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552 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

TABLE 20.9 Sepsis, severe sepsis and MODS definitions 82,84

Term Definition
Infection ● Characterised by an inflammatory response to the presence of microorganisms or the invasion of normally sterile host
tissue by those organisms.
● Bacteraemia: the presence of viable bacteria in the blood.
SIRS ● A non-specific syndrome that results from a wide variety of severe clinical insults; present with two or more of the
following:
● temperature >38°C or <36°C
● heart rate >90 beats/min
● respiratory rate >20 breaths/minute or PaCO 2 <32 mmHg
3
● WBC count >12 000/mm or >10% immature (band) forms.
● Other signs include: altered mental status, positive fluid balance or significant oedema, hyperglycaemia in the absence of
diabetes, raised procalcitonin and/or C reactive protein, hypotension, hypoxaemia, acute oliguria, raised serum creatinine,
coagulation abnormalities, ileus, thrombocytopenia, hyperbilirubinaemia, hyperlactaemia, decreased capillary refill/
mottling.
Sepsis ● Systemic inflammatory response to infection. Manifestations of sepsis are the same as defined for SIRS. Determine if
symptoms are a result of a direct systemic response to an infectious process and represent an acute alteration from
baseline in the absence of other known causes for the abnormalities.
Severe sepsis ● Sepsis associated with organ dysfunction, hypoperfusion or hypotension. Hypoperfusion abnormalities and perfusion
abnormalities may include but are not limited to lactic acidosis, oliguria or acute alteration in mental status.
Septic shock ● A subset of severe sepsis; sepsis-induced hypotension (a systolic blood pressure <90 mmHg or a reduction of ≥40 mmHg
from baseline) in the absence of other causes, despite adequate fluid resuscitation, and perfusion abnormalities (e.g. lactic
acidosis, oliguria, acute alteration in mental status). Patients receiving vasopressor or inotropic agents may not be
hypotensive by the time they manifest hypoperfusion abnormalities or organ dysfunction, but are still considered to have
septic shock.
● Acute circulatory failure with persistent arterial hypotension unexplained by other causes and despite adequate fluid
resuscitation (see also sepsis-induced hypotension).
MODS ● Presence of altered organ function in an acutely ill patient where homeostasis cannot be maintained without intervention.
MODS = multiple organ dysfunction syndrome; SIRS = systemic inflammatory response syndrome.

‘tight glycaemic control’ studies, suggested that the prac- CLINICAL MANIFESTATIONS
tice could increase risk to ICU patients. The more prag-
95
matic approach of maintaining blood glucose levels close Septic shock results when infectious agents or infection-
to normal without inducing hypoglycaemia and other induced mediators in the blood stream produce haemo-
metabolic imbalances is therefore appropriate. The dynamic compromise. Primarily a form of distributive
96
guideline was subsequently modified in 2009 to include shock, it is characterised by ineffective tissue oxygen
findings from NICE-SUGAR. 97 delivery and extraction associated with inappropriate
peripheral vasodilation, despite preserved or increased
98
cardiac output. Hypovolaemia is also associated with
septic shock due to the characteristic increased vasodilata-
tion. This presents a clinical picture of a warm, pink and
Practice tip apparently well-perfused patient in early stages of septic
shock with an elevated cardiac output, in contrast to that
Types of sepsis bundles 137 seen in hypovolaemic or cardiogenic shock patients.
Resuscitation bundle: Unchecked, cellular dysfunction in the presence of a
1. Measure lactate. failing compensatory process leads to cellular membrane
2. Culture prior to administration of antimicrobials. damage, loss of ion gradients, leakage of lysosomal
3. Administer empirical antimicrobials as soon as possible. enzymes, proteolysis due to activation of cellular prote-
4. Volume-load as appropriate. ases and reductions in cellular energy stores which may
5. Use vasopressors for persisting hypotension. result in cell death. Once enough cells from vital organs
6. Maintain directed goals of therapy. have reached this stage, shock becomes irreversible and
death can occur despite eradication of the underlying
Sepsis management bundle: septic focus. About half of the patients who succumb to
1. Use low-dose corticosteroids for septic shock if septic shock die of failure of multiple organs. 98
appropriate.
2. Give drotrecogin alfa if appropriate. The effect of sepsis and septic shock on the cardiovascular
3. Maintain glycaemic control. system is profound; the haemodynamic hallmark is gen-
4. Use protective ventilation strategies. eralised arterial vasodilation with an associated decrease
in systemic vascular resistance. Arterial vasodilation is