Septic Shock Clinical Presentation

  • Author: Michael R Pinsky, MD, CM, FCCP, FCCM; Chief Editor: Michael R Pinsky, MD, CM, FCCP, FCCM   more...
 
Updated: Oct 25, 2011
 

History

Sepsis or septic shock is systemic inflammatory response syndrome (SIRS) secondary to a documented infection (see Background). Detrimental host responses to infection occupy a continuum that ranges from sepsis to severe sepsis to septic shock and multiple organ dysfunction syndrome (MODS). The specific clinical features depend on where the patient falls on that continuum.

Symptoms of sepsis are often nonspecific and include fever, chills, rigors, fatigue, malaise, nausea, vomiting, difficulty breathing, anxiety, or confusion. These symptoms are not pathognomonic for sepsis syndromes and may be present in a wide variety of other conditions. Alternatively, typical symptoms of systemic inflammation may be absent in severe sepsis, especially in elderly individuals.

Fever is a common symptom of sepsis. The hypothalamus resets so that heat production and heat loss are balanced in favor of a higher temperature. Fever may be absent in elderly or immunosuppressed patients. An inquiry should be made about fever onset (abrupt or gradual), duration, and maximal temperature. These features have been associated with increased infectious burden and severity of illness. However, simply mounting a fever is an insensitive indicator of sepsis; in fact, hypothermia is more predictive of illness severity and death.

Chills are a secondary symptom associated with fever, which is a consequence of increased muscular activity that produces heat and raises the body temperature. Sweating occurs when the hypothalamus returns to its normal set point and senses the higher body temperature, stimulating perspiration to evaporate excess body heat.

Alteration in mental function often occurs. Mild disorientation or confusion is especially common in elderly individuals. Apprehension, anxiety, agitation, and, eventually, coma are manifestations of severe sepsis. The exact cause of metabolic encephalopathy is not known; alteration in amino acid metabolism may play a role.

Hyperventilation with respiratory alkalosis is a common feature of patients with sepsis secondary to stimulation of the medullary respiratory center by endotoxins and other inflammatory mediators.

The localizing symptoms referable to organ systems may provide useful clues to the etiology of sepsis and are as follows:

  • Head and neck infections - Severe headache, neck stiffness, altered mental status, earache, sore throat, sinus pain or tenderness, cervical or submandibular lymphadenopathy
  • Chest and pulmonary infections - Cough (especially if productive), pleuritic chest pain, dyspnea
  • Abdominal and gastrointestinal (GI) infections - Abdominal pain, nausea, vomiting, diarrhea
  • Pelvic and genitourinary infections - Pelvic or flank pain, vaginal or urethral discharge, dysuria, frequency, urgency
  • Bone and soft tissue infections - Localized limb pain or tenderness, focal erythema, edema, and swollen joint
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Physical Examination

The hallmarks of severe sepsis and septic shock are changes that occur at the microvascular and cellular level with diffuse activation of inflammatory and coagulation cascades, vasodilation and vascular maldistribution, capillary endothelial leak, and dysfunctional utilization of oxygen and nutrients at the cellular level. The challenge for the clinician is to recognize that this process is under way when it may not be clearly manifested in the vital signs or clinical examination.

The physical examination should first involve assessment of the patient’s general condition, including an assessment of airway, breathing, and circulation (ABCs) and mental status. An acutely ill, flushed, and toxic appearance is observed universally in patients with serious infections.

Examine vital signs, and observe for signs of hypoperfusion. Carefully examine the patient for evidence of localized infection. Ensure that the patient’s body temperature is measured accurately and that rectal temperatures are obtained. Oral and tympanic temperatures are not always reliable. Fever may be absent, but patients generally have tachypnea and tachycardia.

Attention should be paid to skin color and temperature. Pallor, grayish, or mottled skin are signs of poor tissue perfusion seen in septic shock. In the early stages of sepsis, cardiac output is well maintained or even increased. The vasodilation may result in warm skin, warm extremities, and normal capillary refill (warm shock). As sepsis progresses, stroke volume and cardiac output fall. The patients begin to manifest the following signs of poor perfusion: cool skin, cool extremities, and delayed capillary refill (cold shock).

Petechiae or purpura (see the image below) can be associated with disseminated intravascular coagulation (DIC) and are an ominous sign.

A 26-year-old woman developed rapidly progressive A 26-year-old woman developed rapidly progressive shock associated with purpura and signs of meningitis. The blood culture confirmed Neisseria meningitidis. The skin manifestation is characteristic of severe meningococcal infection and is called purpura fulminans.

Tachycardia is a common feature of sepsis and indicative of a systemic response to stress. Tachycardia is the physiologic mechanism of increasing cardiac output and thus increasing oxygen delivery to tissues. It indicates hypovolemia and the need for intravascular fluid repletion; however, tachycardia often persists in sepsis despite adequate fluid repletion. Tachycardia may also be a result of fever itself. Narrow pulse pressure and tachycardia are considered the earliest signs of shock.

Increased respiratory rate is a common and often underappreciated feature of sepsis. Stimulation of the medullary ventilatory center by endotoxins and other inflammatory mediators has been proposed as a cause. As tissue hypoperfusion ensues, the respiratory rate also increases in order to compensate for metabolic acidosis. The patient often feels short of breath or appears mildly anxious.

Notably, tachypnea is the most predictive of the SIRS criteria for adverse outcome. This is likely because tachypnea is also an indicator of pulmonary organ dysfunction and a feature commonly associated with pneumonia and acute respiratory distress syndrome (ARDS), both of which are associated with increased mortality in sepsis.

Altered mental status is another common feature. It is considered a sign of organ dysfunction and is associated with increased mortality. Mild disorientation or confusion is especially common in elderly individuals. Other manifestations include apprehension, anxiety, and agitation. Profound cases may involve obtundation or comatose states. The cause of these mental status abnormalities is not entirely understood, but, in addition to cerebral hypoperfusion, altered amino acid metabolism has been proposed as a causative factor.

In septic shock, it is important to identify any potential source of infection. This is particularly important in cases where a site of infection can be removed or drained, as in certain intra-abdominal infections, soft tissue abscesses and fasciitis, or perirectal abscesses. The following physical signs help to localize the source of an infection:

  • Central nervous system (CNS) infection - Profound depression in mental status, signs of meningismus (neck stiffness)
  • Head and neck infections - Inflamed or swollen tympanic membranes, sinus tenderness, nasal congestion or exudate, pharyngeal erythema and exudates, inspiratory stridor, cervical lymphadenopathy
  • Chest and pulmonary infections - Dullness on percussion, bronchial breath sounds, localized rales, any evidence of consolidation
  • Cardiac infections - Any new murmur, especially in patients with a history of intravenous (IV) drug use
  • Abdominal and GI infections - Abdominal distention, localized tenderness, guarding or rebound tenderness, rectal tenderness or swelling
  • Pelvic and genitourinary infections - Costovertebral angle tenderness, pelvic tenderness, pain on cervical motion, adnexal tenderness or masses, cervical discharge
  • Bone and soft tissue infections - Focal erythema, edema, tenderness, crepitus in necrotizing infections, fluctuance, pain with joint range of motion, joint effusions and associated warmth/erythema
  • Skin infections - Petechiae, purpura, erythema, ulceration, bullous formation, fluctuance
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Complications

Acute respiratory distress syndrome

Acute lung injury (ALI) leading to ARDS is a major complication of severe sepsis and septic shock. The incidence of ARDS is approximately 18% in patients with septic shock, and mortality rates approach 50%. ARDS also leads to prolonged intensive care unit (ICU) stays and an increased incidence of ventilator-associated pneumonia.

ALI and ARDS secondary to severe sepsis demonstrate the manifestations of underlying sepsis and the associated multiple organ dysfunction. Pulmonary manifestations include acute respiratory distress and acute respiratory failure resulting from severe hypoxemia caused by intrapulmonary shunting. Fever and leukocytosis may be present secondary to the lung inflammation.

The severity of ARDS may vary from mild lung injury to severe respiratory failure. The onset of ARDS usually is within 12-48 hours of the inciting event. The patients demonstrate severe dyspnea at rest, tachypnea, and hypoxemia; anxiety and agitation also are present.

Other complications

Acute renal failure (ARF) occurs in 40-50% of patients with septic shock. ARF complicates therapy and worsens the overall outcome. Disseminated intravascular coagulation (DIC) occurs in 40% of patients with septic shock.

Other complications of septic shock include chronic renal dysfunction, mesenteric ischemia, myocardial ischemia and dysfunction, liver failure, and other complications related to prolonged hypotension and organ dysfunction. Prolonged tissue hypoperfusion can lead to long-term neurologic and cognitive sequelae as well.[9]

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Contributor Information and Disclosures
Author

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 School of Medicine, University of Pittsburgh Medical Center

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

Coauthor(s)

Fatima Al Faresi, MD  Dermatologist, Tawam Hospital, Al Ain, UAE

Disclosure: Nothing to disclose.

Barry E Brenner, MD, PhD, FACEP  Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Daniel J Dire, MD, FACEP, FAAP, FAAEM  Clinical Professor, Department of Emergency Medicine, University of Texas Medical School at Houston; Clinical Professor, Department of Pediatrics, University of Texas Health Sciences Center San Antonio

Daniel J Dire, MD, FACEP, FAAP, FAAEM is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American Academy of Pediatrics, American College of Emergency Physicians, and Association of Military Surgeons of the US

Disclosure: Nothing to disclose.

Michael R Filbin, MD  Clinical Instructor, Department of Emergency Medicine, Massachusetts General Hospital

Michael R Filbin, MD is a member of the following medical societies: American College of Emergency Physicians, Massachusetts Medical Society, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Franklin Flowers, MD  Chief, Division of Dermatology, Professor, Department of Medicine and Otolaryngology, Affiliate Associate Professor of Pediatrics and Pathology, University of Florida College of Medicine

Franklin Flowers, MD, is a member of the following medical societies: American College of Mohs Micrographic Surgery and Cutaneous Oncology

Disclosure: Nothing to disclose.

Theodore J Gaeta, DO, MPH, FACEP  Clinical Associate Professor, Department of Emergency Medicine, Weill Cornell Medical College; Vice Chairman and Program Director of Emergency Medicine Residency Program, Department of Emergency Medicine, New York Methodist Hospital; Academic Chair, Adjunct Professor, Department of Emergency Medicine, St George's University School of Medicine

Theodore J Gaeta, DO, MPH, FACEP is a member of the following medical societies: Alliance for Clinical Education, American College of Emergency Physicians, Clerkship Directors in Emergency Medicine, Council of Emergency Medicine Residency Directors, New York Academy of Medicine, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Hassan I Galadari, MD  Assistant Professor of Dermatology, Faculty of Medicine and Health Sciences, United Arab Emirates University

Hassan I Galadari, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, American Medical Student Association/Foundation, and American Society for Dermatologic Surgery

Disclosure: Nothing to disclose.

Paul Krusinski, MD  Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal Medicine, University of Vermont College of Medicine

Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Steven Mink, MD  Head, Section of Pulmonary Medicine, Department of Internal Medicine, St Boniface Hospital; Professor of Medicine, University of Manitoba, Canada

Steven Mink, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

Mark L Plaster, MD, JD  Executive Editor, Emergency Physicians Monthly

Mark L Plaster, MD, JD is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians

Disclosure: M L Plaster Publishing Co LLC Ownership interest Management position

Sat Sharma, MD, FRCPC  Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association

Disclosure: Nothing to disclose.

Vicken Y Totten, MD, MS, FACEP, FAAFP  Assistant Professor, Case Western Reserve University School of Medicine; Director of Research, Department of Emergency Medicine, University Hospitals, Case Medical Center

Vicken Y Totten, MD, MS, FACEP, FAAFP is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Richard P Vinson, MD  Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association

Disclosure: Nothing to disclose.

Eric L Weiss, MD, DTM&H  Medical Director, Office of Service Continuity and Disaster Planning, Fellowship Director, Stanford University Medical Center Disaster Medicine Fellowship, Chairman, SUMC and LPCH Bioterrorism and Emergency Preparedness Task Force, Clinical Associate Progressor, Department of Surgery (Emergency Medicine), Stanford University Medical Center

Eric L Weiss, MD, DTM&H is a member of the following medical societies: American College of Emergency Physicians, American College of Occupational and Environmental Medicine, American Medical Association, American Society of Tropical Medicine and Hygiene, Physicians for Social Responsibility, Southeastern Surgical Congress, Southern Association for Oncology, Southern Clinical Neurological Society, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Specialty Editor Board

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.

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

John L Brusch, MD, FACP  Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance

John L Brusch, MD, FACP is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Dirk M Elston, MD  Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

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 School of Medicine, University of Pittsburgh Medical Center

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

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors R Phillip Dellinger, MD, Ismail Cinel, MD, PhD,Steven Manders, MD, Clara-Dina Cokonis, MD, and Dane Salandy, MD†,to the development and writing of the source articles.

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Venn diagram showing overlap of infection, bacteremia, sepsis, systemic inflammatory response syndrome (SIRS), and multiorgan dysfunction.
A 26-year-old woman developed rapidly progressive shock associated with purpura and signs of meningitis. The blood culture confirmed Neisseria meningitidis. The skin manifestation is characteristic of severe meningococcal infection and is called purpura fulminans.
Gram stain of blood showing presence of Neisseria meningitidis.
Acute respiratory distress syndrome (ARDS), commonly observed in septic shock as a part of multiorgan failure syndrome, is pathologically diffuse alveolar damage (DAD). This photomicrograph shows an early stage (exudative stage) of DAD.
Acute respiratory distress syndrome (ARDS), commonly observed in septic shock as a part of multiorgan failure syndrome, is pathologically diffuse alveolar damage (DAD). This is a high-powered photomicrograph of an early stage (exudative stage) of DAD.
This photomicrograph shows a delayed stage (proliferative or organizing stage) of diffuse alveolar damage (DAD). Proliferation of type II pneumocytes has occurred, hyaline membranes are present, and collagen and fibroblasts are present.
This photomicrograph shows a delayed stage (proliferative or organizing stage) of diffuse alveolar damage (DAD). This is fibrin stain showing collagenous tissue, which may develop into the fibrotic stage of DAD.
Acute respiratory distress syndrome (ARDS) in a patient who developed septic shock secondary to toxic shock syndrome.
Bilateral airspace disease and acute respiratory failure in a patient with gram-negative septic shock The source of sepsis was urosepsis.
A 45-year-old woman is admitted to the intensive care unit with septic shock secondary to spontaneous biliary peritonitis. She subsequently developed acute respiratory distress syndrome (ARDS) and multiorgan failure.
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 is a previous intravenous drug user (HIV-negative status) developed septic shock secondary to bilateral pneumococcal pneumonia.
Table 1. Mediators of Sepsis
TypeMediatorActivity
Cellular mediatorsLipopolysaccharideActivation of macrophages, neutrophils, platelets, and endothelium releases various cytokines and other mediators
Lipoteichoic acid
Peptidoglycan
Superantigens
Endotoxin
Humoral mediatorsCytokinesPotent proinflammatory effect



Neutrophil chemotactic factor



Acts as pyrogen, stimulates B and T lymphocyte proliferation, inhibits cytokine production, induces immunosuppression



Activation and degranulation of neutrophils



Cytotoxic, augments vascular permeability, contributes to shock



Involved in hemodynamic alterations of septic shock



Promote neutrophil and macrophage, platelet activation and chemotaxis, other proinflammatory effects



Enhance vascular permeability and contributes to lung injury



Enhance neutrophil-endothelial cell interaction, regulate leukocyte migration and adhesion, and play a role in pathogenesis of sepsis



TNF-alpha and IL-1β



IL-8



IL-6



IL-10



MIF



G-CSF



Complement
Nitric oxide
Lipid mediators



Phospholipase A2



PAF



Eicosanoids



Arachidonic acid metabolites
Adhesion molecules



Selectins



Leukocyte integrins



G-CSF = Granulocyte colony-stimulating factor; IL = interleukin; MIF = macrophage inhibitory factor; PAF = platelet-activating factor; TNF = tumor necrosis factor.
Table 2. Criteria for Organ Dysfunction
Organ System Mild Criteria Severe Criteria
PulmonaryHypoxia/hypercarbia requiring assisted ventilation for 3-5 dARDS requiring PEEP >10 cm H2 O and FiO2 < 0.5
HepaticBilirubin 2-3 mg/dL or other liver function tests more than twice normal, PT elevated to twice normalJaundice with bilirubin 8-10 mg/dL
RenalOliguria ( < 500 mL/d or increasing creatinine) 2-3 mg/dLDialysis
GastrointestinalIntolerance of gastric feeding for more than 5 dStress ulceration with need for transfusion, acalculous cholecystitis
HematologicaPTT >125% of reference range, platelets < 50-80,000DIC
CardiovascularDecreased ejection fraction with persistent capillary leakHyperdynamic state not responsive to pressors
CNSConfusionComa
Peripheral nervous systemMild sensory neuropathyCombined motor and sensory deficit
aPTT = Activated partial thromboplastin time; ARDS = acute respiratory distress syndrome; CNS = central nervous system; DIC = disseminated intravascular coagulation; FiO2 = fraction of inspired oxygen; PEEP = positive end-expiratory pressure; PT = prothrombin time.
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