Shock refers to the inadequate perfusion of tissues due to the imbalance between oxygen demand of tissues and the body’s ability to supply it. Classically, there are four categories of shock: hypovolemic, cardiogenic, obstructive, and distributive shock. Hypovolemic shock occurs when there is decreased intravascular volume to the point of cardiovascular compromise. The hypovolemic shock could be due to severe dehydration through a variety of mechanisms or from blood loss. The pathophysiology, diagnosis, and treatment of hemorrhagic shock, a subset of hypovolemic shock, will be explored in this article.
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. 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.
Trauma remains a leading cause of death worldwide with approximately half of these attributed to hemorrhage. 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.
The preponderance of hemorrhagic shock cases resulting from trauma is high. During one year, one trauma center reported 62.2% of massive transfusions occur in the setting of trauma. The remaining cases are divided among cardiovascular surgery, critical care, cardiology, obstetrics, and general surgery, with trauma utilizing over 75% of the blood products.
As patients age, physiological reserves decrease the likelihood of anticoagulant use increases and the number of comorbidities increase. Due to this, elderly patients are less likely to handle the physiological stresses of hemorrhagic shock and may decompensate more quickly.
Hemorrhagic shock is due to the depletion of intravascular volume through blood loss to the point of being unable to match the tissues demand for oxygen. As a result, mitochondria are no longer able to sustain aerobic metabolism for the production of oxygen and switch to the less efficient anaerobic metabolism to meet the cellular demand for adenosine triphosphate. In the latter process, pyruvate is produced and converted to lactic acid to regenerate nicotinamide adenine dinucleotide (NAD+) to maintain some degree of cellular respiration in the absence of oxygen.
The body compensates for volume loss by increasing heart rate and contractility, followed by baroreceptor activation resulting in sympathetic nervous system activation and peripheral vasoconstriction. Typically, there is a slight increase in the diastolic blood pressure with narrowing of the pulse pressure. As diastolic ventricular filling continues to decline and cardiac output decreases, systolic blood pressure drops.
Due to sympathetic nervous system activation, blood is diverted away from noncritical organs and tissues to preserve blood supply to vital organs such as the heart and brain. While prolonging heart and brain function, this also leads to other tissues being further deprived of oxygen causing more lactic acid production and worsening acidosis. This worsening acidosis along with hypoxemia, if left uncorrected, eventually causes the loss of peripheral vasoconstriction, worsening hemodynamic compromise, and death.
The body’s compensation varies by cardiopulmonary comorbidities, age, and vasoactive medications. Due to these factors, heart rate and blood pressure responses are extremely variable and, therefore, cannot be relied upon as the sole means of diagnosis.
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.
Recognizing the degree of blood loss via vital sign and mental status abnormalities is important. The American College of Surgeons Advanced Trauma Life Support (ATLS) 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.
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.
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.
In the setting of trauma, an algorithmic approach via the primary and secondary surveys is suggested by ATLS. 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 FAST scan has been reported above 99%, but a negative ultrasound does not rule out intra-abdominal pathology.
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.
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.
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 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.
While hemorrhage is the most common cause of shock in the trauma patient, other causes of shock are to remain on the differential. Obstructive shock can occur in the setting of tension pneumothorax and cardiac tamponade. These etiologies should be uncovered in the primary survey. In the setting of head or neck trauma, an inadequate sympathetic response, or neurogenic shock, is a type of distributive shock that is caused by a decrease in peripheral vascular resistance. This is suggested by an inappropriately low heart rate in the setting of hypotension. Cardiac contusion and infarctions can result in cardiogenic shock. Finally, other causes should be considered that are not related to trauma or blood loss. In the undifferentiated patient with shock, septic shock and toxic causes are also on the differential.
Trauma is the most common cause of hemorrhagic shock, but causes can span multiple systems.
Tachycardia is typically the first abnormal vital sign of hemorrhagic shock. As the body attempts to preserve oxygen delivery to the brain and heart, blood is shunted away from extremities and nonvital organs. This causes cold and modeled extremities with delayed capillary refill. This shunting ultimately leads to worsening acidosis.
The “lethal triad” of trauma is acidosis, hypothermia, and coagulopathy.
Trauma-induced coagulopathy can occur in the absence of the hemodilution of resuscitation.
Damage control resuscitation is based on three principles: permissive hypotension, hemostatic resuscitation, and damage control surgery. Permissive hypotension targets a systolic blood pressure of 90 mmHg accepting suboptimal perfusion to end organs for a limited time to achieve hemostasis.