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Hypotensive resuscitation in a head-injured multi-trauma patient
Journal of Critical Care xxx (2013) xxx–xxx
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Hypotensive resuscitation in a head-injured multi-trauma patient☆ Joshua M. Tobin, MD a,⁎, Richard P. Dutton, MD, MBA b, Jean-Francois Pittet, MD c, Deepak Sharma, MBBS, MD, DM d a
David Geffen School of Medicine at UCLA, Department of Anesthesiology/Division of Critical Care, Los Angeles, CA 90095-7403, USA Clinical Associate, Anesthesia Quality Institute, American Society of Anesthesiologists, Department of Anesthesia & Critical Care, University of Chicago, Chicago, IL, USA Director of the Division of Critical Care Anesthesiology, University of Alabama at Birmingham, Birmingham, AL, USA d Chief of the Division of Neuroanesthesiology and Perioperative Neurosciences, University of Washington, Seattle, WA, USA b c
a r t i c l e
i n f o
Keywords: Resuscitation Trauma Care Traumatic Brain Injury Hypotension
a b s t r a c t The concept of permissive hypotension is a controversial topic in trauma care. While driving blood pressure to “normal” levels with large volume crystalloid infusions is not appropriate, definitive data on the target blood pressure for hypotensive resuscitation are lacking. Indeed, the concept of systolic blood pressure as a marker for resuscitation is arguable. In this case presentation, a panel of experts in trauma resuscitation discusses the merits and limitations of hypotensive resuscitation in the context of a patient who has sustained multiple injuries, including a head injury. The controversies highlighted herein call attention to the role of the intensivist in managing a continuing resuscitation while coordinating the care of other physicians whose therapies can run at cross-purposes to one another. The challenges of the practice of critical care in the 21st century are no more apparent than in the care of a complex trauma patient. © 2013 Published by Elsevier Inc.
A 17-year-old male adolescent is the unrestrained driver in a single car crash in which he veered off the road and hit a bridge abutment. Paramedics initiated a 16-gauge intravenous (IV) line at the scene and have begun infusing one liter of normal saline. The prearrival report states that the patient is disoriented and has a blood pressure of 100/palpation with a heart rate of 120 beats per minute (bpm). He has lacerations to the head and face and does not have any obvious extremity deformities. Paramedics have been unable to assess the patient’s abdomen due to agitation and non-compliance. He is noted at the scene to be moving all four extremities spontaneously. They have placed a cervical collar and full spinal protections with a spine board. Upon arrival in the trauma bay the patient has a blood pressure of 90/56 with a heart rate of 126 bpm. He has a Glasgow Coma Scale of 8 (eyes = 2, verbal = 3, motor = 3). He moves all 4 extremities but remains non-compliant with the remainder of the physical exam. The trauma team elects to intubate the patient’s trachea for airway protection. He is induced via his in situ IV line with etomidate and succinylcholine. Manual in-line stabilization and cricoid pressure are applied as the anesthesiologist uses a Macintosh 3 laryngoscope blade to place a #8 endotracheal tube. End-tidal carbon dioxide is verified
☆ Conflicts of Interest: None to disclose. ⁎ Corresponding author. Tel.: +1 310 206 7496; fax: +1 310 825 2236. E-mail addresses: [email protected], [email protected] (J.M. Tobin), [email protected] (R.P. Dutton), [email protected] (J.-F. Pittet), [email protected] (D. Sharma).
on the side-stream analyzer and breath sounds are confirmed in all lung fields. The epigastrium is silent. After induction the blood pressure is 84/50 and the heart rate is 129. The endotracheal tube is secured and a focused assessment with sonography for trauma (FAST) is performed. The FAST results are equivocal and the patient is transported to the computerized tomography (CT) scanner. A CT scan of the head reveals no intracranial blood and open basal cisterns. There is a zygomatic arch fracture on the left. The CT scan shows no fracture or subluxation of the cervical spine. The abdominal CT scan reveals a significant liver laceration and free fluid in the abdomen. The imaging studies and physical exam findings are otherwise unremarkable. The patient is transported back to the trauma bay where his blood pressure is 78/42 with a heart rate of 130. An infusion of two units of type “O” negative blood is initiated as the patient is emergently transported to the operating room (OR) for an exploratory laparotomy. This case emphasizes a number of important concepts in the management of the trauma patient. Prompt arrival of emergency medical services is a vital first step in improving the survival of the injured patient. Paramedics initiated an IV line and infused a liter of normal saline en route to the hospital. While this remains part of the field management of trauma in many emergency medical services systems, evidence suggests that large volume crystalloid infusions may do more harm than good. More recent data further suggest that chloride rich solutions can worsen acute kidney injury in the intensive care unit [1]. If crystalloid infusions are to be used, it may be appropriate to use chloride-poor solutions (eg, lactated ringers, plasmalyte).
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Please cite this article as: Tobin JM, et al, Hypotensive resuscitation in a head-injured multi-trauma patient, J Crit Care (2013), http:// dx.doi.org/10.1016/j.jcrc.2013.11.017
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J.M. Tobin et al. / Journal of Critical Care xxx (2013) xxx–xxx
Upon arrival in the trauma bay the patient was noted to become increasingly obtunded and tracheal intubation was performed for airway protection. Rapid sequence induction and direct laryngoscopy are a safe and effective means for tracheal intubation in trauma patients [2]. This patient certainly has a mechanism of injury to suggest possible spinal cord injury and a cervical spine collar was appropriately placed by paramedics. Even in patients with documented vertebral body fractures and documented spinal cord injuries, orotracheal intubation remains a safe approach to airway management in trauma [3]. The initial CT scan revealed no cervical spine injury or traumatic brain injury (TBI). While this is reassuring, the patient’s physical exam on presentation suggests a possible TBI and a follow-up CT scan of the head is warranted to evaluate for evolution of any intraparenchymal hematoma or other TBI. The patient is appropriately taken emergently to the OR for exploratory laparotomy due to his liver laceration. The resuscitation in the OR will involve the administration of blood products. Data over the last ten years have demonstrated improved survival with plasma to red blood cell ratios approaching unity, however, the proper ratio of red blood cells to plasma remains a topic of investigation. The goal of resuscitation in the OR is also a subject of debate and on-going research. In hypotensive resuscitation a lower blood pressure is tolerated, with mean arterial pressures approaching 50 mm Hg. The idea is that lower blood pressures will not exacerbate blood loss in the acute/uncontrolled blood loss stage early in resuscitation. There is also a concern of “popping the clot” as larger resuscitation volumes produce higher pressures that overcome the hemostatic benefit of newly formed blood clots. The anesthesiologist is responsible for trauma resuscitation and must manage the, sometimes competing, interests of the neurosurgical and trauma surgical therapies. At the same time the anesthetic must be conducted in parallel with resuscitation of a patient in extremis. To discuss the finer points of such a complex anesthetic/ resuscitation a panel of anesthesiologists with expertise in trauma, critical care and head injury will offer their perspective in the management of this patient. 1. Dr Richard P. Dutton is the Director of the Anesthesia Quality Institute at the American Society of Anesthesiologists and is the former Chief of Anesthesiology at the R Adams Cowley Shock Trauma Center at the University of Maryland. Dr Dutton: What evidence is there to support hypotensive resuscitation in blunt trauma? Penetrating trauma? This patient’s greatest and most-immediate risk is exsanguination from the liver injury. Up to half of all mortality from trauma is due to hemorrhage, either early (about 33% of deaths) or later from the effects of shock and multiple organ system failure. Patients who bleed to death do so during the first three hours in the hospital [4], emphasizing the importance of early intervention. Foremost, of course, is anatomic control of the site of hemorrhage, either through surgery or angiographic embolization. Anesthesiologists play an important role in the logistics of moving patients to definitive care. During this intervention, however, the management of ongoing fluid resuscitation has a significant impact on outcomes. One widely accepted approach is resuscitation to a target blood pressure that is lower than normal for the patient, as a means to avoid the rebleeding associated with blood pressure spikes that wash away fragile extraluminal clots [5]. Deliberate hypotension is common in elective surgery, and is well supported in numerous animal models of uncontrolled hemorrhage [6]. At least three human trials have attempted to validate this approach. Most influential was the trial by Bickell et al in Houston in the early 1990s. [7] Hypotensive patients with penetrating torso trauma were randomized in the field to either customary fluid therapy or none at all; this approach was followed from prehospital transport through emergency department assessment to the operating room
door. The no-fluid group had significantly improved survival (70% vs. 64%; P = .04). A similar protocol was conducted in Baltimore in the late 1990s, randomizing hypotensive patients (either blunt or penetrating) to blood pressure maintenance at 80 mm Hg systolic vs. N 100 mm Hg until definitive control of hemorrhage [8]. No difference in survival was found, despite a higher injury severity in the hypotensive group. Finally, another trial is underway now in Houston; a preliminary report suggests improved outcomes with hypotension [9]. Despite the heterogeneity of patients and injuries in these trials, and concerns about the underlying methodology, deliberate hypotension has been an accepted strategy in penetrating trauma in most major trauma centers since the year 2000. Controversy remains over the best approach to achieving hypotension: whether through fluid restriction (the original Bickell premise) or through simultaneous administration of fluid and anesthetic agents (titrating anestheticinduced vasodilation against vascular filling) [10]. Although scientific evidence is scant, the latter approach is supported by both theories of pathophysiology—vasodilatory hypotension preserving tissue perfusion better than vasoconstricted hypotension—and some limited animal data [5]. A particular concern in this debate is the role of deliberate hypotension in patients who might be vulnerable to ischemic injury. This includes patients with traumatic brain injury (TBI) as well as older patients and those with known coronary artery disease. TBI is especially challenging, because of the well-documented association between episodes of hypotension and bad outcomes in patients with severe injury. It should be recognized, however, that this association is based on observational data and does not prove cause and effect. In fact, it may be that while simultaneous bleeding and TBI predict a bad outcome, the patients in this cohort that do best are the ones that stop bleeding fastest, and are thus able to complete resuscitation. In other words, deliberate hypotension might be MORE important in vulnerable patients. There are some animal data available to support this point of view [11], but definitive human trials are unlikely. In summary, deliberate hypotension is an important tactic for limiting ongoing blood loss and speeding the time to complete resuscitation in patients with traumatic hemorrhage. While numerous questions of clinical application remain open, the core hypothesis that a lower blood pressure will lead to less blood loss has been well established in both pre-clinical and clinical trials. Hypotensive management remains an important tool to facilitate hemostasis and resuscitation in dying trauma patients. 2. Dr Jean-Francois Pittet is a Professor of Anesthesiology at the University of Alabama at Birmingham and the Director of the Division of Critical Care Anesthesiology. Dr Pittet: What are the advantages, if any, of hypotensive resuscitation in trauma? The case presented above emphasizes a number of important concepts in management of the trauma patient. I will focus my comments on pre-hospital and hospital-based hypotensive fluid resuscitation and I will present evidence against the use of hypotensive fluid resuscitation for this particular patient. Recognition of when a trauma patient is bleeding can be difficult. Pulse and arterial blood pressure are neither sensitive nor specific for severe hemorrhage. Young patients may lose more than 30% of their blood volume with little change in their vital signs. Furthermore, the classical cut-off systolic blood pressure (SBP) of 90 mm Hg as a marker of hemorrhagic shock has been based on expert opinion and not on evidence-based data. In fact, a SBP below 110 mm Hg is associated with a significant increase in mortality in blunt major trauma patients with baseline pressure of 130 to 139 mm Hg. Importantly, the mortality rate doubled for a SBP b100 mm Hg, tripled at a SBPb 90 mm Hg and was 5- to 6-fold higher at a SBP b 70 mm Hg [12]. In addition, single, isolated hypotensive SBP measurements of less than 105 mm Hg during trauma resuscitation should not be ignored or dismissed, as
Please cite this article as: Tobin JM, et al, Hypotensive resuscitation in a head-injured multi-trauma patient, J Crit Care (2013), http:// dx.doi.org/10.1016/j.jcrc.2013.11.017
J.M. Tobin et al. / Journal of Critical Care xxx (2013) xxx–xxx
they may suggest the presence of severe injuries that may require immediate operative or endovascular treatment and later admission to a surgical intensive care unit [13]. It should also be pointed out that most of the shock syndromes in trauma patients are hypovolemic, although other causes of shock may be present, such as neurogenic (distributive shock), myocardial contusion (blunt cardiac injury) or obstructive (tension pneumothorax, pneumomediastinum or pericardial tamponade). In the presence of shock following severe trauma, the classical approach was to replace as soon as possible the fluid losses and restore organ perfusion in order to minimize end-organ failure. However, 20 years ago Bickell et al. demonstrated a reduction in mortality in patients with truncal penetrating injuries whose fluid resuscitation was delayed until definitive hemostasis could be achieved [7]. This approach has been developed for modern combat injuries because uncontrolled major hemorrhage from mostly penetrating trauma cannot be treated immediately due to delays in evacuation. To prevent the development of a lethal triad that includes coagulopathy, acidosis and hypothermia, which is associated with administration of large amount of crystalloids, the concept of damage control resuscitation (DCR) was developed and included a hypotensive and hemostatic resuscitation strategy. This therapeutic approach includes a limited amount of volume replacement to achieve a SBP of 80 mm Hg or the return of palpable pulse and hemostatic resuscitation with red blood cells (possibly recently obtained from donors), fresh frozen plasma and platelets in a ratio approximating 1:1:1 [14]. Additional objectives include treatment of hypothermia and acidosis. Although the results of major prospective studies are still missing with this therapeutic approach, initial results suggest a decrease in mortality over standard care in both combat and civilian trauma patients [15,16].
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Investigators Group. This prospective study that includes 1216 severely injured blunt trauma patients, shows that pre-hospital high fluid resuscitation (N 500 mL) provided different results if the patients were hypotensive or not in the pre-hospital setting. In patients with arterial hypotension, high fluid resuscitation (N 500 ml) was associated with correction of hypotension on emergency department arrival and each 1 mm Hg increase in SBP was associated with a 2% increase in survival in subjects with pre-hospital hypotension. In contrast, pre-hospital crystalloid more than 500 mL was associated with worse outcome in patients without hypotension [20]. In summary, the most recent data from the literature indicate that prehospital fluid resuscitation with crystalloids may have a survival advantage for patients with arterial hypotension, however, normotensive patients benefit from a fluid restrictive approach. Ultimately, the classical approach that includes the administration of a large amount of crystalloid fluids in the pre-hospital setting may aggravate coagulopathy and lead to end-organ injury. 5. Dr Deepak Sharma is an Associate Professor of Anesthesiology at the University of Washington and is the Chief of the Division of Neuroanesthesiology and Perioperative Neurosciences. Dr Sharma: Will systolic blood pressures below 90 mm Hg be harmful to a trauma patient with a potential TBI?
The question that needs to be answered for our case is whether the DCR approach can be safely applied to civilian traumatic injuries when its hemostatic component is not always readily available. First, the patient had a Glasgow Coma Scale score of 8 in the pre-hospital setting. This low Glasgow Coma Scale score would preclude a DCR approach as the current guidelines recommend a SBP of at least 90 mm Hg in order to prevent further brain damage [17]. This question will be addressed in detail in the last part of the discussion. Recent data from the Prospective Observational Multicenter Massive Transfusion Study that included 1245 trauma patients, indicate patients who received pre-hospital fluid (median volume 700 ml with interquartile range of 300-1300 ml) had a lower mortality compared to patients who did not receive pre-hospital intravenous fluid. Interestingly, the pre-hospital fluid resuscitation did not increase the SBP in these trauma patients. In fact, the patients who received the pre-hospital fluid resuscitation had a lower SBP than those who did not [18]. This study also indicates that any survival advantage from restrictive fluid resuscitation is conferred from avoidance of the complications associated with a large volume crystalloid resuscitation. This volume threshold was addressed in a recent retrospective investigation of 370 patients that divided the population in a standard (N150 mL) or restrictive (b150 mL) fluid resuscitation group. The patients who underwent restrictive resuscitation demonstrated a survival advantage compared with the standard group [19].
In a classic review published nearly 40 years ago, Trunkey reported that the primary cause of death in trauma victims was brain injury followed by hemorrhage [21]. Decades later, another review of the published literature examining trauma treated in level-1 centers between 1980 and 2008 has reported no considerable changes in the pattern of death. The predominant cause of death after trauma continues to be central nervous system injury followed by exsanguination [22]. Traumatic brain injury (TBI) continues to remain a leading cause of death and disability [3] and is often present in patients with polytrauma. While the severity of brain damage due to the traumatic impact (“primary insult”) largely accounts for mortality after TBI, secondary damage to the injured brain occurs as a result of a variety of physiological perturbations (“secondary insults”) including hypotension, hypoxia, hyper and hypocarbia, increased intracranial pressure and hyperglycemia, leading to poor outcome [23–29]. The essence of modern trauma care is prevention of primary injury and avoidance of secondary injury and hence, rapid correction of secondary insults is a major underpinning of current management of TBI. Impaired cerebral autoregulation due to TBI makes cerebral perfusion dependent on adequacy of systemic blood pressure and systolic blood pressure (SBP) b90 mm Hg early after TBI is associated with up to 150% increase in mortality [24]. Consequently, the Brain Trauma Foundation guidelines recommend prevention and early correction of hypotension (SBP b 90 mm Hg) after severe TBI [30]. Yet, hypotension is a common intraoperative secondary insult in adult and pediatric TBI victims [31,32]. Importantly, this blood pressure goal often conflicts with the “hypotensive resuscitation” approach in polytrauma patients like our index case here. So, is SBP below 90 mm Hg likely to be harmful to a trauma patient with a potential TBI? The answer is yes, and SBP b 90 mm Hg should be avoided because the evidence indicating detrimental effect of hypotension on TBI outcomes is overwhelming and patients with TBI who suffer intraoperative hypotension (during craniotomy or extracranial surgery) may be at higher risk of death and disability [26,29]. Not surprising…the studies examining hypotensive resuscitation during active hemorrhage excluded TBI patients [8,9].
4. Should all trauma patients be resuscitated via the hypotensive approach?
6. What special considerations must be taken into account for patients with TBI?
This important question has recently been addressed in a study conducted by The Inflammation and the Host Response To Injury
While it is obvious that hypotension is detrimental to the injured brain and should be avoided; clinicians are often confronted with at
3. The hypotensive approach seems to offer promise, however, with limitation. What do you see as the limitations of hypotensive resuscitation in this case?
Please cite this article as: Tobin JM, et al, Hypotensive resuscitation in a head-injured multi-trauma patient, J Crit Care (2013), http:// dx.doi.org/10.1016/j.jcrc.2013.11.017
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least two peculiar situations; first, a patient with TBI exsanguinating due to extracranial injury and second, a polytrauma patient where TBI is not evident on admission imaging. In the former situation, hypotension may be unresponsive to treatment and the anesthesiologist may be left with no choice but to transiently tolerate this until the life threatening hemorrhage is controlled. In such a situation, the risk of worsening TBI and neurological impairment clearly exists and the systolic blood pressure should be restored to N90 mm Hg as soon as possible. In the second situation (like our index case), multiple studies have documented that early CT scanning may not demonstrate the post traumatic brain damage in majority of patients and may underestimate the ultimate size of parenchymal contusions [33,34]. The intracranial lesions frequently progress on subsequent imaging and may require intervention. Hence, a “normal” or “unremarkable” head CT performed early after injury should not provide a sense of reassurance in a patient with clinical suspicion of TBI since the brain injury may manifest later. In such patients, the brain remains susceptible to adverse impact of hypotension and it may be prudent to avoid hypotension. The definition of hypotension itself remains somewhat vague. The randomized controlled trial of hypotensive resuscitation in polytrauma patients compared a mean arterial pressure (MAP) target of 50 mm Hg with 65 mm Hg [9,15], while TBI literature refers to SBP b90 mm Hg as hypotension rather than a MAP goal [23–26,29,30,32]. Interestingly, in some situations, clinicians may be able to achieve SBP marginally N 90 mm Hg and yet the MAP may be in the acceptable range of hypotensive resuscitation (MAP 55-65 mm Hg). Our 17-year-old patient in the index case may be considered a pediatric patient and hypotension in pediatric TBI is defined as SBP b 5th percentile for age (70 + 2*Age in years mm Hg) or 90 mm Hg, whichever is lower [31]. While hypotensive resuscitation may be an option for treating life saving hemorrhage in this patient, clinicians should avoid hypotension in infants and young children given the small total circulating volume and limited reserve to compensate for hypovolemia. In any case, the hypotensive resuscitation study included only children N 14 years old [9]. In summary, the use of hypotensive resuscitation in polytrauma victims must account for the possibility of associated TBI. If TBI is suspected clinically even in the absence of initial radiological evidence, SBP b 90 mm Hg should be avoided. When unavoidable, anesthesiologists should strive to minimize the duration of such hypotension and reduce the burden of secondary insult to the injured brain by avoiding simultaneous hypocarbia, which may worsen ischemic cerebral damage [35].
7. Conclusion The contributor’s comments clearly highlight the challenges of the resuscitation consultant. The concept of permissive hypotension dates back, at least, to World War I (not long after intravenous fluid therapy was innovated!) While driving blood pressure to “normal” levels with large volume crystalloid infusions is not appropriate, definitive data on the target blood pressure for hypotensive resuscitation are lacking. Indeed, the concept of systolic blood pressure as a marker for resuscitation is arguable. Perhaps mean arterial pressure, base excess, or some other marker offers a more discrete insight into resuscitation end points. The need for further investigation is clear. Intensivists are often called upon to be the “team captain”. It is the intensivist that orchestrates care from the operating room to the intensive care unit, all the while managing a continuing resuscitation and coordinating the care of other physicians whose therapies can run at crosspurposes to one another. The challenges of the practice of critical care in the 21st century are no more apparent than in the care of a complex trauma patient.
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Please cite this article as: Tobin JM, et al, Hypotensive resuscitation in a head-injured multi-trauma patient, J Crit Care (2013), http:// dx.doi.org/10.1016/j.jcrc.2013.11.017
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Journal of Critical Care journal homepage: www.jccjournal.org
Hypotensive resuscitation in a head-injured multi-trauma patient☆ Joshua M. Tobin, MD a,⁎, Richard P. Dutton, MD, MBA b, Jean-Francois Pittet, MD c, Deepak Sharma, MBBS, MD, DM d a
David Geffen School of Medicine at UCLA, Department of Anesthesiology/Division of Critical Care, Los Angeles, CA 90095-7403, USA Clinical Associate, Anesthesia Quality Institute, American Society of Anesthesiologists, Department of Anesthesia & Critical Care, University of Chicago, Chicago, IL, USA Director of the Division of Critical Care Anesthesiology, University of Alabama at Birmingham, Birmingham, AL, USA d Chief of the Division of Neuroanesthesiology and Perioperative Neurosciences, University of Washington, Seattle, WA, USA b c
a r t i c l e
i n f o
Keywords: Resuscitation Trauma Care Traumatic Brain Injury Hypotension
a b s t r a c t The concept of permissive hypotension is a controversial topic in trauma care. While driving blood pressure to “normal” levels with large volume crystalloid infusions is not appropriate, definitive data on the target blood pressure for hypotensive resuscitation are lacking. Indeed, the concept of systolic blood pressure as a marker for resuscitation is arguable. In this case presentation, a panel of experts in trauma resuscitation discusses the merits and limitations of hypotensive resuscitation in the context of a patient who has sustained multiple injuries, including a head injury. The controversies highlighted herein call attention to the role of the intensivist in managing a continuing resuscitation while coordinating the care of other physicians whose therapies can run at cross-purposes to one another. The challenges of the practice of critical care in the 21st century are no more apparent than in the care of a complex trauma patient. © 2013 Published by Elsevier Inc.
A 17-year-old male adolescent is the unrestrained driver in a single car crash in which he veered off the road and hit a bridge abutment. Paramedics initiated a 16-gauge intravenous (IV) line at the scene and have begun infusing one liter of normal saline. The prearrival report states that the patient is disoriented and has a blood pressure of 100/palpation with a heart rate of 120 beats per minute (bpm). He has lacerations to the head and face and does not have any obvious extremity deformities. Paramedics have been unable to assess the patient’s abdomen due to agitation and non-compliance. He is noted at the scene to be moving all four extremities spontaneously. They have placed a cervical collar and full spinal protections with a spine board. Upon arrival in the trauma bay the patient has a blood pressure of 90/56 with a heart rate of 126 bpm. He has a Glasgow Coma Scale of 8 (eyes = 2, verbal = 3, motor = 3). He moves all 4 extremities but remains non-compliant with the remainder of the physical exam. The trauma team elects to intubate the patient’s trachea for airway protection. He is induced via his in situ IV line with etomidate and succinylcholine. Manual in-line stabilization and cricoid pressure are applied as the anesthesiologist uses a Macintosh 3 laryngoscope blade to place a #8 endotracheal tube. End-tidal carbon dioxide is verified
☆ Conflicts of Interest: None to disclose. ⁎ Corresponding author. Tel.: +1 310 206 7496; fax: +1 310 825 2236. E-mail addresses: [email protected], [email protected] (J.M. Tobin), [email protected] (R.P. Dutton), [email protected] (J.-F. Pittet), [email protected] (D. Sharma).
on the side-stream analyzer and breath sounds are confirmed in all lung fields. The epigastrium is silent. After induction the blood pressure is 84/50 and the heart rate is 129. The endotracheal tube is secured and a focused assessment with sonography for trauma (FAST) is performed. The FAST results are equivocal and the patient is transported to the computerized tomography (CT) scanner. A CT scan of the head reveals no intracranial blood and open basal cisterns. There is a zygomatic arch fracture on the left. The CT scan shows no fracture or subluxation of the cervical spine. The abdominal CT scan reveals a significant liver laceration and free fluid in the abdomen. The imaging studies and physical exam findings are otherwise unremarkable. The patient is transported back to the trauma bay where his blood pressure is 78/42 with a heart rate of 130. An infusion of two units of type “O” negative blood is initiated as the patient is emergently transported to the operating room (OR) for an exploratory laparotomy. This case emphasizes a number of important concepts in the management of the trauma patient. Prompt arrival of emergency medical services is a vital first step in improving the survival of the injured patient. Paramedics initiated an IV line and infused a liter of normal saline en route to the hospital. While this remains part of the field management of trauma in many emergency medical services systems, evidence suggests that large volume crystalloid infusions may do more harm than good. More recent data further suggest that chloride rich solutions can worsen acute kidney injury in the intensive care unit [1]. If crystalloid infusions are to be used, it may be appropriate to use chloride-poor solutions (eg, lactated ringers, plasmalyte).
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Please cite this article as: Tobin JM, et al, Hypotensive resuscitation in a head-injured multi-trauma patient, J Crit Care (2013), http:// dx.doi.org/10.1016/j.jcrc.2013.11.017
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Upon arrival in the trauma bay the patient was noted to become increasingly obtunded and tracheal intubation was performed for airway protection. Rapid sequence induction and direct laryngoscopy are a safe and effective means for tracheal intubation in trauma patients [2]. This patient certainly has a mechanism of injury to suggest possible spinal cord injury and a cervical spine collar was appropriately placed by paramedics. Even in patients with documented vertebral body fractures and documented spinal cord injuries, orotracheal intubation remains a safe approach to airway management in trauma [3]. The initial CT scan revealed no cervical spine injury or traumatic brain injury (TBI). While this is reassuring, the patient’s physical exam on presentation suggests a possible TBI and a follow-up CT scan of the head is warranted to evaluate for evolution of any intraparenchymal hematoma or other TBI. The patient is appropriately taken emergently to the OR for exploratory laparotomy due to his liver laceration. The resuscitation in the OR will involve the administration of blood products. Data over the last ten years have demonstrated improved survival with plasma to red blood cell ratios approaching unity, however, the proper ratio of red blood cells to plasma remains a topic of investigation. The goal of resuscitation in the OR is also a subject of debate and on-going research. In hypotensive resuscitation a lower blood pressure is tolerated, with mean arterial pressures approaching 50 mm Hg. The idea is that lower blood pressures will not exacerbate blood loss in the acute/uncontrolled blood loss stage early in resuscitation. There is also a concern of “popping the clot” as larger resuscitation volumes produce higher pressures that overcome the hemostatic benefit of newly formed blood clots. The anesthesiologist is responsible for trauma resuscitation and must manage the, sometimes competing, interests of the neurosurgical and trauma surgical therapies. At the same time the anesthetic must be conducted in parallel with resuscitation of a patient in extremis. To discuss the finer points of such a complex anesthetic/ resuscitation a panel of anesthesiologists with expertise in trauma, critical care and head injury will offer their perspective in the management of this patient. 1. Dr Richard P. Dutton is the Director of the Anesthesia Quality Institute at the American Society of Anesthesiologists and is the former Chief of Anesthesiology at the R Adams Cowley Shock Trauma Center at the University of Maryland. Dr Dutton: What evidence is there to support hypotensive resuscitation in blunt trauma? Penetrating trauma? This patient’s greatest and most-immediate risk is exsanguination from the liver injury. Up to half of all mortality from trauma is due to hemorrhage, either early (about 33% of deaths) or later from the effects of shock and multiple organ system failure. Patients who bleed to death do so during the first three hours in the hospital [4], emphasizing the importance of early intervention. Foremost, of course, is anatomic control of the site of hemorrhage, either through surgery or angiographic embolization. Anesthesiologists play an important role in the logistics of moving patients to definitive care. During this intervention, however, the management of ongoing fluid resuscitation has a significant impact on outcomes. One widely accepted approach is resuscitation to a target blood pressure that is lower than normal for the patient, as a means to avoid the rebleeding associated with blood pressure spikes that wash away fragile extraluminal clots [5]. Deliberate hypotension is common in elective surgery, and is well supported in numerous animal models of uncontrolled hemorrhage [6]. At least three human trials have attempted to validate this approach. Most influential was the trial by Bickell et al in Houston in the early 1990s. [7] Hypotensive patients with penetrating torso trauma were randomized in the field to either customary fluid therapy or none at all; this approach was followed from prehospital transport through emergency department assessment to the operating room
door. The no-fluid group had significantly improved survival (70% vs. 64%; P = .04). A similar protocol was conducted in Baltimore in the late 1990s, randomizing hypotensive patients (either blunt or penetrating) to blood pressure maintenance at 80 mm Hg systolic vs. N 100 mm Hg until definitive control of hemorrhage [8]. No difference in survival was found, despite a higher injury severity in the hypotensive group. Finally, another trial is underway now in Houston; a preliminary report suggests improved outcomes with hypotension [9]. Despite the heterogeneity of patients and injuries in these trials, and concerns about the underlying methodology, deliberate hypotension has been an accepted strategy in penetrating trauma in most major trauma centers since the year 2000. Controversy remains over the best approach to achieving hypotension: whether through fluid restriction (the original Bickell premise) or through simultaneous administration of fluid and anesthetic agents (titrating anestheticinduced vasodilation against vascular filling) [10]. Although scientific evidence is scant, the latter approach is supported by both theories of pathophysiology—vasodilatory hypotension preserving tissue perfusion better than vasoconstricted hypotension—and some limited animal data [5]. A particular concern in this debate is the role of deliberate hypotension in patients who might be vulnerable to ischemic injury. This includes patients with traumatic brain injury (TBI) as well as older patients and those with known coronary artery disease. TBI is especially challenging, because of the well-documented association between episodes of hypotension and bad outcomes in patients with severe injury. It should be recognized, however, that this association is based on observational data and does not prove cause and effect. In fact, it may be that while simultaneous bleeding and TBI predict a bad outcome, the patients in this cohort that do best are the ones that stop bleeding fastest, and are thus able to complete resuscitation. In other words, deliberate hypotension might be MORE important in vulnerable patients. There are some animal data available to support this point of view [11], but definitive human trials are unlikely. In summary, deliberate hypotension is an important tactic for limiting ongoing blood loss and speeding the time to complete resuscitation in patients with traumatic hemorrhage. While numerous questions of clinical application remain open, the core hypothesis that a lower blood pressure will lead to less blood loss has been well established in both pre-clinical and clinical trials. Hypotensive management remains an important tool to facilitate hemostasis and resuscitation in dying trauma patients. 2. Dr Jean-Francois Pittet is a Professor of Anesthesiology at the University of Alabama at Birmingham and the Director of the Division of Critical Care Anesthesiology. Dr Pittet: What are the advantages, if any, of hypotensive resuscitation in trauma? The case presented above emphasizes a number of important concepts in management of the trauma patient. I will focus my comments on pre-hospital and hospital-based hypotensive fluid resuscitation and I will present evidence against the use of hypotensive fluid resuscitation for this particular patient. Recognition of when a trauma patient is bleeding can be difficult. Pulse and arterial blood pressure are neither sensitive nor specific for severe hemorrhage. Young patients may lose more than 30% of their blood volume with little change in their vital signs. Furthermore, the classical cut-off systolic blood pressure (SBP) of 90 mm Hg as a marker of hemorrhagic shock has been based on expert opinion and not on evidence-based data. In fact, a SBP below 110 mm Hg is associated with a significant increase in mortality in blunt major trauma patients with baseline pressure of 130 to 139 mm Hg. Importantly, the mortality rate doubled for a SBP b100 mm Hg, tripled at a SBPb 90 mm Hg and was 5- to 6-fold higher at a SBP b 70 mm Hg [12]. In addition, single, isolated hypotensive SBP measurements of less than 105 mm Hg during trauma resuscitation should not be ignored or dismissed, as
Please cite this article as: Tobin JM, et al, Hypotensive resuscitation in a head-injured multi-trauma patient, J Crit Care (2013), http:// dx.doi.org/10.1016/j.jcrc.2013.11.017
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they may suggest the presence of severe injuries that may require immediate operative or endovascular treatment and later admission to a surgical intensive care unit [13]. It should also be pointed out that most of the shock syndromes in trauma patients are hypovolemic, although other causes of shock may be present, such as neurogenic (distributive shock), myocardial contusion (blunt cardiac injury) or obstructive (tension pneumothorax, pneumomediastinum or pericardial tamponade). In the presence of shock following severe trauma, the classical approach was to replace as soon as possible the fluid losses and restore organ perfusion in order to minimize end-organ failure. However, 20 years ago Bickell et al. demonstrated a reduction in mortality in patients with truncal penetrating injuries whose fluid resuscitation was delayed until definitive hemostasis could be achieved [7]. This approach has been developed for modern combat injuries because uncontrolled major hemorrhage from mostly penetrating trauma cannot be treated immediately due to delays in evacuation. To prevent the development of a lethal triad that includes coagulopathy, acidosis and hypothermia, which is associated with administration of large amount of crystalloids, the concept of damage control resuscitation (DCR) was developed and included a hypotensive and hemostatic resuscitation strategy. This therapeutic approach includes a limited amount of volume replacement to achieve a SBP of 80 mm Hg or the return of palpable pulse and hemostatic resuscitation with red blood cells (possibly recently obtained from donors), fresh frozen plasma and platelets in a ratio approximating 1:1:1 [14]. Additional objectives include treatment of hypothermia and acidosis. Although the results of major prospective studies are still missing with this therapeutic approach, initial results suggest a decrease in mortality over standard care in both combat and civilian trauma patients [15,16].
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Investigators Group. This prospective study that includes 1216 severely injured blunt trauma patients, shows that pre-hospital high fluid resuscitation (N 500 mL) provided different results if the patients were hypotensive or not in the pre-hospital setting. In patients with arterial hypotension, high fluid resuscitation (N 500 ml) was associated with correction of hypotension on emergency department arrival and each 1 mm Hg increase in SBP was associated with a 2% increase in survival in subjects with pre-hospital hypotension. In contrast, pre-hospital crystalloid more than 500 mL was associated with worse outcome in patients without hypotension [20]. In summary, the most recent data from the literature indicate that prehospital fluid resuscitation with crystalloids may have a survival advantage for patients with arterial hypotension, however, normotensive patients benefit from a fluid restrictive approach. Ultimately, the classical approach that includes the administration of a large amount of crystalloid fluids in the pre-hospital setting may aggravate coagulopathy and lead to end-organ injury. 5. Dr Deepak Sharma is an Associate Professor of Anesthesiology at the University of Washington and is the Chief of the Division of Neuroanesthesiology and Perioperative Neurosciences. Dr Sharma: Will systolic blood pressures below 90 mm Hg be harmful to a trauma patient with a potential TBI?
The question that needs to be answered for our case is whether the DCR approach can be safely applied to civilian traumatic injuries when its hemostatic component is not always readily available. First, the patient had a Glasgow Coma Scale score of 8 in the pre-hospital setting. This low Glasgow Coma Scale score would preclude a DCR approach as the current guidelines recommend a SBP of at least 90 mm Hg in order to prevent further brain damage [17]. This question will be addressed in detail in the last part of the discussion. Recent data from the Prospective Observational Multicenter Massive Transfusion Study that included 1245 trauma patients, indicate patients who received pre-hospital fluid (median volume 700 ml with interquartile range of 300-1300 ml) had a lower mortality compared to patients who did not receive pre-hospital intravenous fluid. Interestingly, the pre-hospital fluid resuscitation did not increase the SBP in these trauma patients. In fact, the patients who received the pre-hospital fluid resuscitation had a lower SBP than those who did not [18]. This study also indicates that any survival advantage from restrictive fluid resuscitation is conferred from avoidance of the complications associated with a large volume crystalloid resuscitation. This volume threshold was addressed in a recent retrospective investigation of 370 patients that divided the population in a standard (N150 mL) or restrictive (b150 mL) fluid resuscitation group. The patients who underwent restrictive resuscitation demonstrated a survival advantage compared with the standard group [19].
In a classic review published nearly 40 years ago, Trunkey reported that the primary cause of death in trauma victims was brain injury followed by hemorrhage [21]. Decades later, another review of the published literature examining trauma treated in level-1 centers between 1980 and 2008 has reported no considerable changes in the pattern of death. The predominant cause of death after trauma continues to be central nervous system injury followed by exsanguination [22]. Traumatic brain injury (TBI) continues to remain a leading cause of death and disability [3] and is often present in patients with polytrauma. While the severity of brain damage due to the traumatic impact (“primary insult”) largely accounts for mortality after TBI, secondary damage to the injured brain occurs as a result of a variety of physiological perturbations (“secondary insults”) including hypotension, hypoxia, hyper and hypocarbia, increased intracranial pressure and hyperglycemia, leading to poor outcome [23–29]. The essence of modern trauma care is prevention of primary injury and avoidance of secondary injury and hence, rapid correction of secondary insults is a major underpinning of current management of TBI. Impaired cerebral autoregulation due to TBI makes cerebral perfusion dependent on adequacy of systemic blood pressure and systolic blood pressure (SBP) b90 mm Hg early after TBI is associated with up to 150% increase in mortality [24]. Consequently, the Brain Trauma Foundation guidelines recommend prevention and early correction of hypotension (SBP b 90 mm Hg) after severe TBI [30]. Yet, hypotension is a common intraoperative secondary insult in adult and pediatric TBI victims [31,32]. Importantly, this blood pressure goal often conflicts with the “hypotensive resuscitation” approach in polytrauma patients like our index case here. So, is SBP below 90 mm Hg likely to be harmful to a trauma patient with a potential TBI? The answer is yes, and SBP b 90 mm Hg should be avoided because the evidence indicating detrimental effect of hypotension on TBI outcomes is overwhelming and patients with TBI who suffer intraoperative hypotension (during craniotomy or extracranial surgery) may be at higher risk of death and disability [26,29]. Not surprising…the studies examining hypotensive resuscitation during active hemorrhage excluded TBI patients [8,9].
4. Should all trauma patients be resuscitated via the hypotensive approach?
6. What special considerations must be taken into account for patients with TBI?
This important question has recently been addressed in a study conducted by The Inflammation and the Host Response To Injury
While it is obvious that hypotension is detrimental to the injured brain and should be avoided; clinicians are often confronted with at
3. The hypotensive approach seems to offer promise, however, with limitation. What do you see as the limitations of hypotensive resuscitation in this case?
Please cite this article as: Tobin JM, et al, Hypotensive resuscitation in a head-injured multi-trauma patient, J Crit Care (2013), http:// dx.doi.org/10.1016/j.jcrc.2013.11.017
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least two peculiar situations; first, a patient with TBI exsanguinating due to extracranial injury and second, a polytrauma patient where TBI is not evident on admission imaging. In the former situation, hypotension may be unresponsive to treatment and the anesthesiologist may be left with no choice but to transiently tolerate this until the life threatening hemorrhage is controlled. In such a situation, the risk of worsening TBI and neurological impairment clearly exists and the systolic blood pressure should be restored to N90 mm Hg as soon as possible. In the second situation (like our index case), multiple studies have documented that early CT scanning may not demonstrate the post traumatic brain damage in majority of patients and may underestimate the ultimate size of parenchymal contusions [33,34]. The intracranial lesions frequently progress on subsequent imaging and may require intervention. Hence, a “normal” or “unremarkable” head CT performed early after injury should not provide a sense of reassurance in a patient with clinical suspicion of TBI since the brain injury may manifest later. In such patients, the brain remains susceptible to adverse impact of hypotension and it may be prudent to avoid hypotension. The definition of hypotension itself remains somewhat vague. The randomized controlled trial of hypotensive resuscitation in polytrauma patients compared a mean arterial pressure (MAP) target of 50 mm Hg with 65 mm Hg [9,15], while TBI literature refers to SBP b90 mm Hg as hypotension rather than a MAP goal [23–26,29,30,32]. Interestingly, in some situations, clinicians may be able to achieve SBP marginally N 90 mm Hg and yet the MAP may be in the acceptable range of hypotensive resuscitation (MAP 55-65 mm Hg). Our 17-year-old patient in the index case may be considered a pediatric patient and hypotension in pediatric TBI is defined as SBP b 5th percentile for age (70 + 2*Age in years mm Hg) or 90 mm Hg, whichever is lower [31]. While hypotensive resuscitation may be an option for treating life saving hemorrhage in this patient, clinicians should avoid hypotension in infants and young children given the small total circulating volume and limited reserve to compensate for hypovolemia. In any case, the hypotensive resuscitation study included only children N 14 years old [9]. In summary, the use of hypotensive resuscitation in polytrauma victims must account for the possibility of associated TBI. If TBI is suspected clinically even in the absence of initial radiological evidence, SBP b 90 mm Hg should be avoided. When unavoidable, anesthesiologists should strive to minimize the duration of such hypotension and reduce the burden of secondary insult to the injured brain by avoiding simultaneous hypocarbia, which may worsen ischemic cerebral damage [35].
7. Conclusion The contributor’s comments clearly highlight the challenges of the resuscitation consultant. The concept of permissive hypotension dates back, at least, to World War I (not long after intravenous fluid therapy was innovated!) While driving blood pressure to “normal” levels with large volume crystalloid infusions is not appropriate, definitive data on the target blood pressure for hypotensive resuscitation are lacking. Indeed, the concept of systolic blood pressure as a marker for resuscitation is arguable. Perhaps mean arterial pressure, base excess, or some other marker offers a more discrete insight into resuscitation end points. The need for further investigation is clear. Intensivists are often called upon to be the “team captain”. It is the intensivist that orchestrates care from the operating room to the intensive care unit, all the while managing a continuing resuscitation and coordinating the care of other physicians whose therapies can run at crosspurposes to one another. The challenges of the practice of critical care in the 21st century are no more apparent than in the care of a complex trauma patient.
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Please cite this article as: Tobin JM, et al, Hypotensive resuscitation in a head-injured multi-trauma patient, J Crit Care (2013), http:// dx.doi.org/10.1016/j.jcrc.2013.11.017