Sepsis: life-threatening organ dysfunction caused by dysregulated responses to infection

Septic shock: a subset of sepsis with profound abnormalities of circulation and cellular/metabolic dysfunction (a subset of distributive shock)

Multiple organ dysfunction syndrome: The dysfunction of two or more organ systems in response to acute injury or illness, affecting the ability to maintain homeostatic control.

Acute respiratory distress syndrome:  Acute lung injury where there is diffuse alveolar injury due to a build-up of fluid.

Systemic inflammatory response syndrome (SIDS): This is a disease where systemic inflammation causes organ dysfunction and organ failure.

The difference between sepsis and SIRS is that the latter can be caused form trauma, burns, haemorrhage and ischaemia, whereas sepsis is caused by an infection from bacteria, parasites, fungi or viruses. The assessment criteria is also different:

                        SIRS                                                   Sepsis

  • Hypo/hyperthermia                            Hypotension <100 systolic
  • Tachycardia                                           Altered mental state <15 GCS
  • Tachypnoea                                           Tachypnoea >22 RR
  • Increased WBC

The assessment tool used to diagnose the presence of sepsis is SOFA

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Risk factors for sepsis include:

  • The young and old
  • Immunosuppressed patients
  • Surgery
  • Impaired skin integrity
  • Indwelling catheters
  • Pregnancy



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Over activation of pro-inflammatory pathways and disruption of anti-inflammatory pathways in response to infection can cause the development of sepsis.


Molecules released from pathogens, pathogen-associated molecular patterns (PAMPs), or damaged body cells, damage-associated molecular patterns (DAMPs); activate the immune response. The release of pro-inflammatory factors further activate immune responses and triggers platelet activation. Platelets trap pathogens by initiating a local coagulation cascade. Furthermore, nitric oxide and c-reactive protein production is induced. Nitric oxide causes systemic vasodilation and contributes to hypotension in sepsis.

Proteins produced from the liver, c-reactive, increase the production of reactive oxygen species (ROS) which damage normal body cells as well as the pathogens. This leads to increased permeability of vessels and allows the shift of intravascular fluids into the interstitial space, furthering hypotension. Oedema impairs gas exchange and waste removal. In response to this, the activated coagulation system causes the formation of blood clots in small vessels, depleting circulation platelets. Disseminated intravascular coagulation damages the small vessels resulting in impaired blood flow, fluid shifts and increased inflammation. Microemboli prevent the exchange of gas and waste in arterioles, venules and capillaries.

Anti-inflammatory signals that are responsible for limiting the activation of the inflammatory response fail in sepsis.

Systemic effects

Cellular metabolism is damaged in the presence of ROS. Mitochondria dysfunction depletes available ATP and causes cells to decrease or stop their normal function. Organ function becomes impaired and MODS occurs which involves

  • AKI
  • Dysfunctional liver
  • Myocardial depression
  • Encephalopathy
  • Lung injury
  • Impaired immune functioning

Damage to the epithelial barrier in the GI tract allows bacteria to enter systemic circulation that worsens inflammation and MODS. Fluid in the lung also leaks due to damaged epithelial cells, which causes pulmonary oedema, acute respiratory distress syndrome.

Blood pressure

Hypotension is caused from the shifting of fluids between compartments. The total circulating volume decreases as fluid escapes in interstitial space. This redistribution is caused from nitric oxide and lactic acid. Compensatory vasoconstriction is altered in their presence and dysregulates the diversion of blood to essential organs. Increased heart rate and cardiac contractility become depressed as sepsis progresses. Hypotension worsens into shock as a result from inadequate perfusion and cellular metabolism dysfunction.

Lactate acid

Hyperlactaemia (>4mmoml/L) causes metabolic acidosis during septic shock. This is due to

  • Inadequate O2 delivery
  • Impaired oxygen use due to damaged mitochondria
  • Stress induce glycolysis
  • Dysfunction of the liver

Lactate continues to accumulate as ARDS and impaired renal function decreases the ability for the body to compensate effectively.

Catabolic state

Stress induced glycolysis causes the rapid destruction of skeletal muscle mass in order to provide energy for the immune response. Hyperglycaemia occurs and the patient becomes insulin resistant.

Sepsis management

  • Antibiotics
  • IV fluids
  • BSL maintained <10.8
  • Blood cultures
  • Vasopressor therapy
  • Nutritional support

Long-term complications

Survivors of sepsis have a high mortality rate for 5 years after diagnosis. One in five will die within 2 years. This is due to residual organ dysfunction and secondary infection. Patients may experience ongoing fatigue, pain, mental impairment, dyspnoea, and depression. Post traumatic stress disorder is common amongst survivors. The persistence of inflammation causes dysfunction in the cardiovascular system leading to MI, hypertension, and heart failure.


This video discusses septic shock and the nurses role

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Casey, G. (2016). “Could this be sepsis?” Kai Tiaki Nursing New Zealand, 22(7), 20–24. Retrieved from

Kelly, M., & Murgo, M. (2008). Nursin management: Shock and multiple organ dysfunction. In D. Brown & H. Edwards (Eds.), Lewis’s medical-surgical nursing: Assessment and management of clinical problems (2nd ed., pp. 1876–1902). Sydney, Australia: Mosby Elsevier.

Kim, W.-S., & Lee, H.-J. (2013). Management of sepsis. Journal of the Korean Medical Association, 56(9), 819. doi: 10.5124/jkma.2013.56.9.819

O’Brien, J. M., Ali, N. A., Aberegg, S. K., & Abraham, E. (2007). Sepsis. The American Journal of Medicine, 120(12), 1012–1022. doi: 10.1016/j.amjmed.2007.01.035