CNS trauma accounts for almost half of all trauma deaths.
CNS trauma consists of both the primary injury, in which tissue is disrupted by mechanical force, and a secondary response, in which the body’s reaction to the injury plays an important role. Mitigation of secondary CNS injury depends on prompt diagnosis and early, goal-directed therapy. Although there is no way to minimize primary CNS injury other than with preventive strategies, secondary brain injury accounts for much of the death and disability that follows trauma.
Trauma produces shear forces that result in primary damage to neuronal cell bodies and axons and to the vasculature.
The pathophysiology of secondary injury include metabolic failure oxidative stress and a cascade of biochemical and molecular events leading to both necrotic and apoptotic cell death. Secondary injury is often exacerbated by tissue hypoxia/ ischemia and by inflammatory responses, and outcomes from TBI are influenced by a large number of interacting factors.      
Classification of head injury into primary injury and secondary injury is useful when considering therapeutic strategies.

• Primary injury is the damage produced by the direct mechanical impact mad the acceleration –deceleration stress onto the skull and the brain tissue, which results in skull fractures (cranial vault, skull base) and intracranial lesion.    
• Secondary injuries develop within minutes, hours, or days of the initial injury and cause further damage to nervous tissue. The common denominators of secondary injury are cerebral hypoxia and ischemia. Secondary injuries are caused by the following disorders.

1 Respiratory dysfunction:- hypoxemia, hypercapnia
2 Cardiovascular instability:- hypotension, low cardiac output (CO)
3 Elevation of ICP

• Metabolic derangements

    The major goal of the perioperative management of patients who have head injuries is to prevent secondary damage. Therapeutic measures based on established guidelines and recommendations must be instituted promptly and continued throughout the perioperative course. Appropriate selection of anesthetics and meticulous general management of respiration, circulation, metabolism, fluid replacement, and temperature are all essential to improve outcome after traumatic brain injury (TBI).
The initial management of these patients can significantly affect outcome. Attention to the ABCDE approach is paramount to successful resuscitation, and the trauma anesthesiologist should be intimately involved in this process.
The perioperative management of patients who have TBI focuses on aggressive stabilization of the patient’s physiologic condition and avoidance of systemic and intracranial insults that cause secondary neuronal injury, these secondary insults, while potentially preventable and treatable, can complicate the course of patients after TBI and adversely affect outcome.
Head injury practice guidelines:- In 1995, the brain trauma foundation approved guidelines for the initial resuscitation and treatment of intracranial hypertension in the severely head-injured patient, recognizing the need to standardize care to improve outcome in these patients. A task force was formed in 1998 to review and update the scientific evidence for the guidelines. These evidence-based guidelines for the management of severe TBI were published in 2000 and were update in 2007.
Recommendations from guidelines for the management of severe traumatic brain injury.
Standards based on class I evidence:- If ICP normal, avoid chronic prolonged hyperventilation therapy (PaCO2< 25mm Hg). The use of steroids is not recommended for improving outcome or reducing ICP. Prophylactic use anticonvulsants does not prevent late post traumatic seizures. Guidelines based on class II evidence:- All regions should have an organized trauma care system. Avoid or correct immediately hypotension (systolic blood pressure <90mm Hg) and hypoxia (SaO2<90% or <60 mm Hg).
 Indications for intracranial pressure (ICP) monitoring include GCS score 3 to 8 with abnormal CT scan or two or more of the following adverse features: age >40y, motor posturing, and systolic blood pressure <90mm Hg. Initiate treatment for ICP at an upper threshold above 20mm Hg. CPP value to target lies within the range of 50 to 70mm Hg. Avoid the use of prophylactic hyperventilation (PaCO2< 25mm Hg) during the first 24h after severe TBI. Mannitol is effective for control of raised ICP after severe TBI in doses ranging from 0.25 to 1 g/kg body weight. High –dose barbiturate therapy may be considered in haemodynamically stable salvageable severe TBI patients who have intracranial hypertension refractory to maximal medical and surgical ICP lowering therapy. Provide nutritional support (140% of resting energy expenditure in non- paralyzed patients and 100% of resting energy expenditure in paralyzed patients) using enteral or parenteral formulas containing at least 15% of calories as protein by day 7 after injury.
Patient with mild TBI (GCS score of 13 to 15) who maintain a stable GCS score for 24 hours after injury are very unlikely to deteriorate further, although they are at risk for a number of “postconcussive” effects, including headache, memory loss, emotional liability, and sleep disturbance .
Moderate TBI (GCS score of 9 to 12) may be accompanied by intracranial lesions that require surgical evacuation, and early CT is strongly indicated. Early intubation, mechanical ventilation, and close observation may be required in the management of patients with moderate TBI because of combative or agitated behavior and the potentially catastrophic consequences of respiratory depression or pulmonary aspiration occurring during diagnostic evaluation. Extubation of the trachea can be undertaken if the patient is haemodynamically stable and appropriately responsive after the diagnostic workup. Treatment of secondary brain injury is accomplished by early correction and subsequent avoidance of hypoxia, prompt fluid resuscitation, and management of associated injuries.
Neurologic monitoring of patients with moderate TBI consists of serial assessment if consciousness and motor and sensory function. Deterioration of the GCS score is an indication for urgent CT to establish the need for craniotomy or invasive monitoring of ICP. Although mortality from moderate TBI is low, almost all patients will suffer significant long-term morbidity.
Serve TBI is classified as a GCS score of 8 or less at the time of admission and carries a significant risk for mortality. Early, rapid management focused on restoration of systemic homeostasis and perfusion-directed care of the injured brain will produce the best possible outcomes in the difficult population.
A single episode of hypoxemia (Pao2 <60 mm Hg) occurring in a patient with serve TBI is associated with nearly a doubling of mortality.
The most challenging of all trauma patients are those with severe TBI and coexisting hemorrhagic shock. A single episode of hypotension defined as systolic blood pressure lower than 90mm Hg, is associated with an increase in morbidity and doubled mortality.after severe TBI. Hypotension together with hypoxia is associated with a threefold increase in mortality. Systolic blood pressure less than 90mm Hg should be avoided, with a goal of greater than 70mm Hg MAP until ICP monitoring is instituted and CPP can be directly targeted. Contrary to practices in the past, current recommendations are to maintain a patient with severe TBI in a euvolemic state. Therefore, fluid resuscitation is the mainstay of therapy, Followed by vasoactive infusions as needed. The ideal fluid has not yet been identified, but increasing evidence suggests that hypertonic saline solutions are optimal. Correction of anemia from blood loss is the first priority, with a goal of maintaining the hematocrit at greater than 30% after the initial ABCD management of a patient with severe TBI, a stepwise approach to maintenance of CPP is initiated, with a currently recommended goal range of 50 to 70mm Hg.
Decompressive craniotomy is a surgical procedure used to control severely elevated ICP.
Decompressive craniotomy is indications for selected anatomic patterns of TBI, such as when CPP cannot be maintained despite vigorous application of the previously described therapies.

Recent evidence suggests that relieving ICP by removal of piece of cranium and use of a dural patch may improve mortality and morbidity in patients who might not otherwise survive.

References

• Miller’s anesthesia- 7th edition.
• Neuroanesthesia – Phillippa Newfield, James Cottrell, 5th edition.
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