Hemorrhagic Shock in Emergency Medicine 

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

Overview

Background

Shock is a state of inadequate perfusion, which does not sustain the physiologic needs of organ tissues. Many conditions, including blood loss but also including nonhemorrhagic 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. See the Medscape articles hemorrhagic shock and hypovolemic shock.[1, 2]

Pathophysiology

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 delivery (ie, DO2), 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.

Epidemiology

Accidental injuries remain the leading cause of death in individuals aged 1-44 years.[3] Hemorrhagic shock is a leading cause of death among trauma patients.[4]

Patient Education

For patient education resources, see the Shock Center, as well as Shock.

 

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.

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.

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]

 

DDx

 

Workup

Laboratory Studies

 

Laboratory studies are essential in management of many forms of hemorrhagic shock. Baseline levels are determined frequently, but these infrequently change the initial management after trauma.

Serial evaluations of the following can help guide ongoing therapy:

  • CBC

  • Prothrombin time and/or activated partial thromboplastin time

  • Urine output rate can help guide adequacy of perfusion

  • ABGs (levels reflect acid-base and perfusion status)

Lactate and base deficit are used in some centers to indicate the degree of metabolic debt. Clearance of these markers over time can reflect the adequacy of resuscitation.

Typed and crossmatched packed red blood cells should be ordered immediately based on clinical suspicion of hemorrhagic shock. Fresh frozen plasma and platelets also may be required to correct or prevent coagulopathies that develop in severe hemorrhagic shock.

Imaging Studies

Cervical spine, chest, and pelvis radiographs are the standard screening images for severe trauma. Other radiographs may be indicated for orthopedic injuries.

Computed tomography can be used to image the appropriate region of suspected injury. CT scanning frequently is the method of choice for evaluating possible intra-abdominal and/or retroperitoneal sources of hemorrhage in stable patients (see the image below). Oral contrast material may not increase the diagnostic yield of abdominal CT scanning in blunt trauma. Scanning should not be delayed to administer oral contrast material.[12]

CT scan of a 26-year-old man after a motor vehicle CT scan of a 26-year-old man after a motor vehicle crash shows a significant amount of intra-abdominal bleeding.

Bedside ultrasonography abdominal ultrasonography can be very useful for the rapid detection of AAA and free intra-abdominal fluid. Thoracic ultrasonographic findings can immediately confirm hemothorax or pericardial tamponade.

Directed angiography may be diagnostic and therapeutic. Interventional radiologists have had good success achieving hemostasis in hemorrhage caused by a variety of vessels and organs.

Other Tests

An ECG can be useful for detecting dysrhythmias and cardiac sequelae of shock.

Tissue oximetry using near infrared spectroscopy (NIRS) shows promise for continuous noninvasive measurement of perfusion in hemorrhagic shock and other conditions.[13]

ADAMTS 13, sP-Selectin, and HSP27 have been investigated as potential prognostic markers in patients with hemorrhagic shock.[14]

Procedures

Tube thoracostomy is necessary in significant hemothorax with or without pneumothorax.

Central venous access facilitates fluid resuscitation and monitoring of central venous pressure and is necessary if peripheral intravenous access is inadequate or impossible to obtain.

Diagnostic peritoneal lavage is used to detect intra-abdominal blood, fluid, and intestinal contents. It is sensitive but not specific for abdominal injury. It is not used to evaluate the retroperitoneum, which can hold significant hemorrhage, and does not identify the source of hemorrhage.

 

Treatment

Prehospital Care

The standard care consists of rapid assessment and expeditious transport to an appropriate center for evaluation and definitive care.

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 elevated lactate levels, and normal saline 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]

Emergency Department Care

Management of hemorrhagic shock should be directed toward optimizing perfusion of and oxygen delivery to vital organs.

Diagnosis and treatment of the underlying hemorrhage must be performed rapidly and concurrently with management of shock.

Supportive therapy, including oxygen administration, monitoring, and establishment of intravenous access (eg, 2 large-bore catheters in peripheral lines, central venous access), should be initiated. Intravascular volume and oxygen-carrying capacity should be optimized. In addition to crystalloids, some colloid solutions, hypertonic solutions, and oxygen-carrying solutions (eg, hemoglobin-based and perfluorocarbon emulsions) are used or being investigated for use in hemorrhagic shock.

Blood products are often required in severe hemorrhagic shock. Replacement of lost components using red blood cells (RBCs), fresh frozen plasma (FFP), and platelets may be essential. The ideal ratio of RBCs to FFP remains undetermined. Recent combat experience has suggested that aggressive use of FFP may reduce coagulopathies and improve outcomes.[15, 9]

Determination of the site and etiology of hemorrhage is critical to guide further interventions and definitive care.

Control of hemorrhage may be achieved in the ED, or control may require consultations and special interventions.

In an Australian study of the long-term outcomes of major-trauma patients who received massive transfusions, massive transfusion was independently associated with unfavorable outcomes. In massively transfused patients, the authors found no significant change in measured outcomes over the study period, with a persistent 23% mortality in hospital, a 52% unfavorable GOSE (Glasgow Outcome Score - extended) at 6 months, and a 44% unfavorable GOSE at 12 months.[8]

Consultations

Consult a general or specialized surgeon, gastroenterologist, obstetrician-gynecologist, interventional radiologist, and others as required.

 

Guidelines

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[16] :

  • 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 TBI (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 hr.

  • Tranexamic acid should be administered to the bleeding trauma patient within 3 hr after injury.

  • 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 TBI. (Grade 2C)

  • Initial dose of 4 to 8 single platelet units or one aphaeresis pack.

 

Medication

Medication Summary

Achievement of hemostasis, fluid resuscitation, and use of blood products are the mainstays of treatment. Pressor agents may be useful in some settings (eg, spinal shock), but these agents should not be substitutes for adequate volume resuscitation and blood product replacement.

Tranexamic acid (TXA) 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.[17] Further studies are planned to determine specific recommendations for TXA administration.

Vasopressors

Class Summary

These agents augment both coronary and cerebral blood flow during the low-flow state associated with shock.

Dopamine (Intropin)

Stimulates both adrenergic and dopaminergic receptors. Hemodynamic effect is dependent on the dose. Lower doses predominantly stimulate dopaminergic receptors that in turn produce renal and mesenteric vasodilation. Higher doses produce cardiac stimulation and renal vasodilation

Norepinephrine (Levophed)

Used in protracted hypotension following adequate fluid-volume replacement. Stimulates beta1-adrenergic and alpha-adrenergic receptors, which, in turn, increase cardiac muscle contractility and heart rate, as well as vasoconstriction; result is increased systemic BP and coronary blood flow.

Vasopressin (Pitressin)

Has vasopressor and ADH activity. Increases water resorption at distal renal tubular epithelium (ADH effect) and promotes smooth muscle contraction throughout the vascular bed of the renal tubular epithelium (vasopressor effects); however, vasoconstriction also is increased in splanchnic, portal, coronary, cerebral, peripheral, pulmonary, and intrahepatic vessels.

Epinephrine (Adrenalin, Bronitin)

Used for hypotension refractory to dopamine. Alpha-agonist effects include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Beta2-agonist effects include bronchodilatation, chronotropic cardiac activity, and positive inotropic effects.