Hemorrhagic Shock Management in the ED Clinical Presentation

Updated: Mar 22, 2022
  • Author: William P Bozeman, MD; Chief Editor: Trevor John Mills, MD, MPH  more...
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Presentation

History and Physical

History taking should address the following:

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

  • A history of bleeding disorders and surgery should be obtained.

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

Findings at physical examination may include the following:

  • Head, ears, eyes, nose, and throat: Sources of hemorrhage usually are apparent. 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 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 at 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.

Next:

Complications

Coagulopathy may occur in severe hemorrhage. Fluid resuscitation, although necessary, may exacerbate coagulopathy. 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. Studies of urban patients with penetrating trauma have shown that mortality increases with these interventions; study findings call these practices into question. [11, 12, 13]  

Resuscitation with crystalloid solutions has been shown to put patients with hemorrhagic shock at risk for marked acidosis and to iatrogenically worsen the lethal triad of coagulopathy, hypothermia, and acidosis. Lactated Ringer’s resuscitation has caused an increase in lactate levels, and normal saline has negatively affected the base deficit. [12, 13, 14, 15, 16, 17]  Reversal of hypotension prior to 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 yet been established.

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 systolic blood pressure, sodium, chloride, and osmolarity at admission, whereas lactate, base deficit, fluid requirement, and hemoglobin levels were similar in all groups. HSD-resuscitated patients had higher international normalized ratio values at admission and greater hypercoagulability. Prothrombotic tissue factor was elevated in shock treated with NS but was depressed in both HS and HSD groups. HSD patients had the worst imbalance between procoagulation/anticoagulation and profibrinolysis/antifibrinolysis, resulting in increased hypocoagulability and hyperfibrinolysis. [13]

Damage control strategies play an important role in trauma management. One such strategy—hypotensive resuscitation—is being increasingly employed. A meta-analysis of literature and randomized controlled and cohort trials revealed significant benefits of hypotensive resuscitation relative to mortality in patients with traumatic hemorrhagic shock. It not only reduced the need for blood transfusions and the incidence of acute respiratory distress syndrome (ARDS) and multiple organ dysfunction; it also caused a nonsignificant incidence of acute kidney injury (AKI). [18]

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