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CCP > Sepsis > Flashcards

Sepsis Flashcards

1
Q

Sepsis causes cellular injury via three mechanisms (tissue ischemia, cytoplasmic injury and altered apoptosis). Describe how it causes tissue ischemia:

A
  • TNFa and IL-1 activate both coagulation and fibrinolysis which leads to microcirculatory lesions and disrupted blood flow.
  • Neutrophils bind to endothelial cells and secrete reactive O2 species, endothelin, NO, platelet activating factor and lytic enzymes which damage endothelial cells and disrupt blood flow.
  • RBCs become rigid
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2
Q

Sepsis causes cellular injury via three mechanisms (tissue ischemia, cytotoxic injury and altered apoptosis). Describe cytotoxic injury:

A

-TNFa and NO cause mitochondrial dysfunction which leads to cell death via histotoxic anemia. Even if there is oxygen present, the cell can’t use it.

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3
Q

Sepsis causes cellular injury via three mechanisms (tissue ischemia, cytoplasmic injury and altered apoptosis). Describe altered apoptosis:

A
  • Proinflammatory cytokines delay apoptosis of dysfunctional cells, prolonging sepsis.
  • Sepsis induces lymphatic and dendritic cell apoptosis which results in decreased clearance of invading microorganisms.
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4
Q

TNFa and IL-1 are the major cytokines in sepsis. What do they cause?

A
  • Fever
  • Hypotension
  • Leukocytosis
  • Induction of other proinflammatory mediators
  • Simultaneous activation of coagulation and fibrinolysis
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5
Q

Causes of worsened hemodynamics in septic patients:

A
  • Prostacyclin and NO secreted by endothelial cells cause vasodilation and loss of metabolic autoregulation.
  • Venodilation decreases preload and CO.
  • Arterial dilation causes decreased MAP and EOP, including decreased coronary perfusion.
  • Microvasculature permeability leads to fluid extravasation.
  • Impaired secretion of ADH
  • Myocardial depressant factors
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6
Q

How does sepsis cause ARDS?

A

Neutrophil entrapment within the lung’s vast microcirculation initiates or amplifies injury to the alveolocapillary membrane which leads to microvascular permeability and leads to interstitial and pulmonary edema.

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7
Q

SIRS Criteria

A

2 of 4:

  • RR > 20 or PaCO2 < 32
  • Temp < 35 to > 38.3
  • WBCs < 4,000 or > 12,000 or > 10% immature forms
  • HR > 90 sinus
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8
Q

qSOFA is a predictive tool that calculates the risk of death from sepsis, not a diagnostic tool. What are it’s three components?

A
  • RR > 22
  • Altered mentation
  • SBP < 100
  • Score of one (3%), two (18%) and three (24%) = risk of mortality.
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9
Q

Define sepsis:

A

SIRS with an infection

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10
Q

Define severe sepsis:

A

Sepsis + organ dysfunction, but negative lactate.

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11
Q

Define MODS:

A

Progressive organ dysfunction such that homeostasis cannot be maintained without intervention.

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12
Q

List some conditions that could make a patient “immunocompromised.”

A
  • Neoplasms
  • Renal failure
  • Hepatic failure
  • AIDS
  • Asplenism
  • Immunosuprression medications
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13
Q

List some circumstances that would put a septic patient at even greater risk of death:

A
  • Infection site is in lungs, GI tract or unk.
  • ABx in the last 90 days
  • Low platelet count
  • Lactate > 4.0
  • Hyperglycemia on admission
  • Nosocomial, instead of community acquired pathogens
  • Being old
  • Hypocoagulability
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14
Q

Key markers to assess when querying MODS:

A
  • P:F ratio (< 300)
  • Platelet count (< 100)
  • Serum total bilirubin (> 4mg/dL)
  • Serum creatinine (increases of > 44)
  • GCS
  • Hypotension and vasopressor requirements
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15
Q

Common causes of non-infectious SIRS:

A
  • Autoimmune disorders
  • Burns
  • Pancreatitis
  • Vasculitis
  • Thromboembolism
  • Surgery
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16
Q

How does sepsis affect the microvasculature?

A
  • Angiopathy -> Platelet consumption -> DIC
  • Mitochondrial toxins -> Histotoxic anemia
  • Fluid extravasation
  • Vasoconstriction (late sign)
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17
Q

How does sepsis affect the macrovascularture?

A
  • Arterial vasodilation -> Low MAP -> Decreased EOP/coronary perfusion
  • Venodilation -> Pooling -> Decreased preload -> Decreased CO
  • Myocardial depressant cytokines -> Decreased contractility
18
Q

Simple equation that sepsis resuscitation can be pulled back to:

A

DO2 = CO x Arterial O2 content

19
Q

List some common sites of infection and whether they’re gram positive or negative:

A
  • Gram positive are often found on the skin and oral mucosa (cellulitis, endocarditis, meningitis , necrotizing fasciitis). Tx with 2g Ceftriaxone and 500mg Azithromycin, +/- Vancomycin.
  • Gram negative are often found in the GI tract (bilary, peritonitis, UTI). Tx with 3.375g Pip/Tazo. If it smells, it’s gram negative.
20
Q

Simple rule of thumb when distinguishing whether to use Ceftriaxone or Pip/Tazo:

A
  • If it’s above the diaphragm, Ceftriaxone (2g)

- If it’s below the diaphragm, Pip/Tazo (3.375g)

21
Q

What’s one lab value you can look at to determine if the sepsis is involved in the muscles and there’s possibly a component of necrotizing fasciitis (surgical disease).

A

CK

22
Q

4 Principles of Sepsis Management:

A
  1. ) Source control
  2. ) Early and aggressive ABx
  3. ) Optimize DO2
  4. ) Ancillary therapies (steroids, glycemic control, albumin therapy, heparin)
23
Q

To optimize DO2 in sepsis, what steps should you complete in order?

A
  1. ) Assess volume status and improve preload (20-30cc/kg). Look at passive leg raise, IVC, CVP trend, skin temp and response to fluid.
  2. ) Levophed, then vasopressin.
  3. ) If still cold peripherally, assess for septic cardiomyopathy (troponins, high CVP/low SvO2, ECG changes) and start Milrinone (high HR) dobutamine (low HR).
24
Q

Well shit, you’re in refractory distributive shock (>50mcg/min of levophed). What do you do?

A
  • Check for reversible causes (PTX, tamponade)
  • Ensure right line, drug, concentration
  • Reassess preload and give them fluid to squeeze
  • Reassess source control
  • Check for metabolic acidemia < 7.10, treat with NaHCO3
  • Check for hypocalcemia <1.0 or hypoalbuminemia
  • Is there too much sedation?
  • Consider 50mg hydrocortisone for adrenal insufficiency
  • Shit! Did you check for anaphylaxis?!
  • All else fails, try methylene blue
25
Q

At what point do you add vasopressin to your levophed infusion?

A

-There’s no set number. Keep cranking up the levophed until you see detrimental Beta-1 effects.

26
Q

Briefly distinguish between DIC, ITP, ITT:

A
  • All have thrombocytopenia, but DIC is the most lethal and will have abnormal PTT and INR.
  • ITP has platelet counts in the single digit range due to antibodies. Tx with prednisone and transfer patient to site that can perform splenectomy.
  • TTP is abnormal platelet adhesion that causes hemolysis. Tx with plasmapherisis and plex
27
Q

Temperature greater than ________ can be detrimental to the brain.

A

40

28
Q

Prophylactic ABx of choice for prehospital trauma:

A

1g of Encef, unless it’s abdominal trauma. Then give Pip/Tazo.

Don’t forget about tetanus.

29
Q

Well this is kinda fucked up… Urea levels > 30 decreases the function of platelets. How do you treat it?

A

DDAVP

30
Q

When you’re facing a MODS situation, what’s one simple strategy to help you gain some ground?

A

Identify the organ that is the most fucked up and target treatments to fix it first.

31
Q

Scenario time…. You’ve got a septic patient with a lactate of 6.2 and elevated transanymase liver enzymes… Do you fluid bolus them?

A

Not necessarily. The liver is dysfunctioning and not breaking down lactate so that could be the reason the lactate is high, not hypo-perfusion.

32
Q

Two types of hyperlacatemia:

A 
Type A (DO2/VO2 mismatch)
-global or focal ischemia, shock liver

Type B (Mitochondrial dysfunction)

  • drugs (propofol, cyanide, metformin, nitroprusside, epinephrine, ASA)
  • lymphoma

*Remember, lactate can also build up due to liver dysfunction.

33
Q

Define Septic Shock:

A

Severe sepsis (organ dysfunction) with elevated lactate despite adequate fluid resuscitation.

34
Q

Your septic patient has an ischemic liver and requires vasoactive support. Will the ischemic liver more likely force you to give higher or lower doses of pressors?

A

Shock liver is associated with vasoplegia and higher doses are often needed. Most vasoactive drugs are not metabolized in the liver anyways.

35
Q

Approach to hypotension?

A
  • IV working?, Right drug/concentration/rate?
  • Use ultrasound to assess for PTX, IVC, tamponade.
  • Too much sedation?
  • Give fluid if IVC collapsing
  • Phenylephrine?
  • Pressors? (check for shock liver/vasoplegia)
  • Inotropes?
  • Calcium?
  • Steroids?
  • Acidemia (correct oxygenation)
36
Q

You got a patient with really fucking low platelets. Is it ITP, TTP or DIC?

A

Both TTP and DIC are sick patients, but DIC will have much worse INR/PTTs. Fibrinogen will also be low in DIC and normal in ITP/TTP.

37
Q

Some studies say little to no benefit for early ABx in sepsis, but one study suggests that for every hour after the onset of sepsis related hypotension, there is a _____% increase in mortality if no ABx are given.

A

7.6

38
Q

Second line agent to increase blood pressure in sepsis is vasopressin. Recent studies have indicated that early use of vasopressin is associated with better mortality and decreased dialysis rates. Why?

A

Compared to other forms of shock, sepsis is thought to inhibit endogenous ADH release, therefore, adding exogenous vasopressin can significantly improve hemodynamics.

It also causes efferent renal arteriole constriction which helps improve GFR and creatinine clearance.

Doses higher than 0.03u/min are associated with mesenteric and coronary ischemia and increased pulmonary artery pressures.

39
Q

How does pH affect ionized (free) calcium levels?

A

Alkalosis will displace H+ from albumin and Ca++ will then bind to it, thus decreasing the level of ionized Ca++.
Acidosis will do the reverse.

It has no affect on total calcium.

40
Q

What’s the NLR?

A
  • Neutrophil to Lymphocyte ratio.
  • In times of stress, neutrophils go up while lymphocytes go down.
  • Stress causes a fast onset of these changes and this is a better acute assay than WBC.
  • Normal NLR: 1-3, mild 6-9, moderate 9-18, severe 18+
41
Q

SARS-CoV-2: To give fluid or not to give fluid?

A
  • Virus directly affects type 2 alveolar cells and damages them causing an alveolitis. It also indirectly affects them with the immune response and interstitial swelling/seepage.
  • Giving them too much fluid will worsen the seepage and result in worsening V/Q mismatching.
42
Q

Will you have a higher or lower LNR in viral patients vs bacteremic patients?

A

Lower. A NLR greater than 3 in a viral patient is concerning where as a bacteremic patient is not considered severe unless it’s greater than 18.

CCP (18 decks)

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