The standard practice in most head injury intensive care units is to elevate the head above the level of the heart in an effort to reduce intracranial pressure by facilitating venous outflow without compromising cerebral perfusion pressure (CPP) and cardiac output (Ng et al. 2004). It has been suggested that head elevation may even slightly improve CPP (Schulz-Stubner & Thiex 2006). Placing patients in an elevated head posture also facilitates early provision of enteral nutrition while also reducing the risk for gastric reflux and pulmonary aspiration when compared with patients kept in the supine position (Ng et al. 2004). However, Ng et al. (2004) note that maintaining individuals with a TBI in a flat position reduces the risk for systemic hypotension inherent in a semi-recumbent posture. Furthermore, some authors argue that a horizontal body position increases CPP, which improves cerebral blood flow (Winkelman 2000).
The EBIC stated that no consensus existed regarding the benefits of head elevation to 30 degrees when compared to the recumbent position (Maas et al. 1997). There are currently no AANS recommendations for head posture.
Table: Head Posture for the Acute Management of ABI
Head elevation was found to significantly reduce ICP when compared to a flat position in numerous studies. Reductions in ICP were observed at 15° elevation (Durward et al. 1983; Ledwith et al. 2010; Moraine et al. 2000; Schneider et al. 1993), 30° elevation (Durward et al. 1983; Feldman et al. 1992; Ledwith et al. 2010; Meixensberger et al. 1997; Moraine et al. 2000; Ng et al. 2004; Park & Ha 1992; Parsons & Wilson 1984; Rosner & Coley 1986; Schneider et al. 1993; Schulz-Stubner & Thiex 2006; Winkelman 2000), 45° elevation (Kenning et al. 1981; Mahfoud et al. 2010; Moraine et al. 2000; Schneider et al. 1993), and 60° elevation (Mahfoud et al. 2010; Ropper et al. 1982). Several studies reported that reductions in ICP following head elevation were correlated with significant improvements in CPP (Ledwith et al. 2010; Mahfoud et al. 2010; Meixensberger et al. 1997; Moraine et al. 2000; Schulz-Stubner & Thiex 2006; Winkelman 2000), although other studies did not find changes in CPP (Durward et al. 1983; Feldman et al. 1992; Ng et al. 2004; Park & Ha 1992; Parsons & Wilson 1984; Rosner & Coley 1986; Schneider et al. 1993). Only one study reported that head elevation did not improve ICP or CPP (March et al. 1990); due to the small sample size, these results should be taken with caution.
In most studies, a greater degree of elevation was associated with a greater reduction in ICP. For example, Rosner and Coley (1986) found that ICP decreased by 1 mmHg with every 10° of elevation. In an earlier study, however, Durward et al. (1983) found no significant difference in ICP reduction between different degrees of elevation. More recently, Ledwith et al. (2010) suggested that no single position is optimal for improving neurodynamic parameters in those who sustain an ABI. Participants were placed into different positions with three levels of head elevation (15°, 30°, and 45°) in a randomized order. The authors reported significant reductions in ICP with head elevations of 30° and 45° in the supine position and 15° in the right and left lateral positions; all of the reductions were similar in magnitude.
In a systematic review, Fan (2004) found 11 studies with a pooled sample of 178 participants. The authors noted that all studies found significant reductions in ICP associated with head elevation, while only six studies found significant improvements in CPP. A meta-analysis by Jiang et al. (2015) examined a total of 10 studies with a pooled sample of 237 participants. The authors found that a head elevation of 30° yielded a large effect in ICP reduction when compared to 0°. In analyses of two studies each, the authors found a moderate effect at 10° and large effects at 15° and 45° when compared to 0°. Large effects were also observed at 30° and 45° when compared to 15°. As well, the authors found no difference in ICP reduction between 30° and 45°.
There is Level 1b evidence that head elevations of 15°, 30°, and 45° effectively reduce elevated intracranial pressure post ABI when compared to a flat position.
There is conflicting (Level 1b and Level 4) evidence as to whether head elevation improves cerebral perfusion pressure post ABI.
Head elevations of 15°, 30°, and 45° can effectively lower elevated intracranial pressure post ABI.
Hypothermia is a neuroprotective treatment that has been explored as a measure to reduce secondary brain injury. It was first proposed as a possible treatment for ABI more than a half a century ago (Fay 1945), and early reports suggested that hypothermia might improve clinical outcomes. It is believed that hypothermia can control elevated ICP and limit the biochemical cascade believed to result in secondary brain injury (Clifton 2004). Neuroprotective effects include reducing cerebral metabolism, decreasing the inflammatory response, and decreasing the release of excitotoxic levels of glutamate and free radicals post ABI (Alderson et al. 2004; Chen et al. 2001; Globus et al. 1995; Marion 1997; Yan et al. 2010). Several methods of therapeutic hypothermic have been suggested. Systemic hypothermia involves cooling the entire body with cooling blankets (Qiu et al. 2007) and occasionally a gastric lavage of cold saline (Marion et al. 1993), while selective hypothermia aims to target the head specifically using a cooling cap and neckband (Liu et al. 2006).
It is important to note that prolonged hypothermia is believed to be associated with various adverse effects including arrhythmias, coagulopathies, sepsis and pneumonia, which could ultimately lead to a poorer clinical outcome (Alderson et al. 2004; Schubert 1995). It has also been suggested that there may be a threshold during rewarming, above which, pressure reactivity may reach damaging levels (Lavinio et al. 2007) and that there is a critical window beyond which hypothermia may be ineffective (Clifton et al. 2009).
The AANS noted that prophylactic hypothermia showed no significant association with improved outcomes relative to normothermic controls (Carney et al. 2017). However, they reported that increased risk of mortality may be seen when target temperatures are achieved within 2.5 hours of injury and maintained for more than 48 hours. There are currently no EBIC recommendations for hypothermia.
In the reviewed studies, therapeutic hypothermia involved cooling patients to 32-36°C for at least 12 hours. The intensity and duration of treatment was specific to each patient, although some studies involved lower temperatures or longer cooling periods. The results of two studies suggested that very mild hypothermia (35-36°C) may be just as effective as mild hypothermia (32-34°C) at improving outcomes with fewer complications (Hayashi et al. 2005; Tokutomi et al. 2009). Similarly, the length of treatment was patient-specific, ranging from one to 14 days. One trial reported that hypothermia delivered over five days showed a greater ICP reduction and more favourable long-term outcomes than a two-day treatment (Jiang et al. 2006). Most studies utilized systemic hypothermia, which was achieved with cooling blankets and/or gastric lavage. Only a few studies delivered selective hypothermia (Harris et al. 2009; Liu et al. 2006; Qiu et al. 2006), which may yield greater improvements in ICP and other outcomes when compared to systemic treatment (Liu et al. 2006).
The majority of reviewed studies found significant reductions in ICP following hypothermia when compared to baseline values (Flynn et al. 2015; Metz et al. 1996; Sahuquillo et al. 2009; Tateishi et al. 1998; Tokutomi et al. 2003) or a normothermia control group (Gal et al. 2002; Jiang et al. 2000; Lee et al. 2010; Liu et al. 2006; Marion et al. 1993; Qiu et al. 2006; Qiu 2007; Shiozaki et al. 1993; Smrcka et al. 2005; Zhao et al. 2011; Zhi et al. 2003). A portion of these studies reported significant increases in CPP accompanying ICP reduction (Gal et al. 2002; Marion et al. 1993; Marion et al. 1997; Shiozaki et al. 1993; Smrcka et al. 2005; Tokutomi et al. 2003). However, some studies did not find any significant improvement in ICP or CPP following therapeutic hypothermia (Andrews et al. 2015; Clifton et al. 2001; Maekawa et al. 2015).
There is less agreement regarding the effectiveness of therapeutic hypothermia in improving long-term outcomes. At three to six months post ABI, some studies reported that patients treated with hypothermia had more favourable outcomes on the GOS/GOS Extended and lower rates of mortality than those treated with normothermia (Hayashi et al. 2005; Jiang et al. 2000; Jiang et al. 2006; Lee et al. 2010; Liu et al. 2006; Marion et al. 1993; Marion et al. 1997; Polderman et al. 2002; Qiu et al. 2006; Qiu et al. 2007; Shiozaki et al. 1993; Smrcka et al. 2005; Yamamoto et al. 2002; Zhi et al. 2003). However, these findings were not replicated in similar studies (Gal et al. 2002; Harris et al. 2009; Shiozaki et al. 2001; Zhao et al. 2011) or in multicentre trials such as the North American Brain Injury Study (Clifton et al. 2001; Clifton et al. 2011), the Japanese Brain Hypothermia Trial (Maekawa et al. 2015), and the European Hypothermia Trial (Andrews et al. 2015). Furthermore, some studies reported that therapeutic hypothermia was associated with increased risk of serious complications (Clifton et al. 2001; Clifton et al. 2011; Qiu et al. 2006; Qiu et al. 2007; Sahuquillo et al. 2009). Pulmonary infections such as pneumonia were noted during cooling, and cardiovascular issues such as arrhythmia and hypotension were noted during rewarming.
Over the past decade, several systematic reviews and meta-analyses have evaluated the effectiveness of therapeutic hypothermia in improving long-term outcomes following ABI. In these reviews, it was reported that hypothermia was associated with a lower likelihood of poor outcome and mortality, but that none of these correlations were statistically significant (Alderson et al. 2004; Georgiou & Manara 2013; Li & Yang 2014; Peterson et al. 2008; Sydenham et al. 2009). Although a recent meta-analysis found significant improvements in long-term outcomes (Crossley et al. 2014), the authors noted significant heterogeneity between the studies and the low methodological quality of some studies. In fact, many of the studies included in these reviews involved small single-centre trials that were non-controlled and unblinded, which tend to overestimate effect size. The results of the high-quality multicentre trials included in the meta-analyses may have been diluted by the cumulative findings of the former studies. As such, therapeutic hypothermia has only been recommended as a treatment option within the confines of well-designed clinical trials.
There is Level 1a evidence that therapeutic hypothermia effectively reduces elevated intracranial pressure post ABI.
There is Level 1a evidence that therapeutic hypothermia is associated with an increased incidence of pneumonia and other complications post ABI.
There is conflicting (Level 1a and Level 2) evidence as to whether therapeutic hypothermia reduces mortality and improves long-term outcomes post ABI.
Therapeutic hypothermia (32-35°C) is an effective intervention for lowering elevated intracranial pressure post ABI, but not for improving long-term outcomes.
Therapeutic hypothermia may increase the risk of complications such as pneumonia.
Controlled hyperventilation to achieve a Partial Pressure of Carbon Dioxide in Arterial Blood (PaCO2) of 30-35 mmHg during the first few days post ABI has been reported to improve outcomes. Hyperventilation causes cerebral vasoconstriction, which leads to decreases in cerebral blood flow and volume, thus leading to a decrease in ICP (Muizelaar et al. 1991). During mild hyperventilation, increased oxygen extraction mechanisms allow compensation for decreases in blood flow and volume, allowing normal cellular metabolism to continue (Diringer et al. 2000).
There is concern that intensive or prolonged hyperventilation may increase metabolic acidosis, which is common following brain injury. Depletion of oxygen forces the injured brain to turn to anaerobic metabolism; the associated increase in lactic acid has been correlated with poor outcomes (De Salles et al. 1987; DeSalles et al. 1986). Since hyperventilation decreases cerebral CO2, this leads to an increase in pH diminishing the detrimental effects of acidosis. However, this process depends on the availability of bicarbonate in the cerebrospinal fluid. Thus prolonged hyperventilation may not be an appropriate therapeutic measure as it may deplete bicarbonate levels favoring ischemia and leading to poorer outcomes. Several studies have also discussed concerns related to pre-hospital intubation leading to inappropriate hyperventilation (Lal et al. 2003; Warner et al. 2007). Targeted hyperventilation to within 30-45 mmHg have been associated with decreased mortality rates, but both precise regulation and proper training are recommended.
The AANS made Level II recommendations against the use of intensive prophylactic hyperventilation (PaCO2<25mmHg) (Carney et al. 2017). Level III recommendations from the previous edition were retracted, as they were based on lower-level evidence. The EBIC recommended mild to moderate hyperventilation (PaCO2=30-35mmHg) to manage high ICP and CPP in association with sedation and analgesia (Maas et al. 1997). If ICP remains uncontrolled, even with osmolar therapy and cerebrospinal fluid (CSF) drainage, then intensive hyperventilation (PaCO2<30mmHg) was recommended (Maas et al. 1997).
The findings of two studies demonstrated that prolonged, moderate hyperventilation can effectively lower elevated ICP in individuals following ABI (Coles et al. 2002; Oertel et al. 2002). In comparing intensive (PaCO2<30mmHg) hyperventilation to moderate (PaCO2>30mmHg) hyperventilation, a higher mortality was found in the former group, but the results were not statistically significant (Mohammed 2013). In another study, it was found that early, brief, moderate hyperventilation did not impair global cerebral metabolism in patients with severe TBI, and thus it is unlikely to cause further neurological injury (Diringer et al. 2000).
Potential detrimental effects following hyperventilation are particularly concerning in ABI, and the issue has been addressed in two earlier studies. In a small retrospective study, Thiagarajan et al. (1998) noted that hyperoxia (PaO2=200-250 mmHg) was able to counteract the reduced cerebral oxygenation following hyperventilation. In a large clinical trial, Muizelaar et al. (1991) evaluated the effects of prolonged hyperventilation in combination with intravenous tromethamine. Long-term outcomes were significantly better in individuals who received the combination therapy than those who received hyperventilation alone and similar to those who received normal ventilation. The authors suggested that the presence of a buffer system can help neutralize cerebral bicarbonate depletion due to hyperventilation.
There is Level 4 evidence that hyperventilation lowers elevated intracranial pressure post TBI.
There is Level 4 evidence that hyperoxia counteracts the detrimental effects of brief hyperventilation post TBI.
There is Level 1b evidence that tromethamine counteracts the detrimental effects of prolonged hyperventilation and yields better outcomes than hyperventilation alone in severe TBI.
Hyperventilation can effectively lower elevated intracranial pressure post TBI.
Tromethamine and hyperoxia may counteract the adverse effects of hyperventilation and lead to better clinical outcomes post TBI.
Cerebrospinal Fluid Drainage
In an attempt to control ICP, ventricular CSF drainage is a frequently used neurosurgical technique. Catheters are generally inserted in to the anterior horn of a lateral ventricle and attached to an external strain gauged transducer (Bracke et al. 1978; March 2005), allowing for concurrent pressure monitoring and fluid drainage. Generally, a few milliliters of fluid are drained from the ventricle at a time, resulting in an immediate decrease in ICP (Kerr et al. 2000). However, ventricular space is often compressed due to associated brain swelling, which limits the potential for drainage as a stand-alone therapy for ICP (James 1979). Criticisms of external ventricular drainage generally surround the intrusiveness of the procedure and the complication of potential infections (Hoefnagel et al. 2008; Zabramski et al. 2003).
When ventricular drainage is not possible, lumbar drainage has been proposed as an alternative method for reducing elevated ICP. Standard practice has been to avoid lumbar drainage for fear of transtentorial or tonsillar herniation. However, technological improvements have renewed interest in its potential for reducing ICP in patients refractory to other treatments (Tuettenberg et al. 2009).
The AANS guidelines made a Level III recommendation for the use of CSF drainage to lower ICP in patients with GCS<6 during the first 12 hours post injury (Carney et al. 2017). As well, the authors noted that an external ventricular system at the midbrain may be more effective with continuous drainage than with intermittent use. According to the EBIC, CSF drainage is an acceptable treatment for ICP reduction post ABI (Maas et al. 1997).
Ventricular drainage of CSF has shown to be an effective intervention for lowering elevated ICP post ABI in small-scale studies (Fortune et al. 1995; Kerr et al. 2000; Timofeev, Dahyot-Fizelier, et al. 2008). While the retrospective studies noted steady increases in ICP after treatment cessation (Fortune et al. 1995; Kerr et al., 2000), the prospective studies found that ICP reductions were maintained for up to 24 hours in select participants (Lescot et al. 2012; Timofeev, Dahyot-Fizelier, et al. 2008). Two of the studies reported significant improvements in CPP associated with ICP reductions (Kerr et al. 2000; Lescot et al. 2012), and only one reported short-term improvements in cerebral blood flow (Fortune et al. 1995). A case-control study examining drainage frequency showed that continuous treatment demonstrated significantly greater reductions in ICP than intermittent treatment. However, both treatments yielded comparable long-term outcomes and required similar therapeutic intensity levels. In a prospective trial evaluating drainage intensity, Kerr et al. (2001) randomized patients to have different amounts of CSF drained. The authors found that all patients experienced significant decreases in ICP and increases in CPP in the short term, regardless of the fluid amount drained. As such, ventricular CSF drainage is a feasible treatment when elevated ICP remains refractory to other interventions.
Lumbar drainage of CSF has shown similar effectiveness in lowering elevated ICP post ABI. The results of two small retrospective studies showed significant reductions in ICP after lumbar drainage (Llompart-Pou et al. 2011; Murad et al. 2008), which were supported by two prospective studies (Murad et al. 2012; Tuettenberg et al. 2009). The rate of favourable long-term outcomes in these studies ranged from 36% (Tuettenberg et al. 2009) to 62% (Llompart-Pou et al. 2011), and one study reported a 70% decrease in therapeutic intensity levels following treatment. Based on these findings, lumbar drainage appears to be a viable alternative when ventricular drainage is not possible.
The effectiveness of an external ventricular drain (EVD) in managing elevated ICP when compared to an intraparenchymal fiberoptic monitor (IPM) is currently unclear. The results from a large retrospective study found the EVD to be inferior to the IPM (Kasotakis et al. 2012). While there were no significant differences between treatments in terms of mortality and long-term outcomes, the EVD had significantly higher rates of surgical decompression and device-related complications. However, the authors also found that the EVD required longer ICP monitoring and ICU stay than the IPM. In a smaller prospective study, the EVD was found to be superior in multiple domains (Liu et al. 2015). The EVD yielded a significantly lower rate of refractory ICP, as well as higher rates of 1-month survival and 6-month favourable outcomes. The rate of surgical decompression was significantly greater with the IPM, although duration of hospital stay and frequency device-related complications were similar in both groups.
There is Level 1b evidence that ventricular cerebrospinal fluid drainage effectively lowers elevated intracranial pressure post ABI.
There is conflicting (Level 2 and Level 3) evidence as to whether an external ventricular drain yields lower intracranial pressure, better long-term outcomes, reduced therapeutic intensity, and fewer complications than an intraparenchymal fiberoptic monitor post ABI.
There is Level 3 evidence that continuous ventricular cerebrospinal fluid drainage is more effective than intermittent drainage at lowering elevated intracranial pressure post ABI.
There is Level 4 evidence that lumbar cerebrospinal fluid drainage effectively lowers elevated intracranial pressure post ABI.
Cerebrospinal fluid drainage can effectively lower elevated intracranial pressure post ABI, using either a ventricular or lumbar device.
Continuous cerebrospinal fluid drainage may be more effective than intermittent drainage at lowering elevated intracranial pressure post ABI.
It is unclear whether external ventricular drainage is more effective than an intraparenchymal fiberoptic monitor in lowering elevated ICP, improving long-term outcomes, reducing therapeutic intensity, and minimizing complications.
It is thought that surgical decompression, the removal of skull sections, improves the damage caused by secondary injury (i.e., delayed brain damage) such as elevated ICP and reduced cerebral oxygenation. Sahuquillo and Arikan (2006) identified two types of surgical decompression: prophylactic/primary decompression and therapeutic/secondary decompressive craniectomy (DC). The former involves performing the surgical procedure as a preventive measure against expected increases in ICP while the latter is performed to control high ICP “refractory to maximal medical therapy” (Sahuquillo & Arikan 2006).
However, debate regarding if and when to perform these surgeries continues. Factors such as age and initial GCS score have been proposed as potential prognostic factors (Guerra et al. 1999). The majority of decompressive techniques are precipitated by evacuation of a mass lesion (Compagnone et al. 2005). Once decompression is decided upon, resection of a larger bone fragment is generally recommended to allow for greater dural expansion with less risk of herniation (Compagnone et al. 2005; Csókay et al. 2001). Therapeutic decompressive craniectomy is typically performed after other therapeutic measures to control ICP have been exhausted (Morgalla et al. 2008).
The AANS reported that there was insufficient evidence to support Level I recommendations regarding DC, although Level II recommendations were provided (Carney et al. 2017). A bifrontal DC was not recommended for improving long-term outcomes in individuals with severe TBI and prolonged, elevated ICP. The authors noted, however, that bifrontal DC demonstrated significant reductions in ICP and ICU stay. As well, a larger frontotempoparietal DC was recommended over a smaller procedure for reduced mortality and improved neurological outcomes. The EBIC suggested that decompressive craniectomy should only be considered in “exceptional situations” (Maas et al. 1997).
The effectiveness of DC following ABI has been examined in numerous retrospective studies. The majority of these studies reported significant decreases in ICP immediately following the procedure (Aarabi et al. 2006; Bao et al. 2010; Daboussi et al. 2009; De Bonis et al. 2011; Eberle et al. 2010; Goksu et al. 2012; Grindlinger et al. 2016; Ho et al. 2008; Howard et al. 2008; Nambiar et al. 2015; Olivecrona et al. 2007; Polin et al. 1997; Schneider et al. 2002; Skoglund et al. 2006; Soustiel et al. 2010; Stiefel et al. 2004; Timofeev et al. 2008; Tuettenberg et al. 2009; Ucar et al. 2005; Whitfield et al. 2001; Williams et al. 2009). Two meta-analyses evaluating the effectiveness of DC in ICP reduction yielded similar results. The earlier study found that postoperative ICP was significantly lower than preoperative values and remained stable for up to 48 hours (Bor-Seng-Shu et al. 2012), while the later study reported that DC resulted in reduced ICP and shorter hospital stay when compared to standard care (Wang et al. 2015). However, both studies were limited by a small sample size, lack of high-quality studies, significant heterogeneity between studies, and absence of a bias assessment.
Few studies have reported an association between decreased ICP and improved long-term outcomes (Chibbaro et al. 2008; Galal 2013; Kim et al. 2009; Nambiar et al. 2015; Skoglund et al. 2006; Williams et al. 2009). Several factors were found to correlate with positive long-term outcomes, including younger age (Chibbaro et al. 2011; Chibbaro et al. 2008; Huang et al. 2013; Limpastan et al. 2013; Meier et al. 2008; Nambiar et al. 2015; Ucar et al. 2005; Williams et al. 2009; Yang et al. 2008; Yuan et al. 2013), higher GCS score (De Bonis et al. 2011; Goksu et al. 2012; Gong J 2014; Ho et al. 2011; Howard et al. 2008; Huang et al. 2013; Limpastan et al. 2013; Meier et al. 2008; Ucar et al. 2005; Williams et al. 2009; Yang et al. 2008; Yuan et al. 2013) earlier DC (Chibbaro et al. 2011; Chibbaro et al. 2008; Girotto et al. 2011; Polin et al. 1997), and larger DC (Li et al. 2008; Skoglund et al. 2006). However, a later prospective study failed to find a significant difference between early (<24hr) and late (>24hr) DC in terms of long-term outcomes (Wen et al. 2011).
Considering the intensiveness of DC and its potential complications, evaluating its long-term outcomes is of particular importance. Some retrospective studies found that DC was associated improved GOS scores and reduced mortality when compared to standard care (Polin et al. 1997; Rubiano et al. 2009), while others did not (Girotto et al. 2011; Nirula et al. 2014; Quintard et al. 2015). The results are similarly mixed when DC is compared to other procedures. An earlier study found that DC yielded more favourable long-term outcomes than craniotomy (Huang et al. 2008), but later studies found that there were no significance differences between the procedures (Chen et al. 2011; Li et al. 2012). In a 2006 Cochrane review, the authors found no evidence to recommend routine use of DC to reduce unfavorable outcomes in adults with uncontrolled ICP (Sahuquillo & Arikan 2006). A recent systematic review reported improved GOS scores and reduced mortality rates associated with DC, particularly in younger individuals with less severe (GCS>5) and more acute (<5hr) injuries (Barthelemy et al. 2016). However, the authors refrained from providing clinical recommendations given a lack of prospective data and significant results.
More recently, researchers have published the results of clinical trials evaluating long-term outcomes following DC. When compared to controlled decompression, one trial found that DC was just as effective in reducing elevated ICP and improving GOS score (Wang et al. 2014). The impact of bone flap size was investigated in two other trials (Jiang et al. 2005; Qiu et al. 2009). Participants received either standard trauma craniectomy with a unilateral frontotemporoparietal bone flap (12x15cm) or limited craniectomy with a routine temporoparietal bone flap (6x8cm). Both studies reported that significantly more patients in the former group showed favourable outcomes on the GOS than those in the latter group at six months (Jiang et al. 2005) and one year (Qiu et al. 2009). As well, ICP fell more rapidly and to a lower level following standard craniectomy than limited craniectomy (Jiang et al. 2005; Qiu et al. 2009).
In a pilot study, Moein et al. (2012) reported than DC was associated with higher GCS and GOS scores when compared to standard care. Although the results were non-significant, the authors noted their small sample size and recommended further investigation. The DECRA trial was a multicentre study evaluating the effectiveness of bifrontotemporoparietal DC over standard care in patients with diffuse TBI (Cooper et al. 2011). The authors found that DC was associated with significantly greater reduction in ICP and shorter stay in the ICU, but yielded significantly lower GOS Extended scores than standard care. The latter results were no longer significant when controlling for age and initial GCS score, and there was no significant difference between groups in mortality. There were a number of concerns regarding the methodological quality of the trial, including time to randomization, length of accrual, initial group differences, timing of DC, and DC technique (Cooper et al. 2011). As well, the ICP threshold was deemed too low (>20mmHg for >15 minutes) such that standard medical management was not fully exhausted.
The recent Rescue ICP trial sought to improve upon the main issues with the DECRA trial, namely utilizing a higher ICP threshold (>25mmHg for >1 hour) and a more comprehensive outcome measure (GOS Extended) (Hutchinson et al. 2016). The results showed significantly lower ICP levels and shorter duration of elevated ICP following DC when compared to standard care, although it yielded a significantly higher rate of adverse events. Unlike the previous trial, DC was associated with more favourable outcomes and lower mortality at both six months and one year. However, similar to the previous trial, the RescueICP trial faced criticism regarding its methodology. In particular, there were concerns regarding the timing of DC and the definition of “favourable outcome”. As well, there was a noted lack of subgroup analyses based on age group, injury severity, and DC technique (bifrontal versus unilateral).
There is Level 1a evidence that decompressive craniectomy effectively reduces elevated intracranial pressure post ABI.
There is conflicting evidence (Level 1a) as to whether decompressive craniectomy is associated with higher Glasgow Outcome Scale scores and lower mortality when compared to standard care.
There is Level 2 evidence that standard craniectomy with a larger bone flap is more effective than limited craniectomy with a smaller bone flap in lowering elevated intracranial pressure and yielding higher Glasgow Outcome Scale scores.
There is conflicting evidence (Level 3) as to whether decompressive craniectomy improves long-term outcomes when compared to craniotomy.
Decompressive craniectomy is an effective intervention for lowering elevated intracranial pressure post ABI.
The effectiveness of decompressive craniectomy in improving long-term outcomes post ABI when compared to standard care or craniotomy is unclear.
Standard craniectomy with a larger bone flap is more effective than limited craniectomy with a smaller bone flap in terms of intracranial pressure reduction and favourable outcome.
Rotational Therapy and Prone Positioning
The concept of continuous lateral rotational therapy has been used for the prevention of secondary complications resulting from immobilization. These complications include pressure ulcers, pneumonia from atelectasis, deep vein thrombosis, pulmonary emboli, muscle atrophy, and contractures. Additionally, there are some indications that continuous rotational therapy may be useful in managing elevations in ICP.
Use of the prone position has been shown to be an effective treatment for patients with acute respiratory insufficiency in the ICU (Pelosi et al. 2002). However, many studies have excluded patients with ABI due to fears of increasing ICP during the rotation process and in the prone position (Johannigman et al. 2000).
The EBIC and the AANS made no recommendations regarding continuous rotational therapy or prone positioning in acute ABI.
A single study has been identified which examined the effects of continuous rotational therapy on ICP (Tillett et al. 1993). The study failed to find any direct benefit of the therapy for managing elevated ICP, but it did not worsen ICP. The authors suggested that care should be taken not to rotate patients with unilateral brain injuries towards the side of the lesion in order to avoid further increments in ICP.
Four case series investigated the effects of prone positioning on various physiological measures. Three studies reported significant increases in ICP during prone positioning (Lee 1989; Nekludov et al. 2006; Roth et al. 2014). Two studies demonstrated increased cerebral oxygenation in patients when they were prone (Nekludov et al. 2006; Thelandersson et al. 2006), which was maintained upon return to the supine position (Thelandersson et al. 2006). One study found increases in CPP and MAP when patients were prone (Nekludov et al. 2006), while other studies reported that these values decreased (Roth et al. 2014) or did not change (Thelandersson et al. 2006). Due to the small sample sizes and retrospective nature of these studies, further prospective research is required to determine the efficacy of prone positioning.
Thelandersson et al. (2006) and Nekludov et al. (2006) studied the effects of the prone position on oxygenation rates in patients with ABI. Both studies showed increased PaO2 levels in the prone position. However, only Thelanderson et al. (2006) reported that increased oxygenation remained after patients returned to the supine position. Nekludov et al. (2006) demonstrated increased CPP associated with increased MAP while in the prone position; of note, ICP also significantly increased in the prone position in this study. Due to the small sample sizes of both papers, additional studies are recommended.
There is Level 4 evidence that continuous rotational therapy does not improve intracranial pressure following severe TBI.
There is Level 4 evidence that the prone position may increase intracranial pressure but improve cerebral oxygenation post ABI.
Continuous rotational therapy does not improve intracranial pressure in individuals with severe TBI.
Prone positioning may increase intracranial pressure but improve cerebral oxygenation post ABI.