Which conditions could be the possible causes of obstructive shock select all that apply?

Shock is a life-threatening condition that occurs when the body is not getting enough blood flow. Lack of blood flow means the cells and organs do not get enough oxygen and nutrients to function properly. Many organs can be damaged as a result. Shock requires immediate treatment and can get worse very rapidly. As many 1 in 5 people in shock will die from it.

Shock can be caused by any condition that reduces blood flow, including:

• Heart problems (such as heart attack or heart failure)
• Low blood volume (as with heavy bleeding or dehydration)
• Changes in blood vessels (as with infection or severe allergic reactions)
• Certain medicines that significantly reduce heart function or blood pressure
• Slow heart rates and changes in blood vessel tone from spinal injuries

Shock is often associated with heavy external or internal bleeding from a serious injury.

Toxic shock syndrome is an example of shock that is caused by an infection.

Take the following steps if you think a person is in shock:

• Call 911 or the local emergency number for immediate medical help.
• Check the person's airway, breathing, and circulation. If necessary, begin rescue breathing and CPR.
• Even if the person is able to breathe on their own, continue to check rate of breathing at least every 5 minutes until help arrives.
• If the person is conscious and DOES NOT have an injury to the head, leg, neck, or spine, place the person in the shock position. Lay the person on the back and elevate the legs about 12 inches (30 centimeters). DO NOT elevate the head. If raising the legs will cause pain or potential harm, leave the person lying flat.
• Give appropriate first aid for any wounds, injuries, or illnesses.
• Keep the person warm and comfortable. Loosen tight clothing.

IF THE PERSON VOMITS OR DROOLS

• Turn the person or their head to one side to prevent choking if you do not suspect an injury to the spine.
• If a spinal injury is suspected, "log roll" the person instead. To do this, keep the person's head, neck, and back in line, and roll the body and head as a unit.

In case of shock:

• DO NOT give the person anything by mouth, including anything to eat or drink.
• DO NOT move the person with a known or suspected spinal injury.
• DO NOT wait for milder shock symptoms to worsen before calling for emergency medical help.

Call 911 or the local emergency number any time a person has symptoms of shock. Stay with the person and follow the first aid steps until medical help arrives.

Learn ways to prevent heart disease, falls, injuries, dehydration, and other causes of shock. If you have a known allergy (for example, to insect bites or stings), carry an epinephrine pen. Your health care provider will teach you how and when to use it.

Angus DC. Approach to the patient with shock. In: Goldman L, Schafer AI, eds. Goldman-Cecil Medicine. 26th ed. Philadelphia, PA: Elsevier; 2020:chap 98.

Puskarich MA, Jones AE. Shock. In: Walls RM, Hockberger RS, Gausche-Hill M, eds. Rosen's Emergency Medicine: Concepts and Clinical Practice. 9th ed. Philadelphia, PA: Elsevier; 2018:chap 6.

Smith SG, Schreiber MA. Shock, electrolytes, and fluid. In: Townsend CM Jr, Beauchamp RD, Evers BM, Mattox KL, eds. Sabiston Textbook of Surgery. 21st ed. St Louis, MO: Elsevier; 2022:chap 4.

Updated by: Jesse Borke, MD, CPE, FAAEM, FACEP, Attending Physician at Kaiser Permanente, Orange County, CA. Also reviewed by David Zieve, MD, MHA, Medical Director, Brenda Conaway, Editorial Director, and the A.D.A.M. Editorial team.

Practice Essentials

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; 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 four 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 (PaCO2) less than 32 mm Hg

• White blood cell (WBC) count of more than 12,000/µL, less than 4000/µL, or more than 10% immature (band) forms

The clinical suspicion of systemic inflammatory response syndrome by an experienced clinician is of utmost importance.

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:

• 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

• 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]

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Author

Klaus-Dieter Lessnau, MD, FCCP Former 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)

Kevin Gerard G Lazo, DO Pulmonologist, Englewood Health Physician Network

Kevin Gerard G Lazo, DO is a member of the following medical societies: American College of Chest Physicians

Disclosure: Nothing to disclose.

Oki Ishikawa, MD Chief Resident Physician, Department of Internal Medicine, Lenox Hill Hospital, Northwell Health

Disclosure: Nothing to disclose.

Ruben Peralta, MD, FACS, FCCM, FCCP Deputy Trauma Medical Director, Professor and Director of Trauma, Emergency and Critical Care Fellowship Program, Senior Consultant in Surgery, Trauma, Emergency and Critical Care Medicine, Associate Director of Trauma Intensive Care Unit, Hamad General Hospital and Hamad Medical Corporation, Weill Cornell Medical College in Qatar

Ruben Peralta, MD, FACS, FCCM, FCCP 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 Medical Society, Society of Critical Care Medicine, Society of Laparoscopic and Robotic Surgeons

Disclosure: Nothing to disclose.

Chief Editor

Ali H Al-Khafaji, MD, MPH, FACP, FCCP, FCCM Professor of Critical Care Medicine, Professor of Surgery, University of Pittsburgh School of Medicine; Medical Director, Transplant Intensive Care Unit, Medical Director, ICU Telemedicine, Department of Critical Care Medicine, University of Pittsburgh Medical Center

Ali H Al-Khafaji, MD, MPH, FACP, FCCP, FCCM is a member of the following medical societies: Allegheny County Medical Society, American College of Chest Physicians, American College of Gastroenterology, American Medical Association, American Thoracic Society, British Medical Association, International Liver Transplantation Society, Royal College of Anaesthetists, Society of Critical Care Anesthesiologists, Society of Critical Care Medicine, Undersea and Hyperbaric Medical Society

Disclosure: Nothing to disclose.

Additional Contributors

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

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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