Assessment and management of hemorrhagic shock
Hemorrhagic shock is a subset of hypovolemic shock that results from a decrease in circulating blood volume
By Kenny Navarro
Preliminary data for 2011 lists unintentional injury as the fifth leading cause of death in the United States for patients of all ages. However, it is the leading cause of death for patients between the ages of 1 and 44 years (Hoyert & Xu, 2012). A significant percentage of those deaths occur as the result of exsanguination (Sauaia et al.,1995), with many occurring before the patient even reaches the hospital.
Hemorrhagic shock is a subset of hypovolemic shock that results from a decrease in circulating blood volume. This decrease can occur because the patient actually loses blood or alternatively, loses only the fluid component of the blood.
While EMS personnel normally associate hypovolemic shock with trauma and bleeding, there are other potential causes of hypovolemic shock. Severe diarrhea, prolonged vomiting, and endocrine disorders can cause significant losses of circulating volume. Hypovolemic shock may also result from internal fluid shifts caused by burns and massive abdominal infections. Always assume hypovolemia as the underlying cause for shock until you can prove otherwise.
The presence of a mechanism of injury should raise the suspicion of bleeding in the traumatized patient (Rossaint et al., 2010). Often, external blood loss in patients with penetrating trauma is the earliest diagnostic clue for developing hemorrhagic shock. However, this sign is absent in patients who suffer blunt trauma which requires EMS personnel to focus on other predictors.
In many shock patients, the rate and depth of ventilation increases in an attempt to compensate for developing tissue acidosis. Radial pulse character (weak or absent), combined with the motor and verbal components of the Glasgow Coma Scale are predictive of the need for lifesaving interventions in non-head-injured trauma patients (Holcomb et al., 2005).
Determining pulse rate alone is a poor predictor of the need for surgery or blood transfusion following a traumatic event (Brasel, Guse, Gentilello, & Nirula, 2007; Demetriades et al., 1998).
In fact, almost half of all patients in one study who presented to the emergency department after suffering penetrating abdominal injuries or severe but isolated extremity trauma had a relative bradycardia, including about 35% of the patients with an initial systolic blood pressure less than 100 mm Hg (Thompson, Adams, & Barrett, 1990).
Historically, clinicians used systolic blood pressure measurement as a significant indicator of hypotension and shock, typically establishing the shock threshold at 90 mm Hg (Kerby & Cusick, 2012).
However, 15% of trauma patients in one study who ultimately required emergency thoracoabdominal surgery and more than five units of pack red blood cells presented to EMS personnel with a systolic blood pressure greater than 100 mm Hg (Luna, Eddy, & Copass, 1989).
Researchers now question whether true tissue hypoperfusion begins at the 90 mm Hg point or whether it is actually much higher (Bruns, Gentilello, Elliott, & Shafi, 2008; Eastridge et al., 2007; Eastridge, Salinas, Wade, & Blackbourne, 2011; Edelman, White, Tyburski, & Wilson, 2007) while others suggest that blood pressure readings are too unreliable for use in the diagnosis of tissue hypoperfusion (Hick, Rodgerson, Heegaard, & Sterner, 2001; McGee, Abernethy, & Simel, 1999).
There is universal agreement that the first step in the management of the hemorrhaging patient is to control blood loss. There is also universal agreement that medics must support the circulatory status of patients exhibiting signs and symptoms of hemorrhagic shock.
Crystalloids, such as lactated Ringer’s solution and saline are the most widely used solutions in the prehospital treatment of traumatic injury. Lactated Ringer’s solution has a theoretic advantage because it can buffer metabolic acidosis and prevent the acidosis resulting from excess chloride ion infusion associated with saline administration (Kobayashi, Costantini, & Coimbra, 2012).
However, outcome advantages is likely only when massive transfusions become necessary (Healey, Davis, Liu, Loomis, & Hoyt, 1998). Research involving mild to moderate hemorrhage demonstrate no outcome advantage provided by one of these solutions compared to the other (Moore et al., 2006; Schreiber, 2011).
The time-honored strategy for pre-hospital fluid resuscitation has followed the American College of Surgeons 3:1 rule – for every unit of blood lost, infuse 3 liters of crystalloid (American College of Surgeons Committee on Trauma, 2008).
However, fluids given before surgical control of hemorrhage may result in clot disruption, thereby allowing continued blood loss (McSwain & Barbeau, 2010). Fluid administration may also dilute coagulation factors (Bickell, Bruttig, Millnamow, O'Benar, & Wade, 1991; Hewson et al., 1985.; Maegele et al., 2007), which slows clot formation.
To prevent these complications, some advocate for a more restrictive fluid replacement strategy in the prehospital period before definitive bleeding control occurs. A permissive hypotension approach minimizes or restricts fluid administration as long as the patient can maintain adequate cerebral perfusion and systolic blood pressures remain above a certain threshold (Kobayashi, Costantini, & Coimbra, 2012).
Delayed fluid resuscitation improved survival in penetrating torso injuries (Bickell et al., 1994), traumatic amputation (Owens, Watson, Prough, Uchida, & Kramer, 1995), while restricting fluid volumes to maintain low mean arterial pressure resulted in lowered postoperative mortality (Morrison et al., 2011).
Animal data suggests that early use of vasoactive agents, particularly before surgical control of blood loss, may result in acceptable blood pressure maintenance without the need for large volume fluid resuscitation and its associated complications (Schwartz & Reid, 1981; Stadlbauer et al., 2003; Voelckel et al., 2003). To date, researchers have completed only one randomized-controlled trial using vasopressin in the acute resuscitation phase (Cohn et al., 2011).
Their results show no significant mortality improvements conferred to fluid + vasopressin administration when compared to standard fluid resuscitation alone. In patients presenting to EMS with blunt traumatic arrest and displaying pulseless electrical activity, researchers prospectively compared a small treatment cohort receiving vasopressin and hydroxyethyl starch solution to a historical control group who received standard resuscitation measures.
The treatment group had significant improvements in return of spontaneous circulation and 24-hour survival (Grmec, Strnad, Cander, & Mally, 2008). On the other hand, three large retrospective studies found that vasopressin administration in severely injured and hypotensive trauma patients increased the risk of death (Collier et al., 2010; Plurad et al., 2011; Sperry et al., 2008). The utility of vasopressin administration in the management of hemorrhagic shock remains unanswered.
Future of shock assessment
Researchers are now testing point-of-care devices that may be a useful tool in helping EMS personnel recognize occult bleeding or as an early indicator of tissue hypoperfusion secondary to blood loss.
For example, one hand held monitor uses a small sample of the patient’s blood to measure the quantity of serum lactate, similar to way glucometers measure blood glucose levels. In one study involving more than 2000 patients who suffered trauma and presented with an initial systolic blood pressure between 90 and 110 mm Hg, serum lactate monitors used in the emergency department were more accurate predictors of both the need for blood transfusion than the patient’s blood pressure and for mortality (Vandromme, Griffin, Weinberg, Rue, & Kerby, 2010).
Serum lactate levels obtained by paramedics in the field during transport of 1000 trauma patients, when added to initial vitals and GCS scores are predictive of the need for urgent surgical care, multiple organ failure syndrome, and mortality (Guyette et al., 2011). A multicenter prehospital trial on the utility of lactate biomarkers in the management of trauma patients is currently underway (Resuscitation Outcomes Consortium, n.d.).
American College of Surgeons Committee on Trauma. (2008). Advanced trauma life support for doctors: Student course manual (8th ed). Chicago: American College of Surgeons.
Bickell, W. H., Bruttig, S. P., Millnamow, G. A., O'Benar, J., & Wade, C. E. (1991). The detrimental effects of intravenous crystalloid after aortotomy in swine. Surgery, 110(3), 529-536.
Bickell, W. H., Wall, W. J., Pepe, P. E., Martin, R. R., Ginger, V. F., Allen, M. K., & Mattox, K. L. (1994). Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. New England Journal of Medicine, 331(17), 1105-1109. doi:10.1056/NEJM199410273311701
Brasel, K. J., Guse, C., Gentilello, L. M., & Nirula, R. (2007). Heart rate: Is it truly a vital sign? Journal of Trauma, 62(4), 812–817. doi:10.1097/TA.0b013e31803245a1
Bruns, B., Gentilello, L., Elliott, A., & Shafi, S. (2008). Prehospital hypotension redefined. Journal of Trauma, 65(6), 1217–1221. doi:10.1097/TA.0b013e318184ee63
Cohn, S. M., McCarthy, J., Stewart, R. M., Jonas, R. B., Dent, D. L., & Michalek, J. E. (2011). Impact of low-dose vasopressin on trauma outcome: Prospective randomized study. World Journal of Surgery, 35(2), 430–439. doi:10.1007/s00268-010-0875-8
Collier, B., Dossett, L., Mann, M., Cotton, B., Guillamondegui, O., Diaz, J., Fleming, S., May, A., & Morris, J. (2010). Vasopressin use is associated with death in acute trauma patients with shock. Journal of Critical Care, 25(1), 173.e9–173.e14. doi:10.1016/j.jcrc.2009.05.003
Demetriades, D., Chan, L. S., Bhasin, P., Berne, T. V., Ramicone, E., Huicochea, F., Velmahos, G., Cornwell, E. E., Belzberg, H., Murray, J., Asensio, J.A. (1998). Relative bradycardia in patients with traumatic hypotension. Journal of Trauma, 45(3), 534–539.
Eastridge, B. J., Salinas, J., McManus, J. G., Blackburn, L., Bugler, E. M., Cooke, W. H., Convertino, V. A., Wade, C. E., & Holcomb, J. B. (2007). Hypotension begins at 110 mm hg: Redefining “hypotension” with data. Journal of Trauma, 63(2), 291–297 [discussion: 297–9]. doi:10.1097/TA.0b013e31809ed924
Eastridge, B. J., Salinas, J., Wade, C. E., & Blackbourne, L. H. (2011). Hypotension is 100 mm Hg on the battlefield. American Journal of Surgery, 202(4), 404–408. doi:10.1016/j.amjsurg.2010.10.012
Edelman, D. A., White, M. T., Tyburski, J. G., & Wilson, R. F. (2007). Post-traumatic hypotension: Should systolic blood pressure of 90-109 mm hg be included? Shock, 27(2), 134–138. doi:10.1097/01.shk.0000239772.18151.18
Grmec, S., Strnad, M., Cander, D., & Mally, S. (2008). A treatment protocol including vasopressin and hydroxyethyl starch solution is associated with increased rate of return of spontaneous circulation in blunt trauma patients with pulseless electrical activity. International Journal of Emergency Medicine, 1(4), 311–316. doi:10.1007/s12245-008-0073-8
Guyette, F., Suffoletto, B., Castillo, J. L., Quintero, J., Callaway, C., & Puyana, J. C. (2011). Prehospital serum lactate as a predictor of outcomes in trauma patients: A retrospective observational study. Journal of Trauma, 70(4), 782–786. doi: 10.1097/TA.0b013e318210f5c9
Healey, M. A., Davis, R. E., Liu, F. C., Loomis, W. H., & Hoyt, D. B. (1998). Lactated ringer’s is superior to normal saline in a model of massive hemorrhage and resuscitation. Journal of Trauma, 45(5), 894–899.
Hewson, J. R., Neame, P. B., Kumar, N., Ayrton, A., Gregor, P., Davis, C., & Shragge, B. W. (1985). Coagulopathy related to dilution and hypotension during massive transfusion. Critical Care Medicine, 13(5), 387–391.
Hick, J. L., Rodgerson, J. D., Heegaard, W. G., & Sterner, S. (2001). Vital signs fail to correlate with hemoperitoneum from ruptured ectopic pregnancy. American Journal of Emergency Medicine, 19(6), 488–491. doi:10.1053/ajem.2001.27133
Holcomb, J. B., Salinas, J., McManus, J. M., Miller, C. C., Cooke, W. H., & Convertino, V. A. (2005). Manual vital signs reliably predict need for life-saving interventions in trauma patients. Journal of Trauma, 59(4), 821-828. doi:10.1097/01.ta.0000188125.44129.7c
Hoyert, D. L., & Xu, J. Q. (2012). Deaths: Preliminary data for 2011. National vital statistics reports, 61(6). Hyattsville, MD: National Center for Health Statistics. Retrieved from http://www.cdc.gov/nchs/data/nvsr/nvsr61/nvsr61_06.pdf
Kerby, J. D., & Cusick, M. V. (2012). Prehospital emergency trauma care and management. Surgical Clinics of North America, 92(4), 823-841. doi:10.1016/j.suc.2012.04.009
Kobayashi, L., Costantini, T. W., & Coimbra, R. (2012). Hypovolemic shock resuscitation. Surgical Clinics of North America, 92(6), 1403–1423. doi:10.1016/j.suc.2012.08.006
Luna, G. K., Eddy, A. C., & Copass, M. (1989). The sensitivity of vital signs in identifying major thoracoabdominal hemorrhage. American Journal of Surgery, 157(5), 512–515. doi:10.1016/0002-9610(89)90649-1
Maegele, M., Lefering, R., Yucel, N., Tjardes, T., Rixen, D., Paffrath, T., Simanski, C., Neugebauer, E., Bouillon, B. & the AG Polytrauma of the German Trauma Society (DGU). (2007). Early coagulopathy in multiple injury: An analysis from the German Trauma Registry on 8724 patients. Injury, 38(3), 298–304. doi:10.1016/j.injury.2006.10.003
McGee, S., Abernethy, W. B., & Simel, D. L. (1999). The rational clinical examination. Is this patient hypovolemic? Journal of the American Medical Association, 281(11), 1022–1029. doi:10.1001/jama.281.11.1022
McSwain, N. Jr., & Barbeau, J. (2010). Potential use of prothrombin complex concentrate in trauma resuscitation. Journal of Trauma, 70(Suppl 5), S53–S56. doi:10.1097/TA.0b013e31821a5e5d
Moore, F. A., McKinley, B. A., Moore, E. E., Nathens, A. B., West, M., Shapiro, M. B., Bankey, P., Freeman, B., Harbrecht, B. G., Johnson, J. L., Minei, J. P., Maier, R. V. & the Inflammation and the Host Response to Injury Collaborative Research Program. (2006). Inflammation and the Host Response to Injury, A large-scale collaborative project: Patient-oriented research core– standard operating procedures for clinical care. III. Guidelines for shock resuscitation. Journal of Trauma, 61(1), 82–89. doi:10.1097/01.ta.0000225933.08478.65
Morrison, C. A., Carrick, M. M., Norman, M. A., Scott, B. G., Welsh, F. J., Tsai, P., Liscum, K. R., Wall, M. J. Jr., & Mattox, K. L. (2011). Hypotensive resuscitation strategy reduces transfusion requirements and severe postoperative coagulopathy in trauma patients with hemorrhagic shock: Preliminary results of a randomized controlled trial. Journal of Trauma, 70(3), 652–663. doi:10.1097/TA.0b013e31820e77ea
Owens, T. M., Watson, W. C., Prough, D. S., Uchida, T., & Kramer, G. C. (1995). Limiting initial resuscitation of uncontrolled hemorrhage reduces internal bleeding and subsequent volume requirements. Journal of Trauma, 39(2), 200–207 [discussion: 208–209].
Plurad, D. S., Talving, P., Lam, L., Inaba, K., Green, D., & Demetriades, D. (2011). Early vasopressor use in critical injury is associated with mortality independent from volume status. Journal of Trauma, 71(3), 565–570 [discussion: 570–572]. doi:10.1097/TA.0b013e3182213d52
Resuscitation Outcomes Consortium. (n.d.). Current studies. Retrieved from https://www.uwctc.org/tiki/current-studies
Rossaint, R., Bouillon, B., Cerny, V, Coats, T. J., Duranteau, J., Fernández-Mondéjar, E., Hunt, B. J., Komadina, R., Nardi, G., Neugebauer, E., Ozier, Y., Riddez, L., Schultz, A., Stahel, P. F., Vincent, J., & Spahn, D. R. (2010). Management of bleeding following major trauma: An updated European guideline. Critical Care, 14(2), R52. doi:10.1186/cc8943
Sauaia, A., Moore. F, A., Moore, E. E., Moser, K. S., Brennan, R., Read, R. A., & Pons, P. T. (1995). Epidemiology of trauma deaths: A reassessment. Journal of Trauma, 38(2), 185–193.
Schreiber, M. A. (2011). The use of normal saline for resuscitation in trauma. Journal of Trauma, 70(Suppl 5), S13–S14. doi:10.1097/TA.0b013e31821a4ba5
Schwartz, J., & Reid, I. A. (1981). Effect of vasopressin blockade on blood pressure regulation during hemorrhage in conscious dogs. Endocrinology, 109(5), 1778–1780. doi:10.1210/endo-109-5-1778
Sperry, J. L., Minei, J. P., Frankel, H. L., West, M. A., Harbrecht, B. G., Moore, E. E., Maier, R. V., & Nirula, R. (2008). Early use of vasopressors after injury: Caution before constriction. Journal of Trauma, 64(1), 9–14. doi:10.1097/TA.0b013e31815dd029
Stadlbauer, K. H., Wagner-Berger, H. G., Raedler, C., Voelckel, W. G., Wenzel, V., Krismer, A. C., Klima, G., Rheinberger, K., Nussbaumer, W., Pressmar, D., Lindner, K. H, & Königsrainer, A. (2003). Vasopressin, but not fluid resuscitation, enhances survival in a liver trauma model with uncontrolled and otherwise lethal hemorrhagic shock in pigs. Anesthesiology, 98(3), 699–704.
Thompson, D., Adams, S. L., & Barrett, J. (1990). Relative bradycardia in patients with isolated penetrating abdominal trauma and isolated extremity trauma. Annals of Emergency Medicine, 19(3), 268–275. doi:10.1016/S0196-0644(05)82042-6
Vandromme, M. J., Griffin, R. L., Weinberg, J. A., Rue, L. W. 3rd., Kerby, J. D. (2010). Lactate is a better predictor than systolic blood pressure for determining blood requirement and mortality: Could prehospital measures improve trauma triage? Journal of the American College of Surgery, 210(5), 861–867, 867–9. doi: 10.1016/j.jamcollsurg.2010.01.012
Voelckel, W. G., Raedler, C., Wenzel, V., Lindner, K. H., Krismer, A. C., Schmittinger, C. A., Herff, H., Rheinberger, K., & Königsrainer, A. (2003). Arginine vasopressin, but not epinephrine, improves survival in uncontrolled hemorrhagic shock after liver trauma in pigs. Critical Care Medicine, 31(4), 1160–1165. doi:10.1097/01.CCM.0000060014.75282.69