17 POSTTRAUMATIC HEMORRHAGIC SHOCK
John B. Moore M.D., Ernest E. Moore M.D.

1. Are hemorrhagic shock and hypovolemic shock the same?

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Yes.

2. What is hemorrhagic shock?

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Shock exists when the cardiovascular system is no longer able to meet the body’s metabolic and oxygen needs-inadequate tissue perfusion.
Hemorrhage is the most common cause of shock after injury. Depletion of the vascular volume results in decrease of the driving pressure returning blood to the heart, decrease of the end-diastolic ventricular volume, and decrease in stroke volume; all result in decrease in cardiac output.

3. What is the initial management of hemorrhagic/hypovolemic shock?

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Prompt and aggressive fluid resuscitation.

4. Describe the cellular manifestations of hemorrhagic shock.

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Inadequately perfused and oxygenated cells are unable to perform normal aerobic metabolism. This inability results in the production of lactic acid, creating a “gap” metabolic acidosis. The production of adenosine triphosphate (ATP) is decreased, and the cell no longer can maintain membrane polarization/integrity. The first evidence of this is swelling of the endoplasmic reticulum, followed by mitochondrial damage, lysozyme rupture, and the entry of sodium and water into the cell. The loss of interstitial water into cells exacerbates the extracellular and the intravascular volume deficit.

5. List the clinical manifestations of hemorrhagic shock.

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* Hemodynamic instability with rapid pulse > 100 beats/min and blood pressure < 90 mmHg.
* Altered mental status with lethargy and confusion.
* Decreases in urine output < 0.5 mL/kg/h, central venous pressure, pulmonary capillary wedge pressure, cardiac output, and mixed venous oxygenation saturation (revealed by invasive monitoring).

6. How can blood volume be estimated in adults and children?

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In adults, multiply the ideal weight in kg × 7% (70 cc/kg).
In children, multiply ideal weight in kg × 9% (90 cc/kg).

7. State the first physiologic response to hypovolemia.

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The patient tries to compensate for the decrease in stroke volume by increasing heart rate (tachycardia).

8. What are the skin manifestations?

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The skin becomes cool, clammy, and pale. The subcutaneous veins collapse (making it hard to start an IV line). Capillary refill is delayed ≥ 2-3 seconds.

9. Can the neck veins tell you anything?

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Lack of pulsations or collapsed external jugular veins indicate low right heart filling pressure (i.e., hypovolemia); conversely, distended veins indicate heart failure or cardiogenic shock.

10. Is the hematocrit a reliable guide for estimating acute blood loss?

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No. A decrease in the hematocrit occurs with refill of the intravascular space from the interstitial space or during administration of exogenous crystalloid resuscitation fluid. This process is not immediate, and serial hematocrits do reflect blood loss.

11. What is the appropriate choice for IV solution during resuscitation?

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Lactated Ringer’s or normal saline. Isotonic crystalloid fluid requirements in hemorrhagic shock are estimated at three times the blood loss (3:1 rule). The initial volume replacement should be directed by the response to therapy rather than relying on estimated blood loss (the amount of blood on the pavement is a guess). Don’t add dextrose to the initial fluids; this just exacerbates the physiologic hyperglycemia and provokes an osmotic diuresis. Dextrose 5% is added to IV solutions after initial resuscitation for its protein-sparing effect in the fasting trauma patient.

12. What is base deficit, and how is it useful during resuscitation?

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Base deficit depends on the hematocrit, pH, and Pco2 and provides information on the metabolic component of acidosis. If you correct the Pco2 back to 40 mmHg, the pH should be 7.40. If your patient is still acidotic, he or she has a base deficit. The worse the base deficit, the lower (less adequate) is your patient’s peripheral perfusion.

13. What are the clinical classifications of shock and the associated clinical manifestations?

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See Table 17-1. But watch out-these estimates are not nearly as accurate or valuable as determining your patient’s response to therapy/resuscitation.
Table 17-1. CLINICAL CLASSIFICATIONS OF SHOCK

14. What are the other types of shock, and how do they differ from hemorrhagic shock?

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In addition to hemorrhagic/hypovolemic shock, there are neurogenic, cardiogenic, and septic shock. Neurogenic shock (this is uncommon) is caused by sudden loss of autonomic vascular tone, resulting in vasodilation. The systolic blood pressure is low, the pulse pressure is low, but the skin remains warm. Cardiogenic shock (less common in young gunslingers and frequent in the country club set) results from pump failure secondary to intrinsic heart muscle damage (myocardial infarction) or mechanical compression (cardiac tamponade). Septic shock (more common in surgical intensive care unit patients) is characterized by hypotension and low systemic vascular resistance.

15. When should fluid resuscitation be initiated on the multiply traumatized patient?

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Immediately! Begin therapy (fluid through big IV lines) while you are doing the primary survey directed at life-threatening injuries. It is inappropriate to wait until the trauma patient fits a precise physiologic classification of shock before starting aggressive volume restoration.
KEY POINTS: CLASSIFICATIONS OF SHOCK

1. Hemorrhagic: most common cause of posttraumatic shock; low filling pressures and cardiac output, low SVO2, high SVR.
2. Neurogenic: uncommon; low SVR with bradycardia; skin remains warm.
3. Cardiogenic: pump failure secondary to intrinsic myocardial damage (infarction) or mechanical compression (tamponade); high filling pressures, low cardiac output, low SVO2.
4. Septic: more common in surgical intensive care unit than in trauma bay; initially high cardiac output, low SVR, high SVO2.

16. What are the potential sources of occult blood loss when trying to figure out a patient’s hemodynamic status?

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The pleural spaces, abdominal cavity, retroperitoneal/pelvic space (pelvic fractures), major long bone fractures, and at the scene externally (”on the sidewalk”). Femur fractures can hide > 1 L of blood, whereas each rib fracture can account for 150 mL.

17. What is the patient called who becomes unstable after the initial resuscitation, and why is it important to recognize this phenomenon?

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This guy is a “transient responder.” This indicates ongoing blood loss! Look for it (more aggressive work-up) or transfer to a trauma center.

18. When is blood transfusion indicated during initial resuscitation?

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If the patient arrives who is not responding to aggressive (”wide open”) crysalloid infusion, the patient should receive uncrossed, O-negative packed red blood cells. Do not wait for type-specific blood if immediate infusion is required-the blood bank is not generally using the same clock (they are not as frightened because they cannot see the patient).

19. How does hemorrhagic shock lead to multiple organ failure (MOF)?

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Severe hemorrhagic shock begins an inflammatory cascade that cannot be reversed in some patients despite adequate resuscitation. During the Vietnam War, the patients in hemorrhagic shock were treated rapidly, but later died as a result of pulmonary failure or adult respiratory distress syndrome (ARDS). Patients with ARDS can be mechanically ventilated but later die from a combination of liver, cardiac, and bone marrow failure or MOF. MOF is the leading cause of late postinjury mortality in 85% of these deaths. In addition to the cellular derangement in ATP synthesis; shock causes the release of platelet-activating factor, interleukin-8, and arachidonic acid metabolites that activate neutrophils to adhere to endothelial cells and release cytotoxic mediators, which blow big holes in the endovasculature, flooding the interstitial space and causing organ damage. The mesenteric circulation is a hotbed of proinflammatory cytokine synthesis (the gut is the “motor for MOF”). In addition to directly activating neutrophils, the mesenteric circulation appears to release agents (probably phospholipases and other toxic lipids) into the mesenteric lymph that cause neutrophil activation and lung injury.

References
WEB SITES

1. http://www.east.org/tpg/endpoints.pdf
2. http://ww.acssurgery.com/abstracts/acs/acs0603.htm
3. http://www.acssurgery.com/abstracts/ascs/acs0501.htm

BIBLIOGRAPHY
1. American College of Surgeons: Shock. In Advanced Trauma Life Support, 6th ed. Chicago, American College of Surgeons, 1997, p 97.
2. Capone AC, Safar P, Stezoski W, et al: Improved outcome with fluid restriction in treatment of uncontrolled hemorrhagic shock. J Am Coll Surg 180:49, 1995.
3. Choi P, Yip G, Quinonez L, Cook D: Crystalloid versus colloids in fluid resuscitation: A systematic review. Crit Care Med 27:200, 1999. Medline Similar articles
4. Holcroft JW: Shock. In American College of Surgeons: Surgery: Principles and Practice. New York, Web/MD, 2002, p 63.
5. Moore EE: Blood substitutes: The future is now. J Am Coll Surg 196:1, 2003. Medline Similar articles
6. National Institutes of Health Consensus Conference: Perioperative red blood cell transfusion. JAMA 260:270, 1988.
7. Peitzman AB: Management of shock. In Moore EE, Mattox KL, Feliciano DV (eds): Trauma, 5th ed. New York, McGraw-Hill, 2003.

• Tags: Acidosis, acute, pulmonary