Distributive Shock Clinical Presentation

  • Author: Lalit K Kanaparthi, MD; Chief Editor: Michael R Pinsky, MD, CM, FCCP, FCCM   more...
 
Updated: May 14, 2012
 

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.

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]

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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.
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Contributor Information and Disclosures
Author

Lalit 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, 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 Thoracic Society, and 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 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, and Society of Laparoendoscopic Surgeons

Disclosure: Nothing to disclose.

Chief Editor

Michael R Pinsky, MD, CM, FCCP, FCCM  Professor of Critical Care Medicine, Bioengineering, Cardiovascular Disease 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, FCCP, FCCM 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, European Society of Intensive Care Medicine, 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

Additional Contributors

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
DiagnosisPulmonary Capillary Wedge PressureCardiac Output
Cardiogenic shock*IncreasedDecreased
Extracardiac obstructive shock



1. Pericardial tamponade†



2. Pulmonary embolism



Increased



Normal or decreased



Decreased



Decreased



Hypovolemic shockDecreasedDecreased
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
DrugDosePrincipal MechanismCardiac OutputBlood PressureSVR
Inotropic agents
Dobutamine2-20 mcg/kg/minBeta 1++++
Dopamine



(low dose)



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



(high dose)



0.21-0.42 mcg/kg/minAlpha >beta 1, beta 2+++++
Norepinephrine0.02-0.25 mcg/kg/minAlpha >beta 1, beta 2+++++
Vasoconstrictors
Phenylephrine0.2-2.5 mcg/kg/minAlpha+++++
Vasopressin0.10-0.40 U/minV1 receptor++++
Vasodilators
Dopamine



(very low dose)



1-4 mcg/kg/minDopamine+/-+/--
Milrinone0.4-0.6 mcg/kg/min after loading dose; 50 mcg/kg bolus over 5 minPhosphodiesterase 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.[47]



Table 3. Empiric Antimicrobial Therapy in Septic Shock Based on Suspected Site of Infection
Suspected SourceRecommended Antibiotic TherapyAlternative Therapy
No source evident in a healthy hostThird-generation cephalosporin, eg, ceftriaxone 2 g IV q12h, ceftizoxime, ceftazidimeNafcillin and aminoglycoside, imipenem, piperacillin/tazobactam
No source evident in an immunocompromised hostCeftazidime 2 g IV q8h plus aminoglycosideImipenem or piperacillin/tazobactam plus aminoglycoside
No source evident in a user of intravenous drugsNafcillin 2 g IV q4h plus aminoglycosideVancomycin plus aminoglycoside, ceftazidime, imipenem, or piperacillin/tazobactam
Bacterial pneumonia, community acquiredCeftriaxone 2 g IV q12-24 h plus macrolideLevofloxacin 750mg IV q24h, cotrimoxazole or imipenem plus macrolide
Bacterial pneumonia, hospital acquiredPiperacillin/tazobactam 4.5 g IV q6h plus aminoglycoside, plus levofloxacin 750 mg IV q24hImipenem plus aminoglycoside, plus macrolide
Urinary tract infectionAmpicillin 2 g IV q4h plus aminoglycosideFluoroquinolone or third-generation cephalosporin plus aminoglycoside
Mixed aerobic and anaerobic abdominal sepsis, aspiration pneumonia, pelvic infection, and necrotizing cellulitisThird-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
MeningitisCeftriaxone 2 g IV q12h plus vancomycinMeropenem plus vancomycin, chloramphenicol plus cotrimoxazole plus vancomycin
Cellulitis/erysipelasNafcillin 2 g IV q4hCefazolin, vancomycin, clindamycin
Toxic shock syndrome (TSS) or streptococcal necrotizing fasciitisClindamycin 600 mg IV q8hCephalosporin, vancomycin, nafcillin
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