TREATMENT Guidelines advocate the early treatment of increased intracranial pressure, since increased severity and longer duration of raised intracranial pressure are associated with a poor outcome.11,12 The accepted threshold for treatment is an intracranial pressure of 20 mm Hg. In all patients with increased intracranial pressure, a repeat CT scan should be considered to exclude surgically treatable lesions. Before initiating therapy to reduce increased intracranial pressure, practitioners need to exclude erroneous measurements and systemic causes that can be rapidly corrected. A practical algorithm is presented in Figure 2FIGURE 2 Algorithm for the Treatment of Increased Intracranial Pressure (ICP). . Medical Therapy During the past 10 years, management of increased intracranial pressure has evolved toward standardized strategies that use a “staircase” approach with an escalating treatment intensity (Figure 3FIGURE 3 Staircase Approach to the Treatment of Increased Intracranial Pressure. ). 24,25 Sedation and analgesia are used to treat pain and agitation26 and to prevent arterial hypertension and patient–ventilator dyssynchrony. Sedation increases the risk of arterial hypotension resulting from vasodilatation, making maintenance of normovolemia a prerequisite. An additional advantage of sedation is to minimize the risk of seizures.27,28 Hyperosmolar agents reduce brain volume and intracranial pressure through multiple mechanisms. In the first minutes of infusion, mannitol and hypertonic saline expand the plasma volume, decrease blood viscosity, and reduce the cerebral blood volume.29 Once plasma osmolarity increases, a gradient across the blood–brain barrier is established, and water is extracted from the brain. This effect may last for up to several hours, until the osmotic equilibrium is reestablished. The integrity of the blood–brain barrier is a prerequisite for the efficacy of hyperosmolar agents. Mannitol is an osmotic diuretic and may cause dehydration and hypovolemia. Hypertonic saline may cause abrupt increases in the sodium plasma concentration. Comparisons between mannitol and hypertonic saline for the treatment of increased intracranial pressure have not shown a clear superiority of one option over the other.29 Induced arterial blood hypocarbia (hyperventilation) reduces intracranial pressure at the expense of decreasing cerebral blood flow as a result of vasoconstriction.30 Hyperventilation carries a serious risk of cerebral ischemia. For this reason, current guidelines recommend additional monitoring for cerebral ischemia (e.g., by the monitoring of oxygen saturation in the jugular bulb and of brain-tissue oxygenation) when hyperventilation is used.31 Barbiturates depress the cerebral metabolism and reduce cerebral blood flow, causing a proportional decrease in cerebral blood volume and a decrease in intracranial pressure. Initial enthusiasm for barbiturate therapy has been tempered by the recognition of serious side effects, including cardiac depression, arterial hypotension, and an increased risk of infection.32 The administration of barbiturates is generally reserved for refractory intracranial hypertension, after other therapies have been tried and have failed.12 Mild hypothermia (32 to 34°C) is effective in decreasing intracranial pressure,33 but studies on the clinical benefit are contradictory, and current evidence does not support its general use in patients with traumatic brain injury.34,35 The effects of hypothermia are complex, and adverse effects are a particular problem in patients with traumatic brain injury who may require cooling for many days to control refractory intracranial hypertension. Surgical Therapy The surgical therapy of raised intracranial pressure includes the evacuation of mass lesions, drainage of cerebrospinal fluid, and decompressive craniectomy. Rapid detection and timely evacuation of an intracranial hematoma is a cornerstone in the management of traumatic brain injury. Guidelines on the surgical management of epidural or acute subdural hemorrhage and of brain contusions have been published, but all of them are based on class III evidence and are heavily focused on volumetric criteria.36 However, the surgical evacuation of an intracerebral or subdural hematoma may be motivated not only by volume or mass effect but also by mitigation of a toxic effect. In a study of experimental rodent models of cerebral contusions, Tanaka et al.37 found metabolic disturbances, with a massive increase in the production of excitatory amino acids and subsequent ischemic damage, in the cortex underlying blood clots. Possible benefits of surgical excision in the clinical situation are suggested by an analysis of 182 patients with cerebral contusions registered in the Japan Neurotrauma Databank.38 Currently, there are no data from randomized, controlled trials to support this approach. Drainage of cerebrospinal fluid is a simple and effective approach to reducing increased intracranial pressure. During withdrawal of cerebrospinal fluid, the pressure reading is determined more by the outflow pressure than by actual brain pressure, so that accurate monitoring of intracranial pressure is not possible with continuous drainage of cerebrospinal fluid.39 New ventricular catheters, including those with a miniature pressure transducer at the tip, may offer more accurate reading during drainage but at a higher monetary cost. Intermittent drainage when the intracranial pressure exceeds 20 mm Hg should be performed against a pressure gradient of approximately 10 cm of water. Drainage of cerebrospinal fluid through lumbar catheters is not recommended in patients with increased intracranial pressure because of the risk of herniation.40 Much interest has focused on decompressive craniectomy. The concept of decompressive craniectomy is to provide a larger reserve to compensate for increased intracranial volume. The actual volume that is gained depends on the diameter of the craniectomy. The presumed benefits of decompressive craniectomy have been challenged by the results of the Decompressive Craniectomy (DECRA) trial.25 In this study, which compared decompressive craniectomy performed within 72 hours after traumatic brain injury with maximal medical therapy in patients with diffuse brain injury whose intracranial pressure exceeded 20 mm Hg for 15 minutes or longer in a 1-hour period, mortality was similar in the two groups. However, the rate of unfavorable neurologic outcomes was significantly higher among patients undergoing decompressive craniectomy. After adjustment for baseline data, such as the reactivity of pupils, the between-group difference in outcome was not significant. The generalizability of these results is limited because of the highly selected patient population and because the study examined the effect only in patients with diffuse injuries. Decompressive craniectomy is not without risk, and adverse effects are common.41 In the ongoing Randomized Evaluation of Surgery with Craniectomy for Uncontrollable Elevation of Intracranial Pressure (RESCUEicp) study (Current Controlled Trials number, ISRCTN66202560),42 which is comparing medical therapy with decompressive craniectomy, patients with a sustained elevation in intracranial pressure (>25 mm Hg for more than 1 hour and up to 12 hours) that is resistant to initial medical therapy are randomly assigned to undergo surgery or intensive medical therapy, including the use of barbiturates. The results of this trial will provide further evidence to define the role of decompressive craniectomy in traumatic brain injury
Posted on: Wed, 22 Oct 2014 10:21:54 +0000