Hemorrhagic Shock Treatment & Management
- Author: John Udeani, MD, FAAEM; Chief Editor: John Geibel, MD, DSc, MSc, MA more...
The primary treatment of hemorrhagic shock is to control the source of bleeding as soon as possible and to replace fluid.
In controlled hemorrhagic shock (CHS), where the source of bleeding has been occluded, fluid replacement is aimed toward normalization of hemodynamic parameters. In uncontrolled hemorrhagic shock (UCHS), in which the bleeding has temporarily stopped because of hypotension, vasoconstriction, and clot formation, fluid treatment is aimed at restoration of radial pulse or restoration of sensorium or obtaining a blood pressure of 80 mm Hg by aliquots of 250 mL of lactated Ringer's solution (hypotensive resuscitation).
When evacuation time is shorter than 1 hour (usually urban trauma), immediate evacuation to a surgical facility is indicated after airway and breathing (A, B) have been secured ("scoop and run"). Precious time is not wasted by introducing an intravenous line. When expected evacuation time exceeds 1 hour, an intravenous line is introduced and fluid treatment is started before evacuation. The resuscitation should occur before, or concurrently with, any diagnostic studies.
Crystalloid is the first fluid of choice for resuscitation. Immediately administer 2 L of isotonic sodium chloride solution or lactated Ringer’s solution in response to shock from blood loss. Fluid administration should continue until the patient's hemodynamics become stabilized. Because crystalloids quickly leak from the vascular space, each liter of fluid expands the blood volume by 20-30%; therefore, 3 L of fluid need to be administered to raise the intravascular volume by 1 L.
Alternatively, colloids restore volume in a 1:1 ratio. Currently available colloids include human albumin, hydroxy-ethyl starch products (mixed in either 0.9% isotonic sodium chloride solution or lactated Ringer’s solution), or hypertonic saline-dextran combinations. The sole product that is avoided routinely in large-volume (>1500 mL/d) restoration is the hydroxy-ethyl starch product mixed in 0.9% isotonic sodium chloride solution because it has been associated with the induction of coagulopathy. The other products have not been so implicated.
In patients with hemorrhagic shock, hypertonic saline has the theoretical benefit of increasing intravascular volume with only small amounts of fluid. The combination of dextran and hypertonic saline may be beneficial in situations where infusion of large volumes of fluid may be harmful, such as in elderly persons with impaired cardiac activity. Additional trials will be required before this combination is accepted as standard of care.
PRBCs should be transfused if the patient remains unstable after 2000 mL of crystalloid resuscitation. For acute situations, O-negative noncrossmatched blood should be administered. Administer 2 U rapidly, and note the response. For patients with active bleeding, several units of blood may be necessary.
There are recognized risks associated with the transfusion of large quantities of PRBCs. As a result, other modalities are being investigated. One such modality is hemoglobin-based oxygen carriers (HBOC). Clinical application has been limited by its toxic effect profile. However, research is ongoing on the use of these products.
In an Australian study of the long-term outcomes of major-trauma patients who received massive transfusions, massive transfusion was independently associated with unfavorable outcomes. In massively transfused patients, the authors found no significant change in measured outcomes over the study period, with a persistent 23% mortality in hospital, a 52% unfavorable GOSE (Glasgow Outcome Score - extended) at 6 months, and a 44% unfavorable GOSE at 12 months.
If at all possible, blood and crystalloid infusions should be delivered through a fluid warmer. A blood sample for type and cross should be drawn, preferably before blood transfusions are begun. Start type-specific blood when available. Patients who require large amounts of transfusion inevitably will become coagulopathic. FFP generally is infused when the patient shows signs of coagulopathy, usually after 6-8 U of PRBCs. Platelets become depleted with large blood transfusions. Platelet transfusion is also recommended when a coagulopathy develops.
In a large, comprehensive cohort study by Levi et al, placebo-controlled trials of recombinant factor VIIIa (rFVIIa) were examined. Off-label treatment with high doses of rFVIIa significantly increased the risk of arterial events but not venous thromboembolic events, especially among elderly patients.
One situation that may arise is the transfusing of massive amounts of blood products into a Jehovah's Witness. This error occurs on occasion. Despite acting in the patient's best interest (prior to knowing that the patient would not want a blood transfusion), this error is a major incident for the patient. In this situation, honesty with the patient and the family member(s) is the rule. Involve the hospital's risk manager early. Family conferencing with a clergy member sometimes is helpful as well.
The decision regarding whether to operate to control bleeding is complicated and beyond the scope of this article. Some generalities, however, may be advanced.
Acute life-threatening bleeding within the abdominal or thoracic cavity is an indication for operation.
Retroperitoneal bleeding is difficult to control operatively and generally is treated nonoperatively.
Severe upper GI bleeds should be managed first by EGD, with the possibility of cauterizing or injecting the bleeding source with epinephrine. Failure of endoscopic management usually is an indication for surgery.
Confirm the location of a lower GI bleed before operative intervention is performed.
Severe vaginal bleeding should prompt early involvement of the gynecologist. Ectopic pregnancies are treated with immediate surgery. Abruptio placenta is a true emergency and should prompt immediate cesarean section.
On occasion, consultation with a hematologist is essential. This is especially true if the coagulopathy fails to be corrected with standard measures. Increasingly recognized are the entities of heparin-induced thrombocytopenia and acquired antibodies to native clotting factors. Consultation is useful in identifying the correct tests to obtain, as well as the full range of useful modalities to correct the underlying defect. These may include IV gamma-globulin infusion, plasmapheresis, or, simply, large-volume clotting factor repletion.
Blalock A. Principle of Surgical Care, Shock, and Other Problems. St Louis: Mosby; 1940.
Mitra B, Gabbe BJ, Kaukonen KM, Olaussen A, Cooper DJ, Cameron PA. Long-term outcomes of patients receiving a massive transfusion after trauma. Shock. 2014 Oct. 42(4):307-12. [Medline].
Levi M, Levy JH, Andersen HF, Truloff D. Safety of recombinant activated factor VII in randomized clinical trials. N Engl J Med. 2010 Nov 4. 363(19):1791-800. [Medline].
Aledort LM. Off-label use of recombinant activated factor VII--safe or not safe?. N Engl J Med. 2010 Nov 4. 363(19):1853-4. [Medline].
Ambrogi MC, Lucchi M, Dini P, et al. Videothoracoscopy for evaluation and treatment of hemothorax. J Cardiovasc Surg (Torino). 2002 Feb. 43(1):109-12. [Medline].
Barber AE, Shires GT. Cell damage after shock. New Horiz. 1996 May. 4(2):161-7. [Medline].
Brown MA, Casola G, Sirlin CB, et al. Blunt abdominal trauma: screening us in 2,693 patients. Radiology. 2001 Feb. 218(2):352-8. [Medline].
Butler K, Winters M. Shock: beyond the "golden hour". Emergency Medicine Reports. 2003. 24:345-356.
Collins JA. The pathophysiology of hemorrhagic shock. Prog Clin Biol Res. 1982. 108:5-29. [Medline].
Dizien O, Held JP, Eyssette M, et al. [Severe cranial trauma in the rehabilitation milieu. Management in the initial phase]. Rev Infirm. 1993 Mar. 43(5):33-8. [Medline].
Domsky MF, Wilson RF. Hemodynamic resuscitation. Crit Care Clin. 1993 Oct. 9(4):715-26. [Medline].
Falk JL, O'Brien JF, Kerr R. Fluid resuscitation in traumatic hemorrhagic shock. Crit Care Clin. 1992 Apr. 8(2):323-40. [Medline].
Hollenberg SM. Cardiogenic shock. Crit Care Clin. 2001 Apr. 17(2):391-410. [Medline].
Kemp SF. Current concepts in pathophysiology, diagnosis, and management of anaphylaxis. Immunol Allergy Clin North Am. 2001. 21:611-634.
Ketcham EM, Cairns CB. Hemoglobin-based oxygen carriers: development and clinical potential. Ann Emerg Med. 1999 Mar. 33(3):326-37. [Medline].
Kramer GC, Kinsky MP, Prough DS, et al. Closed-loop control of fluid therapy for treatment of hypovolemia. J Trauma. 2008 Apr. 64(4 Suppl):S333-41. [Medline].
Krausz MM. Initial resuscitation of hemorrhagic shock. World J Emerg Surg. 2006 Apr 27. 1(1):14.
McCunn M, Karlin A. Nonblood fluid resuscitation: more questions than answers. Anesthesiol Clin North Am. 1999. 17:107-123.
Orlinsky M, Shoemaker W, Reis ED, et al. Current controversies in shock and resuscitation. Surg Clin North Am. 2001 Dec. 81(6):1217-62, xi-xii. [Medline].
Pearl RG. Treatment of shock-1998. Anesthesia and Analgesia. 1998. suppl:75-84.
Peitzman AB, Billiar TR, Harbrecht BG. Hemorrhagic shock. Current Problems in Surgery. 1995. 32:925-1002. [Medline].
Pryor JP, Pryor RJ, Stafford PW. Initial phase of trauma management and fluid resuscitation. Trauma Reports. 2002. 3:1-12.
Schlag G, Krosl P, Redl H. Cardiopulmonary response of the elderly to traumatic and septic shock. Prog Clin Biol Res. 1988. 264:233-42. [Medline].
Shoemaker WC, Peitzman AB, Bellamy R. Resuscitation from severe hemorrhage. Crit Care Med. 1996 Feb. 24(2 Suppl):S12-23. [Medline].