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hemorrhagic shock

Hemorrhagic shock

Hemorrhagic shock is a condition of reduced tissue perfusion, resulting in the inadequate delivery of oxygen and nutrients that are necessary for cellular function 1. Many conditions, including blood loss but also including non-hemorrhagic states such as dehydration, sepsis, impaired autoregulation, obstruction, decreased myocardial function, and loss of autonomic tone, may produce shock or shocklike states.

In hemorrhagic shock, reduced tissue perfusion results in inadequate delivery of oxygen and necessary for cellular function. The state of shock occurs when the cellular oxygen demand outweighs the supply. Whenever cellular oxygen demand outweighs supply, both the cell and the organism are in a state of shock.

Though most commonly thought of in the setting of trauma, there are numerous causes of hemorrhagic shock that span many systems. Blunt or penetrating trauma is the most common cause, followed by upper and lower gastrointestinal sources 2. Obstetrical, vascular, iatrogenic, and even urological sources have all been described. Bleeding may be either external or internal. A substantial amount of blood loss to the point of hemodynamic compromise may occur in the chest, abdomen, or the retroperitoneum. The thigh itself can hold up to 1 L to 2 L of blood. Localizing and controlling the source of bleeding is of utmost importance to the treatment of hemorrhagic shock but beyond the scope of this article 3.

Hemorrhagic shock is a leading cause of death among trauma patients 4. In the United States in 2001, trauma was the third leading cause of death overall, and the leading cause of death in those aged 1 to 44 years. While trauma spans all demographics, it disproportionately affects the young with 40% of injuries occurring in ages 20 to 39 years by one country’s account. Of this 40%, the greatest incidence was in the 20 to 24-year-old range 5.

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.

Classically, there are four categories of shock, as proposed by Alfred Blalock 6:

  • Hypovolemic
  • Vasogenic (septic)
  • Cardiogenic
  • Neurogenic

Hypovolemic shock, the most common type, results from a loss of circulating blood volume from clinical causes to the point of cardiovascular compromise, such as severe dehydration through a variety of mechanisms or from blood loss, penetrating and blunt trauma, gastrointestinal bleeding, and obstetrical bleeding. Hemorrhagic shock is a subset of hypovolemic shock. 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.

Hemorrhagic shock causes

In hemorrhagic shock, blood loss exceeds the body’s ability to compensate and provide adequate tissue perfusion and oxygenation. This frequently is due to trauma, but it may be caused by spontaneous hemorrhage (eg, GI bleeding, childbirth), surgery, and other causes.

Most frequently, clinical hemorrhagic shock is caused by an acute bleeding episode with a discrete precipitating event. Less commonly, hemorrhagic shock may be seen in chronic conditions with subacute blood loss.

Physiologic compensation mechanisms for hemorrhage include initial peripheral and mesenteric vasoconstriction to shunt blood to the central circulation. This is then augmented by a progressive tachycardia. Invasive monitoring may reveal an increased cardiac index, increased oxygen deliver and increased oxygen consumption (ie, VO2) by tissues. Lactate levels, acid-base status, and other markers also may provide useful indicators of physiologic status. Age, medications, and comorbid factors all may affect a patient’s response to hemorrhagic shock.

Failure of compensatory mechanisms in hemorrhagic shock can lead to death. Without intervention, a classic trimodal distribution of deaths is seen in severe hemorrhagic shock. An initial peak of mortality occurs within minutes of hemorrhage due to immediate exsanguination. Another peak occurs after 1 to several hours due to progressive decompensation. A third peak occurs days to weeks later due to sepsis and organ failure.

A key factor in the pathophysiology of hemorrhagic shock is the development of trauma-induced coagulopathy. Coagulopathy develops as a combination of several processes. The simultaneous loss of coagulation factors via hemorrhage, hemodilution with resuscitation fluids, and coagulation cascade dysfunction secondary to acidosis and hypothermia have been traditionally thought to be the cause of coagulopathy in trauma. However, this traditional model of trauma-induced coagulopathy may be too limited. Further studies have shown that a degree of coagulopathy begins in 25% to 56% of patients before initiation of the resuscitation. This has led to the recognition of trauma-induced coagulopathy as the sum of two distinct processes: acute coagulopathy of trauma and resuscitation-induced coagulopathy.

Trauma-induced coagulopathy is acutely worsened by the presence of acidosis and hypothermia. The activity of coagulation factors, fibrinogen depletion, and platelet quantity are all adversely affected by acidosis. Hypothermia (less than 34 °C) compounds coagulopathy by impairing coagulation and is an independent risk factor for death in hemorrhagic shock.

Hemorrhagic shock signs and symptoms

Recognizing the degree of blood loss via vital sign and mental status abnormalities is important. The American College of Surgeons Advanced Trauma Life Support hemorrhagic shock classification links the amount of blood loss to expected physiologic responses in a healthy 70 kg patient. As total circulating blood volume accounts for approximately 7% of total body weight, this equals approximately five liters in the average 70 kg male patient.

  • Class 1 hemorrhagic shock: Volume loss up to 15% of total blood volume or approximately 750 mL. Heart rate is minimally elevated or normal. Typically, there is no change in blood pressure, pulse pressure, or respiratory rate. The patient’s heart rate will typically remain under 100beats per minute, their blood pressure and pulse pressure are stable if not slightly increased due to anxiety. The respiratory rate is stable at 14-20 respiratory rate per minute, and their urine output remains at greater than 30mL/hour.
  • Class 2 hemorrhagic shock: Volume loss from 15% to 30% of total blood volume, from 750 mL to 1500 mL. Heart rate and respiratory rate become elevated (100 to 120 beats per minute; 20 to 24 respiratory rate per minute) and their urine output may drop slightly (20-30mL/hour). Pulse pressure begins to narrow, but systolic blood pressure may be unchanged to slightly decreased, which may be the first sign of the body failing to compensate the sudden blood loss. It is important to note that even outside the realm of shock management, urine output remains the single most important indicator for monitoring fluid status in a patient. Additionally, blood pressure cannot be adequately relied upon to detect the beginning of shock, as the body’s compensatory mechanisms will keep blood pressure typically within normal limits until up to 30% of total blood volume has already been lost.
  • Class 3 hemorrhagic shock: Volume loss from 30% to 40% of total blood volume, from 1500 mL to 2000 mL. A significant drop in blood pressure and changes in mental status occur. Heart rate (more than 120 beats per minute) and respiratory rate (30-40 respiratory rate per minute) are significantly elevated. Urine output declines (urine output decreased to 5-15mL/hour). Capillary refill is delayed.
  • Class 4 hemorrhagic shock (most severe): Volume loss over 40% of total blood volume. Hypotension with narrow pulse pressure (less than 25 mmHg). Tachycardia becomes more pronounced (more than 120 beats per minute) with nonpalpable or thready peripheral pulses, and mental status becomes increasingly altered. The patient’s respiratory rate will have increased to over 35 respiratory rate per minute. Urine output is minimal or absent. Capillary refill is delayed.

Again, the above is outlined for a healthy 70 kg individual. Clinical factors must be taken into account when assessing patients. For example, elderly patients taking beta blockers can alter the patient’s physiologic response to decreased blood volume by inhibiting mechanism to increase heart rate. As another, patients with baseline hypertension may be functionally hypotensive with a systolic blood pressure of 110 mmHg.

Hemorrhagic shock diagnosis

The first step in managing hemorrhagic shock is recognition. Ideally, This should occur before the development of hypotension. Close attention should be paid to physiological responses to low-blood volume. Tachycardia, tachypnea, and narrowing pulse pressure may be the initial signs. Cool extremities and delayed capillary refill are signs of peripheral vasoconstriction 7.

In the setting of trauma, an algorithmic approach via the primary and secondary surveys is suggested by American College of Surgeons Advanced Trauma Life Support. Physical exam and radiological evaluations can help localize sources of bleeding. A trauma ultrasound, or Focused Assessment with Sonography for Trauma (FAST), has been incorporated in many circumstances into the initial surveys. The specificity of a Focused Assessment with Sonography for Trauma scan has been reported above 99%, but a negative ultrasound does not rule out intra-abdominal pathology.

During the primary survey of the patient in hemorrhagic shock, a circulatory assessment should include the insertion of two large bore IVs (16-18 gauge) bilaterally to facilitate the fastest administration of fluids. If this is not available, then a large bore central venous catheter (CVC) such as a Cordis or a standard 7 French triple lumen CVC should be placed. The reason which 2 large bore peripheral IVs is more successful than a CVC in rapid fluid resuscitation is due to Poiseuille’s law which states that fluids passing through a lumen can be transfused most quickly when there is laminar flow (width and length affect velocity). This law also states that the longer the lumen through which the fluids pass, the less laminar flow there is. Therefore, two short peripheral IVs of sufficient diameter are more expedient in transfusions than one large long CVC catheter.

Hemorrhagic shock treatment

With a broader understanding of the pathophysiology of hemorrhagic shock, treatment in trauma has expanded from a simple massive transfusion method to a more comprehensive management strategy of “damage control resuscitation.” The concept of damage control resuscitation focuses on permissive hypotension, hemostatic resuscitation, and hemorrhage control to adequately treat the “lethal triad” of coagulopathy, acidosis, and hypothermia that occurs in trauma 8.

Hypotensive resuscitation has been suggested for the hemorrhagic shock patient without head trauma. The aim is to achieve a systolic blood pressure of 90 mmHg in order maintain tissue perfusion without inducing re-bleeding from recently clotted vessels. Permissive hypotension is a means of restricting fluid administration until hemorrhage is controlled while accepting a short period of suboptimal end-organ perfusion. Studies regarding permissive hypotension have yielded conflicting results and must take into account type of injury (penetrating versus blunt), the likelihood of intracranial injury, the severity of the injury, as well as proximity to a trauma center and definitive hemorrhage control.

The quantity, type of fluids to be used, and endpoints of resuscitation remain topics of much study and debate. For crystalloid resuscitation, normal saline and lactated ringers are the most commonly used fluids. Normal saline has the drawback of causing a non-anion gap hyperchloremic metabolic acidosis due to the high chloride content, while lactated ringers can cause a metabolic alkalosis as lactate metabolism regenerates into bicarbonate.

Initial hemorrhagic shock resuscitation begins with administration of IV fluids, followed transfusion of blood products at a 1:1:1 ratio 8. The initial IV fluids should be a 2L bolus of 0.9% normal saline or two 20mL/kg boluses by patient weight. The patient is then determined to be either a responder, transient responder, or nonresponder to IV fluids based on their improvement. Typically, patients in Class I or II can be treated initially with a trial bolus of crystalloids, but patients in Class III or IV should be getting blood products immediately with the first bolus of crystalloids. The amount of blood transfused depends on a variety of factors, but is specifically centered around the concept of “permissive hypotension”. Permissive hypotension is the idea that a patient in active hemorrhagic shock should be transfused just enough blood products to retain a systolic blood pressure above 70 mmHg. Then, after hemorrhage is controlled, the patient can be transfused to retain a systolic blood pressure above 90 mmHg 9. As a rule of thumb, one can expect roughly a loss of 1L blood with a femur fracture, and at least 1L blood loss with a pelvic fracture. Other long bone fractures such as the humerus, tibia or fibula can also account for as much as 500cc each of blood loss. As such, a patient with bilateral femur fractures or a pelvic fracture can already be assumed to be approaching stage 3 or 4 of hemorrhagic shock. As the saying goes in accounting for blood loss in hemorrhagic shock, “blood on the floor, plus four more”. This phrase meaning basically that a life-threatening amount of blood can be lost as active hemorrhage outside the body, in the thigh compartments of bilateral femur fractures, the pelvis, abdomen, or chest. It should also be noted that no number of transfusions should be used as a substitute for definitive control of an active bleed.

Recent trends in damage control resuscitation focus on “hemostatic resuscitation” which pushes for early use of blood products rather than an abundance of crystalloids in order to minimalize the metabolic derangement, resuscitation-induced coagulopathy, and the hemodilution that occurs with crystalloid resuscitation. The end goal of resuscitation and the ratios of blood products remain at the center of much study and debate. A recent study has shown no significant difference in mortality at 24 hours or 30 days between ratios of 1:1:1 and 1:1:2 of plasma to platelets to packed red blood cells (RBCs). However, patients that received the more balanced ratio of 1:1:1 were less likely to die as a result of exsanguination in 24 hours and were more likely to achieve hemostasis Additionally, reduction in time to first plasma transfusion has shown a significant reduction in mortality in damage control resuscitation.

In addition to blood products, products that prevent the breakdown of fibrin in clots, or antifibrinolytics, have been studied for their utility in the treatment of hemorrhagic shock in the trauma patient. Several antifibrinolytics have been shown to be safe and effective in elective surgery. The CRASH-2 study was a randomized control trial of tranexamic acid versus placebo in trauma has been shown to decrease overall mortality when given in the first eight hours of injury. Follow-up analysis shows additional benefit to tranexamic acid when given in the first three hours after surgery.

Damage control resuscitation is to occur in conjunction with prompt intervention to control the source of bleeding. Strategies may differ depending on proximity to definitive treatment.

Equipment

Packed red blood cells are provided in units of roughly 350cc, and are more concentrated than whole blood with a hematocrit of 65-75%. The plasma and platelets are removed via centrifuge, and the remaining packed red blood cells are stored in a saline-based preservative such as citrate phosphate dextrose adenine (CPDA-1) for increased shelf life. Packed red blood cells (RBCs) can be stored for up to 35 days at 2-4 degrees Celsius. One unit of packed red blood cells is thought to raise a patient’s hemoglobin level by 1g/dL. These products must be typed and matched for ABO and Rh compatibility with patient recipients.

Fresh frozen plasma is given in units of 200-250cc each and contain all coagulation factors, with no red blood cells or platelets. For fresh frozen plasma (FFP) to be therapeutic, it is required to be given at 10-20cc/kg body weight, which would theoretically increase the body’s clotting factor levels by 20-30%. For an increased shelf life of up to 2 years, they are frozen within 8 hours of collection and stored at -40 to -50 degrees Celsius. They are then thawed and must be used immediately as their thawed shelf life is only 5 days before they begin to degrade. Frozen plasma, which is less commonly used, and typically frozen within 24 hours of collection (FP24), has slightly reduced levels of factor V and VIII as compared to fresh frozen plasma (FFP). Fresh frozen plasma is particularly useful for certain coagulopathies or in isolated clotting factor deficiencies. There is some speculation as to the benefit of fresh frozen plasma (FFP) in patients with multiple clotting factor deficiencies or coumadin coagulopathy, but its standard use in the hemorrhagic shock patient remains valid.

Platelets are given in high concentration “6 packs” of platelets with one “6 pack” being equal to one apheresis Unit. 1 Unit is typically 250cc, is stored concentrated in a small volume of plasma, and only has a shelf life of 5 days at 20-24 degrees Celsius. Unlike packed red blood cells, platelets lose what little shelf life they have when they are frozen, and so must remain fresh from collection to administration. 1 Unit of platelets is thought to increase the body’s platelet count by 30,000-60,000 platelets/uL. Roughly 20% of patients can develop antiplatelet antibodies after 10-20 transfusions.

Finally, one other commonly used blood product is cryoprecipitate, which is used in a similar fashion to fresh frozen plasma (FFP). Cryoprecipitate, or Cryo, is gathered by centrifuging plasma and gathering the precipitate, which contains large ratios of vWBF, factor VIII, fibrin (factor XIII), and fibrinogen. Like plasma, Cryo is frozen and can be stored up to 2 years at -30 degrees Celsius. Cryo is typically provided in 10-15cc Units which are then given in 6-10 unit pooled increments.

Hemorrhagic shock guidelines summary

The fourth edition of the guideline on management of major bleeding and coagulopathy following trauma by the pan-European, multidisciplinary Task Force for Advanced Bleeding Care in Trauma includes the following 10:

  • Early imaging (ultrasonography or contrast-enhanced CT) for the detection of free fluid in patients with suspected torso trauma.
  • CT assessment for hemodynamically stable patients.
  • A low initial Hb be considered an indicator for severe bleeding associated with coagulopathy.
  • Use of repeated Hb measurements as a laboratory marker for bleeding, as an initial Hb value in the normal range may mask bleeding.
  • Serum lactate and/or base deficit measurements as sensitive tests to estimate and monitor the extent of bleeding and shock.
  • Repeated monitoring of coagulation, using either a traditional laboratory determination [prothrombin time (PT), activated partial thromboplastin time (APTT), platelet counts, and fibrinogen] and/or a viscoelastic method.
  • Target systolic blood pressure of 80-90 mm Hg until major bleeding has been stopped in the initial phase following trauma without brain injury.
  • In patients with severe traumatic brain injury (GCS ≤8), a mean arterial pressure ≥80 mmHg should be maintained.
  • Fluid therapy using isotonic crystalloid solutions should be initiated in the hypotensive bleeding trauma patient.
  • Excessive use of 0.9 % NaCl solution should be avoided.
  • Hypotonic solutions such as Ringer’s lactate should be avoided in patients with severe head trauma.
  • Use of colloids should be restricted due to the adverse effects on hemostasis.
  • A target Hb of 7-9 g/dl.
  • In the initial management of patients with expected massive haemorrhage, one of the following strategies: Plasma (FFP or pathogen-inactivated plasma) in a plasma-RBC ratio of at least 1:2 as needed; fibrinogen concentrate and RBC according to Hb level.
  • Tranexamic acid should be administered as early as possible to the trauma patient who is bleeding or at risk of significant hemorrhage, at a loading dose of 1 g infused over 10 min, followed by an IV infusion of 1 g over 8 hours. Tranexamic acid should be administered to the bleeding trauma patient within 3 hr after injury. Tranexamic acid is an inexpensive antifibrinolytic drug that promotes blood clotting by preventing blood clots from breaking down. It has been shown to reduce mortality in trauma patients with uncontrolled hemorrhage 11. Further studies are planned to determine specific recommendations for tranexamic acid administration 11.
  • Protocols for the management of bleeding patients should consider administration of the first dose of tranexamic acid en route to the hospital.
  • If a plasma-based coagulation resuscitation strategy is used, plasma (FFP or pathogen-inactivated plasma) should be administered to maintain PT and APTT <1.5 times the normal control.
  • Plasma transfusion should be avoided in patients without substantial bleeding.
  • If a concentrate-based strategy is used, treatment with fibrinogen concentrate or cryoprecipitate if significant bleeding is accompanied by viscoelastic signs of a functional fibrinogen deficit or a plasma fibrinogen level of less than 1.5–2.0 g/L.
  • An initial fibrinogen supplementation of 3-4 g, which is equivalent to 15–20 single donor units of cryoprecipitate or 3-4 g fibrinogen concentrate. Repeat doses must be guided by viscoelastic monitoring and laboratory assessment of fibrinogen levels.
  • Platelets should be administered to maintain a platelet count above 50 × 109/L.
  • Maintenance of a platelet count above 100 × 109/L in patients with ongoing bleeding and/or traumatic brain injury.
  • Initial dose of 4 to 8 single platelet units or one aphaeresis pack.
References
  1. Hemorrhagic shock. https://emedicine.medscape.com/article/432650-overview
  2. Hooper N, Armstrong TJ. Hemorrhagic Shock. [Updated 2019 May 6]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470382
  3. Kornblith LZ, Moore HB, Cohen MJ. Trauma-Induced Coagulopathy: The Past, Present, and Future. J. Thromb. Haemost. 2019 Apr 15
  4. Cocchi MN, Kimlin E, Walsh M, Donnino MW. Identification and resuscitation of the trauma patient in shock. Emerg Med Clin North Am. 2007 Aug. 25(3):623-42, vii.
  5. Eastridge BJ, Holcomb JB, Shackelford S. Outcomes of traumatic hemorrhagic shock and the epidemiology of preventable death from injury. Transfusion. 2019 Apr;59(S2):1423-1428.
  6. Blalock A. Principle of Surgical Care, Shock, and Other Problems. St Louis: Mosby; 1940.
  7. Erdman MO, Chardavoyne P, Olympia RP. School Nurses on the Front Lines of Medicine: The Approach to a Student With Severe Traumatic Bleeding. NASN Sch Nurse. 2019 Mar 28;:1942602X19837525
  8. Kowalski A, Brandis D. Shock Resuscitation. [Updated 2018 Dec 2]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK534830
  9. Pohlman TH, Fecher AM, Arreola-Garcia C. Optimizing transfusion strategies in damage control resuscitation: current insights. J Blood Med. 2018;9:117-133.
  10. Rossaint R, Bouillon B, Cerny V, Coats TJ, Duranteau J, Fernández-Mondéjar E, et al. The European guideline on management of major bleeding and coagulopathy following trauma: fourth edition. Crit Care. 2016 Apr 12. 20 (1):100.
  11. Roberts I, Shakur H, Ker K, Coats T. Antifibrinolytic drugs for acute traumatic injury. Cochrane Database Syst Rev. 2011 Jan 19. 1:CD004896
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