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The 2016 Sepsis-3 consensus shifted the diagnostic emphasis from systemic inflammation to
life-threatening organ dysfunction arising from a dysregulated response to infection.
Fever,
tachycardia and leucocytosis are insufficiently specific to distinguish uncomplicated infection from sepsis
when considered alone.
Sepsis is now defined as life-threatening organ dysfunction caused by a dysregulated
host response to infection.
Operationally,
this means an acute rise of two
or more points in the Sequential Organ Failure Assessment score.
Septic shock is the subset in which, despite adequate fluid resuscitation,
vasopressors are required to maintain a mean arterial pressure of 65 mmHg
or above and the serum lactate exceeds 2 mmol/L.
At the bedside,
the quick SOFA screen flags a systolic pressure of 100 mmHg
or below,
a respiratory rate of 22 or more, and altered mentation.
Two of these three should prompt escalation.
The haemodynamic signature of septic shock follows directly from its molecular chain.
Pathogen-associated molecular patterns, together with damage-associated patterns from injured cells,
are recognised by toll-like receptors, of which TLR4 binds endotoxin.
Recognition activates NF-κB, and macrophages and endothelium release TNF-α,
IL-1β and IL-6 in a cytokine storm.
These cytokines induce nitric oxide synthase,
while complement C5a and platelet-activating factor amplify the injury.
The result is generalised vasodilatation, capillary leak and third-space loss.
Cardiac output is consequently normal or high, systemic vascular resistance collapses,
and the patient presents with warm peripheries
and a bounding pulse despite hypotension.
Lactate accumulates because perfusion, not oxygen content, has failed.
The 2016 Sepsis-3 consensus shifted the diagnostic emphasis from systemic inflammation to
life-threatening organ dysfunction arising from a dysregulated response to infection.
The Surviving Sepsis Campaign condenses the first hour into a bundle
whose order carries its logic.
Lactate is measured first because it reflects perfusion.
Blood cultures are drawn before antibiotics,
since a single dose can sterilise them.
Broad-spectrum antibiotics follow within one hour for probable sepsis or shock,
because each hour of delay increases mortality.
For hypotension or a lactate of 4 mmol/L or above,
30 mL/kg of balanced crystalloid is given rapidly to restore preload.
If pressure remains low after fluid,
vasopressors are titrated to a mean arterial pressure of at least 65 mmHg.
Noradrenaline is the first-line vasopressor.
Vasopressin is added when the noradrenaline dose climbs,
and intravenous hydrocortisone is considered when the requirement persists.
Sodium bicarbonate is not a treatment for hypoperfusion-induced lactic acidosis.
The 2021 guideline reserves it for severe acidaemia with a pH of 7.2
or below in the setting of acute kidney injury.
Source determines the organism, and the organism determines the drug.
In cirrhosis,
a failing gut barrier allows enteric bacteria to translocate into ascites,
so spontaneous bacterial peritonitis is dominated by Gram-negative bacilli such as Escherichia coli
and Klebsiella.
An ascitic neutrophil count of 250 cells per cubic millimetre
or more is diagnostic,
and cefotaxime is the empirical choice.
Albumin at 1.5 g/kg on day one
and 1 g/kg on day three reduces renal failure and mortality.
Cellulitis, by contrast, is diagnosed clinically,
because tissue culture is positive in only 20 to 30 per cent of cases.
The 2016 Sepsis-3 consensus shifted the diagnostic emphasis from systemic inflammation to
life-threatening organ dysfunction arising from a dysregulated response to infection.