Severe head injury

Chapter 67 Severe head injury



Despite improvements in resuscitation and vital organ support, the management of patients with traumatic brain injury in the intensive care unit (ICU) presents a challenge to all members of the critical care team. As head injury is associated with a high mortality and morbidity, the benefits of intensive treatment and care may not become apparent until months or years later during rehabilitation after injury.



EPIDEMIOLOGY


Traumatic brain injury has been termed a ‘silent global epidemic’. It accounts for up to 30% of all trauma-related deaths and is the leading cause of death in young males in developed countries. The impact of mechanisation in developing countries has resulted in a sharp increase in the incidence and mortality from vehicular trauma.


In addition to this high mortality, the cost of survivors in these societies in emotional, social and financial terms is substantial as the effects of the original injury may persist for many years.






PATHOPHYSIOLOGY


Brain injury is a heterogenous pathophysiological process. It encompasses a spectrum of injury that includes the degree of brain damage at the time of injury (primary injury) in addition to insults that occur during the post-injury phase (secondary injury). These processes are depicted in Figure 67.1.



Both primary and secondary injuries are associated with the development of variable degrees of intracranial inflammation and disruption of cerebrovascular autoregulation.


An understanding of these processes is essential in order to quantify the severity of injury, direct appropriate management strategies and interpret information from clinical monitoring systems.






CEREBRAL BLOOD FLOW AND AUTOREGULATION


Normally, cerebral blood flow is maintained at a constant rate in the presence of changing perfusion pressures by myogenic and metabolic autoregulation. These homeostatic mechanisms are impaired following head injury due to neuronal damage and intracranial inflammation. Distinct patterns of cerebral blood flow have been described following head injury that have direct clinical relevance with regard to management2 (Figure 67.2).







RESUSCITATION



INITIAL ASSESSMENT


The resuscitation of head-injured patients should follow the principles outlined in the Advanced Trauma Life Support (ATLS®) guidelines for the early management of severe trauma.6


The initial emphasis is directed at assessing and controlling the airway, ensuring adequate oxygenation and ventilation, establishing adequate intravenous access and correcting haemodynamic inadequacy. Neurological assessment and brain-specific treatment should only follow once cardiorespiratory stability has occurred. Given the direct association between hypotension and hypoxia and adverse outcomes in traumatic brain injury, this is an absolute priority.


With respect to head-injured patients, the following principles in the initial assessment apply.7,8






DISABILITY (= NEUROLOGICAL ASSESSMENT)


Assessment of neurological function following injury is important to quantify the severity of neurotrauma and to provide prognostic information. The level of function may be influenced by associated injuries, hypoxia, hypotension and/or drug or alcohol intoxication. Similarly, recording the mechanism of injury is important, as high velocity injuries are associated with a greater degree of neuronal damage. It is important to review ambulance and emergency personnel and records in order to obtain the most accurate information.






SECONDARY SURVEY


Once the initial assessment is complete and resuscitation underway, a thorough secondary survey adopting a ‘top-to-toe’ approach is mandatory. This is outlined in the ATLS® approach to the traumatised patient.6


The principles outlined in the initial assessment form the basis for prioritising interventions in the secondary survey in traumatic brain injury. Extracranial causes of hypoxia such as pulmonary contusion or haemo/pneumothorax must be excluded and promptly treated. Haemorrhage – both externally from fractures or lacerations and internally from major vascular disruption or visceral injuries – must be aggressively treated until circulatory stability is achieved. There is no place for ‘permissive hypotension’ in head-injured patients as has been advocated in selected cases of penetrating trauma.


Target mean arterial pressure should be estimated in the context of the patient’s premorbid blood pressure. Higher pressures may be necessary in hypertensive or elderly patients. The early use of inotropes such as adrenaline or noradrenaline may be necessary to achieve this.


An approach of ‘damage-control surgery’ is now advocated in head-injured patients to minimise secondary insults. In the initial 24–48 hours following injury, only life- or limb-threatening injuries should be addressed, following which patients are transferred to the ICU for stabilisation and monitoring. Thereafter, semi-urgent surgery such as fixation of closed fractures or delayed plastic repairs may be done. Patients with severe head injury undergoing prolonged emergency surgery should ideally have intracranial pressure monitoring placed as soon as possible.


Routine X-rays of the chest, pelvis and cervical spine and baseline blood tests (including blood alcohol level in appropriate cases) are part of the secondary survey.



BRAIN-SPECIFIC RESUSCITATION


The place of interventions and therapies specifically directed at reducing intracranial pressure has been extensively reviewed in evidence-based guidelines for the management of severe head injury. Whilst there is little evidence for the role of some therapies such as empirical hyperventilation and osmotherapy during resuscitation, they continue to be widely used in clinical practice.




OSMOTHERAPY


Osmotically active agents, such as mannitol, are widely used in the treatment of traumatic brain injury. Theoretically, mannitol is administered to increase plasma osmolality in order to cause net efflux of fluid from areas of damaged, oedematous brain, with resultant reduction in intracranial pressure. An intact blood–brain barrier is necessary for this to occur. Following intravenous administration of mannitol, an immediate plasma expanding effect that reduces haematocrit and viscosity ensues, which temporarily increases cerebral blood flow. Subsequent reductions in intracranial pressure probably result from restoration in cerebral perfusion pressure and rheological changes in cerebral blood flow, rather than specific cerebral dehydration.


Osmotherapy is associated with a number of potentially adverse effects. Mannitol exerts an osmotic effect over a narrow range of plasma osmolality (290–330 mosm/l) above which theoretically beneficial effects may be negated. Mannitol will induce an osmolal gap between measured and calculated osmolality, so that regular measurements of serum osmolality are necessary to monitor the amount administered. This gap may be further increased by alcohol that is frequently present in the acute period. Mannitol will enter the brain where the blood–brain barrier is damaged, thereby potentially increasing cerebral oedema by increasing brain osmolality. Mannitol is a potent osmotic diuretic that may compromise haemodynamic stability by inducing an inappropriate diuresis in a hypovolaemic patient. Consequently, systemic hypotension may ensue which may cause further cerebral ischaemia or subsequent organ dysfunction such as acute renal failure. This effect may be exacerbated by the concomitant administration of catecholamines in order to defend systemic blood pressure.


Given the high risk with minimal benefit during resuscitation, the routine use of mannitol is not recommended in the absence of raised intracranial pressure and in patients where cerebral blood flow is compromised.15


Similarly to hyperventilation, mannitol is considered as an option only in resuscitated patients with unequivocal signs of raised intracranial pressure prior to imaging or evacuation of a mass lesion. Although doses are frequently quoted as 0.25–1.0 g/kg, lower doses are equally as effective as higher doses in terms of improving cerebral perfusion and are associated with a lower incidence of side-effects.


Hypertonic saline (3% solution) exerts similar osmotic plasma expanding effects to mannitol. These solutions do not exert an osmolal gap so that serum sodium reflects serum osmolality allowing easier titration. These solutions have been advocated as ‘small-volume resuscitation fluids’ that may be very effective in restoring systemic and cerebral perfusion in the acute phase following injury. In addition to reducing intracranial pressure, these solutions would appear to be superior to mannitol for resuscitation.16




IMAGING




COMPUTED TOMOGRAPHY (CT SCAN)


CT scanning is the most informative radiological technique in the evaluation of the acute head injury and is now standard in virtually all patients following head injury. CT scanning invariably requires moving the patient to a radiological suite. This must only be done once initial assessment and resuscitation are complete and the patient is stable enough to be transported by appropriately trained and equipped personnel.


The following patients should undergo CT head scan following traumatic brain injury:




Technological advances in imaging now enable quick, high resolution digital images of the brain parenchyma and bony compartments. The most important role of CT scanning is prompt detection of mass lesion such as extradural or subdural haematomas. Thereafter, the degree of brain injury may be quantified by radiological criteria (Table 67.3 and Figure 67.3a).18


Table 67.3 Classification of CT scan appearance following traumatic brain injury.16 Examples are shown in Figure 67.3a
























Category Definition
Diffuse injury (DI) I No visible intracranial pathology seen on CT scan
DI II (diffuse injury) Cisterns are present with midline shift 0–5 mm and/or Lesion densities present No high or mixed density > 25 mm May include bony fragments and foreign bodies
DI III (swelling) Cisterns are compressed or absent with midline shift 0–5 mm No high or mixed density > 25 mm
DI IV (shift) Midline shift > 5 mm No high or mixed density > 25 mm
Evacuated mass lesion Any lesion surgically evacuated
Non-evacuated mass lesion High or mixed density lesion > 25 mm, not surgically evacuated

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Figure 67.3a Computed tomographic classification of diffuse axonal injury (Table 67.3).33 Panel (a) Diffuse injury II; Panel (b) Diffuse injury III; Panel (c) Diffuse injury IV.

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Jul 7, 2016 | Posted by in CRITICAL CARE | Comments Off on Severe head injury

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