Neurocritical Care

3. Medical Care of Traumatic Brain Injury

A 22-year-old patient was in a bar fight and got hit in the head multiple times. He was intubated by a paramedic. On arrival, he is comatose. There are marked bruises in his face and swollen eyelids. His eyes are not opening to pain. Pupils are small, but with good light responses. Corneal reflexes cannot not be obtained, and oculocephalic reflexes cannot not be tested due to uncertainty of associated spine injury. The other brainstem reflexes are intact. There is extensor posturing. CT scan shows evidence of multiple contusions in the frontal and temporal lobes. There is no evidence of a subdural or epidural hematoma. CT of the cervical spine is normal. His alcohol level is markedly increased at 0.3%. Initial examination does not reveal any other systemic injury or fractures, and his vital signs are stable. Arterial blood gas is normal.

What do you do now?

It is of primary importance to understand the causes and consequences of coma in a patient with a traumatic brain injury. Think—at least—of five crucial issues.

First issue: One has to determine whether neurosurgical intervention is needed. Urgent neurosurgical indications are often obvious at the time of arrival and usually involve the presence of a large cerebral contusion creating mass effect and brain tissue displacement. The presence of an acute subdural or epidural hematoma on admission CT scan is always neurosurgical terrain (Figure 3.1). Be warned, these hematomas can emerge quickly, and a normal CT scan after any significant trauma may not mean much. A repeat CT scan should be performed if the clinical examination does not fit the neuroimaging findings, and perhaps the threshold should be even lower in intoxicated patients. A depressed skull fracture will need to be explored by the neurosurgeon.

Second issue: Is the patient actively bleeding? Some patients are on warfarin and this will need to be reversed immediately with vitamin K, and, because of the urgency and possible surgery, with recombinant activated factor VII or prothrombin complex concentrate. Most neurosurgeons prefer an INR of less than 1.5 before surgery.

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FIGURE 3.1 Early CT scan after traumatic brain injury showing major contusional lesions and subdural hematomas with mass effect.

Third issue: There are often major confounders—as it is alcohol intoxication in our case example. A toxicology screen may be needed but a careful history remains most valuable. It is unlikely that the current presentation of extensor posturing is explained by alcohol, but his level of responsiveness could be markedly confounded with such ethanol level in the blood. (This level is lethal in a naive drinker and therefore indicates that the patient is a chronic alcoholic.)

Fourth issue: Any comatose patient after traumatic brain injury (TBI) is at high risk of increased intracranial pressure. Options are an intraparenchymal probe or a ventriculostomy. Most major trauma centers use a fiber-optic device that measures ICP. A ventriculostomy can be placed, but in patients with a small ventricle size and risk of further compression, this is a second target of approach. Placement of an intraparenchymal ICP monitor provides not only an intracranial pressure value, but also the cerebral perfusion pressure (CPP) that can be calculated knowing the mean arterial blood pressure (MAP). The abbreviated formula is CCP = MAP - ICP. The optimal ICP and CPP are currently defined as an ICP less than 20 mmHg and a CPP between 50 and 70 mmHg.

Indications for intracranial monitoring have been well set and include patients with a severe TBI defined as coma, decerebrate, or decorticate posturing, and an abnormal CT scan (contusions, shear lesions, early brain edema). Any patient that will require deep sedation—usually when pulmonary injury is present—is probably best managed by monitoring intracranial pressure. The value of brain tissue oxygen monitoring using an additional intraparenchymal probe to guide the management of TBI has not been established.

Fifth issue: Treatment of increased intracranial pressure first requires mundane interventions such as aggressive oxygenation, avoidance of hypercarbia, treatment of posttraumatic seizures, but also reducing intrathoracic (PEEP values less than 15 mmHg) and intra-abdominal pressure. Fentanyl 1 mg/kg per hour, atracurium 0.5 mg/kg per hour or midazolam 0.1 mg/kg per hour might be necessary to adequately sedate the patient and have the patient synchronize the mechanical ventilator. Although commonly used in TBI, the effect of opiates on ICP is variable, and we have seen patients with reduced intracranial compliance in which the ICP increased after the administration of these drugs. Seizures will have to be treated, and baseline EEG might be necessary if focal seizures have occurred. It is common practice to treat more severely injured stuporous or comatose patient with IV levetiracetam or, less preferably, fosphenytoin (Figure 3.2).

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FIGURE 3.2 Optimizing conditions and treatment for increased intracranial pressure (modified from Wijdicks, The Comatose Patient. Oxford University Press, New York, 2008).

Treatment of intracranial pressure is best first managed with hyperventilation (arterial PCO2 in the 30s) and mannitol using 1 to 2 g/kg. The use of hypertonic saline requires the placement of a central venous catheter, and waiting for that to be in place could markedly delay initial treatment of ICP. In equivalent osmolar doses, mannitol and hypertonic saline appear to have comparable effects on ICP and CPP. However, hypertonic saline can be administered in higher concentrations (23.4%), which can be effective even after mannitol or lower concentrations of hypertonic saline have failed to reduce ICP.

There is controversy whether hypothermia may improve outcome. Earlier studies showed better outcome after aggressive treatment with hypothermia, but this was not confirmed by subsequent larger clinical trials. The effect of hypothermia on ICP management, however, is substantial and has been repeatedly documented. Therefore, moderate hypothermia (33–35 degrees Celsius) is an eloquent way of reducing ICP as an additional treatment to the usual ICP-lowering agents.

Any unsuccessful control of ICP will have to be treated with decompressive craniectomy; either bifrontal craniectomy or hemicraniectomy. In extreme situations, patients with refractory ICP have benefited from abdominal decompression. The initial experience with decompressive craniectomy has shown significant reduction in ICP surges, but a recent randomized trial using bifrontotemporoparietal decompressive surgery found no improvement in outcome (the patient selection in this trial has been criticized because patients could be considered candidates for surgery after already 15 minutes of refractory ICP). Another trial (RESCUEicp) is ongoing.

A long-standing discussion has been whether treatment of traumatic head injury should be “ICP or CPP driven.” Studies have not found any difference between these two approaches. However, treatment of CPP alone with less attention to increased intracranial pressure may be a wrong approach. It is not only cerebral perfusion that matters, and increasing ICP will eventually lead to brainstem displacement and permanent brainstem injury.

Treatment of TBI also involves other aspects of care (Table 3.1). Some have argued that in the most severe cases prophylactic placement of a vena cava filter is a better option than waiting for pulmonary emboli to occur. In many of these patients, treatment with subcutaneous heparin may not suffice and may potentially increase the probability of hemorrhage in blossoming cerebral contusions. There is little consensus on how to proceed in such patients and how to identify those at very high risk of fatal pulmonary emboli. Filter placement may be an option if long-term care is anticipated in polytraumatized patients.

TABLE 3.1 Initial Priorities after Traumatic Brain Injury

Need for ICP Control?

Osmotic diuretics, Mannitol (20%, 1–2 g/kg) or Hypertonic Saline (30 ml of 23%)

Hyperventilation (short term and PaCO2 around 30 mmHg)

Hypothermia (cooling device set to 33–34¡C)

Decompressive surgery (Bifrontotemporoparietal craniectomy; evacuation of subdural hematoma or contusion with mass effect)

Need for seizure control?

Levetiracetam loading 2000 mg IV in cerebral contusions, increased ICP and skull fractures.

Need for better oxygenation?

Endotracheal intubation and mechanical ventilation

Careful use of PEEP

Midazolam infusion for sedation.

Gastrointestinal prophylaxis is essential for patients on a mechanical ventilator who have a substantial risk of gastrointestinal bleeding. Patients should be placed on lansoprazole or famotidine (a component of the “ventilator bundle”).

Much of the treatment in TBI is recognition and early treatment of infections. This includes ventilator-associated pneumonia, urinary tract infections, but also catheter (line) sepsis; all complications that need to be treated appropriately. Early tracheostomy (and reducing time on the ventilator), close monitoring of intravascular catheters and prompt removal when infected or no longer necessary, surveillance for the development of deep venous thrombosis in upper and lower extremities, and early placement of a gastrostomy may all reduce complications and improve the chances of survival and functional outcome in general.

KEY POINTS TO REMEMBER ABOUT TRAUMATIC BRAIN INJURY

· Place an ICP monitor in any comatose patient with early CT scan abnormalities.

· Maintain ICP less than 20 mmHg and CPP between 60 and 70 mmHg (CPP is MAP - ICP).

· Hypertonic saline requires central access and has become a preferred method to quickly and effectively lower ICP.

· Last resort measures are induced hypothermia or decompressive craniectomy in refractory ICP

· Treat infections aggressively.

· Think early about other prophylactic measures (GI protection and surveillance for DVT).

Further Reading

Brain Traumatic Foundation; American Association of Neurological Surgeons; Congress of Neurological Surgeons; Joint section on Neurotrauma and Critical Care, AANS/CNS, Bratton SL, Chestnut RM, Ghajar J, McConnell Hammond FF, Harris OA, Hartl R et al. Guidelines for the management of severe traumatic brain injury. VI. Indications for intracranial pressure monitoring. J Neurotrauma 2008; 24: S37–44.

Cooper DJ, Rosenfeld JV, Murray L, et al. Decompressive craniectomy in diffuse traumatic brain injury. N Engl J Med. 2011;364:1493–1502.

Dietrich WD, Bramlett HM. The evidence for hypothermia as a neuroprotectant in traumatic brain injury. Neurotherapeutics 2010; 7: 43–50.

Hijaz TA, Cento EA, Walker MT. Imaging of head trauma. Radiol Clin North Am 2010; 49:81–103.

Kamel H, Navi BB, Nakagawa K et al. Hypertonic saline versus mannitol for the treatment of elevated intracranial pressure: a meta-analysis of randomized clinical trials. Crit Care Med 2011;39:544–559.

Li LM, Timofeev I, Czosnyka M, Hutchinson PJA. The surgical approach to the management of increased intracranial pressure after traumatic brain injury. Anesth Analg 2010; 111; 736–748.

Lingsma HF, Roozenbeek B, Steyerberg EW et al. Early prognosis in traumatic brain injury: from prophecies to predictions. Lancet Neurol 2010; 9:543–554.

Maas AL, Stocchetti N, Bullock R. Moderate and severe traumatic brain injury in adults. Lancet Neurol 2008; 7: 728–741.

Smith M. Monitoring intracranial pressure in traumatic brain injury. Anesth Analg 2008; 106:240–248.