Haemorrhagic Shock in Trauma
Shock is defined as an abnormality of the circulatory system that results in inadequate organ perfusion and tissue oxygenation. Haemorrhage is the most common cause of shock in trauma patients.
Definition of haemorrhage
Haemorrhage is an acute loss of circulating blood volume. Although it can vary considerably, normal adult blood volume is approximately 7% of body weight. For example, a 70 kg male has a circulating blood volume of approximately 5 L. The blood volume of obese adults is estimated based on their ideal body weight, because calculation based on actual weight can result in significant overestimation. The blood volume for a child is calculated as 8% to 9% of body weight (70–80 mL/kg).
External vs internal haemorrhage
Identify the source of bleeding as external or internal.
- External haemorrhage
- External haemorrhage is identified and controlled during the primary survey.
- Rapid, external blood loss is managed by direct manual pressure on the wound.
- Tourniquets are effective in massive exsanguination from an extremity but carry a risk of ischaemic injury to that extremity. Use a tourniquet only when direct pressure is not effective and the patient’s life is threatened.
- Blind clamping can result in damage to nerves and veins.
- Internal haemorrhage
- The major areas of internal haemorrhage are the chest, abdomen, retroperitoneum, pelvis, and long bones.
- The source of bleeding is usually identified by physical examination and imaging (e.g. chest x-ray, pelvic x-ray, focused assessment with sonography for trauma [FAST], or diagnostic peritoneal lavage [DPL]).
- Immediate management may include chest decompression, and application of a pelvic stabilising device and/or extremity splints.
- Definitive management may require surgical or interventional radiologic treatment and pelvic and long-bone stabilisation.
- Initiate surgical consultation or transfer procedures early in these patients.
Classification of haemorrhagic shock
The physiologic effects of haemorrhage are divided into four classes, based on clinical signs, which are useful for estimating the percentage of acute blood loss. The clinical signs represent a continuum of ongoing haemorrhage and serve only to guide initial therapy. Subsequent volume replacement is determined by the patient’s response to therapy.
Parameter |
Class I |
Class II (mild) |
Class III (moderate) |
Class IV (severe) |
Approximate blood loss |
< 15% |
15 - 30 % |
31 - 40% |
> 40% |
Heart rate |
↔ |
↔/↑ |
↑ |
↑/↑↑ |
Blood pressure |
↔ |
↔ |
↔/↓ |
↓ |
Pulse pressure |
↔ |
↓ |
↓ |
↓ |
Respiratory rate |
↔ |
↔ |
↔/↑ |
↑ |
Urine output |
↔ |
↔ |
↓ |
↓↓ |
Glasgow Coma Scale score |
↔ |
↔ |
↓ |
↓ |
Base deficit |
0 to -2 |
-2 to -6 |
-6 to - 10 |
-10 or less |
Resuscitation required |
Monitor |
Crystalloid fluid |
Crystalloid fluid +/- blood products |
Massive transfusion protocol |
Management of haemorrhagic shock
The diagnosis and treatment of shock must occur almost simultaneously. For most trauma patients, clinicians begin treatment as if the patient has haemorrhagic shock, unless a different cause of shock is clearly evident. The basic management principle is to stop the bleeding and replace the volume loss.
Vascular access
- Obtain access to the vascular system promptly.
- Insert two large caliber (minimum of 18-gauge in an adult) peripheral intravenous catheters. The most desirable sites for peripheral intravenous lines in adults are the forearms and antecubital veins. If peripheral access cannot be obtained, consider placement of an intraosseous needle for temporary access.
- If circumstances prevent the use of peripheral veins, clinicians may initiate large-caliber, central venous (i.e. femoral, jugular, or subclavian vein) access. A chest x-ray must be obtained after attempts at inserting a subclavian or internal jugular line to document the position of the line and evaluate for a pneumothorax or haemothorax. In emergency situations, central venous access is frequently not accomplished under tightly controlled or completely sterile conditions. Therefore, these lines should be changed in a more controlled environment as soon as the patient’s condition permits.
- As intravenous lines are started, draw blood samples for type and crossmatch, appropriate laboratory analyses, toxicology studies, and pregnancy testing for all females of childbearing age. Blood gas analysis (and lactate) also may be performed at this time.
- Use fluid warmers in the presence of massive haemorrhage to prevent hypothermia.
Initial fluid replacement
- The amount of fluid and blood required for resuscitation is difficult to predict on initial evaluation of a patient. Administer an initial, warmed fluid bolus of isotonic fluid. The usual dose is 1 liter for adults and 20 mL/kg for pediatric patients weighing less than 40 kilograms.
- Observe the patient’s response during this initial fluid administration and base further therapeutic and diagnostic decisions on this response. Persistent infusion of large volumes of fluid and blood in an attempt to achieve a normal blood pressure is not a substitute for definitive control of bleeding.
- Early resuscitation with blood and blood products must be considered in patients with evidence of class III and IV haemorrhage. Early administration of blood products at a low ratio of packed red blood cells to plasma and platelets can prevent the development of coagulopathy and thrombocytopenia.
- N.B. Fluid resuscitation and avoidance of hypotension are important principles in the initial management of patients with blunt trauma, particularly those with traumatic brain injury BUT in penetrating trauma with haemorrhage, delaying aggressive fluid resuscitation until definitive control of haemorrhage is achieved may prevent additional bleeding; a careful, balanced approach with frequent reevaluation is required.
- The same signs and symptoms of inadequate perfusion that are used to diagnose shock help determine the patient’s response to therapy. The return of normal blood pressure, pulse pressure, and pulse rate are signs that perfusion is returning to normal, however, these observations do not provide information regarding organ perfusion and tissue oxygenation.
- The volume of urinary output is a reasonably sensitive indicator of renal perfusion; normal urine volumes generally imply adequate renal blood flow, if not modified by underlying kidney injury, marked hyperglycemia or the administration of diuretic agents. For this reason, urinary output is one of the prime indicators of resuscitation and patient response. Adequate volume replacement during resuscitation should produce a urinary output of approximately 0.5 mL/kg/hr in adults, whereas 1 mL/kg/hr is adequate urinary output for pediatric patients. For children under 1 year of age, 2 mL/kg/hr should be maintained. The inability to obtain urinary output at these levels or a decreasing urinary output with an increasing specific gravity suggests inadequate resuscitation.
- Patients in early hypovolemic shock have respiratory alkalosis from tachypnoea, which is frequently followed by mild metabolic acidosis and does not require treatment. However, severe metabolic acidosis can develop from long-standing or severe shock. Metabolic acidosis is caused by anaerobic metabolism, as a result of inadequate tissue perfusion and the production of lactic acid. Persistent acidosis is usually caused by inadequate resuscitation or ongoing blood loss. In patients in shock, treat metabolic acidosis with fluids, blood, and interventions to control haemorrhage. Base deficit and/or lactate values can be useful in determining the presence and severity of shock, and then serial measurement of these parameters can be used to monitor the response to therapy. Do not use sodium bicarbonate to treat metabolic acidosis from hypovolemic shock.
Patient response to intial fluid replacement
- Rapid response
- Patients quickly respond to the intial fluid bolus and become haemodynamically normal
- Blood loss is typically < 15% of blood volume
- No further fluid bolus or immediate blood administration is indicated and clinicians can slow the fluids to maintenance rates
- Typed and crossmatched blood should be kept available
- Transient response
- Patients respond to the initial fluid bolus but begin to show deterioration of perfusion indices as the initial fluids are slowed to maintenance levels indicating either ongoing blood loss or inadequate resuscitation
- Blood loss is typically 15 - 40% of blood volume
- Transfusion of blood and blood products is indicated and patient may require operative or angiographic control of haemorrhage
- A transient response to blood administration identifies patients who are still bleeding and require rapid surgical intervention; consider initiating massive transfusion protocol
- Minimal or no response
- Failure to respond to crystalloid and blood administration in the ED dictates the need for immediate, definitive intervention (i.e. operation or angioembolisation) to control exsanguinating haemorrhage
Blood replacement
- The decision to initiate blood transfusion is based on the patient’s response, as described in the previous section. Patients who are transient responders or nonresponders require pRBCs, plasma and platelets as an early part of their resuscitation.
- Fully crossmatched pRBCs are preferable for this purpose, but the complete crossmatching process requires approximately 1 hour in most blood banks. For patients who stabilise rapidly, crossmatched pRBCs should be obtained and made available for transfusion when indicated.
- If crossmatched blood is unavailable, type O pRBCs are indicated for patients with exsanguinating haemorrhage. AB plasma is given when uncrossmatched plasma is needed. To avoid sensitisation and future complications, Rh-negative pRBCs are preferred for females of childbearing age. As soon as it is available, the use of unmatched, type-specific pRBCs is preferred over type O pRBCs. An exception to this rule is when multiple, unidentified casualties are being treated simultaneously, and the risk of inadvertently administering the wrong unit of blood to a patient is increased.
- A small subset of patients with shock will require massive transfusion, most often defined as > 10 units of pRBCs within the first 24 hours of admission or more than 4 units in 1 hour. Early administration of pRBCs, plasma, and platelets in a balanced ratio to minimise excessive crystalloid administration may improve patient survival. Simultaneous efforts to rapidly control bleeding and reduce the detrimental effects of coagulopathy, hypothermia, and acidosis in these patients are extremely important.
Coagulopathy
- Severe injury and hemorrhage result in the consumption of coagulation factors and early coagulopathy. Such coagulopathy is present in up to 30% of severely injured patients on admission, in the absence of preexisting anticoagulant use. Massive fluid resuscitation with the resultant dilution of platelets and clotting factors, as well as the adverse effect of hypothermia on platelet aggregation and the clotting cascade, contributes to coagulopathy in injured patients.
- Prothrombin time, partial thromboplastin time, and platelet count are valuable baseline studies to obtain in the first hour, especially in patients with a history of coagulation disorders or who take medications that alter coagulation.
- In patients who do not require massive transfusion, the use of platelets, cryoprecipitate, and fresh-frozen plasma should be guided by coagulation studies, along with fibrinogen levels and balanced resuscitation principles.
Causes of non-haemorrhagic shock in trauma
- Cardiogenic shock
- Myocardial dysfunction can be caused by blunt cardiac injury, cardiac tamponade, air embolism or myocardial infarction
- All patients with blunt thoracic trauma need continuous electrocardiographic (ECG) monitoring to detect injury patterns and dysrhythmias
- The shock state may be secondary to myocardial infarction in the elderly and other high-risk patients, such as those with cocaine intoxication
- Cardiac tamponade
- Tachycardia, muffled heart sounds, and dilated, engorged neck veins with hypotension and insufficient response to fluid therapy suggest cardiac tamponade
- Tension pneumothorax
- The presence of acute respiratory distress, subcutaneous emphysema, absent unilateral breath sounds, hyperresonance to percussion, and tracheal shift supports the diagnosis of tension pneumothorax
- Neurogenic shock
- Isolated intracranial injuries do not cause shock unless the brainstem is injured; therefore the presence of shock in patients with head injury necessitates the search for another cause
- Cervical and upper thoracic spinal cord injuries can produce hypotension due to loss of sympathetic tone, which compounds the physiologic effects of hypovolemia; in turn, hypovolemia compounds the physiologic effects of sympathetic denervation
- The classic presentation of neurogenic shock is hypotension without tachycardia or cutaneous vasoconstriction (and without a narrow pulse pressure)
- Patients who have sustained a spinal cord injury often have concurrent torso trauma; therefore, patients with known or suspected neurogenic shock are treated initially for hypovolemia; the failure of fluid resuscitation to restore organ perfusion and tissue oxygenation suggests either continuing haemorrhage or neurogenic shock
- Septic shock
- Shock due to infection immediately after injury is uncommon; however, it can occur when a patient’s arrival at the ED is delayed for several hours.
- Septic shock can occur in patients with penetrating abdominal injuries and contamination of the peritoneal cavity by intestinal contents.
- Patients with sepsis who also have hypotension and are afebrile are clinically difficult to distinguish from those in hypovolemic shock, as patients in both groups can have tachycardia, cutaneous vasoconstriction, impaired urinary output, decreased systolic pressure, and narrow pulse pressure.
- Patients with early septic shock can have a normal circulating volume, modest tachycardia, warm skin, near normal systolic blood pressure, and a wide pulse pressure.