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Distributive Shock
Author: Klaus-Dieter Lessnau, MD, FCCP; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM
more...

Updated: Oct 08, 2015

Background
Distributive shock results from excessive vasodilation and the impaired distribution of
blood flow. Septic shock is the most common form of distributive shock and is
characterized by considerable mortality (treated, around 30%; untreated, probably
>80%). In the United States, this is the leading cause of noncardiac death in intensive
care units (ICUs). (See Pathophysiology, Etiology, Epidemiology, and Prognosis.)

Other causes of distributive shock include systemic inflammatory response syndrome

(SIRS) due to noninfectious inflammatory conditions such as burns and pancreatitis;

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toxic shock syndrome (TSS); anaphylaxis; reactions to drugs or toxins, including

insect bites, transfusion reaction, and heavy metal poisoning; addisonian crisis;
hepatic insufficiency; and neurogenic shock due to brain or spinal cord injury. (See
Pathophysiology and Etiology.)

Types of shock

Shock is a clinical syndrome characterized by inadequate tissue perfusion that results

in end-organ dysfunction. It can be divided into the following 4 categories:

Distributive shock (vasodilation), which is a hyperdynamic process

Cardiogenic shock (pump failure)
Hypovolemic shock (intravascular volume loss)
Obstructive shock (physical obstruction of blood circulation and inadequate
blood oxygenation)

Systemic inflammatory response syndrome

The American College of Chest Physicians/Society of Critical Care Medicine

(ACCP/SCCM) Consensus Conference Committee defined SIRS as the presence of
at least 2 of the following 4 criteria (see Presentation)[1] :

Core temperature of higher than 38°C (100.0°F) or lower than 36°C (96.8°F)
Heart rate of more than 90 beats per minute
Respiratory rate of more than 20 breaths per minute or arterial carbon dioxide
tension (PaCO 2) less than 32mm Hg
White blood cell (WBC) count of more than 12,000/µL, less than 4,000/µL, or
more than 10% immature (band) forms

The clinical suspicion of systemic inflammatory response syndrome by an

experienced clinician is of utmost importance.

Patient education

For patient education information, see Shock and Cardiopulmonary Resuscitation

(CPR).

Pathophysiology
In distributive shock, the inadequate tissue perfusion is caused by loss of the normal
responses of vascular smooth muscle to vasoconstrictive agents coupled with a
direct vasodilating effect. The net result in a fluid-resuscitated patient is a
hyperdynamic, hypotensive state associated with increased mixed venous O2
saturation; however, evidence of tissue ischemia as manifest by an increased serum
lactate, presumably due to intraorgan functional shunts.

Early septic shock (warm or hyperdynamic) causes reduced diastolic blood pressure;
widened pulse pressure; flushed, warm extremities; and brisk capillary refill from
peripheral vasodilation, with a compensatory increase in cardiac output. In late septic
shock (cold or hypodynamic), myocardial contractility combines with peripheral
vascular paralysis to induce a pressure-dependent reduction in organ perfusion. The
result is hypoperfusion of critical organs such as the heart, brain, and liver.

The hemodynamic derangements observed in septic shock and SIRS are due to a
complicated cascade of inflammatory mediators. Inflammatory mediators are
released in response to any of a number of factors, such as infection, inflammation,
or tissue injury. For example, bacterial products such as endotoxin activate the host
inflammatory response, leading to increased pro-inflammatory cytokines (eg, tumor
necrosis factor (TNF), interleukin (IL) –1, and IL-6. Toll-like receptors are thought to
play a critical role in responding to pathogens as well as in the excessive inflammatory
response that characterizes distributive shock; these receptors are considered
possible drug targets.

Cytokines and phospholipid-derived mediators act synergistically to produce the

complex alterations in vasculature (eg, increased microvascular permeability,
impaired microvascular response to endogenous vasoconstrictors such as
norepinephrine) and myocardial function (direct inhibition of myocyte function), which
leads to maldistribution of blood flow and hypoxia. Hypoxia also induces the
upregulation of enzymes that create nitric oxide, a potent vasodilator, thereby further
exacerbating hypoperfusion.

The coagulation cascade is also affected in septic shock. Activated monocytes and
endothelial cells are sources of tissue factors that activate the coagulation cascade;
cytokines, such as IL-6, also play a role. The coagulation response is broadly
disrupted, including impairment of antithrombin and fibrinolysis. Thrombin generated
as part of the inflammatory response can trigger disseminated intravascular
coagulation (DIC). DIC is found in 25-50% of patients with sepsis and is a significant
risk factor for mortality.[2, 3]

During distributive shock, patients are at risk for diverse organ system dysfunction that
may progress to multiple organ failure (MOF). Mortality from severe sepsis increases
markedly with the duration of sepsis and the number of organs failing.

In distributive shock due to anaphylaxis, decreased SVR is due primarily to massive

histamine release from mast cells after activation by antigen-bound immunoglobulin E
(IgE), as well as increased synthesis and release of prostaglandins.

Neurogenic shock is due to loss of sympathetic vascular tone from severe injury to
the nervous system.

Etiology
The most common etiology of distributive shock is sepsis. Other causes include the
following:

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SIRS due to noninfectious conditions such as pancreatitis, burns, or trauma

TSS
Anaphylaxis
Adrenal insufficiency
Reactions to drugs or toxins
Heavy metal poisoning
Hepatic insufficiency
Neurogenic shock

All of these conditions share the common characteristic of hypotension due to

decreased SVR and low effective circulating plasma volume.

Septic shock

The most common sites of infection, in decreasing order of frequency, include the
chest, abdomen, and genitourinary tract.

Septic shock is commonly caused by bacteria, although viruses, fungi, and parasites
are also implicated. Gram-positive bacteria are being isolated more, with their
numbers almost similar to those of gram-negative bacteria, which in the past were
considered to be the predominant organisms. Multidrug-resistant organisms are
increasingly common.[4]

Systemic inflammatory response syndrome

Causes of SIRS include the following:

Infection
Burns
Surgery
Trauma
Pancreatitis
Fulminant hepatic failure

Toxic shock syndrome

TSS can result from infection with Streptococcus pyogenes (group A Streptococcus)
or Staphylococcus aureus.

Adrenal insufficiency

Adrenal insufficiency can result from the following:

Destruction of adrenal glands due to autoimmune disease, infection

(tuberculosis, fungal infection, acquired immunodeficiency syndrome [AIDS]),
hemorrhage, cancer, or surgical removal
Suppression of hypothalamic-pituitary-adrenal axis by exogenous steroid,
usually with doses at 20 mg daily or higher
Hypopituitarism
Metabolic failure in hormone production due to congenital conditions or
drug-induced inhibition of synthetic enzymes (eg, metyrapone, ketoconazole)

Anaphylaxis

Anaphylaxis can develop as a result of the following:

Drugs such as penicillins and cephalosporins

Heterologous proteins such as Hymenoptera venom, foods, pollen, and blood
serum products

Epidemiology
Occurrence in the United States

Sepsis develops in more than 750,000 patients per year in the United States. Angus
and colleagues estimated that, by 2010, 1 million people per year would be
diagnosed with sepsis.[5] From 1979-2000, the incidence of sepsis increased by 9%
per year.

International occurrence

Sepsis is a common cause of death throughout the world and kills approximately
1,400 people worldwide every day.[6, 7]

Age-related demographics

Increased age correlates with increased risk of death from sepsis.

Prognosis
The mortality rate after development of septic shock is 20-80%.[8] Data suggest that
mortality due to septic shock has decreased slightly because of new therapeutic
interventions.[9] Early recognition and appropriate therapy are central to maximizing
good outcomes. Identifying patients with septic shock in the emergency department,
as opposed to identifying them outside of it, results in significantly improved mortality.
In one study, the mortality rate for emergency department-identified patients was
27.7%, compared with 41.1% for patients identified outside of the emergency
department.[10]

Higher mortality rates have also been associated with the following:

Advanced age
The finding of positive blood cultures

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Infection with antibiotic-resistant organisms such as Pseudomonas

aeruginosa
Elevated serum lactate levels
Impaired immune function
Alcohol use
Poor functional status prior to the onset of sepsis.

Mortality rates associated with other forms of distributive shock are not well
documented.

Complications

Duration of delirium is an independent predictor of long-term cognitive impairment. At

3-month and 12-month follow-up, as many as 79% and 71% of patients have
cognitive impairment. About one third remain severely impaired.[11, 12, 13]

Clinical Presentation

Contributor Information and Disclosures

Author
Klaus-Dieter Lessnau, MD, FCCP Clinical Associate Professor of Medicine, New York University School of
Medicine; Medical Director, Pulmonary Physiology Laboratory; Director of Research in Pulmonary Medicine,
Department of Medicine, Section of Pulmonary Medicine, Lenox Hill Hospital

Klaus-Dieter Lessnau, MD, FCCP is a member of the following medical societies: American College of Chest
Physicians, American College of Physicians, American Medical Association, American Thoracic Society, Society of
Critical Care Medicine

Disclosure: Nothing to disclose.

Coauthor(s)
Ruben Peralta, MD, FACS Professor of Surgery, Anesthesia and Emergency Medicine, Senior Medical Advisor,
Board of Directors, Program Chief of Trauma, Emergency and Critical Care, Consulting Staff, Professor Juan
Bosch Trauma Hospital, Dominican Republic

Ruben Peralta, MD, FACS is a member of the following medical societies: American Association of Blood Banks,
American College of Surgeons, American Medical Association, Association for Academic Surgery, Massachusetts
Medical Society, Society of Critical Care Medicine, Society of Laparoendoscopic Surgeons, Eastern Association
for the Surgery of Trauma, American College of Healthcare Executives

Disclosure: Nothing to disclose.

Chief Editor
Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM Professor of Critical Care Medicine, Bioengineering,
Cardiovascular Disease, Clinical and Translational Science and Anesthesiology, Vice-Chair of Academic Affairs,
Department of Critical Care Medicine, University of Pittsburgh Medical Center, University of Pittsburgh School of
Medicine

Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM is a member of the following medical societies: American
College of Chest Physicians, Association of University Anesthetists, European Society of Intensive Care Medicine,
American College of Critical Care Medicine, American Heart Association, American Thoracic Society, Shock
Society, Society of Critical Care Medicine

Disclosure: Received income in an amount equal to or greater than $250 from: Masimo<br/>Received honoraria
from LiDCO Ltd for consulting; Received intellectual property rights from iNTELOMED for board membership;
Received honoraria from Edwards Lifesciences for consulting; Received honoraria from Masimo, Inc for board
membership.

Additional Contributors
Lalit K Kanaparthi, MD Attending Physician, North Florida Lung Associates

Lalit K Kanaparthi, MD is a member of the following medical societies: American College of Chest Physicians,
American Medical Association, American Thoracic Society

Disclosure: Nothing to disclose.

Acknowledgements
Cory Franklin, MD Professor, Department of Medicine, Rosalind Franklin University of Medicine and Science;
Director, Division of Critical Care Medicine, Cook County Hospital

Cory Franklin, MD is a member of the following medical societies: New York Academy of Sciences and Society of
Critical Care Medicine

Disclosure: Nothing to disclose.

Sarah C Langenfeld, MD Assistant Professor, Department of Psychiatry, University of Massachusetts Medical

School; Attending Psychiatrist, Community HealthLink

Sarah Langenfeld, MD is a member of the following medical societies: American Medical Association, American
Psychiatric Association, and Massachusetts Medical Society

Disclosure: Nothing to disclose.

Scott P Neeley, MD Medical Director, Intensive Care Unit, St Alexius Medical Center

9 of 12 18/10/2016 22:21
Distributive Shock: Background, Pathophysiology, Etiology http://emedicine.medscape.com/article/168689-overview#showall

Scott P Neeley, MD is a member of the following medical societies: American College of Chest Physicians,
American College of Physician Executives, American College of Physicians, American Thoracic Society, Phi Beta
Kappa, and Sigma Xi

Disclosure: Nothing to disclose.

Daniel R Ouellette, MD, FCCP Associate Professor of Medicine, Wayne State University School of Medicine;
Consulting Staff, Pulmonary Disease and Critical Care Medicine Service, Henry Ford Health System

Daniel R Ouellette, MD, FCCP is a member of the following medical societies: American College of Chest
Physicians and American Thoracic Society

Disclosure: Nothing to disclose.

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

Disclosure: Medscape Salary Employment

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