American Brain Injury Consortium

ABIC PATIENT CARE GUIDELINES

May 1, 2010 To optimize the care of head injured patients and to standardize their treatment at ABIC centers insofar as possible, we provide the following summary of management of these patients based on GUIDELINES FOR THE MANAGEMENT OF SEVERE HEAD INJURY published by the American Association of Neurological Surgeons and the Brain Trauma Foundation. All ABIC centers must agree to treat patients within the boundaries of these guidelines. While the guidelines list some of the treatments as options, we believe the specified options are the best available from the literature and should be taken as treatment guides for ABIC centers. TREATMENT IN THE EMERGENCY DEPARTMENT 1. Patients are resuscitated according to the American College of Surgeons Committee on Trauma (ACS-COT) Advanced Trauma Life Support (ATLS) protocol. Adequate oxygenation and ventilation must be achieved (SaO2 > 95% or PaO2 > 100 mm Hg); intubation and mechanical ventilation usually are necessary in comatose patients. If patients are intubated, paralytic agents should be used only as necessary to ventilate, transport and manage the patient safely. Paralysis with long-lasting agents can complicate neurological evaluation, and their use should be restricted to the ICU after the patient has clinically stabilized. Normocarbia (PaCO2 > 30 mmHg) should be maintained in the absence of clinical evidence of herniation (pupillary dilatation or asymmetric reactivity, motor posturing, coma). Fluids should be given to the point of apparent euvolemia as estimated by a normal systolic arterial pressure (SAP) 120 mmHg, central venous pressure (CVP) (5-10 mmHg) or adequate urine output. Hypotension (SAP < 90 mmHg) and hypoxia (PaO2 < 60 mmHg) must be avoided. No treatment for intracranial hypertension should be given unless patients deteriorate clinically or show signs of herniation or CT evidence of elevated ICP (e.g., compressed or absent cisterns). Mannitol and hyperventilation should not be used prophylactically. If there is neurological deterioration or signs of herniation, the patient should be hyperventilated (PaCo2 to 30 torr) and/or given mannitol (1 gm/kg). Early intensive hyperventilation can worsen cerebral hypoperfusion soon after injury. A CT scan should be done promptly in stable patients. CT scans should be done emergently in comatose patients or those who deteriorate clinically.

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TREATMENT IN THE OPERATING ROOM 1. Acute extracerebral hematomas > 1 cm in thickness (or estimated to be greater than 25cc in volume) should promptly be evacuated by craniotomy. The neurosurgeon should consider acute removal of intracerebral hematomas causing substantial mass effect. If unstable comatose patients are taken immediately from the Emergency Department for surgery for intrathoracic or intraabdominal injury, a decision must be made in the OR to perform diagnostic bur holes or establish intracranial pressure monitoring if there is a significant scalp injury or signs of herniation. There are insufficient data to allow a consensus on the specifics of operative management of cranial or cerebral traumatic lesions (e.g. bone flap replacement, hemicraniectomy, use of prophylactic antibiotics, etc.) and the individual neurosurgeon should exercise his or her judgment regarding surgical treatment. It is imperative that adequate oxygenation and blood pressure be maintained as described in the Emergency Department section. Pressors should be used in addition to restoration of euvolemia to maintain systolic arterial pressure (SAP) > 120 mmHg. Intracranial pressure (ICP) monitoring should be established before or after surgical management in all comatose head-injured patients with an abnormal CT scan, or with two or more of the following features at admission: age > 40 years, motor posturing, or systolic blood pressure < 90 mmHg. In this trial, all comatose patients should have monitoring of ICP, optimally by ventriculostomy although other methods are acceptable. INTENSIVE CARE MANAGEMENT 1. Treatment of ICP should be initiated at an upper threshold of 20-25 mmHg. Interpretation and treatment of ICP should be corroborated by frequent clinical examinations. Repeat CT scanning should be done when there is a delayed rise of ICP or persistent intracranial hypertension despite treatment. Cerebral perfusion pressure (CPP = MAP-ICP) should be maintained above 60 mmHg. This will be accomplished usually by a combination of therapies for lowering ICP below 25 mmHG, and vasopressors (e.g. dopamine, epinephrine) to increase MAP such that CPP > 60 mmHg. If a ventricular catheter is in place, CSF drainage can be used to lower ICP until ventricular collapse precludes further fluid removal.

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Osmotic therapy (mannitol and hypertonic saline) can be used to lower ICP. Patients should be maintained at euvolemia, and mannitol should not be used when serum osmolarity > 320 mOsm. Sedation with intravenous narcotics (morphine, fentanyl), azepams (diazepam, Versed), or shortacting anesthetic agents (propofol) can facilitate the management of patients, particularly those who are agitated, and can lower ICP in some patients. Short-acting paralytic agents (vecuronium) can be used when patients must be clinically evaluated serially. Longer-acting agents (pancuronum) can be used in patients who are stable and need be examined less frequently. Chronic extreme hyperventilation (PaCO2 < 25) is harmful and should not be used. Cerebral blood flow is reduced early after severe head injury. Hyperventilation may increase the risk of ischemia and should be avoided in the first day after injury. Thereafter, it can be used for relative short periods to reduce intracranial hypertension until mannitol, sedation, paralysis or ventricular fluid drainage can lower ICP. Hyperventilation may be required for longer periods or to PaCO2 < 30 in patients with refractory intracranial hypertension; in such circumstances, jugular venous O2 saturation or cerebral blood flow monitoring may be used to monitor for cerebral ischemia. Induced barbiturate coma should be considered for persistent intracranial hypertension refractory to all other treatment including surgical decompression (partial lobectomy, hemicraniectomy, removal of craniotomy bone) if the latter is considered of potential benefit by the neurosurgeon. Considerable caution must be exercised to prevent hypotension (CPP < 60) with barbiturate use. Patients should receive 100-140% of resting metabolism expenditure of calories within 7 days of injury, preferably by an oro-jejunal or gastrojejunal route. Prophylactic anticonvulsants reduce the incidence of post-traumatic seizures during the first week after injury. Although such a reduction has not been shown to improve outcome, it is the consensus of ABIC investigators (Minneapolis 4/96) that the increased metabolism caused by seizures might be harmful and that anticonvulsants should be used for at least one week after severe head injury. TREATMENTS NOT TO BE USED

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Corticosteroids at any dose have not been shown to be beneficial and are not to be used routinely in any ABIC-associated studies. Patients in ABIC-associated trials should not be entered into any other trials.

REFERENCES 1. Guidelines for the management of severe head injury. Brain Trauma Foundation. Bullock R, Chesnut RM, Clifton G, Ghajar J, Marion DW, Narayan RK, Newell DW, Pitts LH, Rosner MJ, Wilberger JW. Medical College of Virginia, USA. Eur J Emerg Med. 1996 Jun; 3(2):109-27.

2. Guidelines for the Surgical Management of Traumatic Brain Injury Bullock, M Ross; Chesnut, Randall; Ghajar, Jamshid; Gordon, David; Hartl, Roger; Newell, David W.; Servadei, Franco; Walters, Beverly C.; Wilberger, Jack E. Neurosurgery. 58(3): Supplement, March 2006.

3. Guidelines for the management of severe traumatic brain injury. Brain Trauma Foundation; American Association of Neurological Surgeons; Congress of Neurological Surgeons; Joint Section on Neurotrauma and Critical Care, AANS/CNS, Carney NA. J Neurotrauma. 2007; 24 Supple 1