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).

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.

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