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Distributive Shock Clinical Presentation

  • Author: Klaus-Dieter Lessnau, MD, FCCP; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM  more...
Updated: Oct 08, 2015


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.

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 be another cause of distributive shock; expect symptoms of abdominal pain that radiate to the back, as well as nausea and vomiting. Burns also have been described as a cause of distributive shock.

Adrenal insufficiency

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 patients infected with the human immunodeficiency virus (HIV), although this incidence varies with the criteria used to diagnose adrenal insufficiency.[14]


Physical Examination

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 (101°F)
  • Hypothermia - Core body temperate less than 36°C (96.8°F)
  • Pulse oximetry - Relative hypoxemia
  • Decreased urine output

Clinical symptoms of the underlying infections found in distributive shock include the following:

  • Pneumonia - Dullness to percussion, rhonchi, crackles, bronchial breath sounds
  • Urinary tract infection - Costovertebral angle tenderness, suprapubic tenderness, dysuria and 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 and ulceration, desquamating rash, areas of subcutaneous necrosis

Anaphylaxis is characterized by the following clinical symptoms:

  • Respiratory distress
  • Wheezing
  • Urticarial rash
  • Angioedema

TSS is characterized by the following clinical symptoms:

  • 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. Occasionally, it can progress explosively within hours.

Adrenal insufficiency is characterized by the following clinical symptoms:

  • 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.
Contributor Information and Disclosures

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.


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.


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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An 8-year-old boy developed septic shock secondary to Blastomycosis pneumonia. Fungal infections are a rare cause of septic shock.
A 28-year-old woman who was a previous intravenous drug user (human immunodeficiency virus [HIV] status: negative) developed septic shock secondary to bilateral pneumococcal pneumonia.
Microcirculatory abnormalities in distributive shock. Each image represents a venule (large, curved tube) and 2 capillaries (smaller tubes) and demonstrates the 2 main capillary flow patterns found in each class of microcirculatory abnormality, as they occur in distributive shock. This classification system was introduced by Elbers and Ince. Elbers P, Ince C. Bench-to-bedside review: mechanisms of critical illness—classifying microcirculatory flow abnormalities in distributive shock. Crit Care. July 19 2006;10(4):221.
Table 1. Pulmonary Artery Catheter Findings in Common Shock States
Diagnosis Pulmonary Capillary Wedge Pressure Cardiac Output
Cardiogenic shock* Increased Decreased
Extracardiac obstructive shock

1. Pericardial tamponade†

2. Pulmonary embolism


Normal or decreased



Hypovolemic shock Decreased Decreased
Distributive shock

1. Septic shock

2. Anaphylactic shock

Normal or decreased

Normal or decreased

Increased or normal

Increased or normal

*In cardiogenic shock due to a mechanical defect, such as mitral regurgitation, forward cardiac output is reduced, although the measured cardiac output may be unreliable. Large V waves are commonly observed in the pulmonary capillary wedge tracing in mitral regurgitation.

†The hallmark finding is equalization of right atrial mean, right ventricular end-diastolic, pulmonary artery (PA) end-diastolic, and pulmonary capillary wedge pressures.

Table 2. Vasoactive Drugs in Sepsis and the Usual Hemodynamic Responses
Drug Dose Principal Mechanism Cardiac Output Blood Pressure SVR
Inotropic agents
Dobutamine 2-20 mcg/kg/min Beta 1 ++ + +

(low dose)

5-10 mcg/kg/min Beta 1, dopamine ++ + +
Epinephrine (low dose) 0.06-0.20 mcg/kg/min Beta 1, beta 2 >alpha ++ + +
Inotropic agents and vasoconstrictors
Dopamine (high dose) >10 mcg/kg/min Alpha, beta 1, dopamine ++ ++ +

(high dose)

0.21-0.42 mcg/kg/min Alpha >beta 1, beta 2 ++ ++ +
Norepinephrine 0.02-0.25 mcg/kg/min Alpha >beta 1, beta 2 + ++ ++
Phenylephrine 0.2-2.5 mcg/kg/min Alpha + ++ ++
Vasopressin 0.10-0.40 U/min V1 receptor + + ++

(very low dose)

1-4 mcg/kg/min Dopamine +/- +/- -
Milrinone 0.4-0.6 mcg/kg/min after loading dose; 50 mcg/kg bolus over 5 min Phosphodiesterase inhibitor + +/- -
Alpha and beta refer to agonist activity at these adrenergic receptor sites.

Beta 1-adrenergic effects are inotropic and increase contractility.

Beta 2-adrenergic effects are chronotropic.[51]

Table 3. Empiric Antimicrobial Therapy in Septic Shock Based on Suspected Site of Infection
Suspected Source Recommended Antibiotic Therapy Alternative Therapy
No source evident in a healthy host Third-generation cephalosporin, eg, ceftriaxone 2 g IV q12h, ceftizoxime, ceftazidime Nafcillin and aminoglycoside, imipenem, piperacillin/tazobactam
No source evident in an immunocompromised host Ceftazidime 2 g IV q8h plus aminoglycoside Imipenem or piperacillin/tazobactam plus aminoglycoside
No source evident in a user of intravenous drugs Nafcillin 2 g IV q4h plus aminoglycoside Vancomycin plus aminoglycoside, ceftazidime, imipenem, or piperacillin/tazobactam
Bacterial pneumonia, community acquired Ceftriaxone 2 g IV q12-24 h plus macrolide Levofloxacin 750mg IV q24h, cotrimoxazole or imipenem plus macrolide
Bacterial pneumonia, hospital acquired Piperacillin/tazobactam 4.5 g IV q6h plus aminoglycoside, plus levofloxacin 750 mg IV q24h Imipenem plus aminoglycoside, plus macrolide
Urinary tract infection Ampicillin 2 g IV q4h plus aminoglycoside Fluoroquinolone or third-generation cephalosporin plus aminoglycoside
Mixed aerobic and anaerobic abdominal sepsis, aspiration pneumonia, pelvic infection, and necrotizing cellulitis Third-generation cephalosporin or ampicillin 2 g IV q4h plus aminoglycoside plus clindamycin 600 mg IV q8h or metronidazole 500 mg IV q6h Fluoroquinolone plus clindamycin, imipenem, piperacillin/tazobactam
Meningitis Ceftriaxone 2 g IV q12h plus vancomycin Meropenem plus vancomycin, chloramphenicol plus cotrimoxazole plus vancomycin
Cellulitis/erysipelas Nafcillin 2 g IV q4h Cefazolin, vancomycin, clindamycin
Toxic shock syndrome (TSS) or streptococcal necrotizing fasciitis Clindamycin 600 mg IV q8h Cephalosporin, vancomycin, nafcillin
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