Lecture 8 - Sepsis Flashcards
Sepsis
life threatening organ dysfunction caused by a dysregulated host response to infection
Septic shock
sepsis with circulatory and cellular/metabolic abnormalities profound enough to substantially increase mortality (type of distributive shocks)
SIRS criteria
must have >/= 2:
- Fever of more than 38C (100.4) or less than 36 (96.8)
- HR >90/min
- RR >20/min or PaCO2 <32mmHg
- WBC >12,000 or <4,000 or >10% bands
What is the clinical criteria for sepsis -3, 2016?
sepsis: suspected or documented infection and an acute increase of >/= 2 sequential (sepsis related) organ failure assessment (SOFA) points (a proxy for organ dysfunction)
- at the bedside: use the quick SOFA (qSOFA)
Septic shock: sepsis and vasopressor therapy needed to elevated MAP >/= 65mmHg and lactate > 2mmol/L after adequate fluid resuscitation
qSOFA
used at the bedside for sepsis
1 point each:
RR >22/min
AMS
Systolic BP <100mmHG
qSOFA >/= 2 identifies pts with suspected infection who are likely to have prolonged ICU stay or die in hospital
What is the pathophysiology behind sepsis?
bacteria invades tissue
macrophages are triggered and release:
-proinflammatory mediators (TNF, IL 1, 2, 6)
-antiinflammatory mediators (inhibitors of above)
sepsis occurs when the release of proinflammatory mediators in response to infection in unbalanced and exceeds the boundaries of the local environment
“malignant intravascular inflammation”
Endotoxin
cell wall component on Gram negative organisms
contributes to progression of local infection to sepsis
activates the complement, coagulation and fibrinolytic system
basically there are certain bacteria that are more likely to cause sepsis
Which bacteria are more likely to cause sepsis?
Endotoxin (see in gram negative)
Gram Positive: Staph Enterotoxin B (staph aureus) TSS toxin -1 (staph aureus) Pseudomonas exotoxin Group A strep M protein
What signs qualify as end organ damage in sepsis?
hypotension from vasodilation, hypoperfusion of all organs
ARDS
encephalopathy
liver dysfunction/shock liver, elevated bili, clotting factors not made
acute renal failure, dec or absent urine output
systolic and diastolic ventricular dysfunction
DIC
White out on CXR
ARDS
ARDS
acute respiratory distress syndrome
predominantly a hypoxemic respiratory failure caused by alveolar edema
inability of the respiratory system to meet the oxygenation requirements
management: ventilate with low tidal volume (6mL/kg), control inflammatory response, prevent volume overload that can further congest lungs
What is the management of ARDS?
ventilate with low tidal volume (6mL/kg), control inflammatory response, prevent volume overload that can further congest lungs
DIC
Disseminated intravascular coagulation
“consumption coagulopathy”
coagulation and fibrinolysis become abnormally over-activated
- coagulation: formation of clot
- fibrinolysis: break down of clot
- overactive clotting stimulation depletes coagulation factors which causes further bleeding
risk of thrombosis and hemorrhage
Acute vs chronic DIC
acute: more symptomatic with bleeding/thrombosis
chronic: often from cancer. less symptomatic; with evidence of DIC on labs
What causes DIC?
stimulated by a procoagulant (tissue factor, bacterial lipopolysaccharides, procaogulant enzymes)
bacterial infection cancer obstetrical complication trauma to tissues hemolysis from blood transfusion reaction
How do pts with DIC present?
bleeding (sites of trauma, nose, drains, catheters)
thrombosis (DVT, PE, CVA, MI, microvascular)
thrombocytopenia
coagulopathy with long PT/INR, PTT
organ damage (kidneys, lungs, liver, brain)
clinical exa,: ecchymoses, petechiae, bleeding
What labs do you expect to see for DIC?
PT/INR: elevated (extrinsic coagulation factors)
aPTT: elevated (intrinsic coagulation factors)
fibrinogen: low in DIC (might be high in the acute phase)
D-Dimer: elevated
Platelets: low (thrombocytopenia)
schistocytes
How is DIC managed?
treat symptomatology:
if the pt is bleeding - treat by giving products (FFP, cryo)
if pt is clotting - give anticoagulation (heparin drip)
you basically have to sacrifice one for the other
replace lost blood volume with PRBCs
support pt: vasopressors, oxygen, ventilator
How can you tell the difference between DIC and TTP?
TTP has a normal PT/INR and PTT because it does not involve coagulation factors
but you will still have (in both):
low fibrinogen, elevated d-dimer, thrombocytopenia, schistocytes
What is the clinical presentation for sepsis?
ill-appearing fever rigors AMS tachycardia tachypnea hypotension elevated WBC, left shift/bandemia pain
NOT EVERY SPETIC PT HAS A FEVER
How do you manage septic shock?
stabilize respiration and establish venous access
identify source of infection
Labs: CBC, chemistry, LFTs, coags, lactate, ABG
give empiric antibiotics
admit to ICU
treat infection source
GET BLOOD CULTURE to narrow ABX therapy later
What is an example of empiric antibiotic therapy for sepsis?
vancomycin + carbapenem +/- fluoroquinolone or aminoglycoside
Hypovolemia
septic shock is associated with:
peripheral vasodilation
intra to extravascular fluid shifts
assess preload by exam and ancillary testing
bolus balanced crystaloid solution (LR, 0.9% NS) and reassess
watch for pulmonary edema, CHF
add pressors after euvolemic
Hypotension
prolonged hypotension results in: tissue ischemia/anaerobic metabolism, inefficient ATP production and lactic acidosis
maintain MAP >/=65
select norepi as first line vasporessor
add “stress steroids” for shcok refractory to vasporessor therapy
Lactate
sign of tissue hypoxia
lactate is a byproduct of anaerobic metabolism. cells go into anaerobic metabolism when there is not enough oxygen to complete aerobic metabolism
- lactic acidosis is a sign of hypoperfusion and hypooxygenation
- trending lactates can help determine severity of illness and prognosis. if pt is unable to clear lactate (down to a normal range of <2), this indicates poor prognosis
What are the causes of septic shock?
PNA: most common
intra-abdominal infection
UTI
bacteremia: blood cultures are positive in 30-45% of septic pts
in up to 1/3 - 1/2 of cases, cultures from all sites are negative (“culture negative sepsis”)
Most common: gram negative
-e.coli, klebsiella, pseudomonas, enterobacter
gram +: staph aureus , strep pneumo
fungi: candida
What are the components of SOFA?
respiration (PaO2) coagulation (platelets) liver (bili) cardio (MAP) GCS Renal (Cr + urine output)
to be considered sepsis (post 2016 criteria) a person must have 2+ of these + suspected infection
septic shock:
2+ SOFA + suspected infection + vasopressors needed to get MAP >/=65mmHg + lactate >2 mmol/L
