Hemorrhagic Shock Case File

Hemorrhagic Shock Case File

Eugene C. Toy, MD, Barry C. Simon, MD, Terrence H. Liu, MD, MHP, Katrin Y. Takenaka, MD, Adam J. Rosh, MD, MS

Case 7

A 23-year-old man is transported to your emergency department (ED) from the scene of a rollover motor vehicle collision (MVC). He was found approximately 1 hour after the accident had occurred. At the scene, the patient was awake and complained of pain in his back and legs. In the ED, he is awake, his speech is clear and appropriate, and he has normal breath sounds over bilateral lung fields. He has palpable, equal bilateral femoral pulses. His temperature is 35.6°C (96.1°F) (rectally), pulse rate is 106 beats per minute, blood pressure is 110/88 mm Hg, respiratory rate is 24 breaths per minute, and Glasgow coma scale is 15. Multiple abrasions are noted over the neck, shoulders, abdomen, and legs. His chest wall is nontender. His abdomen is mildly tender. The pelvis is stable, but he has extensive swelling and tenderness of the right thigh. He has a deep scalp laceration over his right temporal area that continues to ooze. A focused abdominal sonographic examination trauma (FAST) is performed revealing free fluid in Morison pouch and no other abnormalities. The patient’s initial complete blood count (CBC) reveals a white blood cell count (WBC) of 14,800 cells/mm3, hemoglobin of 11.2 g/dL, and hematocrit of 34.4%.

⯈ What is the next step in the evaluation of this patient?

⯈ If this patient becomes hypotensive, what is the most likely cause?

ANSWER TO CASE 7:

Hemorrhagic Shock

Summary: A healthy 23-year-old man presents following a motor vehicle accident with mild tachycardia, scalp laceration, femur fracture, and a tender abdomen with a positive FAST examination.

• Next step: The Emergency Medicine approach to every critically ill patient begins with evaluation and stabilization of the airway, breathing, and circulation (ABC). This approach is also advocated by Advanced Trauma Life Support (ATLS) guidelines. Once the ABCs are stabilized, a thorough secondary survey, consisting of a detailed physical examination, should follow. In this patient, the ABCs are stable and the secondary survey reveals abdominal pain and a likely right femur fracture with intact pulses. Immediately subsequent to the secondary survey, the ultrasound examination demonstrates free fluid in the hepatorenal potential space known as Morison pouch. Presence of fluid in the hepatorenal space indicates intra-abdominal hemorrhage likely secondary to solid organ injury. Since this patient is hemodynamically stable, a computed tomography (CT) scan of the abdomen and pelvis should be done to identify and grade the severity of the injuries. In addition to estimating the amount of intraperitoneal free fluid, the CT scan can aid in identifying the source of bleeding and the presence of other injuries that may have not been appreciated on clinical examination. The limitations of CT scans in blunt trauma—mainly the lower sensitivity for hollow organ injuries and bowel wall hematomas—should be kept in mind when reviewing a CT scan in this setting.
• Most likely cause of hypotension: Hemorrhagic shock. The probable sources of blood loss in this patient are thigh, abdomen, and scalp laceration. Other possible causes or contributors to his hypotension are cardiogenic shock secondary to myocardial contusion or spinal shock secondary to injury to the spinal cord. The latter can easily be ruled out by performing a neurologic examination during the secondary survey, or even as part of the disability evaluation during the primary survey.

ANALYSIS

Objectives

1. Learn the basics of initial assessment of a trauma patient (Figure 7–1).
2. Learn the definitions and pathophysiology of shock and hemorrhagic shock.
3. Learn the advantages and disadvantages of base deficit, serum lactate, hemoglobin/ hematocrit, and pulmonary artery catheter application for shock identification and patient resuscitation.
4. Learn the initial approach to managing and treating the patient with hemorrhagic shock.

Figure 7–1. Algorithm for assessment/management of the trauma patient.

Initial Assessment of the Trauma Patient

The first priorities in the evaluation of any trauma patient are the ABCs. Airway is assessed by asking the patient to state his or her name, followed by noting the presence or absence of tracheal deviation. If the patient is unable to protect his airway because of confusion, loss of consciousness, or an extrinsic threat to the airway (ie, expanding neck hematoma), the patient should be intubated with an endotracheal tube. Next, breathing is assessed by listening to the chest for the presence of equal

bilateral breath sounds and by observing the symmetry of chest wall expansion. The unstable patient with clinical signs of pneumothorax or tension pneumothorax should be treated with immediate needle decompression followed by placement of a chest tube. Finally, circulation is assessed via the vital signs and by palpation of bilateral femoral, radial, or pedal pulses. Any suggestion of cardiovascular instability requires immediate crystalloid or colloid resuscitation through two large bore peripheral IVs.

Next, the patient’s ability to follow commands should be evaluated and an overall assessment of his/her level of functioning should be made. This consists of assigning a score on the Glasgow coma scale, ranging from 3 to 15 (see also Table I–1 in Section I). Subsequently, a focused history should be quickly elicited. The mnemonic “AMPLE” is useful for guiding the history taking (Table 7–1).

Based on the capability of your hospital and trauma or emergency services, bedside ultrasound can be incorporated into the initial evaluation of the trauma patient.

Aside from the FAST examination (assessment for free fluid in Morison pouch, splenorenal and supra-splenic space, pelvis, and pericardial space), ultrasound can be used for rapid identification of pneumothorax, hemothorax, cardiac activity, and central line placement if needed. The use of ultrasound in the trauma patient is operator-dependent.

The secondary survey follows, in which the patient is examined from head to toe. In the presence of severe, obvious injuries, it is appropriate to start the examination at the affected sites. However, one must be cautious and diligent to complete a thorough physical examination to preclude missing any less obvious but equally important or potentially life-threatening injuries. Additional history from paramedics, and emergency medical technicians (EMTs) should also be elicited.

In this patient, the entire history is very concerning. In addition to being ejected from a vehicle involved in a collision at high speed, and therefore at risk for multisystem injuries secondary to a high kinetic energy transfer, the patient was found 1 hour following the incident. The risk for hypothermia and a diminished ability to respond to hemorrhagic shock is great.

Approach To:

Hemorrhagic Shock

DEFINITIONS

SHOCK: Insufficient cellular perfusion/inability to deliver sufficient oxygen to the tissues.

HEMORRHAGIC SHOCK: Inadequate tissue oxygenation resulting from a blood volume deficit. In this situation, the loss of blood volume decreases venous return, cardiac filling pressures, and cardiac output. End-organ perfusion is subsequently decreased as blood flow is preferentially preserved to the brain and heart.

CLINICAL APPROACH

In shock, the lack of oxygen available to cells results in an inability of mitochondria to generate adequate ATP. Instead, anaerobic metabolism dominates, leading to an accumulation of pyruvate that is converted to lactate.

Shock is divided into three stages: Compensated, progressive, and irreversible. Shock is initially compensated by control mechanisms that return cardiac output and arterial pressure back to normal levels. Within seconds, baroreceptors and chemoreceptors elicit powerful sympathetic stimulation that vasoconstricts arterioles and increases heart rate and cardiac contractility. After minutes to hours, angiotensin constricts the peripheral arteries while vasopressin constricts the veins to maintain arterial pressures and improve blood return to the heart. Angiotensin and vasopressin also increase water retention, thereby improving cardiac filling pressures. Locally, vascular control preferentially dilates vessels around the hypoxic tissues to increase blood flow to injured areas. The normal manifestations of shock do not apply to pregnant women, athletes, and individuals with altered autonomic nervous systems (older patients, those taking β-blockers).

As shock evolves into the progressive stage, arterial pressure falls. This leads to cardiac depression from decreased coronary blood flow, and, in turn, further decreases arterial pressure. The result is a feedback loop that becomes a vicious cycle toward uncontrolled deterioration. Inadequate blood flow to the nervous system eventually results in complete inactivation of sympathetic stimulation. In the microvasculature, low blood flow causes the blood to sludge, amplifying the inadequate delivery of oxygen to the tissues. This ischemia results in increased microvascular permeability, and large quantities of fluid and protein move from the intravascular space to the extravascular compartment, which exacerbates the already decreased intravascular volume. The systemic inflammatory response syndrome caused by severe injury and shock may progress to multiorgan failure. Pulmonary edema, acute respiratory distress syndrome (ARDS), poor cardiac contractility, loss of electrolyte and fluid control, and inability to metabolize toxins and waste products set in. Cells lose the ability to maintain electrolyte balance, metabolize glucose, maintain mitochondrial activity, and prevent lysosomal release of hydrolases. Resuscitation during this progressive stage of tissue ischemia can cause reperfusion injury from the burst of oxygen-free radicals.

Finally, the patient enters the irreversible stage of shock, and any therapeutic efforts become futile. Despite transiently elevated arterial pressures and cardiac output, the body is unable to recover, and death becomes inevitable.

Pathophysiology and Stages of Hemorrhagic Shock

Hemorrhagic shock is the most common cause of death in trauma patients aside from traumatic brain injury. A high level of suspicion for hemorrhage and hemorrhagic shock should dominate evaluation of a trauma patient, especially as vital signs may not become abnormal until a significant amount of hemorrhage has occurred. Hemorrhagic shock is classified by the advanced trauma life support (ATLS) into four categories to further emphasize the progression of vital sign instability in response to blood loss (Table 7–2). Additional clinical signs that indicate hemorrhagic shock include skin pallor/coolness, delayed capillary refill, weak distal pulses, and anxiety.

As demonstrated by the ATLS classification of stages of hemorrhagic shock, the clinician must not rely solely on vital signs for determination of extent of hemorrhage. This patient obviously has had some blood loss from his femur fracture, and the focused abdominal sonography for trauma (FAST) examination suggests intra-abdominal solid organ injury associated with additional hemorrhage.

Additionally, his scalp laceration must be evaluated as a potential source for serious exsanguination. Despite these multiple sources of hemorrhage, our patient has a normal blood pressure and only a slightly elevated heart rate, which places him in Class II hemorrhagic shock.

DIAGNOSTIC APPROACH

Identify the Source of Bleeding

A trauma patient should be carefully screened to locate the source of blood loss. In this patient, the possibility of bleeding should be assessed in five areas: (1) external bleeding (eg, scalp/extremity lacerations); (2) thorax (eg, hemothorax, aortic injury); (3) peritoneal cavity (eg, solid organ lacerations, large vessel injury); (4) pelvis/ retroperitoneum (eg, pelvic fracture); and (5) soft-tissue compartments (eg, longbone fractures). Adjunctive studies that should be obtained in blunt trauma patients early during their evaluation include chest and pelvic roentgenograms and computed tomography (CT) scans of the head, chest, abdomen, and pelvis. Chest roentgenograms can identify a hemothorax and potential mediastinal bleeding. Pelvic films can demonstrate pelvic fractures as a source of pelvic blood loss. Films of any affected extremity, in this case the femur, should also be obtained. Fractures are not only associated with blood loss from the bone and adjacent soft tissue, but their presence indicates significant energy transfer (often referred to as a significant mechanism of injury) and should increase the clinical suspicion for intra-abdominal and retroperitoneal bleeding. Typically, tibial or humeral fractures can be associated with 750 mL of blood loss (1.5 units of blood), whereas femur fractures can be associated with up to 1500 mL of blood (3 units of blood) in the thigh. Pelvic fractures may result in even more blood loss—up to several liters can be lost into a retroperitoneal hematoma.

Laboratory Evaluation

Laboratory studies that aid (but are not necessary) in evaluating acute blood loss are hemoglobin, hematocrit, base deficit, and lactate levels. In the setting of acute 

hemorrhage, hemoglobin and hematocrit levels may or may not be decreased. These values measure concentration, not absolute amounts. Hemoglobin is measured in grams of red blood cells per deciliter of blood; hematocrit is the percentage of blood volume that is red blood cells. Loss of whole blood will not decrease the red blood cell concentration or the percentage of red cells in blood. The initial minor drops in hemoglobin and hematocrit levels are the results of mechanisms that compensate for blood loss by drawing fluid into the vascular space. To see significant decreases in these values, blood loss must be replaced with crystalloid solution; therefore, most decreases in hemoglobin and hematocrit values are not seen until patients have received large volumes of crystalloid fluid for resuscitation.

With the ongoing metabolic acidosis of hemorrhagic shock, an increased base deficit and lactate level will be seen. Both lactate and base deficit levels are laboratory values that indicate systemic acidosis, not local tissue ischemia. They are global indices of tissue perfusion and normal values may mask areas of under perfusion as a consequence of normal blood flow to the remainder of the body. These laboratory tests are not true representations of tissue hypoxia. It is, therefore, not surprising that lactate and base deficit are poor prognostic indicators of survival in patients with shock. Although absolute values of these laboratory results are not predictors of survival in patients with shock, the baseline value and trends can be used to determine the extent of tissue hypoxia and adequacy of resuscitation. Normalization of base deficit and serum lactate within 24 hours after resuscitation is a good prognostic indicator of survival. Of note, given that lactate is hepatically metabolized, it is not a reliable value in patients with liver dysfunction.

Central Monitoring

The approach to central monitoring in the trauma patient has changed dramatically. The benefit of central monitoring is to most accurately determine cardiac preload, given that preload, or end-diastolic sarcomere length, is the driving force behind the cardiac output as defined by the Starling Curve. Previously, placement of a pulmonary artery catheter was used to measure the pulmonary capillary occlusion (wedge) pressure. This number was used as an approximation of left atrial pressure, which in turn was an indirect measurement of left ventricular end-diastolic pressure and volume. Left-ventricular end-diastolic volume is considered the best clinical estimate of preload. However in recent years, the invasive nature of PA catheters has raised concern about their placement. Clinical practice varies, but in general has shifted towards the use of central venous catheters recording central venous pressure (CVP) to estimate volume status. Even more recently, ultrasound has been used to assess intravascular volume status by examining the respiratory variation of the inferior vena cava (more variation signifying low intravascular volume), or by calculation a ratio of the diameter of the IVC to the aorta. The adoption of these techniques is highly institution-specific.

Management of Hemorrhagic Shock

Resuscitation The most common and easily available fl uid replacements are isotonic crystalloid solutions such as normal saline or lactated Ringer solution. For each liter of these solutions that is infused, approximately 300 mL stays in the intravascular space while the remainder leaks into the interstitial space. This distribution has led to the guideline of 3 mL crystalloid replacement for each 1 mL of blood loss. A blood transfusion is indicated if the patient persists in shock despite the rapid infusion of 2 to 3 L of crystalloid solution, or if the patient has had such severe blood loss that cardiovascular collapse is imminent. When possible, typed and cross-matched blood is optimal; however, in the acute setting, this is often unfeasible. Type-specific unmatched blood is the next best option, followed by O-negative blood in females and O-positive blood in males. Blood is generally administered as packed erythrocytes or packed red blood cells (PRBCs). Crystalloids, fresh-frozen plasma (FFP), and/or platelets may need to be transfused if massive blood volumes have been given. Transfusion protocols differ by institution regarding the ratio of FFP to platelets to PRBCs that should be administered. Colloid solutions such as albumin and hetastarch or dextran are not superior to crystalloid replacement in the acute setting and have the potential for large fluid shifts and pulmonary or bowel wall edema. Hypertonic solutions such as 7.5% saline have the advantage of retaining as much as 500 mL in the intravascular space and may be useful in trauma situations with no access to blood products, such as in military settings.

The concept of permissive hypotension is now more widely accepted in trauma care. The central tenet is that patients suffering from hemorrhagic shock (excluding intracranial hemorrhages) may benefit from judicious fluid administration. In permissive hypotension, the patient’s blood pressure is not resuscitated to their normal blood pressure, or to what physicians consider a normal blood pressure. Instead, the blood pressure is allowed to remain low (mean arterial pressures of 60-70 mm Hg or a systolic blood pressure of 80-90 mm Hg). Permissive hypotension is thought to be effective in hemorrhagic shock because it is thought that post-hemorrhage, the artificially increased blood pressure by aggressive fluid resuscitation may disrupt endogenous clot formation and promote further bleeding. Also, crystalloid is often administered at room temperature, which is actually colder than the body temperature and can result in hypothermia following excessive administration. Crystalloid can also dilute the endogenous clotting factors and erythrocyte concentration, resulting in poorer control of bleeding and also diminished oxygen carrying capacity. Though shown to have great benefits in animal models, human studies of permissive hypotension are few. However, this concept is becoming more accepted in trauma centers. Patients in whom permissive hypotension should not be practiced are: patients with traumatic brain injuries who require maintenance of their cerebral perfusion pressure; patients with a history of hypertension, congestive heart failure, or coronary artery disease, in whom hypotension will be poorly tolerated and may produce other medical problems such as strokes or myocardial infarctions.

Controlling Hemorrhage Achieving hemostasis is paramount in managing the trauma patient with hemorrhagic shock. Wounds amenable to local tamponade with direct pressure, dressings, or tourniquet application should be managed as such. For other injuries that require operative repair, such as intra-abdominal injuries, or for pelvic fractures that require advanced therapies such as interventional radiology (IR)–guided embolization, the appropriate specialists should be contacted immediately. While contacting and arranging for further definitive care, appropriate resuscitation of the patient should be initiated.

COMPREHENSION QUESTIONS

7.1 A 32-year-old man was involved in a knife fight and had stab injuries to his abdomen, although it is unclear how deep these injuries are. He is brought into the emergency room with a heart rate of 110 beats per minute and blood pressure of 84/50 mm Hg. Based on the clinical assessment, which of the following is the amount of acute blood loss he has experienced?

A. 250 mL

B. 500 mL

C. 1000 mL

D. 1500 mL

7.2 Which of the following is an advantage of the FAST examination in a patient with hemorrhagic shock?

A. Can identify retroperitoneal hematomas

B. Can be performed quickly at bedside

C. Can identify the specific site of injury

D. Can quantify the exact amount of blood loss

7.3 A 20-year-old man involved in a motor vehicle accident is brought into the emergency room having lost much blood at the accident scene. His initial blood pressure is 80/40 mm Hg and heart rate 130 beats per minute. He is given 3 L of normal saline intravenously and is still hypotensive. Which of these statements most accurately describes the pathophysiology of his condition?

A. Insufficient cardiac preload

B. Insufficient myocardial contractility

C. Excessive systemic vascular resistance

D. Excessive IL-6 and leukotrienes

7.4 A 35-year-old man has been involved in a motor vehicle accident, and is found to be hypotensive. Which of the following locations of bleeding can cause significant complications but does not explain the hypotension?

A. Chest and abdomen

B. Pelvic girdle and soft-tissue compartments

C. External bleeding

D. Intracranial bleeding

ANSWERS

7.1 D. Blood pressure at rest typically does not decrease until class III hemorrhagic shock, when 1500 to 2000 mL of blood is lost (30%-40% of blood volume). Class I hemorrhagic shock is well compensated associated with 750 mL EBL or less, with no effect on blood pressure and minimal effect on heart rate. Class II shock, associated with 750 to 1500 mL EBL, is associated with tachycardia but normal blood pressure at rest, and low urine output.

7.2 B. DPL and FAST cannot rule out retroperitoneal injury or identify the specific site of injury, but they can be performed quickly at bedside on unstable trauma patients. To fi nd the specific site of injury and rule out retroperitoneal injury, a CT scan can be done; however, the trauma patient must be hemodynamically stable to be transported to the CT scan suite.

7.3 A. In situations of trauma and hemorrhage, persistent hypotension is caused by blood loss unless otherwise proven. Hypotension is caused by lack of preload. Preload is end-diastolic sarcomere length, and insufficient circulating volume does not allow for sufficient venous return or cardiac output.

7.4 D. It is important to systematically check for bleeding sources in the chest, abdomen, pelvic girdle, soft-tissue compartments (long-bone fractures), and external bleeding. Intracranial bleeding, although a significant injury, is usually not the cause of hypotension. The exception to this is the patient who is moribund secondary to a head injury.

CLINICAL PEARLS

⯈ Evaluation of a trauma patient begins with assessment and stabilization of the ABCs.

⯈ Hypotension in a trauma patient is hemorrhage until proven otherwise.

⯈ A trauma patient should be assessed systematically for the source of hemorrhage.

⯈ Laboratory evaluation is not as sensitive as the combination of history, clinical examination, physical examination findings, and vital sign abnormalities for the diagnosis of hemorrhagic shock.

⯈ Therapy must be initiated promptly with fluid and/or blood product administration.

⯈ Definitive therapy for control of hemorrhage should be arranged as soon as possible.

References

Holcroft JW. Shock—approach to the treatment of shock. In: Wilmore DW, Cheung LY, Harken AH, et al, eds. ACS Surgery. New York, NY: Webmed Professional Publishers; 2003:61-74. 

Mullins RJ. Management of shock. In: Mattox KL, Feliciano DV, Moore EE, eds. Trauma. New York, NY: McGraw-Hill; 1999:195-234. 

Rossaint R, Bouillon B, Cerny V, et al. Management of bleeding following major trauma: an updated European guideline. Crit Care Med. (London, England). 2010;14:R52. 

Spahn DR, Cerny V, Coats TJ, et al. Management of bleeding following major trauma: a European guideline. Crit Care. 2007;11(1):R17. 

Wilson M, Davis DP, Coimbra R. Diagnosis and monitoring of hemorrhagic shock during the initial resuscitation of multiple trauma patients: a review. J Emerg Med. 2003;24(4):413-422.

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