from aneurysmal rupture, since aneurysmal bleeds are managed differently, though both carry a risk of cerebral vasospasm [6].

• Diffuse axonal injury (DAI), also called traumatic axonal injury or shear injury, is caused by rotational acceleration–deceleration injury to the white matter tracts, producing primary axotomy or functional or anatomical disruption of those pathways; in severe cases the primary axotomy is followed by a secondary axotomy of apoptosis and degeneration over the subsequent 6 to 12 hours [6].
• Visible lesions on MRI and CT are believed to be just the tip of the iceberg of the actual injury, so it is virtually impossible to know the true incidence and prevalence of DAI with current clinical neuroimaging [6].
• DAI should be on the differential in a patient who fails to improve after evacuation of a subdural or epidural haematoma, or who remains unconscious despite the absence of haemorrhage on CT, although the utility of pursuing clinical MRI is uncertain given its weak correlation with outcomes [6].

Secondary brain injury

• Secondary brain injury is driven by a self-perpetuating cycle of raised ICP, reduced cerebral perfusion, hypoxia, deranged autoregulation, and increased metabolic demand from seizure, pyrexia, and inflammation [1].
• Sabiston's account adds the mechanism and the epidemiology: at least half of all patients hospitalised with TBI have polytrauma or other associated injuries, which both raises their risk of secondary injury and forces competing life-threatening injuries to be managed simultaneously [6].
• Severe TBI disrupts cerebral vessel autoregulation, and adding systemic hypotension to impaired autoregulation reduces cerebral blood flow and produces relative ischaemia; that cycle is exacerbated by systemic hypoxia, intracranial hypertension and cerebral inflammation, leading to excitotoxicity, calcium influx and Na⁺/K⁺-ATPase dysfunction, and culminating in neuronal dysfunction and death [6].
• Elevated ICP is a global measure that may reflect oedema, cerebral venous outflow obstruction, hyperaemia from loss of autoregulation, mass effect or disturbed CSF circulation, but crucially, secondary brain injury may occur even in the absence of intracranial hypertension [6].
• At least 3% of dementia cases in the general population are attributable to TBI, and Sabiston regards this as likely an underestimate [6].

Clinical features

• Extradural haematoma classically produces transient loss of consciousness followed by a lucid interval, then rapid deterioration with contralateral hemiparesis, reduced conscious level, and ipsilateral pupillary dilatation; this "talk and die" pattern occurs in only about one-third of cases but is critical to recognise [1][3].
• Chronic subdural haematoma, common in older adults with cerebral atrophy and stretched bridging veins, presents with gradual deterioration over days to weeks, often after a trivial or unrecalled impact, especially on antiplatelet or anticoagulant therapy [1].
• Signs of basal skull fracture include Battle's sign, mastoid bruising associated with a middle fossa fracture and facial nerve injury; "raccoon eyes", periorbital bruising indicating an anterior fossa fracture; haemotympanum; and CSF rhinorrhoea or otorrhoea [1][3][4].
• A dilated or "blown" pupil suggests ipsilateral uncal herniation compressing the oculomotor nerve [1][3].
• Concussion presents with confusion and amnesia, without necessarily any loss of consciousness; post-concussive syndrome comprises persistent headache, dizziness, and neurocognitive disturbance [1].
• Cushing's reflex of bradycardia, hypertension and altered or Cheyne-Stokes respiration is a late sign of impending herniation [3].

The pupil examination

• Sabiston treats the pupils as a formal part of the assessment rather than an incidental sign, to be performed at the same time as the GCS once ABC has been stabilised [6].
• The normal light reflex requires a functioning lens, retina, optic nerve, brainstem and oculomotor nerve, and the consensual response assesses the function of the contralateral oculomotor nerve [6].
• Absence or asymmetry of these reflexes may indicate herniation or brainstem ischaemia; new pupillary changes or anisocoria, defined as unequal pupils with more than 1 mm of difference, may indicate a rise in ICP requiring reimaging or intervention [6].
• A unilateral fixed and dilated pupil may represent herniation, whereas bilateral fixed and dilated pupils may reflect global anoxia and a dismal prognosis [6].
• The examination may be unreliable after traumatic globe rupture or other ophthalmological trauma, and metabolic, pharmacological, toxic, surgical or genetic causes can all produce pupillary abnormality, but Sabiston's rule is that pupillary abnormalities should be presumed to indicate a primary brain injury until proven otherwise [6].

Etiology

• Road traffic accidents are the leading cause of head injury, up to 50% of cases, followed by falls and assault; firearms are the third leading cause in the USA [1].
• Oxford gives the same three as the commonest reasons in the UK: falls, road traffic accidents and assaults [4].
• Non-accidental injury must be considered in children and vulnerable adults, suggested by delayed presentation, injuries of disparate age, retinal haemorrhages, bilateral chronic subdural haematomas, multiple skull fractures, and neurological injury without external signs of trauma [1].
• Intracerebral or intraparenchymal haematoma, usually frontal or temporal, is the most common brain injury in blunt trauma [3].
• Diffuse axonal injury is a form of primary injury seen in high-energy accidents, usually rendering the patient comatose, and is associated with poor outcomes [1][3].

Diagnosis

• On CT, extradural haematoma appears as a lentiform, biconvex hyperdense collection constrained by dural attachments to the skull; acute subdural haematoma appears as a diffuse concave, crescent-shaped collection free to spread over the brain surface because the dura is not adherent to the brain; chronic subdural haematoma appears diffusely hypodense [1][3].
• Diffuse axonal injury shows haemorrhagic foci in the corpus callosum and dorsolateral rostral brainstem on CT, but MRI is more sensitive, showing blurring of grey-white matter and multiple small punctate haemorrhages, classically as multifocal hyperintense lesions at the grey-white matter interfaces, graded in increasing severity with involvement of the cerebral lobes, corpus callosum and brainstem [1][3][6].
• A cervical spine fracture is found in up to 10% of moderate-to-severe TBI and must be presumed until excluded [1].
• Indications for head CT in the ABSITE account include suspected skull penetration, CSF or blood discharge from nose or ear, haemotympanum, intoxication, altered consciousness, focal signs, any loss of consciousness, and head injury with additional trauma; GCS 14 or less warrants head CT, and GCS 8 or less warrants intubation and ICP monitoring [3].

• Sabiston sets out what the non-contrast head CT is being read for: presence or absence of fracture, intracranial haemorrhage, midline shift, and the appearance of the basal and perimesencephalic cisterns, with routine scanning of the cervical spine at the same time to exclude acute fractures or traumatic dislocations [6].
• If life-threatening injuries in a polytrauma patient mandate immediate operative exploration for haemorrhage control, CT should be delayed until after stabilisation, and an intraoperatively placed ICP monitor can be a useful adjunct where there is concern about undiagnosed intracranial injury or an extended operating time [6].
• Where a polytrauma patient has an impaired GCS and a suspected unilateral intracranial mass lesion evidenced by a unilateral fixed and dilated pupil, an exploratory burr hole may be performed in theatre concurrently with laparotomy or thoracotomy, but Sabiston stresses this situation should rarely occur, because CT neuroimaging is best used to guide emergent evacuation of epidural and subdural haematomas [6].
• The same scenario is the one ABSITE Review describes as an unstable patient with a blown pupil, in whom hypotension from abdominal or pelvic bleeding should be addressed before head CT, with a burr hole considered only if CT access will be significantly delayed [3].

Scoring and Severity

• The Glasgow Coma Scale sums eye-opening (1–4), verbal (1–5), and motor (1–6) responses; intubated patients receive a verbal score of "1T", so the best possible score for an intubated patient is 11T [1][3][4][6].
• Of the three components, the motor score carries the most prognostic weight [1][6].
• Sustained ICP above 20–25 mmHg is associated with poor outcome; target parameters in neurointensive care include PaCO₂ 4.5–5.0 kPa, PaO₂ above 11 kPa, MAP 80–90 mmHg, ICP below 20 mmHg, CPP above 60 mmHg, and sodium above 140 mmol/L [1][3].
• Craniotomy is generally indicated for significant neurological deterioration or midline shift greater than 5 mm on imaging [3].
• Skull fracture surgical indications include depression greater than 1 cm, contamination in an open fracture, or persistent CSF leak unresponsive to conservative treatment [3].
• Peak ICP and brain swelling typically occur 48–72 hours after injury [3].
• The Glasgow Outcome Scale (good recovery, moderate disability, severe disability, persistent vegetative state, death) quantifies long-term recovery [1].

Physiological targets and how the GCS is used over time

Sabiston tabulates the Brain Trauma Foundation and American College of Surgeons TQIP targets separately for the prehospital and emergency department phase and for the intensive care unit [6]:

Table reformats the goals of treatment for traumatic brain injury [6]. Two thresholds in that table differ from the numbers taught elsewhere: hypotension is defined at a systolic below 100 mmHg, not 90 mmHg, and intracranial hypertension is defined as persistent elevation above 22 mmHg rather than 20 [6].

• The GCS is a repeated measure, not a single number: it should be determined at least every 30 minutes in the prehospital setting and whenever there is an apparent change in mental status, and should be measured before sedative or paralytic drugs are given if the patient's stability allows [6].
• An initially depressed GCS may reflect true injury severity, but may equally reflect haemorrhagic shock with poor cerebral perfusion, hypoglycaemia, seizure activity, sedatives or other ingestions, all of which may improve the score once addressed [6].
• The Simplified Motor Score and Simplified Verbal Score are also in some prehospital use [6].

Sabiston uses the Glasgow Outcome Scale-Extended (GOSE) as its main outcome metric, an eight-point scale running from 1 dead, 2 vegetative state, 3 lower severe disability with complete dependence, 4 upper severe disability with dependence for some activities, 5 lower moderate disability with inability to return to work or social activities, 6 upper moderate disability with return to work or social function at reduced capacity, 7 lower good recovery with minor social or mental deficits, to 8 upper good recovery [6]. Acute-phase scales include the Rancho de Los Amigos Scale and the Galveston Orientation and Amnesia Test [6].

Treatment and Management

• Resuscitation follows ATLS principles, beginning with airway and cervical spine control, with hypoxia and hypotension avoided to prevent secondary injury; blood glucose is checked early to exclude reversible hypoglycaemia [1].
• ICP is controlled first by simple measures, raising the head of the bed, loosening a tight collar, and controlling seizures and pyrexia, before escalating to sedation, analgesia, and paralysis [1][3].
• Mannitol, loaded at 1 g/kg then 0.25 g/kg every 4 hours, or hypertonic saline, can be used to temporise or treat raised ICP by an osmotic effect [1][3].
• Modest relative hyperventilation to a PaCO₂ of 30–35 mmHg or 4.5–5.0 kPa produces cerebral vasoconstriction to lower ICP, but excessive hyperventilation risks cerebral ischaemia [1][3].
• Routine, non-directed corticosteroids in severe head injury increase mortality and are not recommended [1].
• Prophylactic antiepileptics such as phenytoin, fosphenytoin or levetiracetam for about a week are given to patients at high risk of early seizures with moderate-to-severe TBI [1][3].
• Blind nasogastric or nasotracheal tube placement is contraindicated with suspected skull base fracture [1][3].
• Anticoagulation should be reversed with vitamin K, prothrombin complex concentrate or DOAC-specific reversal agents in patients on anticoagulants with an abnormal head CT; a normal CT still warrants a repeat scan at 8 hours because of the risk of delayed bleeding [1][3].
• Enteral nutrition should begin within 72 hours of injury [1].
• Second impact syndrome, malignant brain swelling after a repeat and apparently trivial injury while still symptomatic, means symptomatic athletes must not return to play [1].
• Oxford adds that systemic analgesia should be avoided until full neurological assessment is made, and that an anaesthetist should be involved for airway management in a patient with a GCS below 8 or an AVPU score of P or U [4].

The three prehospital pitfalls

• Sabiston frames prehospital management around three things to be anticipated, prevented and avoided in any patient with suspected TBI: hypoxia (saturation below 90%), hypotension (systolic below 100 mmHg), and hyperventilation (end-tidal CO₂ below 35), with monitoring at least every 5 minutes, or continuously where available [6].
• Preventing those three pitfalls is what the Excellence in Prehospital Injury Care Study implemented across more than 130 EMS systems in Arizona, improving TBI outcomes [6].
• Ventilation of patients with altered consciousness should target an end-tidal CO₂ of 35 to 45 mmHg, and both hypothermia and hyperthermia should be avoided [6].

• The single exception to the ban on hyperventilation is a patient with a prehospital GCS below 9 and signs of imminent herniation, Cushing's triad, posturing or lateralising findings, or unilateral or bilateral fixed dilated pupils, in whom hyperventilation should temporarily target an end-tidal CO₂ of 30 to 35 mmHg [6].
• Two other prehospital points are stated as negatives: hyperosmolar therapy with mannitol or hypertonic saline should not be given for the prophylactic treatment of suspected elevated ICP in the prehospital setting, having shown no benefit in large randomised trials, and the evidence for hypertonic fluids prehospital is weak [6].
• Prehospital tranexamic acid is described only as used empirically in some practice settings for clot stabilisation in patients with suspected intracranial haemorrhage or elevated ICP [6].
• Patients with suspected moderate to severe TBI should be transported directly from the scene to the highest-level trauma centre available, and any patient with suspected TBI of any type, particularly with polytrauma, should go directly to the nearest trauma centre rather than being stabilised at a non-trauma centre first [6].

Critical care management

• Goal-directed treatment extends from the prehospital and emergency department phases into the ICU.
• Systolic and mean arterial pressure should be tracked closely to avoid hypotension and optimise CPP; body temperature, glucose and electrolytes should be kept in the normal range; and hyponatraemia should specifically be avoided because of the risk of cerebral oedema [6].
• Patients with severe TBI merit frequent monitoring of serum sodium and osmolality because they are at risk of developing diabetes insipidus or SIADH [6]. Paroxysmal sympathetic hyperactivity, or "storming", can occur after severe TBI, is associated with elevated catecholamines producing hypertension and other negative effects, and is commonly treated with beta-blockade, though evidence for benefit is variable [6].

• ICP monitoring is indicated for comatose patients with a GCS of 8 or less and evidence of structural brain injury on CT, or in patients judged at high risk of progression because of large contusions or coagulopathy, and may also be considered in moderate TBI undergoing urgent extracranial surgery [6].
• The external ventricular drain's advantage over an intraparenchymal bolt is the ability to drain CSF and thereby lower ICP; subdural and epidural monitors tend to be less accurate and are used less [6].
• Sabiston's caveat is important: monitoring should not replace careful, repeated neurological assessments and prompt repeat CT imaging in cases of neurological deterioration, and in under-resourced settings reasonably good outcomes from severe TBI can still be obtained using institutional protocols of empiric treatment of elevated ICP, repeat imaging and meticulous clinical examination [6].

Treatment of intracranial hypertension follows a three-tier approach [6]. Tier 1 elevates the head of the bed to 30 degrees with the head neutral to improve cerebral venous outflow, taking care that cervical immobilisation devices do not obstruct jugular venous flow, adds short-acting sedation such as propofol or fentanyl in intubated patients to allow frequent reassessment off sedation, and uses intermittent CSF drainage where an EVD is in place. Tier 2 adds hyperosmolar therapy with mannitol or hypertonic saline, with serum sodium and osmolality checked every 6 hours and treatment held if levels reach 160 mEq/L or 320 mOsm/L respectively; a single test dose of neuromuscular paralysis is given, with continuous infusion only if the test dose reduces ICP; and hyperventilation to a PaCO₂ of 30–35 mmHg may be considered although brain hypoxia may result from the reduced cerebral blood flow. Tier 3 comprises decompressive bilateral craniectomy, continuous neuromuscular blockade if the tier 2 test dose worked, or barbiturate coma with continuous EEG titrated to burst suppression; hypothermia is not recommended as salvage treatment for intracranial hypertension [6]. In a deeply sedated patient, the pupillary examination and the ICP measurement are all that remain, and a persistently elevated ICP or a new blown pupil necessitates emergent CT neuroimaging [6].

Sabiston tabulates eleven treatments that should be avoided in severe TBI: mannitol by non-bolus continuous infusion; scheduled infusion of hyperosmolar therapy every 4–6 hours; lumbar drainage of CSF; furosemide; routine use of steroids; routine therapeutic hypothermia to below 35 °C; high-dose propofol to attempt EEG burst suppression; hyperventilation to a PaCO₂ below 30 mmHg; routinely raising CPP above 90 mmHg; platelet transfusion in adults on antiplatelet therapy; and antibiotic prophylaxis for external ventricular drain placement [6].

• Other supportive measures: nutritional support should begin within 24 to 48 hours of injury with full nutrition by 7 days at the latest, enterally by preference, because the hypermetabolic and hypercatabolic state lasts from 1 week to several months [6].
• Anticonvulsant prophylaxis is given to prevent early post-traumatic seizures within the first week [6]. Once there is no evidence of ongoing intracranial haemorrhage, pharmacological VTE prophylaxis should be started as soon as 24 to 48 hours after injury, because of high VTE rates in this population [6].
• The dopamine agonist amantadine may improve cognitive function, especially when given within the first week [6].
• Early tracheostomy within the first 5 to 7 days should be considered in patients requiring mechanical ventilation, to reduce ventilator-associated pneumonia and other complications [6].
• Coagulopathy should be reversed when apparent on laboratory testing or from a history of anticoagulant use, to limit expansion of intracranial bleeding, using prothrombin complex concentrate for anticoagulants and desmopressin for non-aspirin antiplatelet agents [6].

Surgeries

• Significant extradural haematoma requires urgent transfer for surgical evacuation, typically via craniotomy, in deteriorating or comatose patients or those with large bleeds; smaller bleeds may be observed with serial imaging [1].
• Acute subdural haematoma from high-energy injury with significant midline shift or deteriorating neurology requires urgent evacuation, typically by craniotomy or craniectomy [1].
• Chronic subdural haematoma is generally drained through burr holes; if clinically stable, a 7–10 day delay may be used to allow platelet function to normalise after stopping antiplatelet agents, and liquefaction of clot over 7–10 days can allow less invasive burr-hole evacuation even of some acute collections [1].
• ICP monitoring uses an intraparenchymal bolt or an external ventricular drain, which also allows therapeutic CSF drainage, indicated for GCS 8 or less with head injury, suspected raised ICP, or inability to follow the clinical examination, as when the patient is intubated [1][3].
• Depressed skull fractures, where bone is displaced inward by at least the thickness of the skull and which are usually compound, require exploration and elevation, especially with intracranial air suggesting a dural breach; fractures through air sinuses are managed as open fractures with broad-spectrum antibiotics with or without exploration [1].
• Traumatic intraventricular haemorrhage causing hydrocephalus requires ventriculostomy [3].

Operative thresholds and the craniectomy question

• Sabiston gives explicit volumetric criteria. An epidural haematoma of more than 30 mL, in association with neurological deficits or radiographic signs of midline shift or effacement of the basal cisterns, is commonly accepted as the criterion for emergent craniotomy
• A subdural haematoma of at least 1 cm in size, or with any midline shift, in combination with a decline in neurological examination should also prompt evacuation [6].
• Regardless of examination findings, a large mass lesion should be evacuated before neurological deterioration develops, if that accords with the patient's goals of care [6].
• Both types are treated with a formal craniotomy centred on the clot, rather than a burr hole, and depending on brain swelling the neurosurgeon may elect to leave the bone flap off (a craniectomy) to allow the brain to heal before coverage.
• A recent international trial reached equipoise on routine craniectomy versus craniotomy [6].
• ICP monitors are often placed at the time of craniotomy, particularly for a preoperative GCS below 8, at the operating surgeon's discretion [6].

• Decompressive craniectomy is considered when ICP cannot be controlled medically, though evidence for long-term outcome benefit is limited [1][3].
• Sabiston states the trial evidence behind that caution: decompressive craniectomy for intracranial hypertension in the absence of mass lesions is performed at some institutions as tier 3 management but is not well supported by the literature
• The 2011 randomised DECRA trial showed that the successful reduction in ICP achieved by decompressive craniectomy was associated with worse neurological outcomes at 6 months, with similar findings in the 2016 RESCUEicp trial [6].

Burr holes, maxillofacial and spinal injury in Schwartz's account

• Schwartz keeps ICP under 20 mmHg (normal upper limit 10) with cerebral perfusion pressure above 60, evacuates haematomas on clot volume, shift over 5 mm (not absolute), location, GCS and ICP, small posterior fossa clots for brainstem compression, small clots to relieve refractory ICP, and treats open or depressed fractures and penetrating wounds operatively; the general surgeon without neurosurgical cover must know burr-hole placement for a life-threatening epidural haematoma, whose course is loss of consciousness, a lucid interval and recurrent coma with an ipsilateral fixed dilated pupil as the temporal lobe compresses the third nerve and brainstem: epidurals need evacuation within 70 minutes while subdurals may wait, the hole is made on the side of the dilated pupil, external carotid branches are usually ligated for access, no attempt is made to control intracranial bleeding through the hole, the head is wrapped in a bulky dressing and the patient transferred for craniotomy [11].
• Secondary injury is limited by avoiding systolic under 100 mmHg, PaO₂ under 60 or saturation under 90%, keeping PCO₂ 35–40 (hyperventilation below 30 only briefly for acute hypertension), using sedation, osmotic diuresis, paralysis, ventricular drainage and barbiturate coma in sequence, noting that moderate hypothermia (32–33°C) helped experimentally but not clinically and decompressive craniectomy remains controversial after a multicentre trial, and giving 7 days of prophylactic anticonvulsants [11].
• Maxillofacial injury is divided into upper (frontal sinus and brain), mid (orbits, nose, zygomaticomaxillary complex) and lower (mandible) face, high energy fracturing frontal sinus, orbital rims and mandible and low energy nose and zygoma; bleeding from facial fractures is controlled by nasal packing, Foley tamponade of the posterior nose and oropharyngeal packing with prompt angioembolisation for exsanguination, tooth-bearing fractures are open fractures needing antibiotics and semi-urgent repair for airway, occlusion and aesthetics, orbital fractures threaten vision, cause diplopia and enophthalmos, nasoethmoid fractures threaten the lacrimal system and cribriform plate with CSF rhinorrhoea, and three-dimensional CT follows a cranial nerve examination [11].
• Cervical spine injuries are reduced and stabilised by supervised axial traction with tongs or, more often, a halo vest, or braced; fusion is performed for neurological deficit, angulation over 11° or translation over 3.5 mm, or persistent instability, immediate surgery for deterioration or fracture-dislocation with incomplete deficit, and urgent decompression for bilateral locked facets with incomplete tetraplegia or deterioration, surgery within 24 hours shortening stay and complications; methylprednisolone (24-hour infusion within 3 hours, 48-hour within 3–8 hours) is no longer recommended, complete injuries are essentially untreatable, and about 3% of flaccid quadriplegics have concussive injury and recover [11].

Complications

• Depressed skull fractures carry a high incidence of infection, neurological deficit, and late-onset epilepsy [1].
• Skull base fractures may be complicated by pituitary dysfunction, arterial dissection, and cranial nerve deficits including anosmia, facial palsy and hearing loss; persistent CSF leak can result in meningitis [1].
• Electrolyte disturbance is common in TBI: cerebral salt wasting and SIADH both cause hyponatraemia, which worsens brain swelling, so hypotonic fluids are avoided, while impaired ADH secretion causes diabetes insipidus with hypernatraemia [1].
• Post-traumatic seizure cumulative probability ranges from 2% in mild TBI to 60% in severe TBI, with risk factors including intracerebral haemorrhage, depressed skull fracture and dural tear [1].
• Coagulopathy after TBI results from release of tissue thromboplastin [3].
• Cervical collars, especially if ill-fitting, may increase ICP and impair airway management [2].

Prognosis

• Prompt evacuation of extradural haematoma without associated primary brain injury carries an excellent prognosis [1].
• Chronic subdural haematoma in the elderly is a common and treatable cause of acute neurological deterioration [1].
• Diffuse axonal injury carries a very poor prognosis [3].
• Penetrating head injury has the worst survival of all head injury types [3].
• UK trauma audit data show higher mortality when severe TBI is managed at non-neurosurgical centres, supporting early transfer regardless of the ultimate need for surgery [1].
• Reduced CPP results in secondary traumatic brain injury and worsens outcomes; hypotension and hypoxia are the principal preventable drivers of secondary injury [2][3].

Prognostication and the 72-hour rule

• Sabiston is unusually direct about the limits of prognostication and its consequences.
• After discharge, TBI recovery is varied and poorly understood, with predictions limited to 6 months; it is unknown at what point recovery plateaus, and in some patients post-TBI neuroplasticity continues for multiple years [6]. Currently available prognostic models do not adequately predict long-term outcomes for individual patients and should be used with caution when making treatment-limiting decisions: despite broad acceptance in research, the IMPACT and CRASH-TBI models are infrequently used clinically and predict only 35% of the variance in patient outcomes [6].
• The one exception is the Baylor score for penetrating intracranial gunshot wounds, which does adequately predict mortality and functional outcomes to inform goals-of-care discussions acutely [6].

• From that follows the practical rule.
• Clinical fluctuations during the first 72 hours after injury may help inform prognosis and trajectory, and patients with severe TBI should receive full treatment for at least 72 hours unless their goals of care do not align with a trial of full treatment [6].
• There is a growing consensus that premature withdrawal of life-sustaining measures, meaning within 72 hours, can lead to a self-fulfilling prophecy of fatalism or inappropriate therapeutic nihilism, and that a substantial minority of patients with seemingly devastating TBI can recover to independent functional status [6].
• The chapter closes on Hippocrates: no head injury is too severe to despair of, nor too trivial to ignore [6].

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