REVIEW URRENT C OPINION
Multicompartment management of patients with severe traumatic brain injury Margaret H. Lauerman and Deborah M. Stein
Purpose of review Intracranial pressure (ICP) control is a mainstay of traumatic brain injury (TBI) management. However, development of intracranial hypertension (ICH) may be affected by factors outside of the cranial vault in addition to the local effects of the TBI. This review will examine the pathophysiology of multiple compartment syndrome (MCS) and current treatment considerations for patients with TBI given the effects of MCS. Recent findings Elevated intra-abdominal pressure (IAP) is associated with ICP elevation, and decompressive laparotomy in patients with concurrent elevations in IAP and ICP can reduce ICP. Elevated intrathoracic pressure may be similarly associated with ICP elevation, although the ideal ventilator management strategy for TBI patients when considering MCS is unclear. Summary In MCS, intracranial, intrathoracic and intra-abdominal compartment pressures are interrelated. TBI patient care should include ICP control as well as minimization of intrathoracic and intra-abdominal pressure as clinically possible. Keywords abdominal hypertension, multiple compartment syndrome, traumatic brain injury
INTRODUCTION Traumatic brain injury (TBI) is a prevalent condition [1]. Modern management of TBI utilizes a multimodal approach, incorporating both medical and surgical therapy as well as treatment of intracranial and extracranial factors. This review will elucidate how pressure elevation in extracranial body compartments can affect intracranial pressure (ICP), and how treatment of patients with TBI can be optimized with the knowledge of multiple compartment syndrome (MCS).
EPIDEMIOLOGY OF TRAUMATIC BRAIN INJURY Each year, 1.7 million patients are diagnosed with a TBI. Although the clinical spectrum of TBI is broad, 250 000 TBIs are severe enough to merit hospital admission annually [1]. TBI is also a mortal condition, with over 53 000 deaths from TBI each year [2]. Long-term disability occurs in many survivors of TBI [3]. Outcomes for patients with TBI have improved, with mortality decreasing 8.2% over the past decade [2].
OVERVIEW OF MULTIPLE COMPARTMENT SYNDROME Much of the improvement in TBI outcomes may be because of increased understanding of the pathophysiology of TBI, such as awareness of MCS. MCS is a condition in which pressure in one body compartment, or treatment of pressure in one body compartment, can affect pressure in another body compartment [4 ]. In a patient with a TBI, the end result of MCS can be intracranial hypertension (ICH) [4 ], which has been associated with poor neurologic outcomes [3,5,6]. Fortunately, development of MCS is uncommon, with a 2% incidence of MCS during a 4-year period at our institution. Mortality for MCS patients, however, is higher than &&
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Program in Trauma, University of Maryland School of Medicine, Baltimore, Maryland, USA Correspondence to Deborah M. Stein, MD, MPH, Program in Trauma, University of Maryland School of Medicine, 22 South Greene St, Baltimore, MD 21201, USA. Tel: +1 410 328 3495; e-mail: [email protected] Curr Opin Anesthesiol 2014, 27:219–224 DOI:10.1097/ACO.0000000000000044
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KEY POINTS MCS develops because of the physiologic interactions between ICP, intra-abdominal pressure (IAP), and intrathoracic pressure (ITP). Elevations in ICP with concurrent intra-abdominal hypertension should be treated with a decompressive laparotomy, even without the development of abdominal compartment syndrome (ACS). Although there is no consensus currently for ventilator management in TBI, ITP should be limited as clinically possible, as ITP may contribute to elevations in ICP. Management of elevated ICP should include medical ICP therapy and consideration of decompressive craniectomy if medical therapy fails.
mortality for those undergoing decompressive craniectomy alone [4 ]. Optimization of patients with TBI not only involves treatment of intracranial disorders, but also optimizing other organ systems cognizant of possible central nervous system effects. Conventional ICP management targets decreasing cranial vault compartment pressure through brain tissue edema reduction, appropriate reductions in cerebral blood flow (CBF), cerebrospinal fluid drainage, or decompressive craniectomy. However, ICP is not only influenced by cranial vault contents, as ICP has been shown to have a complex relationship with both intra-abdominal pressure (IAP) and intrathoracic pressure (ITP) [4 ,7,8]. &&
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absence of evacuatable mass lesion, target cranial vault size. ICP can be lowered with decompressive craniectomy, which allows the brain parenchyma to expand further than previously limited by the cranial vault [4 ]. Decompressive craniectomy is associated with improved intracranial physiology, as decompressive craniectomy increases macrovascular and microvascular circulation. In a prospective study of 19 TBI patients, internal carotid artery and middle cerebral artery flow velocity improved significantly after decompressive craniectomy [11]. In another study of six TBI patients, microvascular blood flow, measured by microbubble contrast enhanced ultrasound, significantly improved following decompressive craniectomy [12]. In addition to improving CBF, decompressive craniectomy also improves brain tissue oxygenation, which can be compromised in TBI. In a prospective study of nine TBI patients, low or declining brain tissue oxygen levels were noted in all patients prior to decompressive craniectomy, but significantly improved after decompressive craniectomy [13]. In addition to the improvement in blood flow and brain tissue oxygenation [11–13], decompressive craniectomy may improve clinical outcomes. In one study of 50 patients undergoing decompressive craniectomy for refractory ICP, good functional outcomes were seen in 40% of patients [14]. Decompressive craniectomy, much like ICP monitoring, has become recently controversial, as a randomized trial of 155 patients with TBI demonstrated worse outcomes for decompressive craniectomy patients, although mortality was not significantly affected [15 ]. However, this trial of decompressive craniectomy is limited by its bifrontal surgical approach, variation in preoperative pupillary exam between groups, and exclusion of patients requiring surgery for mass lesions [16]. Given these limitations, and the good functional outcomes seen after decompressive craniectomy, our institution continues to consider decompressive craniectomy for refractory ICP patients or patients with primary surgical indications. &&
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INTRACRANIAL PRESSURE MANAGEMENT ICP monitoring is often used in TBI patient care, and many therapies for TBI use ICP as their treatment target. ICP is elevated at levels over 20 mmHg [9], and is associated with neurologic deterioration, disability, and mortality [3,5,6]. Although ICP monitoring has recently become controversial, with a randomized trial failing to show benefit to invasive ICP monitoring for functional recovery or mortality [10 ], ICP monitoring continues to be the standard of care in most large volume centers, including our own institution. Medical strategies for decreasing ICP include sedation and pain control, temperature control, hyperosmolar therapy with mannitol or hypertonic saline, and barbiturate coma induction [9]. These medical strategies for ICP management target intracranial contents, decreasing CBF and subsequent intracranial blood volume, or brain tissue volume. Surgical strategies for the treatment of ICH, in the &&
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INTRATHORACIC PRESSURE TBI patients often present with concurrent thoracic trauma [17]. Pulmonary injury can require ventilator manipulation and higher ventilator pressures, such as an increase in positive end expiratory pressure (PEEP) [17]. Other concurrent pulmonary issues, such as pulmonary edema development from fluid resuscitation, pneumonia, and acute respiratory distress syndrome can increase ventilator pressure requirements. Development of acute Volume 27 Number 2 April 2014
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Multicompartment management in severe traumatic brain injury Lauerman and Stein
lung injury in patients with TBI is associated with poorer neurologic outcome [18]. High tidal volumes are correlated with acute lung injury in patients with TBI as well [19], suggesting that a high pressure, low tidal volume ventilation approach may be preferable. However, high-pressure ventilation may have deleterious effects on ICP due to effects of MCS. Increases in ITP are associated with increases in ICP in animal models. When ITP and ICP were measured during cardiopulmonary resuscitation (CPR), ICP elevation was seen with CPR-induced ITP increases [8]. PEEP can also be used as a surrogate for ITP, as it represents a constant minimum of ITP throughout the respiratory cycle. Ventilator manipulation with PEEP increased ICP, even in the presence of baseline elevated ICP. The increase in ICP was less with underlying ICH, although it still may have significant effects in animal models [20]. However, the relationship between ITP and ICP in humans remains unclear. In one review of patients with TBI, as PEEP was increased up to 15 cm H2O, ICP decreased incrementally [17]. Another review of TBI and subarachnoid hemorrhage (SAH) patients failed to show association between ICP and PEEP [21], whereas another review does note a positive correlation between PEEP and ICP in patients with TBI [22]. The effect of PEEP on CBF is similarly unclear. In patients with SAH, there was a significant mean arterial pressure (MAP)-induced decrease in CBF with increasing PEEP [23], whereas in another review of TBI patients, CPP did not change in any specific pattern with increasing PEEP [17]. Choice of ventilator mode may influence ICP, although data are limited. Inverse ratio ventilation, although associated with a longer period of elevated ITP during the respiratory cycle, did not significantly increase ICP in patients with TBI [24]. Airway pressure release ventilation (APRV), another ventilation mode with a prolonged inspiratory time, similarly did not increase ICP and actually improved carotid blood flow, a surrogate marker of CBF, in a SAH patient with hypoxemia [25]. In an animal model, use of APRV with spontaneous breathing, as opposed to altering pressure and rate for constant minute ventilation without spontaneous breathing, was associated with higher cerebral perfusion [26]. Recruitment maneuvers are also often performed in patients with hypoxemia to increase alveolar expansion, and have a high set pressure. Recruitment maneuvers, when performed with escalating PEEP, increased ICP in 75% of patients with TBI, with resolution of the ICP elevation at recruitment maneuver completion [27 ]. Although low tidal volume, high-pressure ventilation has been shown beneficial in the acute lung injury population, higher CO2 levels are seen with &
lower tidal volumes [28]. This elevation in CO2, and potential cerebral vasoconstriction, is another deleterious effect of high-pressure ventilation for patients with TBI, in addition to high-pressure ventilation potentially increasing ICP. In patients who are difficult to oxygenate or ventilate, ICP optimization may be sacrificed for increased ITP, as poor oxygenation is also detrimental to TBI patients [29]. However, no recommendations have been formalized for TBI patients thus far regarding ventilator strategies or settings [9].
INTRAABDOMINAL PRESSURE Elevated IAP is a common condition, with a 32.1% overall incidence of elevated IAP in ICU patients [30]. Elevations in IAP are often brought on by intraabdominal fluid accumulation or visceral organ edema, with compensation for this edema constrained by the diaphragm, abdominal wall, and bony structures, only some of which are distensible [31]. IAP is typically monitored through bladder pressure measurement at end expiration [4 ,31, 32 ]. IAP is considered elevated when greater than 12 mmHg [32 ] and abdominal compartment syndrome (ACS) develops at a pressure of 20 mmHg when combined with organ failure [31]. Elevated IAP affects the function of many abdominal visceral organs, including the renal, hepatic, and gastrointestinal systems [31]. There are many options for the treatment of elevated IAP, including sedation, paralysis, gastric and rectal decompression, paracentesis, diuretics or dialysis. However, should ACS develop, decompressive laparotomy is recommended [32 ]. Much as the effect of ITP extends beyond the thoracic cavity, the effect of elevated IAP is not limited to the abdominal cavity [31]. In an animal model of elevated IAP, stepwise increases in IAP induced stepwise increases in ICP. With these increases in ICP, CPP decreased as well [33]. This association between IAP and ICP holds true in humans. Induction of elevated IAP in human patients with TBI, through placement of an external water bag on the abdomen, increased ICP significantly. The clinical implication of the elevated ICP is unclear, as despite the numeric increase in ICP, cerebral oxygen extraction was maintained in this study [34]. Just as increasing IAP induced elevations in ICP, therapy to relieve increased IAP through decompressive laparotomy can resolve ICP elevation. In a review of 102 patients who underwent decompressive craniectomy for ICP elevation, 24% also underwent decompressive laparotomy for MCS. IAP was elevated at the time of decompressive laparotomy, with a mean IAP of 28 mmHg. Decompressive
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laparotomy initially relieved the ICP elevation, with mean ICP significantly decreasing from 28 to 19 mmHg. Unfortunately, this ICP decrease after decompressive laparotomy was transient in the days following decompressive laparotomy [4 ]. Decompressive laparotomy has also been used successfully without decompressive craniectomy for the treatment of elevated ICP in the setting of MCS [35–36]. In one patient with elevated IAP and ICP, decompressive laparotomy alone was performed with a decrease in ICP, and the patient subsequently had an excellent functional outcome despite the malignant ICH [36]. Physiologic changes associated with ACS do not need to occur for IAP to elevate ICP. In one series of 17 patients undergoing decompressive laparotomy for refractory ICP, no patient had progressed to ACS prior to decompressive laparotomy. Increased airway pressures were not evident, as patients had a mean airway pressure of 29.5 mmHg. Renal function was similarly maintained, with a mean urine output of 2.7 l over 12 h. Some patients did require pressers, although this is difficult to interpret in the multiply injured patient. Despite the lack of clinical ACS signs, mean IAP was elevated, ranging from 21 to 35 mmHg prior to decompression [35]. Overall, elevations in IAP should be treated according to the World Society for the Abdominal Compartment Syndrome algorithm. Sedation, paracentesis, and fluid removal through diuretics or dialysis for elevated IAP must be undertaken with caution in TBI patients to avoid hypotension, and a subsequent decrease in CPP due to a decreased MAP from hypovolemia. Progression to ACS should be treated with decompressive laparotomy in patients with TBI as it is in non-TBI patients [32 ]. However, decompressive laparotomy should be performed prior to development of the physiologic changes with ACS in the setting of intractable ICH with elevated IAP. &&
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cardiac compliance and cardiac output [31], all of which could potentially exacerbate ICP if venous return is limited [4 ]. Animal models have examined the relationship between ICP, ITP, and IAP. In an animal model measuring effects of balloon insufflation-induced increases of IAP on ICP and ITP, both ITP and ICP increased with higher IAP. Cardiac index decreased with higher IAP, as did CPP. However, there is some evidence that the relationship between IAP and ICP may be mediated through ITP. When a median sternotomy and pleuropericardotomy was performed with the balloon insufflation, the increase of ICP with elevated IAP was no longer seen [7]. Another animal model looking at the effect of CPR on ICP affirmed the interplay of ITP and IAP in affecting ICP. Although ICP rose with increased ITP during CPR, placement of an abdominal binder heightened the amount of ICP increase a set change in ITP induced [8]. The complex relationship between IAP, ITP, and ICP holds true in human studies as well. In patients who underwent decompressive laparotomy after decompressive craniectomy for elevated ICP, IAP predictably decreased, but so did ITP. With both the decrease in ITP and IAP, ICP elevation resolved [4 ]. In addition to therapies targeting reduction of intracranial contents for ICP control, modern ICP reduction strategies also treat the relationship between ICP, ITP, and IAP. Positional therapy for refractory ICP elevation, through standing the patient (Fig. 1), allows relief of the mechanical effect of IAP on ICP and minimization of ITP from ventilator pressures through increased pulmonary recruitment. Extracorporeal membrane oxygenation (ECMO) has also been used in patients with TBI and respiratory failure [38], and may be an additional therapy to reduce ITP in patients with &&
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PHYSIOLOGY OF MULTIPLE COMPARTMENT SYNDROME The true physiology behind the interplay of IAP, ITP, and ICP in MCS is unknown. Much of the effect of ITP and IAP on ICP may be mediated through an association between IAP and ITP, as well as the cardiovascular system. Elevated IAP directly compresses the thoracic cavity, inducing higher peak airway pressures while decreasing functional residual capacity, lung volume, and chest wall compliance [31]. As pleural pressure rises in ventilated patients, pulmonary artery occlusion pressure increases [37], indicating an afterload increase on the cardiac system. Elevated IAP also decreases 222
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FIGURE 1. Positional therapy being used in a TBI patient. Volume 27 Number 2 April 2014
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Multicompartment management in severe traumatic brain injury Lauerman and Stein
elevated ICP. Positional therapy is used at our institution with combined refractory ICP and respiratory failure, whereas ECMO is used in trauma patients with severe hypoxemia unresponsive to all other measures.
FACTORS CONTRIBUTING TO MULTIPLE COMPARTMENT SYNDROME It is difficult to elucidate factors contributing to MCS given the small number of patients in the literature. MCS patients were more critically injured on admission, with higher Injury Severity Score and mean ICP at the time of decompressive craniectomy. Fluid resuscitation may also contribute to MCS development. Patients with MCS received 23 liters more fluid in the first seven hospital days than those undergoing decompressive craniectomy without developing MCS [4 ]. Ascites was seen in almost all patients at the time of decompressive laparotomy for MCS [35–36]. CPP maintenance, correction of sedation-induced hypotension, and hypertonic saline ICP therapy were associated with increased fluid administration [4 ], and thus may contribute to the development of MCS. &&
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OUTCOMES IN MULTIPLE COMPARTMENT SYNDROME Outcomes in patients developing MCS are worse than those with elevated ICP alone. There was a 12% absolute increase in mortality for patients undergoing decompressive craniectomy and decompressive laparotomy compared with those undergoing decompressive craniectomy alone, although this was not significant. ICU length of stay and hospital length of stay were both significantly increased in patients with MCS [4 ]. Overall survival of MCS patients ranges from 58 to 65% [4 ,35]. The only significant predictor of survival in MCS is younger age. Higher initial ICP, higher initial Glascow Coma Score, lower volume fluid resuscitation required, shorter time to decompressive laparotomy, avoidance of decompressive craniectomy, and avoidance of barbiturate coma were all associated with survival in MCS, although these did not reach statistical significance [35]. In patients with both IAP and ICP elevation, the order of decompressive craniectomy and decompressive laparotomy did not have a significant effect on mortality or length of stay [4 ]. &&
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CONCLUSION TBI patients should be closely monitored for MCS development, with ICP monitoring, bladder
pressure monitoring, and serial abdominal exams. Fluid resuscitation should be administered judiciously to avoid exacerbating MCS through pulmonary edema, ascites, and bowel edema elevating IAP and ITP. Sedating medications should be dosed to avoid hypotension and the subsequent need for fluid administration for CPP maintenance. Ventilator mode and pressure should be selected to limit ITP as clinically possible. Should maximal medical ICP therapy fail, decompressive craniectomy should be considered. IAP elevation concurrent with refractory ICP elevation should prompt decompressive laparotomy. Generally at our institution, decompressive laparotomy is considered in patients with elevated IAP in the setting of ICH. Physiologic compromise of ACS is not required for decompressive laparotomy to be considered. Overall, treatment of intracranial, intrathoracic, and intra-abdominal disorders cannot be undertaken without consideration of the effects on other compartments, specifically ICP in TBI patients [4 ]. &&
Acknowledgements No funding was received. Conflicts of interest There are no conflicts of interest.
REFERENCES AND RECOMMENDED READING Papers of particular interest, published within the annual period of review, have been highlighted as: & of special interest && of outstanding interest 1. Faul M, Xu L, Wald MM, et al. Traumatic brain injury in the United States: emergency department visits, hospitalizations, and deaths, 2002–2006 [Internet]. Atlanta, GA: Centers for Disease Control and Prevention, National Center for Injury Prevention and Control; 2010 March. http://www.cdc.gov/ traumaticbraininjury/pdf/blue_book.pdf. [Accessed 2 July 2013] 2. Coronado VG, Xu L, Basavaraju SV, et al. Surveillance for traumatic brain injury: related deaths – United States, 1997–2007 [Internet]. Atlanta, GA: Centers for Disease Control and Prevention. 2011 May. http://www.cdc.gov/ mmwr/preview/mmwrhtml/ss6005a1.htm?s_cid=ss6005a1_w. [Accessed 13 May 2013] 3. Juul N, Morris GF, Marshall SB, Marshall LF. Intracranial hypertension and cerebral perfusion pressure: influence on neurological deterioration and outcome in severe head injury. The Executive Committee of the International Selfotel Trial. J Neurosurg 2000; 92:1–6. 4. Scalea TM, Bochicchio GV, Habashi N, et al. Increased intraabdominal, && intrathoracic and intracranial pressure after severe brain injury: multiple compartment syndrome. J Trauma 2007; 62:647–656. This series of patients undergoing decompressive laparotomy for refractory ICP elevation is the largest in the literature, and showed a decrease in ICP with decompressive laparotomy. 5. Miller JD, Butterworth JF, Gedeman SK, et al. Further experience in the management of severe head injury. J Neurosurg 1981; 54:289–299. 6. Narayan RK, Greenberg RP, Miller JD, et al., Improved confidence of outcome prediction in severe head injury. A comparative analysis of the clinical examination, multimodality evoked potentials, CT scanning, and intracranial pressure. J Neurosurg 1981; 54:751–762. 7. Bloomfield GL, Ridings PC, Blocher CR, et al. A proposed relationship between increased intraabdominal, intrathoracic, and intracranial pressure. Crit Care Med 1997; 25:496–503. 8. Guerci AD, Shi AY, Levin H, et al. Transmission of intrathoracic pressure to the intracranial space during cardiopulmonary resuscitation in dogs. Circ Res 1985; 56:20–30.
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Trauma and transfusion 9. Bratton SL, Chestnut RM, Ghajar J, et al., Brain Trauma Foundation, American Association of Neurologic Surgeons, Congress of Neurologic Surgeons. Guidelines for the management of severe traumatic brain injury. J Neurotrauma 2007; 24 (Suppl 1):S1–106. 10. Chesnut RM, Temkin N, Carney N, et al. A trial of intracranial-pressure && monitoring in traumatic brain injury. N Engl J Med 2012; 367:2471–2481. This is a randomized controlled trial examining the effect of ICP monitoring on clinical outcomes, with ICP monitoring failing to show a mortality benefit. 11. Bor-Seng-Shu E, Hirsch R, Teixeira MJ, et al. Cerebral hemodynamic changes gauged by transcranial Doppler ultrasonography in patients with posttraumatic brain swelling treated by surgical decompression. J Neurosurg 2006; 104:93–100. 12. Heppner P, Ellegala DB, Durieux M, et al. Contrast ultrasonographic assessment of cerebral perfusion in patients undergoing decompressive craniectomy for traumatic brain injury. J Neurosurg 2006; 104:738–745. 13. Stiefel MF, Heuer GD, Smith MJ, et al. Cerebral oxygenation following decompressive hemicraniectomy for the treatment of refractory intracranial hypertension. J Neurosurg 2004; 101:241–247. 14. Aarabi B, Hesdorffer DC, Ahn ES, et al. Outcome following decompressive craniectomy for malignant swelling due to severe head injury. J Neurosurg 2006; 104:469–479. 15. Cooper DJ, Rosenfeld JV, Murray L, et al. Decompressive craniectomy in && diffuse traumatic brain injury. N Eng J Med 2011; 364:1493–1502. This is a randomized controlled trial examining the effect of decompressive craniectomy in patients with refractory ICP elevation, which showed similar mortality but worse Glascow Outcomes Scale scores for patients undergoing decompressive craniectomy. 16. Timmons SD, Ullman JS, Eisenberg HM. Craniectomy in diffuse traumatic brain injury. N Eng J Med 2011; 365:373. 17. Huynh T, Messer M, Sing RF, et al. Positive end-expiratory pressure alters intracranial and cerebral perfusion pressure in severe traumatic brain injury. J Trauma 2002; 53:488–493. 18. Holland MC, Mackersie RC, Morabito D, et al. The development of acute lung injury is associated with worse neurologic outcome in patients with severe traumatic brain injury. J Trauma 2003; 55:106–111. 19. Mascia L, Zavala E, Bosma K, et al. High tidal volume is associated with the development of acute lung injury after severe brain injury: an international observational study. Crit Care Med 2007; 35:1815–1820. 20. Huseby JS, Luce JM, Cary JM, et al. Effects of positive end-expiratory pressure on intracranial pressure in dogs with intracranial hypertension. J Neurosurg 1981; 55:704–705. 21. Caricato A, Conti G, Corte FD, et al. Effects of PEEP on the intracranial system of patients with head injury and subarachnoid hemorrhage: the role of respiratory system compliance. J Trauma 2005; 58:571–576. 22. Cooper KR, Boswell PA, Choi SC. Safe use of PEEP in patients with severe head injury. J Neurosurg 1985; 63:552–555. 23. Muench E, Bauhuf C, Roth H, et al. Effects of positive end-expiratory pressure on regional cerebral blood flow, intracranial pressure, and brain tissue oxygenation. Crit Care Med 2005; 33:2367–2372.
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24. Clarke JP. The effects of inverse ratio ventilation on intracranial pressure. Intensive Care Med 1997; 23:106–109. 25. Marik PE, Young A, Sibole S, Levitov A. The effect of APRV ventilation on ICP and cerebral hemodynamics. Neurocrit Care 2012; 17:219–223. 26. Kreyer S, Putensen C, Berg A, et al. Effects of spontaneous breathing during airway pressure release ventilation on cerebral and spinal cord perfusion in experimental acute lung injury. J Neurosurg Anesthesiol 2010; 22:323–329. 27. Zhang XY, Yang ZJ, Wang QX, Fan HR. Impact of positive end-expiratory & pressure on cerebral injury patients with hypoxemia. Am J Emerg Med 2011; 29:699–703. This is a study looking at effects of recruitment maneuvers, which showed that in most patients, increased PEEP was associated with increased ICP. 28. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Eng J Med 2000; 342:1301– 1308. 29. Chesnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury in determining outcome from severe head injury. J Trauma 1993; 34:216–222. 30. Malbrain ML, Chiumello D, Pelosi P, et al. Incidence and prognosis of intraabdominal hypertension in a mixed population of critically ill patients: a multiple-center epidemiological study. Crit Care Med 2005; 33:315–322. 31. Malbrain ML, Cheatham ML. Definitions and pathophysiologic implications of intra-abdominal hypertension and abdominal compartment syndrome. Am Surg 2011; 77:s6–11. 32. Kirkpatrick AW, Roberts DJ, De Waele J, et al. Intraabdominal hypertension & and the abdominal compartment syndrome: updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care Med 2013; 39:1190–1206. This is a practice guideline for the management of intra-abdominal hypertension from the World Society of the Abdominal Compartment Syndrome, including practice algorithms. 33. Saggi BH, Bloomfield GL, Sugerman HJ, et al. Treatment of intracranial hypertension using nonsurgical abdominal decompression. J Trauma 1999; 46:646–651. 34. Citerio G, Vascotto E, Villa F, et al. Induced abdominal compartment syndrome increases intracranial pressure in neurotrauma patients: a prospective study. Crit Care Med 2001; 29:1466–1471. 35. Joseph DK, Dutton RP, Aarabi B, Scalea TM. Decompressive laparotomy to treat intractable intracranial hypertension after traumatic brain injury. J Trauma 2004; 57:687–693. 36. Miglietta MA, Salzano LJ, Chiu WC, Scalea TM. Decompressive laparotomy: a novel approach in the management of severe intracranial hypertension. J Trauma 2003; 55:551–554. 37. Bellemare P, Goldberg P, Magder SA. Variations in pulmonary artery occlusion pressure to estimate changes in pleural pressure. Intensive Care Med 2007; 33:2004–2008. 38. Biderman P, Einav S, Fainblut M, et al. Extracorporeal life support in patients with multiple injuries and severe respiratory failure: a single center experience? J Trauma Acute Care Surg 2013; 75:907–912.
Volume 27 Number 2 April 2014
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Multicompartment management of patients with severe traumatic brain injury Margaret H. Lauerman and Deborah M. Stein
Purpose of review Intracranial pressure (ICP) control is a mainstay of traumatic brain injury (TBI) management. However, development of intracranial hypertension (ICH) may be affected by factors outside of the cranial vault in addition to the local effects of the TBI. This review will examine the pathophysiology of multiple compartment syndrome (MCS) and current treatment considerations for patients with TBI given the effects of MCS. Recent findings Elevated intra-abdominal pressure (IAP) is associated with ICP elevation, and decompressive laparotomy in patients with concurrent elevations in IAP and ICP can reduce ICP. Elevated intrathoracic pressure may be similarly associated with ICP elevation, although the ideal ventilator management strategy for TBI patients when considering MCS is unclear. Summary In MCS, intracranial, intrathoracic and intra-abdominal compartment pressures are interrelated. TBI patient care should include ICP control as well as minimization of intrathoracic and intra-abdominal pressure as clinically possible. Keywords abdominal hypertension, multiple compartment syndrome, traumatic brain injury
INTRODUCTION Traumatic brain injury (TBI) is a prevalent condition [1]. Modern management of TBI utilizes a multimodal approach, incorporating both medical and surgical therapy as well as treatment of intracranial and extracranial factors. This review will elucidate how pressure elevation in extracranial body compartments can affect intracranial pressure (ICP), and how treatment of patients with TBI can be optimized with the knowledge of multiple compartment syndrome (MCS).
EPIDEMIOLOGY OF TRAUMATIC BRAIN INJURY Each year, 1.7 million patients are diagnosed with a TBI. Although the clinical spectrum of TBI is broad, 250 000 TBIs are severe enough to merit hospital admission annually [1]. TBI is also a mortal condition, with over 53 000 deaths from TBI each year [2]. Long-term disability occurs in many survivors of TBI [3]. Outcomes for patients with TBI have improved, with mortality decreasing 8.2% over the past decade [2].
OVERVIEW OF MULTIPLE COMPARTMENT SYNDROME Much of the improvement in TBI outcomes may be because of increased understanding of the pathophysiology of TBI, such as awareness of MCS. MCS is a condition in which pressure in one body compartment, or treatment of pressure in one body compartment, can affect pressure in another body compartment [4 ]. In a patient with a TBI, the end result of MCS can be intracranial hypertension (ICH) [4 ], which has been associated with poor neurologic outcomes [3,5,6]. Fortunately, development of MCS is uncommon, with a 2% incidence of MCS during a 4-year period at our institution. Mortality for MCS patients, however, is higher than &&
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Program in Trauma, University of Maryland School of Medicine, Baltimore, Maryland, USA Correspondence to Deborah M. Stein, MD, MPH, Program in Trauma, University of Maryland School of Medicine, 22 South Greene St, Baltimore, MD 21201, USA. Tel: +1 410 328 3495; e-mail: [email protected] Curr Opin Anesthesiol 2014, 27:219–224 DOI:10.1097/ACO.0000000000000044
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KEY POINTS MCS develops because of the physiologic interactions between ICP, intra-abdominal pressure (IAP), and intrathoracic pressure (ITP). Elevations in ICP with concurrent intra-abdominal hypertension should be treated with a decompressive laparotomy, even without the development of abdominal compartment syndrome (ACS). Although there is no consensus currently for ventilator management in TBI, ITP should be limited as clinically possible, as ITP may contribute to elevations in ICP. Management of elevated ICP should include medical ICP therapy and consideration of decompressive craniectomy if medical therapy fails.
mortality for those undergoing decompressive craniectomy alone [4 ]. Optimization of patients with TBI not only involves treatment of intracranial disorders, but also optimizing other organ systems cognizant of possible central nervous system effects. Conventional ICP management targets decreasing cranial vault compartment pressure through brain tissue edema reduction, appropriate reductions in cerebral blood flow (CBF), cerebrospinal fluid drainage, or decompressive craniectomy. However, ICP is not only influenced by cranial vault contents, as ICP has been shown to have a complex relationship with both intra-abdominal pressure (IAP) and intrathoracic pressure (ITP) [4 ,7,8]. &&
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absence of evacuatable mass lesion, target cranial vault size. ICP can be lowered with decompressive craniectomy, which allows the brain parenchyma to expand further than previously limited by the cranial vault [4 ]. Decompressive craniectomy is associated with improved intracranial physiology, as decompressive craniectomy increases macrovascular and microvascular circulation. In a prospective study of 19 TBI patients, internal carotid artery and middle cerebral artery flow velocity improved significantly after decompressive craniectomy [11]. In another study of six TBI patients, microvascular blood flow, measured by microbubble contrast enhanced ultrasound, significantly improved following decompressive craniectomy [12]. In addition to improving CBF, decompressive craniectomy also improves brain tissue oxygenation, which can be compromised in TBI. In a prospective study of nine TBI patients, low or declining brain tissue oxygen levels were noted in all patients prior to decompressive craniectomy, but significantly improved after decompressive craniectomy [13]. In addition to the improvement in blood flow and brain tissue oxygenation [11–13], decompressive craniectomy may improve clinical outcomes. In one study of 50 patients undergoing decompressive craniectomy for refractory ICP, good functional outcomes were seen in 40% of patients [14]. Decompressive craniectomy, much like ICP monitoring, has become recently controversial, as a randomized trial of 155 patients with TBI demonstrated worse outcomes for decompressive craniectomy patients, although mortality was not significantly affected [15 ]. However, this trial of decompressive craniectomy is limited by its bifrontal surgical approach, variation in preoperative pupillary exam between groups, and exclusion of patients requiring surgery for mass lesions [16]. Given these limitations, and the good functional outcomes seen after decompressive craniectomy, our institution continues to consider decompressive craniectomy for refractory ICP patients or patients with primary surgical indications. &&
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INTRACRANIAL PRESSURE MANAGEMENT ICP monitoring is often used in TBI patient care, and many therapies for TBI use ICP as their treatment target. ICP is elevated at levels over 20 mmHg [9], and is associated with neurologic deterioration, disability, and mortality [3,5,6]. Although ICP monitoring has recently become controversial, with a randomized trial failing to show benefit to invasive ICP monitoring for functional recovery or mortality [10 ], ICP monitoring continues to be the standard of care in most large volume centers, including our own institution. Medical strategies for decreasing ICP include sedation and pain control, temperature control, hyperosmolar therapy with mannitol or hypertonic saline, and barbiturate coma induction [9]. These medical strategies for ICP management target intracranial contents, decreasing CBF and subsequent intracranial blood volume, or brain tissue volume. Surgical strategies for the treatment of ICH, in the &&
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INTRATHORACIC PRESSURE TBI patients often present with concurrent thoracic trauma [17]. Pulmonary injury can require ventilator manipulation and higher ventilator pressures, such as an increase in positive end expiratory pressure (PEEP) [17]. Other concurrent pulmonary issues, such as pulmonary edema development from fluid resuscitation, pneumonia, and acute respiratory distress syndrome can increase ventilator pressure requirements. Development of acute Volume 27 Number 2 April 2014
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Multicompartment management in severe traumatic brain injury Lauerman and Stein
lung injury in patients with TBI is associated with poorer neurologic outcome [18]. High tidal volumes are correlated with acute lung injury in patients with TBI as well [19], suggesting that a high pressure, low tidal volume ventilation approach may be preferable. However, high-pressure ventilation may have deleterious effects on ICP due to effects of MCS. Increases in ITP are associated with increases in ICP in animal models. When ITP and ICP were measured during cardiopulmonary resuscitation (CPR), ICP elevation was seen with CPR-induced ITP increases [8]. PEEP can also be used as a surrogate for ITP, as it represents a constant minimum of ITP throughout the respiratory cycle. Ventilator manipulation with PEEP increased ICP, even in the presence of baseline elevated ICP. The increase in ICP was less with underlying ICH, although it still may have significant effects in animal models [20]. However, the relationship between ITP and ICP in humans remains unclear. In one review of patients with TBI, as PEEP was increased up to 15 cm H2O, ICP decreased incrementally [17]. Another review of TBI and subarachnoid hemorrhage (SAH) patients failed to show association between ICP and PEEP [21], whereas another review does note a positive correlation between PEEP and ICP in patients with TBI [22]. The effect of PEEP on CBF is similarly unclear. In patients with SAH, there was a significant mean arterial pressure (MAP)-induced decrease in CBF with increasing PEEP [23], whereas in another review of TBI patients, CPP did not change in any specific pattern with increasing PEEP [17]. Choice of ventilator mode may influence ICP, although data are limited. Inverse ratio ventilation, although associated with a longer period of elevated ITP during the respiratory cycle, did not significantly increase ICP in patients with TBI [24]. Airway pressure release ventilation (APRV), another ventilation mode with a prolonged inspiratory time, similarly did not increase ICP and actually improved carotid blood flow, a surrogate marker of CBF, in a SAH patient with hypoxemia [25]. In an animal model, use of APRV with spontaneous breathing, as opposed to altering pressure and rate for constant minute ventilation without spontaneous breathing, was associated with higher cerebral perfusion [26]. Recruitment maneuvers are also often performed in patients with hypoxemia to increase alveolar expansion, and have a high set pressure. Recruitment maneuvers, when performed with escalating PEEP, increased ICP in 75% of patients with TBI, with resolution of the ICP elevation at recruitment maneuver completion [27 ]. Although low tidal volume, high-pressure ventilation has been shown beneficial in the acute lung injury population, higher CO2 levels are seen with &
lower tidal volumes [28]. This elevation in CO2, and potential cerebral vasoconstriction, is another deleterious effect of high-pressure ventilation for patients with TBI, in addition to high-pressure ventilation potentially increasing ICP. In patients who are difficult to oxygenate or ventilate, ICP optimization may be sacrificed for increased ITP, as poor oxygenation is also detrimental to TBI patients [29]. However, no recommendations have been formalized for TBI patients thus far regarding ventilator strategies or settings [9].
INTRAABDOMINAL PRESSURE Elevated IAP is a common condition, with a 32.1% overall incidence of elevated IAP in ICU patients [30]. Elevations in IAP are often brought on by intraabdominal fluid accumulation or visceral organ edema, with compensation for this edema constrained by the diaphragm, abdominal wall, and bony structures, only some of which are distensible [31]. IAP is typically monitored through bladder pressure measurement at end expiration [4 ,31, 32 ]. IAP is considered elevated when greater than 12 mmHg [32 ] and abdominal compartment syndrome (ACS) develops at a pressure of 20 mmHg when combined with organ failure [31]. Elevated IAP affects the function of many abdominal visceral organs, including the renal, hepatic, and gastrointestinal systems [31]. There are many options for the treatment of elevated IAP, including sedation, paralysis, gastric and rectal decompression, paracentesis, diuretics or dialysis. However, should ACS develop, decompressive laparotomy is recommended [32 ]. Much as the effect of ITP extends beyond the thoracic cavity, the effect of elevated IAP is not limited to the abdominal cavity [31]. In an animal model of elevated IAP, stepwise increases in IAP induced stepwise increases in ICP. With these increases in ICP, CPP decreased as well [33]. This association between IAP and ICP holds true in humans. Induction of elevated IAP in human patients with TBI, through placement of an external water bag on the abdomen, increased ICP significantly. The clinical implication of the elevated ICP is unclear, as despite the numeric increase in ICP, cerebral oxygen extraction was maintained in this study [34]. Just as increasing IAP induced elevations in ICP, therapy to relieve increased IAP through decompressive laparotomy can resolve ICP elevation. In a review of 102 patients who underwent decompressive craniectomy for ICP elevation, 24% also underwent decompressive laparotomy for MCS. IAP was elevated at the time of decompressive laparotomy, with a mean IAP of 28 mmHg. Decompressive
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Trauma and transfusion
laparotomy initially relieved the ICP elevation, with mean ICP significantly decreasing from 28 to 19 mmHg. Unfortunately, this ICP decrease after decompressive laparotomy was transient in the days following decompressive laparotomy [4 ]. Decompressive laparotomy has also been used successfully without decompressive craniectomy for the treatment of elevated ICP in the setting of MCS [35–36]. In one patient with elevated IAP and ICP, decompressive laparotomy alone was performed with a decrease in ICP, and the patient subsequently had an excellent functional outcome despite the malignant ICH [36]. Physiologic changes associated with ACS do not need to occur for IAP to elevate ICP. In one series of 17 patients undergoing decompressive laparotomy for refractory ICP, no patient had progressed to ACS prior to decompressive laparotomy. Increased airway pressures were not evident, as patients had a mean airway pressure of 29.5 mmHg. Renal function was similarly maintained, with a mean urine output of 2.7 l over 12 h. Some patients did require pressers, although this is difficult to interpret in the multiply injured patient. Despite the lack of clinical ACS signs, mean IAP was elevated, ranging from 21 to 35 mmHg prior to decompression [35]. Overall, elevations in IAP should be treated according to the World Society for the Abdominal Compartment Syndrome algorithm. Sedation, paracentesis, and fluid removal through diuretics or dialysis for elevated IAP must be undertaken with caution in TBI patients to avoid hypotension, and a subsequent decrease in CPP due to a decreased MAP from hypovolemia. Progression to ACS should be treated with decompressive laparotomy in patients with TBI as it is in non-TBI patients [32 ]. However, decompressive laparotomy should be performed prior to development of the physiologic changes with ACS in the setting of intractable ICH with elevated IAP. &&
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cardiac compliance and cardiac output [31], all of which could potentially exacerbate ICP if venous return is limited [4 ]. Animal models have examined the relationship between ICP, ITP, and IAP. In an animal model measuring effects of balloon insufflation-induced increases of IAP on ICP and ITP, both ITP and ICP increased with higher IAP. Cardiac index decreased with higher IAP, as did CPP. However, there is some evidence that the relationship between IAP and ICP may be mediated through ITP. When a median sternotomy and pleuropericardotomy was performed with the balloon insufflation, the increase of ICP with elevated IAP was no longer seen [7]. Another animal model looking at the effect of CPR on ICP affirmed the interplay of ITP and IAP in affecting ICP. Although ICP rose with increased ITP during CPR, placement of an abdominal binder heightened the amount of ICP increase a set change in ITP induced [8]. The complex relationship between IAP, ITP, and ICP holds true in human studies as well. In patients who underwent decompressive laparotomy after decompressive craniectomy for elevated ICP, IAP predictably decreased, but so did ITP. With both the decrease in ITP and IAP, ICP elevation resolved [4 ]. In addition to therapies targeting reduction of intracranial contents for ICP control, modern ICP reduction strategies also treat the relationship between ICP, ITP, and IAP. Positional therapy for refractory ICP elevation, through standing the patient (Fig. 1), allows relief of the mechanical effect of IAP on ICP and minimization of ITP from ventilator pressures through increased pulmonary recruitment. Extracorporeal membrane oxygenation (ECMO) has also been used in patients with TBI and respiratory failure [38], and may be an additional therapy to reduce ITP in patients with &&
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PHYSIOLOGY OF MULTIPLE COMPARTMENT SYNDROME The true physiology behind the interplay of IAP, ITP, and ICP in MCS is unknown. Much of the effect of ITP and IAP on ICP may be mediated through an association between IAP and ITP, as well as the cardiovascular system. Elevated IAP directly compresses the thoracic cavity, inducing higher peak airway pressures while decreasing functional residual capacity, lung volume, and chest wall compliance [31]. As pleural pressure rises in ventilated patients, pulmonary artery occlusion pressure increases [37], indicating an afterload increase on the cardiac system. Elevated IAP also decreases 222
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FIGURE 1. Positional therapy being used in a TBI patient. Volume 27 Number 2 April 2014
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Multicompartment management in severe traumatic brain injury Lauerman and Stein
elevated ICP. Positional therapy is used at our institution with combined refractory ICP and respiratory failure, whereas ECMO is used in trauma patients with severe hypoxemia unresponsive to all other measures.
FACTORS CONTRIBUTING TO MULTIPLE COMPARTMENT SYNDROME It is difficult to elucidate factors contributing to MCS given the small number of patients in the literature. MCS patients were more critically injured on admission, with higher Injury Severity Score and mean ICP at the time of decompressive craniectomy. Fluid resuscitation may also contribute to MCS development. Patients with MCS received 23 liters more fluid in the first seven hospital days than those undergoing decompressive craniectomy without developing MCS [4 ]. Ascites was seen in almost all patients at the time of decompressive laparotomy for MCS [35–36]. CPP maintenance, correction of sedation-induced hypotension, and hypertonic saline ICP therapy were associated with increased fluid administration [4 ], and thus may contribute to the development of MCS. &&
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OUTCOMES IN MULTIPLE COMPARTMENT SYNDROME Outcomes in patients developing MCS are worse than those with elevated ICP alone. There was a 12% absolute increase in mortality for patients undergoing decompressive craniectomy and decompressive laparotomy compared with those undergoing decompressive craniectomy alone, although this was not significant. ICU length of stay and hospital length of stay were both significantly increased in patients with MCS [4 ]. Overall survival of MCS patients ranges from 58 to 65% [4 ,35]. The only significant predictor of survival in MCS is younger age. Higher initial ICP, higher initial Glascow Coma Score, lower volume fluid resuscitation required, shorter time to decompressive laparotomy, avoidance of decompressive craniectomy, and avoidance of barbiturate coma were all associated with survival in MCS, although these did not reach statistical significance [35]. In patients with both IAP and ICP elevation, the order of decompressive craniectomy and decompressive laparotomy did not have a significant effect on mortality or length of stay [4 ]. &&
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CONCLUSION TBI patients should be closely monitored for MCS development, with ICP monitoring, bladder
pressure monitoring, and serial abdominal exams. Fluid resuscitation should be administered judiciously to avoid exacerbating MCS through pulmonary edema, ascites, and bowel edema elevating IAP and ITP. Sedating medications should be dosed to avoid hypotension and the subsequent need for fluid administration for CPP maintenance. Ventilator mode and pressure should be selected to limit ITP as clinically possible. Should maximal medical ICP therapy fail, decompressive craniectomy should be considered. IAP elevation concurrent with refractory ICP elevation should prompt decompressive laparotomy. Generally at our institution, decompressive laparotomy is considered in patients with elevated IAP in the setting of ICH. Physiologic compromise of ACS is not required for decompressive laparotomy to be considered. Overall, treatment of intracranial, intrathoracic, and intra-abdominal disorders cannot be undertaken without consideration of the effects on other compartments, specifically ICP in TBI patients [4 ]. &&
Acknowledgements No funding was received. Conflicts of interest There are no conflicts of interest.
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