Brain Injury Symposium Management of Moderate and Severe Head Injuries
The European Brain Injury Consortium. Nemo solus satis sapit: nobody knows enough alone. Acta Neurochir (Wien). 1997;139(9):797-803 With globalization, goods, capital, culture, and knowledge readily diffuse across borders, but political and social institutions often lag a step behind. Infection and inequalities: The modern plagues. Farmer P (ed). Berkley: Universityof California Press, 1999
ATLS Procedures A: Airway with cervical spine control B: Breathing C: Circulation (MAP and capillar refill) D: Neurological deficit (GCS)
GCS (After resuscitation) GCS < 8 GCS > 8 Pupillary asimetry Isocoria Intubation HV Mannitol (0.25 a 0.5 mg/kg/bolo) CT ? Neurosurgery Intubation CT ICU Neurosurgery GCS 9 - 13 GCS 14 -15 CT Intensive - Intermediate Care Neurosurgery? Italian Guidelines for Minor Head Injury
Glasgow 9 - 13 Clinical observation 48 hs, CT and neurosurgical consultation No intracranial lesion Intracranial lesion New CT in 48 hs TCDB III Temporal Contusion TCDB I - II Contusion NICU ICP NINCU Hourly GCS
Gidelines for the management of severe traumatic brain injury Trauma Systems Initial management Resuscitation of blood pressure and oxygenation Indications for intracranial pressure monitoring Intracranial pressure treatment threshold Recommendations for intracranial pressure monitoring technology Guidelines for cerebral perfusion pressure Hyperventilation Hyperventilation Use of mannitol Use of barbiturates in the control of intracranial hypertension Rol of steroids Critical pathway for the treatment of established intracranial hypertension Nutrition Rol of antiseizure prophylaxis following head injury
Classification of evidence Class I evidence: Prospective randomized controlled trials , the (Standards) gold standard of clinical trials. However some may be poorly designed, lack sufficient patient numbers or suffer from other methodological inadequacies. Class II evidence: Clinical studies in which the data was (Guidelines) collected prospectively, and retrospective analyses that were based on clearly reliable data (observational, cohort, prevalence and case control studies) Class III evidence: Most studies based on retrospectively collected (Options) data (clinical series, databases or registries, case reviews, case report) Expert opinion.
Trauma systems Guidelines: All regions should have an organized trauma care system Options: Neurosurgeons should have an organized and responsive system of care for patients with neurotrauma. They should initiate neurotrauma care planning, including pre-hospital management and triage, direct trauma center transport, maintain appropriate call schedules, review trauma care records for quality improvement and participate in trauma education programs Trauma facilities treating neurotrauma must have a neurosurgery service, an in-house trauma surgeon, a continuously staffed and available operating room, intensive care unit and laboratory. A CT scanner must be immediately available. In rural or weather-bound communities without a neurosurgeon, a surgeon should be trained to perform accurate neurological assessment, including training to perform life-saving surgical treatment of an extracerebral hematoma in a deteriorating patient.
Initial management Severe Head Injury (GCS 8 or less) ATLS Evaluation Emergency diagnostic or therapeutic procedures as indicated Intubation 52 patients Ventilation (PCO 2 ca 35) 16 pleural drainages Fluid resuscitation 2228 ml crystalloids 1350 ml colloids Oxygenation Sedation (midazolam 52 patients) Neuromuscular paralysis (pancuronion 47 patients) Hyperventilation (8) Mannitol (1 g/kg) (7) CT 52 patients No Surgery (20) Yes ICU ICP monitoring 49 patients Yes Surgical lesion? Resolution? Yes Herniation? Deterioration?
Resuscitation of blood pressure and oxygenation
Hypotension (SBP < 90 mmHg) or hypoxia (apnea, cyanosis or SaO 2 < 90%) must be avoided and scrupulously avoided, if possible, or corrected immediately in severe TBI patients.
The MAP should be maintained above 90 mmHg through the infusion of fluids throughout the patient’s course to attempt to maintain CPP > 70 mmHg. Patients with GCS < 9 who are unable to maintain their airway or who remain hypoxemic despite supplemental O2 required that their AW be secured, preferably by endotraqueal intubation.
Differences in the incidence of hypoxia and hypotension in the Emergency Room, between 1987 and 1997 (p 0.01). Incidence of hypoxia and hypotension
GOS according to the presence of hypotension Modified from Chesnut R. Acta Neurochir Suppl 1993;59:121.
Initial Hypotension and GOS p 0.008 p 0.29 p 0.01
GOS according to the presence of hypoxia Modified from Chesnut R. J Trauma 1993;34:206
Indications for intracranial pressure monitoring Guidelines: Comatose head injury patients (GCS 3-8) with abnormal CT scans should undergo ICP monitoring. Comatose patients with normal CT scans have a much lower incidence of intracranial hypertension unless they have two or more of the following features at admission: age over 40, unilateral or bilateral motor posturing, or a systolic blood pressure of less than 90 mm Hg. ICP monitoring in patients with a normal CT scan with two or more of these risk factors is suggested as a guideline. Routine ICP monitoring is not indicated in patients with mild or moderate head injury. However, it may be undertaken in certain conscious patients with traumatic mass lesions at the discretion of the treating physician.
Intracranial pressure monitoring Differences in the use of intracranial pressure monitoring devices between 1987 and 1997.
An absolute ICP threshold that is uniformly applicable is unlikely to exist. Current data, however, support 20-25 mm Hg as an upper threshold above which treatment to lower ICP should generally be initiated.
Interpretation and treatment of ICP based on any threshold should be corroborated by frequent clinical examination and CPP data.
Recommendations for intracranial pressure monitoring technology
In patients who require ICP monitoring, a ventricular catheter connected to an external strain gauge transducer or catheter tip pressure transducer device is the most accurate reliable method of monitoring ICP and enables therapeutic CSF drainage. Clinically significant infections or hemorrhage associated with ICP devices causing patient morbidity are rare and should not deter the decision to monitor ICP. Parenchymal catheter tip pressure transducer devices measure ICP similar to ventricular ICP pressure but have the potential for significant measurement differences and drift due to the inability to recalibrate. These devices are advantageous when ventricular ICP is not obtained or if there is obstruction in the fluid couple. Subarachnoid or subdural fluid coupled devices and epidural ICP devices are currently less accurate
Maintenance of a CPP above 70 mm Hg is a therapeutic option that may be associated with a substantial reduction in mortality and improvement in quality of survival and is likely to enhance perfusion to ischemic regions of the brain following severe TBI. No study has demonstrated that the incidence of intracranial hypertension, morbidity, or mortality is increased by the active maintenance of CPP above 70 mm Hg, even if this means normalizing the intravascular volume or inducing systemic hypertension
CPP and outcome Statistical differences (two tails) for CPP were found for: GOS 2 - 5 against GOS 1 (p < 0.01), GOS 4 - 5 against GOS 1 - 3 (p < 0.01), GOS 5 against GOS 3 (p 0.02), GOS 5 against GOS 2 (p 0.01) and GOS 5 against GOS 1 (p < 0.01).
Effectiveness of raising CPP with dopamine * * p < 0.05 * * * * * Modified from Unterberg AW, J Trauma 1997;42Supp:S33
Effectiveness of head position * * p < 0.05 * Modified from Unterberg AW, J Trauma 1997;42Supp:S33
In the absence of increased ICP chronic prolonged HV therapy (PaCO 2 < 25 mmHg) should be avoided after TBI.
The use of prophylactic HV (PaCO 2 < 30 mmHg) during the first 24 hs after severe TBI should be avoided because it can compromise cerebral perfusion during a time when CBF is reduced.
HV may be necessary for brief periods when there is acute neurological deterioration or for longer periods if there is refractory intracranial hypertension. SjO2, AJDO2, PtiO2 and CBF monitoring may help to identify cerebral ischemia if HV is necessary.
The effect of hyperventilation * * p < 0.05 * * * * Modified from Unterberg AW, J Trauma 1997;42Supp:S33
Mannitol is effective for control of raised ICP after severe TBI. Effective doses range from 0.25 to 1 g/kg/body weight.
Indications to it use prior to ICP monitoring are signs of transtentorial herniation or neurological worsening not attributable to extracranial explanations. Hypovolemia should be avoided by fluid replacement.
Serum osmolarity should be kept below 300 mOsm because of concern for renal failure.
Euvolemia should be maintained by adequate fluid replacement. A Foley catheter is essential in these patients.
Intermittent boluses may be more effective than continuous infusion.
Effectiveness of mannitol 0.5 g/kg/bolus administration Modified from Unterberg AW, J Trauma 1997;42Supp:S33 * p < 0.05 SjO2 basal 69%, Pti O2 basal 39 mmHg, * *
Use of barbiturates in the control of intracranial hypertension
High-dose barbiturate therapy is efficacious in lowering ICP and decreasing mortality in the setting of uncontrollable ICP refractory to all other conventional medical and surgical ICP-lowering treatments, in salvageable TBI patients. Utilization of barbiturates for the prophylactic treatment of ICP is not indicated.
Replace 140% of resting metabolism expenditure in nonparalyzed patients and 100% in paralized patients using enteral or parenteral formulas containing at least 15% of calories as protein by day 7 after injury.
The preferable option is use of jejunal feeding by gastrojejunostomy due to ease of use and avoidance of gastric intolerance.
Role of antiseizure prophylaxis following head injury Standard: Prophylactic use of phenytoin, carbamazepine, phenobarbital or valproate, is not recommended for preventing late posttraumatic seizures. Options: Anticonvulsivants may be used to prevent early PTS in patients at risk. This prevention does not indicate an improvement in outcome.
Hospital Fernández, Buenos Aires, Severe Head Injury mortality rates from 1987 to 1999