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Management of Shock 551

● hyperglycaemia due to the stress response to acute
illness, and in response to sympathomimetic TABLE 20.8 PIRO acronym 85
administration
● bicarbonate levels decline due to pH buffering, but Predisposition Factors that dispose certain patient groups
replacement therapy is not routinely undertaken to be more susceptible to infection and
unless the arterial pH is life-threatening organ dysfunction, including genetic
● urea and creatinine to detect the onset of acute renal predisposition, age, and comorbidities
like alcohol use and diabetes.
failure due to renal hypoperfusion.
Infection Type of infecting organism. How is it
Haemofiltration-based therapies (as slow continuous diagnosed? How severe is the infection?
ultrafiltration, continuous veno-venous haemofiltration Is it local or general? What is the site of
or haemodialysis) are used for fluid and electrolyte infection and the related outcomes?
control when renal function suffers or as acute method Hospital/ICU or community-acquired?
for unloading fluid from the circulation (see Chapter 18). Response Stratify severity, using biomarkers (e.g. IL-6
or procalcitonin) to gauge severity of the
inflammatory/immune responses, and to
DISTRIBUTIVE SHOCK STATES predict how patients will respond and
potential outcomes. Also assess ABGs,
Distributive shock states result in impaired oxygen and lactate levels, WBC, temperature, C
nutrient delivery to the tissues as a result of failure of the reactive protein.
vascular system (the blood distribution system). While Organ dysfunction Describe using either physiological levels
there may be additional factors (e.g. infection) beyond or level of intervention. Use scoring
simple failure to provide sufficient perfusion to the capil- systems to quantify level (mild,
moderate, severe) and predict outcomes.
lary bed due to widespread vascular dilation, the common
factor for all underlying causes of distributive shock is
widespread failure of the vasculature. The most common
categories of distributive shock are associated with sys-
temic inflammatory response syndrome, anaphylaxis and the critical care literature, and led to a worldwide cam-
neurogenic shock. paign in 2002 to reduce the mortality from sepsis.

SEPSIS AND SEPTIC SHOCK The Surviving Sepsis Campaign
Systemic Inflammatory Response Syndrome (SIRS) was a The Surviving Sepsis campaign is an international collab-
term developed to describe the clinical manifestations of orative formed after the Barcelona Declaration in 2002 to
many processes characterised by systemic inflammation reduce the mortality of sepsis by 25% over a 5-year period,
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including sepsis, burns, pancreatitis and trauma. This by increasing awareness and developing treatment guide-
definition was however limited and problematic as it lines for severe sepsis and shock, including a comprehen-
89,90
described general signs and was non-specific. 83,84 Despite sive list of graded recommendations.
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a revision in 2001, SIRS was viewed as a valid descriptor Various recommendations were combined to form ‘care
but not useful for clinical diagnosis in that form. It was bundles’ (‘a group of interventions related to a disease
however noted that the use of the SIRS definition in sepsis process that, when executed together, result in better out-
to aid in early identification was important. Signs and comes than when implemented individually’) 91, p.5 and
symptoms were subsequently added to SIRS in response promulgated through professional organisations (e.g.
to infection (sepsis): hyperglycaemia, altered mentation, Institute of Healthcare Improvement [IHI]). Bundles have
generalised oedema, as well as a number of inflamma- been introduced to change processes of care and as
tory, haemodynamic, organ dysfunction and tissue per- quality or benchmarking measures (see Chapter 3).
fusion variables. A staging system (PIRO) was also Although the first version of the sepsis guidelines was
introduced to profile the processes in septic patients supported by ANZICS, the subsequent and much
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(see Table 20.8). expanded version was not, as many of the recommenda-
tions were based on research involving non-ICU and/or
Severe sepsis and septic shock is a leading cause of admis-
sion to ICU and has an associated high mortality. The non-sepsis patients. Further research and evaluation is
terms ‘severe sepsis’ and ‘septic shock’ were defined and needed as mortality benefits of ‘care bundles’ may be a
then refined during international consensus meetings result of increased clinician awareness rather than the
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that also described SIRS 82,84 (see Table 20.9 and Chapter impact of treatment changes.
21). The incidence of severe sepsis in Australia and New An example of a refuted bundle relates to tight glycaemic
Zealand was 11.8% of ICU admissions, with median ICU control. The recommendation in the surviving sepsis
and hospital stays of 6 days and 18 days respectively, and guidelines supported tight glycaemic control and origi-
corresponding mortality rates of 32% at 28 days and an nated from research where the glycaemic control practice
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in-hospital mortality of 40%. A Victorian epidemiologi- differed from Australia and New Zealand. The NICE-
87
cal study reflected similar results. More recent Australian SUGAR study subsequently concluded that measures
data shows mortality remaining relatively high but in to maintain blood glucose level of ≤10 mmol/L
decline. 36,88 The consequence of this high mortality increased mortality particularly in relation to severe
focused attention on sepsis and its associated sequelae in hypoglycaemia. A recent meta analysis of 26 ICU related
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