Click on Guidelines for the Management of Severe Traumatic Brain Injury of the Brain Trauma Foundation, American Association of Neurological Surgeons and Congress of Neurological Surgeons for the 2007 guidelines.

     The primary objectives of the intensive care unit are to optimize cerebral perfusion and brain tissue oxygenation, minimize brain swelling, and avoid medical and surgical complications while the brain recovers by:

1. Continuing to monitor blood pressure and brain oxygenation
   • Maintain CPP (cerebral perfusion pressure) above 70 mmHg. This is 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 (Brain Trauma Foundation, 2000i)
   • Maintain arterial pO2 above 98 mmHg
   • If the MABP/ICP slope is less than 0.13, then hypertensive CPP therapy is likely to produce a better outcome than ICP therapy (Howells, et al 2005).
   • In severe TBI
     • Measure CBF with the xenon technique, several times a day and measure AVdO2 with blood samples from a catheter in the jugular bulb, several times a day. The product of the CBF and AVdO2 is an estimate of the cerebral metabolic rate for oxygen.  In severe TBI, cerebral hypoxia is common, even with CPP > or = 70; is associated with GCS score, CT scan severity, and mortality; and is related to cerebral hypoperfusion (Dunham, et al 2004).

       Although jugular bulb oximetry is the most widely used method of monitoring cerebral oxygenation, a multiparameter sensor inserted into the brain tissue may better reflect regional brain oxygenation (Gupta, et al 1999; Haselman & Fox, 2000) and is associated with a normalization of cerebral metabolism (Stahl, et al 2001). Transcranial cerebral oximetry is a non-invasive method that uses near-infrared technology to measure cerebral saturation (Dunham, et al 2002). A new ultrasonic device for blood flow volume assessment supports bedside assessment comparable to xenon technique (Soustiel, et al 2003).

       Although jugular venous oxygen saturation (Sjvo2) is used to monitor global oxygenation, brain tissue Po2 (Pbto2) is used to monitor local oxygenation (Gopinath, et al 1999). Cerebral autoregulation can be monitored continuously, graded, and reliably assessed using a moving correlation analysis of CPP and CBF velocity (Lang, et al 2002)

     • Administer narcotic sedation, systemic neuromuscular paralysis, osmotic or loop diuretics, moderate hyperventilation, or barbiturates, only if necessary to control brain swelling
     • Hyperbaric oxygenation therapy may improve aerobic metabolism (Rockswold, et al 2001). The addition of HBOT significantly reduces the risk of death but not of favourable clinical outcome. The routine application of HBOT cannot be justified (Bennett, et al 2004). There is insufficient evidence to prove effectiveness or ineffectiveness for HBOT in TBI (McDonagh, et al 2004).
     • The effect of normobaric hyperoxia is controversial, but in patients with severe TBI it can improve indices of brain oxidative metabolism (Tolias, et al 2004), but it may not (Diringer, et al 2007).

2. Continuing to monitor ICP
   • Patients
     • Monitor ICP for all patients with severe head injury, i.e. with a Glasgow Coma Scale score of 3-8 after cardiopulmonary resuscitation, who also:
       • Have an abnormal CT scan, i.e. a scan that reveals hematomas, contusions, edema, or compressed basal cisterns, OR
       • Have a normal CT scan but 2 or more of the following features upon admission: over 40 years of age, unilateral or bilateral motor posturing, systolic blood pressure < 90 mm Hg (Brain Trauma Foundation, 2000l)
       • Monitor ICP for patients with large posttraumatic intracranial lesions (Marion, 1998)
       • Monitor ICP selectively for conscious patients with mild or moderate head injury and traumatic mass lesions

   • Methods
     • The ventriculostomy system is still considered the most reliable because it enables CSF to be drained periodically, monitors pressure throughout the ventricles, and detects immediate changes in ICP. Percutaneous computed tomographic (CT)-controlled ventriculostomy (PCV) may be more efficient and allow exact catheter positioning (Ruchholtz, et al 1998; Brain Trauma Foundation, 2000j)
     • The fiberoptic ICP monitor avoids problems associated with the ventriculostomy system, such as difficulty inserting a catheter into the ventricles, hemorrhage, and infection, but does not allow drainage of CSF for control of elevated ICP and has higher costs
     • The use of external ventricular drainage catheters impregnated with minocycline and rifampin can significantly reduce the risk of catheter-related infections (Zabramski, et al 2003)

3. Treating ICP - although an ICP threshold that is uniformly applicable is unlikely to exist, current data support 20-25 mm Hg as an upper threshold above which treatment to lower ICP should be generally initiated (Brain Trauma Foundation, 2000j; Chesnut, 1997). ICP-oriented therapy should be used in patients whose slope of the MABP/ICP regression line is at least 0.13, that is, in pressure-passive patients (Howells, et al 2005). Greater systolic ICP wavefront slope during inspiration after TBI is consistent with prior observations in subjects with hydrocephalus. The strong correlation between ICP slope and simultaneous mean ICP suggests that increasins ICP slope might indicate loss of intracranial compliance after TBI. (Westhout et al, 2008).
   • Analgesics, Sedatives, and Neuromuscular Blockade
     • Narcotics, such as morphine sulfate, are recommended as the first level of therapy in severe TBI, since they also can achieve airway reflex depression
     • Narcotics can be supplemented with sedatives, such as benzodiazepines or propofol, which also facilitate diagnostic and therapeutic procedures, such as neuromuscular blockade
     • Neuromuscular blockade (particularly patients who are agitated or confused during transport), with short-acting paralytics for the least interference with the neurologic exam; may not be effective as a routine sedation strategy for patients with severe TBI (Juul, et al 2000)

   • Intermittent Ventricular CSF Drainage

   • Mannitol
     • Indicated prior to ICP monitoring only if there are signs of transtentorial herniation or progressive neurological deterioration not attributable to systemic pathology
     • After ICP monitoring, only if documented intracranial hypertension, but then:
       • as quickly as possible
       • as a bolus if possible, and
       • without repeated doses, if possible, due to potential renal toxicity. However, intermittent boluses of mannitol have been administered following intermittent CSF drainage (Marion, 1998); a normal osmole gap, found at trough times, indicates sufficient clearance for a new mannitol dose (Garcia-Morales, et al 2004)
     • Mannitol therapy for raised ICP may have a beneficial effect on mortality when compared with pentobarbital (Schierhout & Roberto, 2002)
     • High-dose mannitol appears to be preferable to conventional-dose mannitol in the pre-operative management of patients with acute intracranial haematomas (Roberts, et al 2003)
     • Long term administration of mannitol can induce significent increases in cerbrospinal fluid osmolarity in patients with severe head injury; CSF osmolarity should be measured regularly in all patients receiving mannitol for longer than 24 hrs. If CSF osmolarity increases, discontinuation or tapering of mannitol therapy should be considered (Polderman, et al 2003)

   • Hypothermia for 24 hours can reduce elevated ICP (Marion, 1998) and hasten neurologic recovery (Marion, et al 1997) if there do not appear to be other systemic effects (Chesnut, 1997). Mild hypothermia can prevent ICP elevation in patients without diffuse brain swelling and with ICP > 20 mm Hg but < 40 mm Hg after conventional therapy (Shiozadi, et al 1998). Hypothermia to a target temperature between 32 degrees C and 33 degrees C, a duration of 24 hours, and rewarming within 24 hours were all associated with reduced risks of poor neurologic outcome compared with normothermia (McIntyre, et al 2003)
     
     Compared with short-term mild hypothermia, long-term mild hypotermia, long-term mild hypothermia significantly improves sthe outcome of severe traumatic brain injured patients with cerebral contusion and intracranial hypertension without significant complications. Data suggest that 5 day of short-term cooling when mild hypothermia is used to control refractory intracranial hypertension in patients with severe traumatic brain injury (Jiang, et al 2006).
     
     However, treatment with hypothermia, with the body temperature reaching 33 degrees C within 8 hours after injury, is not effective in patients with severe TBI (Clifton, et al 2001). Hypothermia is not thought to be beneficial in the management of severe head injury (Harris, et al 2002)

   • Hyperventilation - Recommended only when the ICP elevation has proved refractory to other treatments, or for catastrophic ICP until the cause of ICP can be determined and the ICP directly treated. Early, brief, moderate hyperventilation does not impair global cerebral metabolism in patients with severe TBI (Diringer, et al 2000). Aggressive hyperventilation produces a marked reduction in cerebral blood flow and can exacerbate, rather than reduce, secondary brain injury (Yundt & Diringer, 1997). In brain tissue adjacent to cerebral contusions or underlying subdural hematomas, even brief periods of hyperventilation can significantly increase extracellular concentrations of mediators of secondary brain injury, especially during the first 24-36 hours after injury (Marion, et al 2002). Hyperventilation therapy should be avoided during the first 5 days after severe TBI and particularly during the first 24 hours (Brain Trauma Foundation, 2000h). The data available are inadequate to assess any potential benefit or harm that might result from hyperventilation in severe head injury (Roberts & Schierhout, 2005).

   • Decompressive craniectomy should be routinely performed before irreversible ischemic brain damage occurs when there is progressive therapy-resistant ICP correlated with GCS score, decebrate posturing, dilating of pupils, electrophysiological parameters, and CT findings (Guerra, et al 1999). Decompressive craniectomy, when applied as part of protocol-driven therapy, yields a satisfactory rate of favorable outcome (Timofeev, et al 2006; Arabi, et al 2006). Decompressive laparotomy can be a useful adjunct in the treatment of ICH failing maximal therapy following TBI (Joseph, et al 2004).

   • High-dose barbiturate therapy is efficacious in lowering ICP and decreasing mortality for uncontrollable ICP refractory to other conventional and surgical ICP-lowering treatments (Brain Trauma Foundation, 2000g). However, there is no evidence that barbiturate therapy in patients with severe head injury improves outcome. Barbiturate therapy results in a fall in blood pressure in 1 in 4 patients, and this hypotensive effect will offset any ICP lowering effect on cerebral pefusion pressure (Roberts, 2000)

4. Identifying and correcting abnormalities in glucose, electrolyte, and body temperature levels
   • Treat hyponatremia, the most common electrolyte abnormality (due to causes such as inappropriate antidiuretic hormone and cerebral salt-wasting (Zafonte, et al 1997)) with hydration and salt replacement (Zafonte & Mann, 1997)

   • Maintain body temperature between 37 and 38 degrees C, to avoid hyperthermia. However, hypothermia may be a safe and effective means of managing ICP (see Hypothermia before Hyperventilation above)

5. Providing nutritional supplementation - early feeding may be associated with a trend towards better outcomes in terms of survival and disability (Yanagawa, et al 2002)
   • Within 48 hours of injury provide supplementation to meet the increased need for protein and calories, preferably with an enteral feeding tube (or with parenteral intravenous hyperalimentation if enteral feeding is not well tolerated) to reduce the degree of protein wasting in severe TBI. Gastrostomy or jejunostomy tubes are indicated in the acute phase of severe TBI, because enteral feedings are often not well tolerated, probably due to impaired gastric emptying or increased ICP.
     • Provide 2 - 2.3 g protein/kg/d as small peptides if renal function is normal; 40%-70% above basal needs as total calories, with 30%-40% of calories as lipid to minimize hyperglycemia, or with a carbohydrate-free diet to prevent hyperglycemia; and a lipid source with 50% - 70% medium-chain triglycerides and an omega-6 to omega-3 ratio of 2:1 - 8:1 (Twyman, 1997; Ritter, et al 1996).
     • Zinc supplementation may also be indicated in severe TBI during the immediate postinjury period (Young, et al 1996)

   • Within 72 hours provide full-strength, full-rate feedings via nasojejunal or percutaneous endoscopic jejunostomy or gastrostomy feeding tubes (Twyman, 1997). Nasogastric tubes should be used as soon as the patient is stable, but may contribute to regurgitation and pharyngeal irritation.  Total parenteral nutrition (TPN) is another safe, alternative route for minimally responsive patients

   • Within 7 days postinjury replace 140% of resting metabolism expenditure in nonparalyzed patients and 100% of resting metabolism expenditure in paralyzed patients, with at least 15% of calories as protein. The preferred method is jejunal feeding by gastrojejunostomy because of ease of use and avoidance of gastric intolerance (Brain Trauma Foundation, 1996)

   • By day 7 institute full nutritional replacement, based on the level of nitrogen wasting in TBI and the nitrogen sparing effect of feeding (Brain Trauma Foundation, 2000f)

6. Administering anticonvulsant therapy only to patients who:
   • Had a seizure during the acute period. Seizures occur in >1 in 5 patients during the 1st week after moderate-to-severe TBI (Vespa, et al 1999). Anti-epileptics are effective in reducing early seizures, but not late seizures (Schierhout & Roberts, 2001)
   • Have severe TBI (Chang, et al 2003); click on Practice parameter: Antiepileptic drug prophylaxis in severe traumatic brain injury.
   • Have a nonpenetrating injury and a history of seizures
   • Are at high risk for posttraumatic seizures (PTS).
   • Have a penetrating brain injury; in these cases, anti-seizure medication should be administered only in the first week to prevent early posttraumatic seizures (click Antiseizure Prophylaxis for Penetrating Brain Injury)
   • Are diagnosed with epilepsy. Prolonged video electroencephalogram (VEEG) monitoring can distinguish epileptic and nonepileptic seizures following TBI (Hudak, et al 2004).

   Prophylactic use of phenytoin, carbamazepine, sodium valproate, or phenobarbital is not recommended for preventing late PTS, i.e. seizure occurring > 1 week postinjury, in patients who have no history of seizures and a nonpenetrating injury and patients with a penetrating injury (Brain Injury Special Interest Group, 1998). Phenytoin or carbamazepine can be used to prevent seizures in high-risk patients during the first week post injury (Brain Trauma Foundation, 2000 e) and for provoked seizures after TBI (Temkin, 2001)
   • Phenytoin is one of the least sedating anticonvulsants that can be administered intravenously. Although it can effectively reduce the incidence of early PTS, this reduction is not associated with a reduction in mortality (Haltiner, et al 1999)
   • Phenobarbitol can cause sedation but not the idiopathic febrile response caused by phenytoin in some patients
   • Carbamazepine has fewer cognitive and visumotor side effects and is recommended for patients who can tolerate enteral medications
   • Valproate therapy shows no benefit over short-term phenytoin therapy for prevention of early seizures and neither treatment prevents late seizures; the trend toward higher mortality among valproate-treated patients suggests that valproate should not be routinely used to prevent posttraumatic seizures (Temkin, et al 1999); valproate is ruled out for unprovoked seizures following TBI (Temkin, 2001) and does not have a positive effect on cognition (Dikmen, et al 2000)

7. Assessing physical, cognitive, and neurobehavioral impairments following TBI
   • Physical impairments of TBI are numerous and include:
     • Nutrition and hemorrhage of the GI system
     • Hypoxia, trauma to the chest wall, acute lung injury, respiratory infection, and neurogenic pulmonary edema
     • Fluid-electrolyte imbalance and hypothalamic-pituitary dysfunction
     • Anemia, bleeding diathesis, and thromboembolic disease
     • Neurogenic bladder, stricture, and genitourinary infection
     • Fracture, joint instability, and heterotopic ossification
     • Arrhythmia, ischemia, contusion, hypotension, and hypertension
     • Neurologic impairments, such as spasticity, rigidity, monoparesis-plegia, hemiparesis-plegia, triparesis-plegia, quadraparesis-plegia, ataxia, tremor, autonomic dysfunction, causalgia, entrapment neuropathy, field cuts, diplopia, dysphagia, and hearing loss

   • Cognitive impairments include arousal, attention, orientation, memory, apraxia, agnosia, aphasia, and abstraction

   • Neurobehavioral impairments include apathy, impulsivity, irritability, aggressiveness, anxiety, depression, emotional lability, and lack of initiative

8. Preventing complications, such as infections, DVT, pulmonary complications, and pressure sores by:
   • Mobilizing the patient frequently and daily physical therapy
   • Performing aggressive pulmonary toilet several times each day
   • Administering low-dose warfarin sodium, preferably, or pneumatic compression stockings and subcutaneous heparin

9. Repeating CT scan within 24 hours postinjury, particularly if ICP increases unexpectedly (Marion, 1998), if admission CT demonstrates evidence of a diffuse injury (Servadei, et al 2000), or if patient has coagulopathy, hypotension, ICP elevation, or marked increase in GCS score (Kaups, et al 2004).

10. Transferring the patient from ICU when brain swelling subsides (usually within 4-5 days)
    • Extubate and transfer patients who have regained consciousness. Delaying extubating patients when impaired neurologic status is the only concern prolonging intubation is not supported (Coplin, et al 2000)
    • Place a tracheostomy and a gastrostomy tube in patients who remain comatose

     A physiatrist and/or other rehabilitation specialists should be consulted when the patient is admitted to ICU, and an initial physiatric evaluation should be done within 24 hours after the injury. Acute short-term care provided in a trauma center, as opposed to a general hospital, and early initiation of rehabilitation strategies ensure the best medical and functional outcomes with the shortest possible lengths of stay. Multicenter findings support assertions that increased therapy intensity, particularly physical and psychologic therapies, enhances functional outcomes (Cifu, et al 2003)