Sepsis and septic shock Flashcards
define sepsis
Sepsis is defined as life-threatening organ dysfunction caused by dysregulated host response to infection, an organism enters the bloodstream creating a septic state.
define septic shock
Septic shock can be identified with a clinical construct of sepsis with persisting hypotension requiring vasopressors to maintain MAP >65mmHg and having a serum lactate of >2mmol/l despite adequate volume resuscitation
what does qSOFA consist of?
hypotension <100 systolic, altered mental status, tachypnea >22RR. A SCORE OF 2 OR MORE SUGGESTS A GREATER RISK OF A POOR OUTCOME
what is a SOFA score?
pao2, GCS, MAP, serum creatinine or urine output, bilirubin, platelet count.
despite adequate fluid resucitation when should you suspect sespis has progressed to septic shock?
vassopressors required to maintain MAP over 65mmhg, serum lactate over 2
how much does mortality increase for each hours delay of abx administration in septic shock?
7.60%
pathophysiology of sepsis
similar to immunosuppression: loss of hypersensitivity, inability to clear infection, predisposition to nosocomial infection
what are the 3 phases in the pathogenesis of sepsis?
release of bascterial toxins, release of mediators, effects of specific excessive mediators
describe what happens in phase 1
Bacterial invasion into body tissues is a source of dangerous toxins, May or may not be neutralised and cleared by existing immune system
what are commonly released toxins
Gram negative = Lipopolysaccharide (LPS)
Gram positive = Microbial-associated molecular pattern (MAMP), Lipoteichoic acid, Muramyl dipeptides, Superantigens = Staphylococcal toxic shock syndrome toxin (TSST), Streptococcal exotoxins
describe what happens in phase 2
effects of infection due to endo/exo toxin release, mediator role on sepsis (endo - LTA don’t need binding proteins to bind to macrophages) (exo - pro-inflammatory response)
what do proinflammatory mediators do? (inflammatory response that characterises sepsis)
Promote endothelial cell – leukocyte adhesion, Release of arachidonic acid metabolites, Complement activation, Vasodilatation of blood vessels by NO, Increase coagulation by release of tissue factors and membrane coagulants, Cause hyperthermia
what is a compensatory anti-inflammatory reaction?
can cause immunoparalysis
what do anti-inflammatory mediators do?
Inhibit TNF alpha, Augment acute phase reaction, Inhibit activation of coagulation system, Provide negative feedback mechanisms to pro-inflammatory mediators
what are the Clinical features of sepsis?
• Fever >38 degrees – chills, rigors, flushes, cold sweats, night sweats
• Hypothermia < 36 degrees – especially in elderly and children (anti-inflammatory response)
• Tachycardia >90bpm
• Tachypnoea >20/min
• Altered mental state
• Hyperglycaemia >8mmol/l
Arterial hypotension (systolic <90mmHg or MAP <70mmHg)
SvO2 >70%
what are thhe changes in inflammatory variables in sepsis
Leucocytosis (WCC > 12,000/ml) Leucopenia (WCC < 4,000/ml) Normal WCC with greater than 10% immature forms High CRP High procalcitonin
what are the changes in organ dysfunction variables in sepsis?
Arterial hypoxaemia (PaO2/FiO2 < 50mmHg), Oliguria (<0.5ml/kg/h), Creatinine increase compared to baseline, Coagulation abnormalities (PT >1.5 or APTT >60s), Ileus, Thrombocytopenia (<150,000/ml), Hyperbilirubinaemia.
tissue perfusion variables…
high lactate and skin mottling and reduced capillary perfusion
factors affecting sy and sx of sepsis…
gram of bacteria, age, comorbidities, immunosupression, previous surgery, occupation, travel
What is the SEPSIS 6?
Take –> blood cultures, blood lactate, measure urine output
Give –> o2 aim for sats off 94-98%, iv abx, iv fluid. (type of empirical ABX given depending on the situation -amox, penc, metrondiazole, if ellegies give vanc)
what is lactate a marker of?
generalised hypoperfusion, severe sepsis, pooer prognosis. Type a - hypoperfusion, type b - Mitochondrial toxins, Alcohol, Malignancy, metabolism errors
how much fluid is appropriate?
30ml/kg e.g. 2.1L 70kg patient
what to consider when giving abx…
allergies, mrsa, esbl, cpe, abx toxicity, interactions.
when to consider HDU referral?
low bp responsive to fluids, lactate over 2 despite fluids, elevated creatinine, oliguria, liver dysfunction, bilateral infiltrates, hypoxaemia.
Case 1
55m, DM, smoker, IHD, Admitted through Emergency Department with fever, nausea, vomiting and abdominal pain x 4 hours, riased bp, pulse and resp rate, tender epigastrium, no rebound, BS present, WCC 15,600, tx in a and e - sepsis 6, Started on Amoxicillin, Gentamicin and Metronidazole for intra-abdominal sepsis
6 hours later patient failed to improve
Admitted with SIRS, On post-take round another blood test was carried out, Serum amylase 1450, Diagnosed as Acute pancreatitis, Antibiotics stopped and patient transferred to surgery for further management
Case 2
68 year old woman admitted with worsening shortness of breath
History of IHD, CVA and bed bound
On examination: Alert, Temp 38oC, Resp rate 26/min, pulse 120/min irreg, BP 85/60, Chest dullness right base
Pneumonia CURB65 score - confusion, >7ureaN2, >30RR, DIASTOLIC <60 SYSTOLIC <90, over 65yo. out of 5, 3/5 is high risk of death.