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Shock, Distributive

Author: Lalit K Kanaparthi, MD, Fellow in Pulmonary Medicine, Lenox Hill Hospital
Coauthor(s): 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; 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; Sarah Guzofski, MD, Staff Physician, Department of Psychiatry, University of Massachusetts Medical School; Scott P Neeley, MD, Medical Director, Intensive Care Unit, St Alexius Medical Center; Consulting Staff, Chest Medicine Consultants
Contributor Information and Disclosures

Updated: Mar 4, 2009

Introduction

Background

Shock is a clinical syndrome characterized by inadequate tissue perfusion that results in end-organ dysfunction. Shock 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 (blood vessels and heart)

This article discusses distributive shock.

Distributive shock has several causes. Septic shock is the most common form of distributive shock, with considerable mortality. In the United States, this is the leading cause of noncardiac death in intensive care units (ICUs). Other causes of distributive shock include systemic inflammatory response syndrome (SIRS) due to noninfectious inflammatory conditions like burns & pancreatitis; toxic shock syndrome (TSS); anaphylaxis; drug or toxin reactions, including insect bites, transfusion reaction, and heavy metal poisoning; Addisonian crisis; hepatic insufficiency; and neurogenic shock due to brain or spinal cord injury.

Pathophysiology

In distributive shock, the inadequate tissue perfusion is caused by decreased systemic vascular resistance (SVR) and a high cardiac output.  The early changes are primarily characterized by the evolution of changes in contractility and dilation of peripheral small vessels and the impact of resuscitation efforts. Early septic shock (warm or hyperdynamic) causes reduced diastolic blood, 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)-1b, 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 a possible drug targets.

Cytokines and phospholipids-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 American College of Chest Physicians/Society of Critical Care Medicine (ACCP/SCCM) Consensus Conference Committee defined the following 4 clinical subcategories of systemic inflammatory response:1

  • Systemic inflammatory response with 2 or more of the following:
    • A core temperature of higher than 38° C or lower than 36° C
    • A heart rate of more than 90 beats per minute; respiratory rate of more than 20 breaths per minute; WBC count of more than 12,000 103/µL, less than 4,000 103/µL, or more than 10% bands.
  • Systemic inflammatory response with sepsis - Meets criteria for SIRS, source of infection is presumed or confirmed
  • Systemic inflammatory response with severe sepsis - Sepsis plus hypoperfusion and dysfunction or organs, as evidenced by hypotension (systolic blood pressure of more than 90 mm Hg or a decrease of more than 40 mm Hg from baseline), lactic acidosis, oliguria, a change in mental status
  • Systemic inflammatory response with septic shock - Severe sepsis in a patient who does not respond to intravenous fluid resuscitation and vasopressors   

The coagulation cascade is also affected.  In septic shock, activated monocytes and endothelial cells are sources of tissue factor that activates 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 nervous system.

Frequency

United States

Sepsis develops in more than 750,000 patients per year. Angus and colleagues have estimated that, by 2010, 1 million people per year will be diagnosed with sepsis.4 From 1979-2000, the incidence of sepsis has increased by 9% per year.

International

Sepsis is a common cause of death throughout the world and kills approximately 1,400 people worldwide every day.5,6

Mortality/Morbidity

  • The mortality rate after development of septic shock is 20-80%.7 Recent data suggest that mortality due to septic shock has decreased slightly from new therapeutic interventions.8
  • Higher mortality rates have been associated with advanced age, the finding of positive blood cultures, infection with antibiotic-resistant organisms such as Pseudomonas aeruginosa, elevated serum lactate levels, impaired immune function, alcohol use, and poor functional status prior to the onset of sepsis.
  • Mortality rates associated with other forms of distributive shock are not well documented.

Age

Increased age correlates with increased risk of death from sepsis.

Clinical

History

  • Patients with shock frequently present with tachycardia, tachypnea, hypotension, altered mental status changes, and oliguria.
  • Patients with septic shock or systemic inflammatory response syndrome (SIRS) may have prior symptoms that suggest infection or inflammation of the respiratory tract, urinary tract, or abdominal cavity.
  • Septic shock occurs frequently in hospitalized patients with risk factors such as indwelling catheters or venous access devices, recent surgery, or immunosuppressive therapy.
  • Patients with anaphylaxis commonly have recent iatrogenic (drug) or accidental (bee sting) exposure to an allergen and coexisting respiratory symptoms, such as wheezing and dyspnea, pruritus, or urticaria.
  • Adrenal insufficiency as a cause of shock should be considered in any patient with hypotension who lacks signs of infection, cardiovascular disease, or hypovolemia.
    • Long-term treatment with corticosteroids may result in inadequate response of the adrenal axis to stress, such as infection, surgery, or trauma, and subsequent onset or worsening of shock.
    • If the clinical picture is consistent with adrenal insufficiency in a person without this diagnosis, consider that this could be the first presentation of this disorder.
    • There is a high incidence of adrenal insufficiency in critically ill HIV-infected patients that varies with the criteria used to diagnose adrenal insufficiency.9
    • Staphylococcal toxic shock syndrome (TSS) is still observed most commonly in women who are menstruating, but it is also associated with recent soft tissue injury, cutaneous infections, postpartum and cesarean delivery, wound infections, pharyngitis and focal staphylococcal infections, such as abscess, empyema, pneumonia, and osteomyelitis. Patients often have a history of influenzalike illness (fever, arthralgias, myalgias) and a desquamating rash.
    • Pancreatitis may also be a cause of distributive shock; expect symptoms of abdominal pain that radiate to the back and nausea and vomiting.
    • Burns have been described as a cause of distributive shock.

Physical

  • Cardinal features of distributive shock include the following:
    • Change in mental status
    • Heart rate - Greater than 90 beats per minute (Note that heart rate elevation is not evident if the patient is on a beta-blocker.)
    • Hypotension - Systolic blood pressure less than 90 mm Hg or a reduction of 40 mm Hg from baseline
    • Respiratory rate - Greater than 20 breaths per minute
    • Extremities - Frequently warm with bounding pulses and increased pulse pressure (systolic minus diastolic blood pressure) in early shock (Late shock may present as critical organ dysfunction.)
    • Hyperthermia - Core body temperature greater than 38.3° C or 101° F
    • Hypothermia - Core body temperate less than 36° C or 96.8° F
    • Pulse oximetry - Relative hypoxemia
    • Decreased urine output
  • Underlying infection
    • Pneumonia
      • Dullness to percussion
      • Rhonchi
      • Crackles
      • Bronchial breath sounds
    • Urinary tract infection
      • Costovertebral angle tenderness
      • Suprapubic tenderness
      • Dysuria & polyuria
    • Intra-abdominal infection or acute abdomen
      • Focal or diffuse tenderness to palpation
      • Diminished or absent bowel sounds
      • Rebound tenderness
    • Gangrene or soft tissue infection
      • Pain out of proportion to lesion
      • Skin discoloration & ulceration
      • Desquamating rash
      • Areas of subcutaneous necrosis
  • Anaphylaxis
    • Respiratory distress
    • Wheezing
    • Urticarial rash
    • Angioedema
  • Toxic shock syndrome
    • High fever
    • Diffuse rash with desquamation on the palms and soles over a subsequent 1-2 weeks
    • Hypotension (may be orthostatic) and evidence of involvement of 3 other organ systems
    • Streptococcal TSS more frequently presents with focal soft tissue inflammation and is less commonly associated with diffuse rash.
  • Adrenal insufficiency
    • Hyperpigmentation of skin, oral, vaginal, and anal mucosal membranes may be present in chronic adrenal insufficiency.
    • In acute or acute-on-chronic adrenal insufficiency brought on by physiologic stress, hypotension may be the only physical sign.

Causes

The most common etiology of distributive shock is sepsis. Other causes include SIRS due to noninfectious conditions such as pancreatitis, burns and trauma, TSS, anaphylaxis, adrenal insufficiency, drug or toxin reactions, heavy metal poisoning, hepatic insufficiency, and neurogenic shock. All these conditions share the common characteristic of hypotension due to decreased systemic vascular resistance 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 the gram-negative bacteria which in the past were considered to be the predominant organisms. Multidrug-resistant organisms are increasingly common.10
  • SIRS (see ACCP/SCCM definition in the Pathophysiology section)
    • Infection
    • Burns
    • Surgery
    • Trauma
    • Pancreatitis
    • Fulminant hepatic failure
  • Toxic shock syndrome
    • Streptococcus pyogenes (group A Streptococcus)
    • Staphylococcus aureus
  • Adrenal insufficiency
    • Destruction of adrenal glands due to autoimmune disease, infection (tuberculosis, fungal infection, AIDS), hemorrhage, cancer, or surgical removal
    • Suppression of hypothalamic-pituitary-adrenal axis by exogenous steroid
    • Hypopituitarism
    • Metabolic failure in hormone production due to congenital conditions or drug-induced inhibition of synthetic enzymes (eg, metyrapone, ketoconazole)
  • Anaphylaxis
    • Drugs such as penicillins and cephalosporins
    • Heterologous proteins such as Hymenoptera venom, foods, pollen, and blood serum products

More on Shock, Distributive

Overview: Shock, Distributive
Differential Diagnoses & Workup: Shock, Distributive
Treatment & Medication: Shock, Distributive
Follow-up: Shock, Distributive
References
[ CLOSE WINDOW ]

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Further Reading

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Keywords

distributive shock, end-organ dysfunction, hypotension, systemic vascular resistance, SVR, septic shock, systemic inflammatory response syndrome, SIRS, toxic shock syndrome, TSS, anaphylaxis, drug reactions, toxin reactions, transfusion reaction, heavy metal poisoning, addisonian crisis, hepatic insufficiency, neurogenic shock

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Contributor Information and Disclosures

Author

Lalit K Kanaparthi, MD, Fellow in 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, and American Thoracic Society
Disclosure: Nothing to disclose.

Coauthor(s)

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 Society for Artificial Internal Organs, American Thoracic Society, Physicians for Social Responsibility, and Society of Critical Care Medicine
Disclosure: sepracor Ownership interest None

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 College of Surgeons, American Medical Association, Association for Academic Surgery, Eastern Association for the Surgery of Trauma, Massachusetts Medical Society, Society of Critical Care Medicine, and Society of Laparoendoscopic Surgeons
Disclosure: Nothing to disclose.

Sarah Guzofski, MD, Staff Physician, Department of Psychiatry, University of Massachusetts Medical School
Sarah Guzofski, 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; Consulting Staff, Chest Medicine Consultants
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.

Medical Editor

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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

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: Boehringer Ingleheim Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching

CME Editor

Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians
Disclosure: Nothing to disclose.

Chief Editor

Michael R Pinsky, MD, CM, Professor of Critical Care Medicine, Bioengineering, Cardiovascular Diseases and Anesthesiology, University of Pittsburgh School of Medicine, University of Pittsburgh Medical Center
Michael R Pinsky, MD, CM is a member of the following medical societies: American College of Chest Physicians, American College of Critical Care Medicine, American Heart Association, American Thoracic Society, Association of University Anesthetists, Shock Society, and Society of Critical Care Medicine
Disclosure: LiDCO Ltd Honoraria Consulting; iNTELOMED Intellectual property rights Board membership; Edwards Lifesciences Honoraria Consulting; Applied Physiology, Ltd Honoraria Consulting; Cheetah Medical Consulting fee Consulting

 
 
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