Sepsis and SIRS
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Before discussing SIRS along with the various sepsis syndromes, it is important to understand some basic definitions.
  • Infection: This is the inflammatory response initiated by the presence of a micro-organisms in normally sterile tissue.
  • Bacteraemia: The presence of live bacteria in the blood stream. This can occur in a healthy individual and present with no symptoms. Common causes include surgery, dental procedures and even tooth brushing.
  • Septicaemia: Often misused to describe sepsis, septicaemia is the presence of a pathogen in the blood stream leading to sepsis.
  • Systemic Inflammatory Response Syndrome (SIRS): This syndrome consists of a set of clinical signs in response to systemic inflammation. These symptoms will be discussed shortly. SIRS can be triggered by many causes including infection, surgery, trauma, malignancy and chronic inflammatory diseases.
  • Sepsis: This is defined as SIRS triggered by a primary localised infection. Bacterial, fungal, viral and parasitic infections can all cause sepsis.
  • Sepsis can progress to severe sepsis and septic shock, which will be discussed later.

Signs and Symptoms

Table 1: Signs of SIRS, sepsis and septic shock.
Clinical Signs.
Two or more of the following:
  1. Temperature <36oC or >38oC.
  2. Tachycardia = HR >90bpm
  3. Respiratory rate >20 per minute or PaCO2 <4.3 kPa
  4. White Cell Count >12 x 109/L or <4 x 109/L
Two or more of the above signs resulting from infection.
Severe Sepsis
Sepsis along with signs of organ hypo-perfusion.
Signs include hypoxemia, oliguria, lactic acidosis or acute alteration in mental state.
Septic Shock
Severe sepsis with hypotension (systolic BP <90 mmHg or a decrease of >40mmHg from baseline) – OR  – the requirement for vasoactive drugs – despite adequate fluid resuscitation.


SIRS can be caused by many events. Common triggers include infection, trauma, burns, pancreatitis and malignancies such as lymphoma.
There are several potential sites of infection, which can lead to sepsis. It is helpful to divide these up into two categories: causes in a healthy adult and causes in a hospitalised patient.

1.     Potential sites of infection causing sepsis in a healthy adult (+ example of organism).

  • Skin – staphylococcus aureus
  • Respiratory tract – streptococcus pneuomoniae
  • Gall bladder / Bowel – Escherichia coli, enterococcus faecalis,
  • Pelvic viscera – Neisseria gonorrhoeae

2.     Potential sources of infection in hospitalised patients

  • Burns – gram +ve cocci
  • IV catheter (cannula, arterial line etc) – S. aureus, S. epidermidis, Pseudomonas spp, Candida albicans
  • Wound infection (trauma, post-surgical) – S. aureus, E. coli
  • Peritoneal catheter (ascites drain, peritoneal dialysis) – S. epidermidis
  • Urinary catheter – E. coli, Proteus spp, Klebsiella spp
  • Immuno-compromised – most pathogens.
This is something you should not get too tied down with. The actual mechanism is not fully understood and a whole bunch of immune modulators are responsible for the signs observed.
It is thought the mechanisms behind SIRS and sepsis are much the same, despite the varying aetiologies.
The principal molecules involved in the development of SIRS / sepsis are cytokines. Many cytokines have been implicated including:
  • Interleukins (1b, 4, 6, 8, 10)
  • TNF alpha
  • TGF beta
The cascade begins with the release of TNF-alpha and IL-1b – predominantly from mononuclear leukocytes (macrophages) in response to endotoxins. This stimulates the release of other cytokines – IL-6, 8 and 10 as well as causing fever and initiating clotting cascades.
The mass release of pro-inflammatory cytokines exerts systemic effects, causing tissue injury, which leads to dysfunction of many organ systems. Tissue injury is mediated mainly by polymophs – predominantly neutrophils.
The main effects systemic effects by system are shown in table 2 below.
Table 2. Multi-organ complications of SIRS, sepsis and septic shock. (items marked with * indicate specific complications of septic shock).
Tachycardia, hypotension
Cytokines stimulate nitric oxide synthesis, which causes vasodilatation, and a drop in SVR. Tachycardia is initiated as a response to a drop in SVR.
Tachypnoea, hypoxemia, respiratory alkalosis. ARDS*
In ARDS, dysfunction (leakiness) of pulmonary capillaries causes alveolar oedema and neutrophil activation.
Cytokine-mediated vasodilation and hypotension cause decreased renal perfusion
Disseminated intravascular coagulation (DIC)
Cytokine mediated activation of extrinsic coagulation cascade.

In addition, lactic acidosis is caused by tissue hypoxia. The hypoxia results from tissue hypoperfusion as a result of hypotension and arteriovenous shunting.


If you are clinically suspicious of SIRS or sepsis, investigations should be used to identify the trigger. These should include:
  • Chest X-ray
  • Blood cultures
  • Other routine bloods – FBC, U+E, LFT’s
  • Arterial blood gas
  • Urine dipstick


Initial managment:
The sepsis six:
  1. Give high flow oxygen
  2. Take blood cultures
  3. Give empirical IV antibiotics
  4. IV fluid resuscitation
  5. Check Hb and lactate (ABG or VBG)
  6. Monitor urine output accurately

(An easy way to remember this is – give 3 and take 3; i.e. take cultures, ABG and urine and give O2, fluids and antibiotics).

If sepsis is suspected, empirical antimicrobial therapy should be commenced before a causative organism is identified.
  • My local trust guidelines recommend prescribing benzylpenicillin 1.2g IV QDS + Gentamicin 5mg/kg IV OD (maximum 400mg gentamicin per day).
  • In patients with penicillin allergy vancomycin 1g can be given i nstead of the penicillin
  • Always check your local guidelines
Once a causative organisms has been identified, targeted antibiotic therapy should be started as dictated by the local trust guidelines.
Severe Sepsis and Septic Shock
Cases of severe sepsis and septic shock should be referred to ITU. As with sepsis, a causative organism should be identified and treated.
However, other supportive treatment is required with two main aims; 1 – to restore cardiac output and BP; and 2 – ensure adequate ventilation and oxygenation.
Ventilation and Oxygenation
Cardiac output and BP
·      Maintain patent airway. Patient may require:
  • Oropharyngeal airway
  • Endotracheal tube
  • Emergency tracheostomy (rare).
·      High flow oxygen
  • Expand circulating volume:
    • Colloids
    • Crystalloids
    • Blood (If haemorrhage).
  • Cardiovascular function support:
    • Inotropes
    • Vasopressors
    • Vasodilators
Monitoring Required
  • Arterial line – to monitor BP and ABG
  • ECG
  • Insert catheter to monitor urine output
  • Temperature probe
  • Central venous catheter
Aims of supportive treatment:
  • Mean arterial pressure >65 mmHg
  • Central venous pressure >8-12 mmHg
  • Urine output >0.5 ml/kg/hour


  1. Clinical Medicine 7th Ed. (2009) by Kumar and Clark.
  2. Paterson, RL., Webster, NR. (2000). Sepsis and the systemic inflammatory response syndrome. J.R.Coll.Surg.Edinb., 45, 178-182
  3. Oxford Handbook of Clinical Medicine 7th Ed. (2008). Longmore et al.

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Dr Tom Leach

Dr Tom Leach MBChB DCH EMCert(ACEM) FRACGP currently works as a GP and an Emergency Department CMO in Australia. He is also a Clinical Associate Lecturer at the Australian National University, and is studying for a Masters of Sports Medicine at the University of Queensland. After graduating from his medical degree at the University of Manchester in 2011, Tom completed his Foundation Training at Bolton Royal Hospital, before moving to Australia in 2013. He started almostadoctor whilst a third year medical student in 2009. Read full bio

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