Lecture 8: Sepsis Flashcards
How does bacteremia differ from sepsis
Which one can cause the other
Bacteremia = infxn in the bloodstream
Sepsis = over-response of the immune system
Bacteremia may lead to sepsis
A pt recently had dental procedure done, however their were complications and their mucosa was injured. What type of infxn is this pt now at risk for?
GI mucosa injury –> risk for Bacteremia
- Infxns (UTI, PNA)
- Surgery
- Catheters (CVCs, Urinary)
- Depressed immune sys (steroids, chemo, etc)
- Skin breakdown/wounds/bites
- Fluid collections (kidney stone, obstruction)
- GI mucosa injury
- Ischemic tissue
Are all RFs for _________
RFs for Bacteremia
- Infxns (UTI, PNA)
- Surgery
- Catheters (CVCs, Urinary)
- Depressed immune sys (steroids, chemo, etc)
- Skin breakdown/wounds/bites
- Fluid collections (kidney stone, obstruction)
- GI mucosa injury
- Ischemic tissue
Old Definition: Sepsis 2
- How many of the criteria need to be met to fufill SIRS?
- Sepsis = SIRS + _____
- Severe Sepsis = above + _____
- Septic Shock = above + _____
Old Definition: Sepsis 2
- 2+ criteria to fufill SIRS
- Sepsis = SIRS + infxn
- Severe Sepsis = above + organ damage
- Septic Shock = above + HoTN
What type of shock is septic shock?
Distributive shock
Life threatening organ dysfxn caused by exaggerated/dysregulated immune response
definition of Sepsis
What clinical criteria used for defining sepsis (newer)
SOFA
qSOFA at bedside: Clinical criteria for sepsis
- what are the 3 parameters (+ values) included?
- pt has 2+ what does that indicate?
qSOFA at bedside: Clinical criteria for sepsis
- RR > 22, AMS, SBP < 100
- pt has 2+ –> likely prolonged hospital stay or die
When vasopressor therapy needed to elevate MAP to 65+ and lactate > 2 after adequate fluid resuscitation what state in the continuum is this pt in?
Septic Shock
What is the only effective tx for sepsis
Tx for sepsis
- IV ABXs
- supportive care (IV fluids, etc)
Pathophys of sepsis:
once the bacteria invade the tissue what does cells become triggered and what do these cells then rel?
Pathophys of sepsis:
bacteria invade tissue –> macrophages triggered and rel pro inflammatory mediators (TNFs, ILs)
Pathophys of sepsis:
- How does Sepsis occur once the pro inflammatory mediators (TNFs, ILs) are released? (answer before looking below)
- Once the bacteria are in the bloodstream what do they do the blood vessels that ultimately cause organ hypoperfusion
Pathophys of sepsis:
- Sepsis occurs when pro-inflam > anti-inflam mediators –> infxn spread to bloodstream
- bacteria get in bloodstream –> leaky blood vessels –> impaired blood flow –> organ hypoperfusion
What are the 4 main bacterial causes of Sepsis
Bacterial Causes of Sepsis
- Gram (-)s w/ENDOTOXIN
- Staph aureus
- Pseudomonas exotoxin
- Strep (GAS M protein)
Bacterial Causes of Sepsis:
- How do endotoxins contribute to the progression of local infxn to sepsis (what do they activate)
Bacterial Causes of Sepsis:
Endotoxins activate the compliment, coag and fibrinolytic systems
Bacterial Causes of Sepsis:
- What are 2 toxins produced by Staph aureus that
contribute to sepsis
Bacterial Causes of Sepsis: Staph aureus toxins
- Staph enterotxin B
- TSS toxin-1
Sequelae of Sepsis: End Organ dysfunction seen w/:
- Circulation system
- lungs
- Brain
- Liver (3)
- Kidney (2)
- Heme
Sequelae of Sepsis: End Organ dysfunction seen w/:
- Circulation system vasodilation–> HoTN –> Hypoperfusion of all organs
- lungs –> ARDs
- Brain –> swelling –> Encephalopathy
- Liver –> liver dysfxn, incr Bili, clotting factors not made
- Kidney –> renal failure, decr/no UO
- Heme –> DIC
Manifestation of systemic inflammatory response
ARDS
What is the hypoxemic respiratory failure in ARDS caused by
pulm/alveolar edema
How do pro-inflam cytokines (caused MC by sepsis) ultimately cause pulm/alveolar edema that is a/w ARDS
pro inflam cytokines –> diffuse alveolar damage –> incr permeability of alveolar-capillary barrier –> pulm/alveolar edema + influx of fluid into alveoli –> decr blood oxygenation
ARDS
- Hallmark S/s of ARDS
- Classic sign on CXR
- what is the PCWP a/w ARDS (high or low, value)
- Hallmark = severe, hypoxemia that is refractory to 100% O@2
- CXR = WHITE OUT
- LOW PCWP ( < 18)
Pt in sepsis presents sudden onset of dyspnea. You obtain labs and a CXR. Labs reveal severe hypoxemia. You put her on 100% O2 but no improvement is seen. Her CXR shows diffuse bilateral infiltrates sparing the costophrenic angles.
Dx?
ARDS
- Main form of management for ARDs
2. what should be given for HoTN
- Ventilation
2. HoTN –> fluids
Tx of ARDs: Ventilation
- what are 2 types (general)
- what are 2 specific methods of ventilating
Tx of ARDs: Ventilation
- non-invasive and mechanical ventilation
- PEEP or CPAP
Septic Shock: infectious
- what is the MC infectious cause
- 3 other causes
Septic Shock: infectious
- MC infectious cause = PNA
- others = Intra-abd infxn, UTI, Bacteremia
Septic shock: bacterial/fungal causes
- Which is more common cause: Gram - or +
- What are the 2 types of gram + likely to cause septic shock
- What fungus causes septic shock
Gram (-) Exs: E coli, Klebsiella, Enterobacter, Pseudomonas
Septic shock: bacterial/fungal causes
- MC = Gram (-)
- Gram (+) = s. aureus, strep pneumo
- Fungus = Candida
ill appearing pt presents to ER w/ AMS and rigors. RR = 22, HR = 115, BP 95/50. Labs show incr WBC and lactate.
Dx?
Septic Shock
Septic shock
- what should be obtained to identify the source of infxn (1 big thing)
Septic shock
- get cultures to identify source of infxn
Septic Shock
- initial labs you should order (5)
+/- ABGs
Septic Shock: initial labs
- CBC
- CMP
- LFTs
- Coag studies (PT/PTT)
- Lactate
What type of ABX Tx do pts need
and what should be covered
EARLY broad spectrum empiric ABXs, cover gram + and -
Pt confirmed to be in septic shock. What is an example of good Tx combo that should be initiated ASAP?
Septic Shock Tx
Vanco + Carbepenem (maybe add fluroquinolone or aminoglycoside)
alt: Zosyn + (Ceftriaxone or Imipenem)
What are 3 major signs of sepsis that need to be managed
Signs of Sepsis/Management
- Hypovolemia
- HoTN
- incr Lactate
Signs of Sepsis/Management: #1 Hypovolemia
- how should you assess pts preload at bedside?
- what result indicated hypovolemia - What types of fluids should be given to hypovolemic pts (gen + spp)
- once a pt becomes euvolemic what can be added to assist w/txting their Hypovoemia
Signs of Sepsis/Management: #1 Hypovolemia
- asses preload w/bedside US
- IVC collapse on inspiration = hypovolemia - Fluids for hypovolemia = isotonic crytalloids
- 1 L bolus of NS or LR - euvolemic –> add pressors
how do you know a pt is no longer hypovolemic
IVC not collapsing = euvolemic
note: BP NOT AN INDICATOR OF VOL STATUS
What is the 1st line pressor for Septic pts
NE = 1st line pressor for septic pts
Signs of Sepsis/Management: HoTN
what does prolonged HoTN lead to (2 steps)
Signs of Sepsis/Management: HoTN
prolonged HoTN –> tissue ischemia + anaerobic metab –> lactate production/lactic acidosis
Signs of Sepsis/Management: HoTN
- what do you what at pts MAP to be above/equal to?
- if pts refractory to NE as pressor what can be added
Signs of Sepsis/Management: HoTN
- MAP 65+
- if pts refractory to NE–> stress dose steroids
What is lactic acidosis a sign of (2 things)
Hypoperfusion/oxygenation
5 y/o ill appearing kid presents w/rigors, AMS, tacypnea, tachycardia and HoTN to ER. Should you wait for labs, etc to begin treating him for suspected shock? why/why not?
dont wait, tx immed b/c HoTN - late sign of shock in kids
Why is DIC called a consumptive coagulopathy
OVERactivate coag cascade –> widepsread microthrombi CONSUME coags factors/plts –> thrombocytopenia + diffuse bleeding
“clotting and bleeding at the same time”
in DIC pts are “clotting and bleeding at the same time” so what are they at risk for
clotting and bleeding at the same time
- risk for thrombosis and hemorrhage simultaneously
What stimulates/causes the overactivation of the clotting cascade that triggers DIC
procoagulant
- stimulates/causes the overactivation of the clotting cascade that triggers DIC
Pt in ICU presents w/ new onset of bleeding of nose and blood in urinary catheter. On exam you notice various ecchymoses and petechiae. Her L leg is swollen and when you get a doppler US you Dx a DVT. Her labs reveal incr PT/PTT, INR, and D-dimer. Platelets, Hb, and fibrinogen are low. On blood smear Schistocytes are seen.
Dx?
DIC
Tx of DIC
what does the tx depend on?
what should be given to replace blood loss
Tx of DIC
- depends on Sxs (clotting vs bleeding)
- PRBCS to replace blood loss
Tx of DIC
- if pt is primarily bleeding what should you give
- if pt is primarily clotting what should you give
Tx of DIC
- if pt is primarily bleeding –> FFP/cryo
- if pt is primarily clotting –> heparin
