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Hemorrhagic Shock


Original Editor ­ Narayani Nagare Top Contributors - Narayani Nagare and Khloud Shreif


Hemorrhagic Shock

Hemorrhagic shock is a critical medical condition that results from significant blood loss, leading to inadequate tissue perfusion and oxygen delivery. This condition can rapidly progress to organ failure and death if not promptly recognized and treated. Hemorrhagic shock is a subset of hypovolemic shock, characterized by a severe reduction in circulating blood volume due to acute hemorrhage. This leads to a decrease in cardiac output and insufficient oxygen supply to meet the metabolic demands of tissues and organs.[1]

Causes of Hemorrhagic Shock

Hemorrhagic shock can result from any condition leading to significant blood loss. The most common causes include:

  1. Trauma: This is the most common cause of hemorrhagic shock globally. It encompasses both blunt trauma, such as car accidents, and penetrating trauma, like gunshot or stab wounds. Such injuries can lead to massive external or internal bleeding, especially in areas like the abdomen, thorax, and pelvis.[2]
  2. Surgical Complications: Another very common cause of this is uncontrolled bleeding at or following the time of surgical intervention. Highly risky conditions are complex surgeries on major blood vessels or organs.
  3. Obstetric Emergencies: These are life-threatening hemorrhages from the complications of pregnancy and the puerperium, such as postpartum hemorrhage, uterine rupture, placental abruption, and ectopic pregnancy.[3]
  4. Gastrointestinal Bleeding: Gastrointestinal bleeding resulting from peptic ulcer disease, esophageal varices, or diverticular disease. The conditions are extremely common in people with a history of alcoholism, liver disease, or chronic intake of nonsteroidal anti-inflammatory drugs (NSAIDs).[4]
  5. Ruptured Aneurysms: Severe internal hemorrhage and very rapid onset of hemorrhagic shock might occur due to the rupture of a large blood vessel, such as the aorta, known as an abdominal aortic aneurysm.[5]
  6. Coagulopathies: Diseases that disrupt coagulation of normal blood; such as hemophilia or Disseminated intravascular coagulation (DIC), predispose to uncontrollable hemorrhage.[6]

Mechanism of Hemorrhagic Shock

The pathophysiology of hemorrhagic shock involves complex hemodynamic and cellular changes. It can be divided into the following phases:

  1. Acute Blood Loss: Due to significant blood loss, the circulating blood volume reduces, which further lead to decreased venous return to the heart. This decreases the preload, stroke volume, and cardiac output due to which blood supply to vital organs is compromised.[7]
  2. Compensatory Mechanisms: The sympathetic nervous system is activated to sustain blood pressure and perfusion:
    • Tachycardia: Increases heart rate in order to increase cardiac output.
    • Peripheral Vasoconstriction: Blood flow to the brain, heart, and kidneys is shunted at the expense of the less vital tissues such as the skin and the gastrointestinal organs.
    • Activation of the Renin-Angiotensin-Aldosterone System (RAAS): It promotes vasoconstriction and sodium/water retention to conserve intravascular volume.[8]
  3. Decompensation: When blood loss increases, compensatory mechanisms fail. This will lead to hypotension, decreased oxygen delivery, and a result metabolic acidosis, causing cellular hypoxia and dysfunction.
  4. Irreversible Shock: Long-term cell injury due to oxygen deprivation, multi-organ failure, and death may occue if untreated.[9]

Signs and Symptoms

The clinical presentation of hemorrhagic shock varies depending on the degree and rate of blood loss.

The clinician employs these classifications to determine priorities and estimate the severity of underlying blood loss. For instance, a patient in mild shock may only need fluid resuscitation, while one in severe shock may require immediate surgical intervention or even massive transfusion protocols to stabilize the patient.

These signs and symptoms can be classified as follows:

Mild Hemorrhagic Shock:

  • Tachycardia (heart rate >100 bpm)
  • Normal or low blood pressure
  • Cool, clammy skin
  • Restlessness or agitation
  • Delayed capillary refill [10]

Moderate Hemorrhagic Shock:

  • Tachycardia (more than 120 bpm)
  • Hypotension (systolic blood pressure <90 mmHg)
  • Oliguria (urine output <30 mL/hour)
  • Restlessness with rapid, shallow breathing
  • Agitation or confusion [11]

Severe Hemorrhagic Shock:

  • Hypotension (systolic blood pressure <70 mmHg)
  • Bradycardia, a late finding
  • Cyanosis that may show discoloration of skin and mucous membranes
  • Coma or unresponsiveness [12]

Management and Treatment

Effective management of hemorrhagic shock includes rapid recognition, control of bleeding, and restoration of both circulating volume and tissue perfusion. A team approach by a surgeon, an emergency physician, an intensivist, and a nursing staff helps to ensure overall and timely patient care. These steps outline treatment in detail below:

  • Initial Assessment and Resuscitation: Using the "ABCDE" approach for the initial treatment.[13]
    • Airway: Maintain an open airway and administer supplemental oxygen at high concentration if required. Look for signs of airway obstruction and treat it as a medical emergency.
    • Breathing: Administer high-flow oxygen and monitor saturation. Assessment of breathing is important.
    • Circulation: Evaluate hemodynamic stability and begin resuscitation.
    • Disability: Use an antagonist (such as naloxone for opioid toxicity) when appropriate. Assess consciousness using the ACVPU scale (Alert, Confusion, Voice, Pain, Unresponsive) or Glasgow Coma Scale. Obtain blood glucose to exclude hypoglycaemia and give glucose if present. In unconscious patients, nurse in lateral position if the airway is unprotected.
AVPU Scale
Glasgow Coma Scale
Glasgow Coma Scale
  • Exposure: Full exposure of the body may be necessary for proper examination. Respect the patient’s dignity and minimise heat loss.
  • Insert two large-bore intravenous (IV) catheters for rapid fluid administration.

  • Hemorrhage Control:
    • External bleeding: Apply direct pressure, wound packing, or tourniquets.
    • Internal bleeding: Surgical intervention (e.g., laparotomy) or endovascular procedures (e.g., embolization) may be necessary to control bleeding sources.[14]
  • Fluid Resuscitation:
    • Begin with crystalloids (e.g., normal saline or lactated Ringer's solution) to restore intravascular volume.
    • Transition to blood products as needed. Employ the Massive Transfusion Protocol (MTP), which uses a balanced ratio of PRBCs, FFP, and platelets (1:1:1) to manage massive hemorrhage.
    • Avoid excessive fluids to prevent dilutional coagulopathy and worsening acidosis.[15]
  • Pharmacological Interventions:
    • Administer tranexamic acid (TXA) within three hours of injury to inhibit fibrinolysis and improve survival outcomes .
    • Correct hypocalcemia during massive transfusions by administering calcium gluconate or chloride.
    • If hypotension is persistent, then use vasopressors, such as norepinephrine, very judiciously and only after adequate volume resuscitation.[11][16]
  • Monitoring and Adjunctive Therapies:
    • Maintain continuous monitoring of blood pressure, heart rate, urine output, and arterial blood gases.
    • Lethal triad of trauma:
      • Hypothermia: Use active warming techniques
      • Acidosis: Improve perfusion and administer bicarbonate, if necessary.
      • Coagulopathy: Clotting factors or fibrinogen concentrates should be administered based on results of TEG or ROTEM.[17]
      • Once stabilized, they often need to be admitted to an intensive care unit (ICU) for close monitoring. Multidisciplinary care involving surgeons, intensivists, and rehabilitation specialists is important for full recovery.
References
  1. ↑ Guyton AC, Hall JE.Textbook of Medical Physiology. 13th ed. Philadelphia: Elsevier; 2015.
  2. ↑ American College of Surgeons. Advanced Trauma Life Support (ATLS): Student Course Manual. 10th ed. Chicago: ACS; 2018.https://www.facs.org/atls
  3. ↑ Pacheco LD, Saade GR, Hankins GD. Severe obstetric hemorrhage: concepts and current perspectives. Obstet Gynecol Clin North Am. 2010;37(2):269-282.
  4. ↑ Lau JYW, Barkun A, Fan DM, et al. Challenges in the management of acute peptic ulcer bleeding. Lancet. 2013;381(9882):2033-2043.
  5. ↑ Chaikof EL, Brewster DC, Dalman RL, et al. The care of patients with an abdominal aortic aneurysm. J Vasc Surg. 2009;50(4):880-896.
  6. ↑ Levi M, Hunt BJ. Thrombosis and coagulopathy in critical care. N Engl J Med. 2015;373(3):147-160.
  7. ↑ Mutschler M, Paffrath T, Wolfl C, et al. The ATLS® classification of hypovolemic shock: a reappraisal. Resuscitation. 2013;84(3):299-304.
  8. ↑ Vincent JL, De Backer D. Circulatory shock. N Engl J Med. 2013;369(18):1726-1734.
  9. ↑ Kauvar DS, Wade CE. The epidemiology and modern management of traumatic hemorrhage: US and international perspectives. Crit Care. 2005;9(Suppl 5):S1-S9.
  10. ↑ Holcomb JB, Tilley BC, Baraniuk S, et al. Transfusion of plasma, platelets, and red blood cells in a 1:1:1 ratio and mortality in patients with severe trauma. JAMA. 2015;313(5):471-482.
  11. ↑ 11.0 11.1 Duchesne JC, McSwain NE Jr, Cotton BA, et al. Damage control resuscitation: the new face of damage control. J Trauma. 2010;69(4):976-990.
  12. ↑ Moore HB, Moore EE, Gonzalez E, et al. Postinjury fibrinolysis shutdown: rationale for selective tranexamic acid J Trauma Acute Care Surg. 2015;78(6):1246-1252.
  13. ↑ Resuscitation Council UK. The ABCDE Approach. Published October 2015, reviewed May 2021, updated July 2024.
  14. ↑ Brohi K, Singh J, Heron M, et al. Acute traumatic coagulopathy. J Trauma. 2003;54(6):1127-1130.
  15. ↑ Spinella PC, Holcomb JB. Resuscitation and transfusion principles for traumatic hemorrhagic shock. Blood Rev. 2009;23(6):231-240.
  16. ↑ CRASH-2 Trial Collaborators. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant hemorrhage: a randomised, placebo-controlled trial. Lancet. 2010;376(9734):23-32.
  17. ↑ Moore HB, Moore EE, Gonzalez E, et al. Postinjury fibrinolysis shutdown: rationale for selective tranexamic acid. J Trauma Acute Care Surg. 2015;78(6):1246-1252.
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