Hemorrhagic Shock and Resuscitation



Hemorrhagic Shock and Resuscitation


Christopher P. Michetti

Timothy A. Emhoff



I. GENERAL PRINCIPLES

A. Definition.

1. Shock is a condition in which the amount of oxygen delivered to tissues is inadequate to maintain normal cellular function, that is, aerobic metabolism.

2. Hemorrhagic shock (HS) results from tissue hypoperfusion due to hypovolemia from blood loss.

B. Epidemiology.

1. Of those with severe, life-threatening injuries who survive to medical care, exsanguination is second to severe brain injury as the cause of death in the first hour.

C. Outcome.

1. Outcome is proportional to the duration and severity of shock.

2. Rapid identification of shock and initiation of treatment before hypotension occurs are essential to minimize morbidity.

3. Trauma patients with HS have improved outcomes when treated at a level I trauma center (highest level) as soon as possible after injury.

II. PATHOPHYSIOLOGY

A. Physiologic alterations.

1. Hypoperfusion after hemorrhage leads to tissue ischemia, a shift from aerobic to anaerobic metabolism, production of lactate release of inorganic phosphates, and metabolic acidosis.

a. Depletion of adenosine triphosphate (ATP), oxygen radical formation, and other processes of anaerobic metabolism result in cellular injury and eventually cell death.

2. The hypothalamic-pituitary-adrenal axis is activated by shock and results in release and elevation of several hormones.

a. Increased cortisol leads to hyperglycemia and insulin resistance, muscle breakdown, and lipolysis.

b. Release of vasopressin causes sodium and water retention.

c. Activation of the renin-angiotensin system produces angiotensin II, a vasoconstrictor.


3. Activation of the systemic inflammatory response results in release of proinflammatory mediators that can cause cell and organ dysfunction.

a. Ischemia and reperfusion of tissues, especially gut, activate systemic inflammatory response.

b. Cytokines such as tumor necrosis factor, interleukins 1 and 6 are released.

c. Complement system is activated.

d. Endothelial cells allow adhesion of activated neutrophils and their transmigration into tissues, where they cause tissue injury by releasing oxygen radicals and proteolytic enzymes. Loss of endothelial barrier function leads to transudation and intravascular fluid depletion.

B. Fluid shifts.

1. Triphasic response.

a. Initial phase: response to bleeding is fluid shift from the interstitial space into capillaries to compensate for lost intravascular volume.

i. Lasts from start of bleeding until bleeding controlled.

ii. These fluid shifts occur in minutes after blood loss.

b. Second phase: with resuscitation, fluid shifts from the intravascular space back to the interstitial space (the “third space”).

i. Lasts one to several days.

ii. Interstitial space sequesters large amounts of fluids (the “capillary leak” phenomenon).

iii. Patients become severely edematous and simultaneously intravascularly depleted.

iv. Fluid intake markedly exceeds output.

v. Fluid sequestration and resultant edema are obligatory and necessary in resuscitation from HS.

c. Third phase: with restoration of endothelial integrity, fluid moves from the interstitial space to the intravascular space and is filtered through the kidneys, and diuresis occurs.

i. Starts 3 to 5 days after injury.

ii. Key sign of recovery from shock.

2. Common mistake among those inexperienced in shock resuscitation is to misinterpret the edema and highly positive fluid balance of shock patients as signs of increased hydrostatic pressure from congestive heart failure.

a. Fluid intake/output balance is irrelevant in acute HS resuscitation.

b. Tissue edema and increased body water are the natural result of successful HS resuscitation.

c. Forced diuresis exacerbates tissue hypoperfusion by depleting intravascular volume.

d. Overhydration, however, can lead to abdominal compartment syndrome, increased lung water, and poor tissue healing, further exacerbating trauma morbidity.

III. DIAGNOSIS

A. Classifications of HS.

1. Total circulating blood volume is 70 to 80 mL/kg in the adult.


2. Class I hemorrhage.

a. Loss of up to 15% of total blood volume (0 to 750 mL in a 70-kg person).

b. Characterized by normal vital signs and urine output, slight tachypnea, and slight anxiety.

3. Class II hemorrhage.

a. Loss of 15% to 30% of total blood volume (750 to 1,500 mL).

b. Characterized by normal blood pressure (BP), tachycardia, mild tachypnea, decreased urine output, and mild anxiety.

4. Class III hemorrhage.

a. Loss of 30% to 40% of total blood volume (1,500 to 2,000 mL).

b. Characterized by hypotension, tachycardia, tachypnea, decreased urine output, and anxiety and confusion.

5. Class IV hemorrhage.

a. Loss of >40% of total blood volume (>2,000 mL).

b. Characterized by severe hypotension and tachycardia, tachypnea, negligible urine output, and lethargy.

6. Note that BP is normal until significant blood loss occurs (Class III).

7. Tachycardia and decreased pulse pressure (systolic-diastolic) are the earliest reliable signs of shock.

B. Sources of hemorrhage.

1. There are only five locations of blood loss that can result in HS.

a. Thorax.

i. Hemothorax (blood in pleural cavity: 1,500 to 2,000 mL).

ii. Diagnosis by chest radiograph, trauma-room ultrasound, or computed tomography (CT) scan.

iii. Ninety percent of thoracic injuries can be treated with thoracostomy tube alone: evacuating the blood and reexpanding the lung (tamponading the bleeding source).

b. Abdomen.

i. Usually due to liver, spleen injury, or tears in the bowel mesentery.

ii. Diagnosis by ultrasound (FAST exam), CT scan, or diagnostic peritoneal lavage.

iii. Physical examination is not adequate to exclude bleeding in the abdomen.

iv. Significant injuries (bowel rupture) and hemoperitoneum may be present with a normal abdominal examination.

c. Pelvis and retroperitoneum.

i. Exsanguination can result from pelvic fractures, especially posterior fractures.

ii. Renal or major vascular injuries (pelvic veins/arteries) can result in significant retroperitoneal blood loss.

iii. CT scan (with IV contrast) best exam for retroperitoneal hemorrhage from pelvic fracture, renal injury.

d. Multiple long bone fractures.

i. Can lose up to 1,500 mL of blood in each thigh from femur fractures.


ii. Can lose up to 750 mL of blood from humerus or tibia fracture.

iii. Diagnosis by radiography and physical exam.

e. External sites.

i. Bleeding from scalp lacerations, deep soft tissue wounds, major vascular injuries, and open fractures can all result in HS.

ii. Diagnosis by history (from scene) and physical examination of all wounds.

iii. Wounds should be carefully explored and never blindly probed (to avoid dislodging a hemostatic clot and rebleeding).

iv. Exsanguination from an external wound is best controlled with point pressure or tourniquet and then exploration in the operating room.

2. Intracranial bleeding or brain injuries do not cause shock unless so severe that brain death is imminent and hormonal imbalance has occurred.

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Jun 11, 2016 | Posted by in CRITICAL CARE | Comments Off on Hemorrhagic Shock and Resuscitation

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