Sepsis

Question 1

Sepsis

Answer 1

• Life threatening organ dysfunction caused by dysregulated host response to infection

Atleast 2 qSOFA plus evidence or suspected infection

SIRS criteria
SBP < 90
RR > 22
Altered mental status

Question 2

Septic shock

Answer 2

• Subset of sepsis with circulatory and metabolic dysfunction
  Type of distributive shock characterised by peripheral vasodilation and shunting away from major organs, which is made worse by endothelial damage and increased permeability
• Characterised by fluid-unresponsive hypotension, vassopressor reliance to maintain MAP > 65 and serum lactate > 2mmol/L (decreased clearance)

Question 3

Pathophysiology of sepsis

Answer 3

• Begins as an exaggerated immune response to microbial invasion
• Pathogen binding to immune cells causes massive release of inflammatory modulators and NO that causes a loss of intracellular Ca and severe peripheral vasodilation
• Maldisribution of blood flow now occurs which worsens hypoxia
• Myocardial dysfunction occurs due to reduced cardiac output, and vascular damage leads to oedema which also puts strain on the heart
• The response also activated a coagulation cascade = release of tissue factor, that leads to the production of thrombin, which converts fibrinogen to fibrin = causes microvascular thrombi that worsens sepsis by causing ischaemia and hypoxia

Question 4

Risk factors

Answer 4

• Recent trauma, surgery, invasive procedure
• Impaired immunity (DM, steroids, chemo)
• Indwelling lines, broken skin
• DM, substance abuse, organ dysfunction, AIDs, burns
• Majority is from bacteria, most common source is respiratory

Question 5

Effect of sepsis on the respiratory system

Answer 5

• Proinflammatory cytokines during inflammatory response leads to acute lung injury and development of ARDS (increased pulmonary permeability)
• Crackles on auscultation from pulmonary oedema

Question 6

Effect of sepsis on the renal system

Answer 6

• Peripheral vasodilation during sepsis causes the release of vassopressin and activation of RAAS
• This leads to renal vasocontriction, Na and water retention and thus oliguria
• Reduction in renal blood flow and secondary tubular epithelial injury + from inflammatory mediators contribute to AKI

Question 7

Clinical presentation

Answer 7

• Fever (most common)
• Tachycardia
• Rapid breathing
• Cool extremeties/delayed CRT
• Colour changes (non-blanching mottled skin, rash)
• Hypotension (< 90 or > 40 drop)
• O2 required to maintain sats
• UO < 0.5ml/kg/h
• Acute confused state
• Lactate >2mmol/l & lactic acidosis due to anarobic respiration

Question 8

Signs of late state sepsis in children

Answer 8

• Hypotension
• Mental status changes
• Anuria

Question 9

Warm vs cold shock

Answer 9

Warm (adults): low svr, high co, tachy, warm extremities, fast cap refil, low bp

Cold (children and uncompensated adults): high svr, low co, tachy, cool extremities, slow cap refil, sustained then low BP

Question 10

Diagnostic tests

Answer 10

• Bloods: FBC, WCC, U&E, LVF, aPTT, PT
• Blood cultures, urine and sputum specimen, wound swabs
• BGL, lactate
• Scans
  *

Question 11

Treatment

Answer 11

• Fluid resus + monitor MAP & BP (arterial line) and CVP (via CVC) - keep up with FBC
• Antibiotics
• Vasoactive agents
• Mechanical ventilation and/or O2
• Glucose and lactate control
• Monitor Hb and urine output
• NPO until gut hypoxia ruled out - nutritional support
• IVIg and corticosteroids to help immune modulation
• Temperature control (antipyretics)

Question 12

Treatment - fluid resus

Answer 12

• Crystalloids are the fluid of choice (isotonic - usually hartmanns)
• Albumin given in addition when substantial fluid replacement is required
• Goal to maintain CVP 8-12, MAP >65, and urina output >0.5ml/kg/h
• Use lactate levels as a guide for resus (marker of tissue hypoperfusion)
• early aggressive resus in children is often required in children with normal BP as they tend to maintain BP despite significant volume depletion (look for signs of dehydration: dry mucous membranes, no tears, prolonged CRT, abnormal appearance)

Question 13

Antibiotics - Treatment

Answer 13

• IV antimicrobial initiated asap, ideally within 1h of recognition
• Recommended to use combination therapy of atleast 2 antibiotics of different classes

Question 14

Treatment - Vasoactive agents

Answer 14

• Noradrenaline is the first choice for counteracting septic vasodilation
• Others include adrenaline (in cold shock), dopamine, vassopressin,

Question 15

Treatment - Mechanical ventilation

Answer 15

• Intervention to maintains airways (inflammatory damage to lungs causes accumulation of fluid and decreased oxygen exchange)
• Recommended to use higher PEEP in sepsis-induced mod-sev ARDS
• Supplemental O2 therapy included
• PaO2 > 70

Question 16

Treatment - glucose control

Answer 16

• Commence insulin dosing when 2 consecutive BGLs are >7mmol
• Then monitored every 1-2h until values and infusion rates stabilise, then every 4h

Question 17

Complications - Disseminated intravascular coagulation

Answer 17

• Widespread and ongoing activation of clotting due to exessive tissue factor and reduction of clotting factors
• This results in blockages and ischaemia, which worsens DIC and MODS

Question 18

Complications - multiorgan dysfunction syndrome (MODS)

Answer 18

• altered organ fuction that cannot self correct without intervention
• Either occurs primary from direct insult or secondary as a host response

Question 19

Noradrenaline

Answer 19

• IV catecholamine that binds alpha and beta receptors in the heart to cause peripheral vasoconstriction and dilation of coronary arteries = increase BP
• 4mg in 50mls BS or 5% dextrose (preferred) infused to maintain MAP or SBP

Question 20

Piperacilin-Tazobactim

Answer 20

• IVAB, pip is a broad spectrum AB that inhibits cell wall synthesis, taz is a beta lactamase that inhibits beta-lactamase (inhibits ABs)
• 4.5mg reconstituted in 20ml WFT, diluted in 50ml NS infused over 30min