Hemorrhagic Shock: Practice Essentials, Pathophysiology, Epidemiology (original) (raw)

Overview

Practice Essentials

Hemorrhagic shock is a condition of reduced tissue perfusion, resulting in the inadequate delivery of oxygen and nutrients that are necessary for cellular function. Whenever cellular oxygen demand outweighs supply, both the cell and the organism are in a state of shock.

On a multicellular level, the definition of shock becomes more difficult because not all tissues and organs will experience the same amount of oxygen imbalance for a given clinical disturbance. Clinicians struggle daily to adequately define and monitor oxygen utilization on the cellular level and to correlate this physiology to useful clinical parameters and diagnostic tests.

The 4 classes of shock, as proposed by Alfred Blalock, are as follows [1, 2] :

Hypovolemic shock, the most common type, results from a loss of circulating blood volume from clinical etiologies, such as penetrating and blunt trauma, gastrointestinal bleeding, and obstetrical bleeding. (See the image below.) Humans are able to compensate for a significant hemorrhage through various neural and hormonal mechanisms. Modern advances in trauma care allow patients to survive when these adaptive compensatory mechanisms become overwhelmed.

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.

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Pathophysiology

Well-described responses to acute loss of circulating volume exist. Teleologically, these responses act to systematically divert circulating volume away from nonvital organ systems so that blood volume may be conserved for vital organ function. Acute hemorrhage causes a decreased cardiac output and decreased pulse pressure. These changes are sensed by baroreceptors in the aortic arch and atrium. With a decrease in the circulating volume, neural reflexes cause an increased sympathetic outflow to the heart and other organs. The response is an increase in heart rate, vasoconstriction, and redistribution of blood flow away from certain nonvital organs, such as the skin, gastrointestinal tract, and kidneys.

Concurrently, a multisystem hormonal response to acute hemorrhage occurs. Corticotropin-releasing hormone is stimulated directly. This eventually leads to glucocorticoid and beta-endorphin release. Vasopressin from the posterior pituitary is released, causing water retention at the distal tubules. Renin is released by the juxtamedullary complex in response to decreased mean arterial pressure, leading to increased aldosterone levels and eventually to sodium and water resorption. Hyperglycemia commonly is associated with acute hemorrhage. This is due to a glucagon and growth hormone–induced increase in gluconeogenesis and glycogenolysis. Circulating catecholamines relatively inhibit insulin release and activity, leading to increased plasma glucose.

In addition to these global changes, many organ-specific responses occur. The brain has remarkable autoregulation that keeps cerebral blood flow constant over a wide range of systemic mean arterial blood pressures. The kidneys can tolerate a 90% decrease in total blood flow for short periods of time. With significant decreases in circulatory volume, intestinal blood flow is dramatically reduced by splanchnic vasoconstriction. Early and appropriate resuscitation may avert damage to individual organs as adaptive mechanisms act to preserve the organism.

Etiology

Hemorrhagic shock is caused by the loss of both circulating blood volume and oxygen-carrying capacity. The most common clinical etiologies are penetrating and blunt trauma, gastrointestinal bleeding, and obstetrical bleeding.

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Epidemiology

United States statistics

Hemorrhagic shock is the leading cause of preventable death in patients with traumatic injury. Most of the potentially preventable deaths after trauma are related to hemorrhage and occur early after injury, with the greatest number of deaths occurring before the patient arrives at the hospital. [3, 4]

Hemorrhagic shock is tolerated differently, depending on the preexisting physiologic state and, to some extent, the age of the patient. Very young and very old people are more prone to early decompensation after loss of circulating volume.

Pediatric patients have smaller total blood volumes and, therefore, are at risk to lose a proportionately greater percentage of blood on an equivalent-volume basis during exsanguination compared to adults. The kidneys of children younger than 2 years are not mature; they have a blunted ability to concentrate solute. Younger children cannot conserve circulating volume as effectively as older children. Also, the body surface area is increased relative to the weight, allowing for rapid heat loss and early hypothermia, possibly leading to coagulopathy.

Elderly people may have both altered physiology and preexisting medical conditions that may severely impair their ability to compensate for acute blood loss. Atherosclerosis and decreased elastin cause arterial vessels to be less compliant, leading to blunted vascular compensation, decreased cardiac arteriolar vasodilation, and angina or infarction when myocardial oxygen demand is increased. Older patients are less able to mount a tachycardia in response to decreased stoke volume because of decreased beta-adrenergic receptors in the heart and a decreased effective volume of pacing myocytes within the sinoatrial node. Also, these patients frequently are treated with a variety of cardiotropic medications that may blunt the normal physiological response to shock. These include beta-adrenergic blockers, nitroglycerin, calcium channel blockers, and antiarrhythmics.

The kidneys also undergo age-related atrophy, and many older patients have significantly decreased creatinine clearance in the presence of near-normal serum creatinine. Concentrating ability may be impaired by a relative insensitivity to antidiuretic hormone. These changes in the heart, vessels, and kidneys can lead to early decompensation after blood loss. All of these factors in concert with comorbid conditions make management of elderly patients with hemorrhage quite challenging.

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Prognosis

Prognosis is related to the ability to be resuscitated from shock, as well as the underlying illness or injury, not the presentation of hemorrhagic shock.

Complications

The primary complication is death.

The entire spectrum of organ failures may be the sequelae of resuscitated hemorrhagic shock.

The cascade of systemic inflammatory response syndrome (SIRS) progressing to multiple organ failure syndrome (as described by the late Roger Bone, MD) complicates the cases of approximately 30-70% of patients who present with hemorrhagic shock and survive their initial resuscitation.

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Author

John Udeani, MD, FAAEM Assistant Professor, Department of Emergency Medicine, Charles Drew University of Medicine and Science, University of California, Los Angeles, David Geffen School of Medicine

John Udeani, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians

Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment.

Chief Editor

John Geibel, MD, MSc, DSc, AGAF Vice Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, Professor, Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director of Surgical Research, Department of Surgery, Yale-New Haven Hospital; American Gastroenterological Association Fellow; Fellow of the Royal Society of Medicine

John Geibel, MD, MSc, DSc, AGAF is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, Society for Surgery of the Alimentary Tract

Disclosure: Nothing to disclose.

Additional Contributors

Lewis J Kaplan, MD, FACS, FCCM, FCCP Professor of Surgery, Division of Trauma, Surgical Critical Care, and Emergency Surgery, Department of Surgery, Perelman School of Medicine at the University of Pennsylvania; Section Chief, Surgical Critical Care, Philadelphia Veterans Affairs Medical Center

Lewis J Kaplan, MD, FACS, FCCM, FCCP is a member of the following medical societies: American Association for the Surgery of Trauma, American College of Surgeons, Association for Academic Surgery, Association for Surgical Education, Connecticut State Medical Society, Eastern Association for the Surgery of Trauma, International Trauma Anesthesia and Critical Care Society, Society for the Advancement of Blood Management, Society of Critical Care Medicine, Surgical Infection Society

Disclosure: Nothing to disclose.