Hemorrhagic Shock in Emergency Medicine Clinical Presentation

Updated: May 06, 2016
  • Author: William P Bozeman, MD; Chief Editor: Trevor John Mills, MD, MPH  more...
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Presentation

History

History taking should address the following:

  • Specific details of the mechanism of trauma or other cause of hemorrhage are essential.

  • Inquire about a history of bleeding disorders and surgery.

  • Prehospital interventions, especially the administration of fluids, and changes in vital signs should be determined. Emergency medical technicians or paramedics should share this information.

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Physical

Findings at physical examination may include the following:

  • Head, ears, eyes, nose, and throat

    • Sources of hemorrhage usually are apparent.

    • The blood supply of the scalp is rich and can produce significant hemorrhage.

    • Intracranial hemorrhage usually is insufficient to produce shock, except possibly in very young individuals.

  • Chest

    • Hemorrhage into the thoracic cavities (pleural, mediastinal, pericardial) may be discerned at physical examination. Ancillary studies often are required for confirmation.

    • Signs of hemothorax may include respiratory distress, decreased breath sounds, and dullness to percussion.

    • Tension hemothorax, or hemothorax with cardiac and contralateral lung compression, produces jugular venous distention and hemodynamic and respiratory decompensation.

    • With pericardial tamponade, the classic triad of muffled heart sounds, jugular venous distention, and hypotension often is present, but these signs may be difficult to appreciate in the setting of an acute resuscitation.

  • Abdomen

    • Injuries to the liver or spleen are common causes of hemorrhagic shock. Spontaneous rupture of abdominal aortic aneurysm (AAA) may also cause severe intra-abdominal hemorrhage and shock.

    • Blood irritates the peritoneal cavity; diffuse tenderness and peritonitis are common when blood is present. However, the patient with altered mental status or multiple concomitant injuries may not have the classic signs and symptoms at physical examination.

    • Progressive abdominal distention in hemorrhagic shock is highly suggestive of intra-abdominal hemorrhage.

  • Pelvis

    • Fractures can produce massive bleeding. Retroperitoneal bleeding must be suspected.

    • Flank ecchymosis may indicate retroperitoneal hemorrhage.

  • Extremities

    • Hemorrhage from extremity injuries may be apparent, or tissues may obscure significant bleeding.

    • Femoral fractures may produce significant blood loss.

  • Nervous system

    • Agitation and combativeness may be seen in the initial stages of hemorrhagic shock.

    • These signs are followed by a progressive decline in level of consciousness due to cerebral hypoperfusion or concomitant head injury.

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Complications

Coagulopathies may occur in severe hemorrhage. Fluid resuscitation, while necessary, may exacerbate coagulopathies. Sepsis and multiple organ system failure may occur days after acute hemorrhagic shock. Death may result.

Intravenous access and fluid resuscitation are standard. However, this practice has become controversial. For many years, aggressive fluid administration has been advocated to normalize hypotension associated with severe hemorrhagic shock. Recent studies of urban patients with penetrating trauma have shown that mortality increases with these interventions; these findings call these practices into question. [5, 6, 7]  

Resuscitation with crystalloid solutions has been shown to put patients with hemorrhagic shock at risk for marked acidosis and iatrogenically worsen the lethal triad of coagulopathy, hypothermia, and acidosis. Lactated Ringer’s resuscitation has caused and increase in lactate levels, and normal saline has negatively affected the base deficit. [8, 6, 7, 9, 10, 11]  Reversal of hypotension prior to the achievement of hemostasis may increase hemorrhage, dislodge partially formed clots, and dilute existing clotting factors. Findings from animal studies of uncontrolled hemorrhage support these postulates. These provocative results raise the possibility that moderate hypotension may be physiologically protective and should be permitted, if present, until hemorrhage is controlled. These findings should not yet be clinically extrapolated to other settings or etiologies of hemorrhage. The ramifications of permissive hypotension in humans remain speculative, and safety limits have not been established yet.

In a study of patients who received 7.5% NaCl (HS), 7.5% NaCl/6% Dextran 70 (HSD), or 0.9% NaCl (normal saline [NS]) in the prehospital setting, treatment with HS/HSD led to higher admission systolic blood pressure, sodium, chloride, and osmolarity, whereas lactate, base deficit, fluid requirement, and hemoglobin levels were similar in all groups. The HSD-resuscitated patients had higher admission international normalized ratio values and more hypocoagulable patients. Prothrombotic tissue factor was elevated in shock treated with NS but depressed in both HS and HSD groups. The HSD patients had the worst imbalance between procoagulation/anticoagulation and profibrinolysis/antifibrinolysis, resulting in more hypocoagulability and hyperfibrinolysis. [7]

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