Background

Hemorrhagic shock is a condition of reduced tissue perfusion, resulting in the inadequate delivery of oxygen and nutrients that are necessary for cellular function. Whenever cellular oxygen demand outweighs supply, both the cell and the organism are in a state of shock. On a multicellular level, the definition of shock becomes more difficult because not all tissues and organs will experience the same amount of oxygen imbalance for a given clinical disturbance. Clinicians struggle daily to adequately define and monitor oxygen utilization on the cellular level and to correlate this physiology to useful clinical parameters and diagnostic tests. The 4 classes of shock, as proposed by Alfred Blalock, are as follows:

Hypovolemic Vasogenic (septic) Cardiogenic Neurogenic

Hypovolemic shock, the most common type, results from a loss of circulating blood volume from clinical etiologies, such as penetrating and blunt trauma, gastrointestinal bleeding, and obstetrical bleeding. Humans are able to compensate for a significant hemorrhage through various neural and hormonal mechanisms. Modern advances in trauma care allow patients to survive when these adaptive compensatory mechanisms become overwhelmed.

Pathophysiology
Well-described responses to acute loss of circulating volume exist. Teleologically, these responses act to systematically divert circulating volume away from nonvital organ systems so that blood volume may be conserved for vital organ function. Acute hemorrhage causes a decreased cardiac output and decreased pulse pressure. These changes are sensed by baroreceptors in the aortic arch and atrium. With a decrease in the circulating volume, neural reflexes cause an increased sympathetic outflow to the heart and other organs. The response is an increase in heart rate, vasoconstriction, and redistribution of blood flow away from certain nonvital organs, such as the skin, gastrointestinal tract, and kidneys. Concurrently, a multisystem hormonal response to acute hemorrhage occurs. Corticotropin-releasing hormone is stimulated directly. This eventually leads to glucocorticoid and beta-endorphin release. Vasopressin from the posterior pituitary is released, causing water retention at the distal tubules. Renin is released by the juxtamedullary complex in response to decreased mean arterial pressure, leading to increased aldosterone levels and eventually to sodium and water resorption. Hyperglycemia commonly is associated with acute hemorrhage. This is due to a glucagon and growth hormoneinduced increase in gluconeogenesis and glycogenolysis. Circulating catecholamines relatively inhibit insulin release and activity, leading to increased plasma glucose. In addition to these global changes, many organ-specific responses occur. The brain has remarkable autoregulation that keeps cerebral blood flow constant over a wide range of systemic mean arterial blood pressures. The kidneys can tolerate a 90% decrease in total blood flow for short periods of time. With significant decreases in circulatory volume, intestinal blood flow is dramatically reduced by splanchnic vasoconstriction. Early and appropriate resuscitation may avert damage to individual organs as adaptive mechanisms act to preserve the organism.

Medical Care
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 Ringers 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 Ringers solution), or hypertonic saline dextran combinations. The sole product that is avoided routinely in large-volume (>1500 mL/d) restoration is the hydroxyethyl 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. 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 [2] 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.

Special concern
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.

Source: http://emedicine.medscape.com/article/432650-overview#showall http://emedicine.medscape.com/article/432650-treatment#showall