Sepsis

Question 1

What is the definition of sepsis?

Answer 1

Life threatening organ dysfunction caused by dysregulated host response to infection. Overall dysregulated inflammatory response.

Question 2

What is septic shock?

Answer 2

Patient meets definition of sepsis, has persistently dec BP despite adequate fluid replacement, lactate is greater than or equal to 2, requires vasopressors to maintain a MAP of greater than or equal to 65

Question 3

What can sepsis and septic shock progress into? Can SIRS progress into MODS?

Answer 3

MODS. Yes.

Question 4

What is SIRS? What are the SIRS criteria?

Answer 4

Normal inflammatory response gone out of control. Non-infectious and infectious causes. Temp >38 or <36, HR >90, RR >20 or PaCO2 <32, WBC >12000; <4000 or 10% band cells (immature cells)

Question 5

What are some predisposing factors to sepsis?

Answer 5

Age extreme <1 or >65, chronic conditions (HF, diabetes), malignancies, burns, immobilized pt, skin breakdown, meds (not finishing abx, multiple abx, immunosuppressants), trauma, bacterial colonization, VAP

Question 6

What are the steps during the normal inflammatory response?

Answer 6

Vascular response, immune response, platelets, plasma protein response

Question 7

What occurs during the vascular response of inflammatory process? What process of ABCCs of sepsis does this line up with? What are signs we might see in a patient during this step?

Answer 7

Release of histamines, bradykinin and prostaglandins result in increased cap permeability and vasodilation. Lines up with Arachnoidic Acid and Bradykinin steps. Pain and fever (due to prostaglandins)

Question 8

What occurs during the immune response of normal inflammatory process? What might we see in a patient in this phase? What process of ABCCs of sepsis does this line up with?

Answer 8

Neutrophils, monocytes/macrophages, Ab and Ag work to kill bacteria. Exudate formation. This phase lines up with complement of ABCCs of sepsis.

Question 9

What occurs during the platelets phase of the normal inflammatory response? What might we see occur in a patient during this phase? What does this phase line up with in the ABCCs of sepsis?

Answer 9

Coagulation, fibrinolysis = clotting. Patient stops bleeding. This lines up with coagulation phase.

Question 10

What occurs during the plasma protein response during normal inflammation? What phases does this line up with in ABCCs?

Answer 10

Promotes inflammatory response via bradykinin and complement. Bradykinin and complement.

Question 11

What is the role of mast cells?

Answer 11

Degranualte and release histamine which results in vasodilation and increased cap perm (supports extravasation of neutrophils), inc gastric acid secretion, inc airway mucous production

Question 12

What is the role of cytokines? What types are there? What are their specific roles?

Answer 12

Mediate inflm response. Interleukin 1/6 you get fever. Tissue necrosis factor you get dec BP (and dec EOP) and increased cap perm.

Question 13

What are the main points during the Arachnoidic Acid phase during sepsis? What are the two main pathways? What are the important compounds in each pathway? What are the roles of these compounds? What is the overall effect on O2 S and D?

Answer 13

Prostaglandin (inflm mediator) is activated by hypoxia, ischemia, endotoxins, catecholamines, and tissue injury. This results in vasodilation, increased cap perm and pain. On a systemic level it leads to haphazard vasoconstriction and vasodilation which results in maldistribution of blood (leading to compromised organ tissue oxygenation). The widespread increased cap perm leads to fluid shifts (if fluid shifts into lungs pateint with have issues with vent/oxygenation). Lipoxygenase and cylooxygenase are the two main pathways. Leukotrienes and lipotoxins are released from lipooxygenase, COX 1 and 2 are released from cyclooxygenase (which include prostaglandin and thromboxane for COX 1 and prostaglandin for COX 2. Lipoxygenase - increased cap permability, vasoconstriction, bronchoconstriction. Cyclooxygenase - pain and vasodilation from prostaglandin and platelet aggregation from thromboxane. Maldistribution of BF (from simultaneous vasoconstricting and vasodilating) results in decreasd preload which results in an O2 S and D imbalance.

Question 14

What are the main points of the Bradykinin pathway? What other pathways does this one stimulate? What are the major O2 S and D issues that arise from the Bradykinin pathway?

Answer 14

Hageman factor (factor 12) is stimulated by tissue damage. It is a potent vasodilator and results in increased capillary permeability leading to decreased afterload and fluid shifts leading to decreased preload. It stimulates mast cells which stimulate the AA pathway, also stimulates complement and coagulation system.

Question 15

What are the main O2 S and D outcomes of the coagulation cascade?

Answer 15

Cytokines inhibit plasmin production leading to reduced clots being broken down and more being formed = micro emboli in vasculature leading to a maldistribution of BF and organ dysfunction from decreased O2 supply

Question 16

What are the main outcomes for complement pathway?

Answer 16

Three main pathways, lectin, classical, and alternative stimulate C3 production which leads to C3 B. C3B results in opsonization which means leukocytes are attracted to area of injury to partake in phagocytosis. C3 combines with C5 to create C5 a and b. C5a results in chemotaxis and histamine production and C5b results in the membrane attack complex (MAC) allowing water to rush into a pore in the membrane of pathogens causing them to explode, their content cause further inflammation in the body.

Question 17

Where is MDF produced? What does it do?

Answer 17

Produced from an under-perfused pancreas. Leads to myocardial contractility depression.

Question 18

What is the qSOFA meant to assess? What is the scoring criteria? What does it mean if someone has a score of greater than or equal to 2?

Answer 18

Assess for severity of organ dysfunction. RR greater than or equal to 22, altered mentation (GCS <15), systolic hypotension SBP less than or equal to 100. Score of greater than or equal to 2 indicates the individual is at a greater risk of death/prolonged ICU stays

Question 19

Describe the Hour 1 bundle for sepsis/septic shock management?

Answer 19

1. Measure lactate level (re-measure if lactate was >2 initially)
2. Obtain BCX before ABX
3. Broad spectrum ABX administered
4. Rapid administration of crystalloid 30 ml/kg for dec BP or lactate greater than or equal to 4 (approx 2 L)
5. Vasopressor if dec BP during or after fluid resuscitation to maintain MAP greater than or equal to 65

Question 20

What are the main goals after the Hour 1 bundle is complete?

Answer 20

Maintain MAP greater than 65
Normalize lactate (aka achieve adequate tissue oxygenation)

Question 21

What is the most accurate way to assess preload?

Answer 21

Bedside ultrasound, PLR, fluid challenge

Question 22

What is a fluid challenge? How does it assess preload?

Answer 22

250-500 cc NS. If patient is “fluid responsive” (i.e. has more room for fluid) then we will see improvement in hemodynamics (dec HR, inc MAP).

Question 23

How does PLR assess preload?

Answer 23

Patient is laying flat, raised legs increase venous return to heart, if patient has “room” for fluid/fluid responsive we will see improvement in their hemodynamic numbers (dec HR, inc MAP). This allows us to check the same as if we were going to do a fluid challenge but without giving them the extra fluid.

Question 24

What does a bedside US visualize?

Answer 24

LV wall motion and change in ventricular size between systole and diastole which gives us a sense of SV and can estimate EF. If patient is not vented, we can look at size of IVC and make a correlation with the degree of collapse during inspiration to the degree of dec preload (more collapse = less preload)

Question 25

SCVO2 and lactate both tell us what?

Answer 25

Indicators of tissue perfusion

Question 26

If we have given our patient in septic shock fluids, and their preload is satisfactory, but we are still having issues with their BP and MAP, what drug might we start (what is the first drug of choice?). Why is it important to ensure that we are only giving this drug when we know preload is adequate?

Answer 26

Levophed (norepi). Giving this only when preload is adequate as it will cause too much increased workload on the heart if preload is low (contractility will be low) and then we will increase afterload to increase BP.

Question 27

Why might we decide to as vasopressin if our MAP is greater than or equal to 65 while we have Levo running? What other drug could we add instead of vasopressin?

Answer 27

To decrease the amount of Levo we are giving. Epinephrine.

Question 28

What are “lung protective” strategies to consider when we have a patient with sepsis/in septic shock who is vented?

Answer 28

Lower Vt (6 cc/kg)
Higher PEEP (PRN to support gas exchange)
Limiting plateau pressure to 30
Use of NMBA PRN to facilitate mech vent and O2 S and D balance (should be limited to <48 hr)

Question 29

What is something we can give to treat preload, afterload, contractility issues in sepsis/septick shock?

Answer 29

Fluids, vasopressors, inotropes.

Question 30

AABCDDs of sepsis?

Answer 30

A- artificial airway PRN to support vent/gas exchange
A- antibiotics, obtain cultures first, start broad then narrow
B- breathing, mech vent PRN, lung protective strategies, consider fluid status and diffusion issues, manage bronchospasm (leukotrienes in AA pathway))
C- cardiac output. Preload assessment and fluid therapy. Consider levophed, vasopressin, or dopamine (at high dose) to support afterload. Consider dobutamine to support contractility.
D- decrease demand - RASS goals, adequate analgesia, weight benefits of inc temp, anticipate shivering if cooling.
D- drugs. Glycemic control (glucose 6-10), steroids, stress ulcer prophylaxis (if at inc risk), nutrition (oral/enteral as tolerated, TPN if not tolerated).