Distributive Shock. Medscape. Pinsky M

7/29/2019 Distributive Shock. Medscape. Pinsky M

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Distributive Shock

Author: Lalit K Kanaparthi, MD; Chief Editor: Michael R Pinsky, MD, CM, FCCP, FCCM more...

Updated: Feb 12, 2013

Background

Distributive shock results from excessive vasodilation and the impaired distribution of blood flow. Septic shock is themost common form of distributive shock and is characterized by considerable mortality. In the United States, this isthe 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 noninfectiousinflammatory conditions such as burns and pancreatitis; toxic shock syndrome (TSS); anaphylaxis; reactions to drugsor toxins, including insect bites, transfusion reaction, and heavy metal poisoning; addisonian crisis; hepaticinsufficiency; 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. Itcan be divided into the following 4 categories:

Distributive shock (vasodilation), which is a hyperdynamic processCardiogenic 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 38C (100.0F) or lower than 36C (96.8F)Heart rate of more than 90 beats per minuteRespiratory rate of more than 20 breaths per minute or arterial carbon dioxide tension (PaCO2) less than

32mm HgWhite blood cell (WBC) count of more than 12,000/ L, less than 4,000/ L, or more than 10% immature (band)forms

The clinical suspicion of systemic inflammatory response syndrome by an experienced clinician is also important.

Patient education

For patient education information, see Shock and Cardiopulmonary Resuscitation (CPR).

Pathophysiology

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In distributive shock, the inadequate tissue perfusion is caused by loss of the normal responses of vascular smoothmuscle to vasoconstrictive agents coupled with a direct vasodilating effect. The net result in a fluid-resuscitatedpatient 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 functionalshunts.

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

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

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 asnorepinephrine) 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. In septic shock, activated monocytes and endothelial cellsare sources of tissue factor that activates the coagulation cascade; cytokines, such as IL-6, also play a role. Thecoagulation response is broadly disrupted, including impairment of antithrombin and fibrinolysis. Thrombin generatedas part of the inflammatory response can triggerdisseminated 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 multipleorgan failure (MOF). Mortality from severe sepsis increases markedly with the duration of sepsis and the number oforgans 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 ofprostaglandins.

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:

SIRS due to noninfectious conditions such as pancreatitis, burns, or traumaTSSAnaphylaxisAdrenal insufficiencyReactions to drugs or toxins

Heavy metal poisoningHepatic insufficiencyNeurogenic shock

All of these conditions share the common characteristic of hypotension due to decreased SVR and low effectivecirculating plasma volume.

Septic shock

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

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 increasinglycommon.[4]




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Systemic inflammatory response syndrome

Causes of SIRS include the following:

InfectionBurnsSurgery

TraumaPancreatitisFulminant hepatic failure

Toxic shock syndrome

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

Adrenal insufficiency

Adrenal insufficiency can result from the following:

Destruction of adrenal glands due to autoimmune disease, infection (tuberculosis, fungal infection, acquiredimmunodeficiency syndrome [AIDS]), hemorrhage, cancer, or surgical removal

Suppression of hypothalamic-pituitary-adrenal axis by exogenous steroid, usually with doses at 20 mg daily orhigherHypopituitarismMetabolic failure in hormone production due to congenital conditions or drug-induced inhibition of syntheticenzymes (eg, metyrapone, ketoconazole)

Anaphylaxis

Anaphylaxis can develop as a result of the following:

Drugs such as penicillins and cephalosporinsHeterologous proteins such as Hymenoptera venom, foods, pollen, and blood serum products

EpidemiologyOccurrence 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 sepsisincreased 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 centralto maximizing good outcomes. Identifying patients with septic shock in the emergency department, as opposed toidentifying them outside of it, results in significantly improved mortality. In one study, the mortality rate for emergencydepartment-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 ageThe finding of positive blood culturesInfection with antibiotic-resistant organisms such as Pseudomonas aeruginosa




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Elevated serum lactate levelsImpaired immune functionAlcohol usePoor 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 are severely impaired.[11, 12, 13]

Contributor Information and DisclosuresAuthorLalit K Kanaparthi, MD Senior Fellow, Department of Pulmonary Medicine, Lenox Hill Hospital

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

Disclosure: Nothing to disclose.

Coauthor(s)Klaus-Dieter Lessnau, MD, FCCP Clinical Associate Professor of Medicine, New York University School ofMedicine; 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 ChestPhysicians,American College of Physicians,American Medical Association,American Thoracic Society, andSociety of Critical Care Medicine


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 JuanBosch Trauma Hospital, Dominican Republic

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


Chief EditorMichael R Pinsky, MD, CM, FCCP, FCCM Professor of Critical Care Medicine, Bioengineering, CardiovascularDisease and Anesthesiology, Vice-Chair of Academic Affairs, Department of Critical Care Medicine, University ofPittsburgh Medical Center, University of Pittsburgh School of Medicine

Michael R Pinsky, MD, CM, FCCP, FCCM is a member of the following medical societies:American College ofChest Physicians, American College of Critical Care Medicine,American Heart Association,American Thoracic

Society, Association of University Anesthetists, European Society of Intensive Care Medicine, Shock Society, andSociety of Critical Care Medicine

Disclosure: LiDCO Ltd Honoraria Consulting; iNTELOMED Intellectual property rights Board membership;Edwards Lifesciences Honoraria Consulting

Additional ContributorsCory 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 ofCritical Care Medicine


Sarah C Langenfeld, MDAssistant Professor, Department of Psychiatry, University of Massachusetts MedicalSchool; Attending Psychiatrist, Community HealthLink




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


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

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


Daniel R Ouellette, MD, FCCPAssociate 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 ChestPhysicians andAmerican Thoracic Society


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

Disclosure: Medscape Salary Employment

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Distributive Shock. Medscape. Pinsky M