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ID Exam 3 B

Berman Sepsis and Septic Shock

QuestionAnswer
Sepsis is defined as life threatening conditions caused by dysregulated host response to infection, resulting in ORGAN DYSFUNCTION
septic shock is subset of sepsis with PROFOUND circulatory, cellular, and metabolic abnormalities, presenting as fluid-refractory hypotension requiring vasopressor therapy with associated tissue hypoperfusion
Septic shock is CLINICALLY defined as requirement of ________ to maintain MAP >/= to _________ and lactate _________ after adequate fluid resuscitation vasopressors; 65 mmHg; >2 mmol/L
Simplifed version of sepsis/septic shock--> 2 things 1. endothelial cells are releasing a lot of cytokines 2. macrophages are activating all parts of the immune system and that can even affect the clotting cascade *(overwhelming response of our pro-inflammatory cytokines that is suppose to target pathogen but we start damaging our organs (hence ORGAN DYSFUNCTION
How we recognize sepsis is through the ________ effect hemodynamic
Hemodynamic effect: Sepsis and Septic shock are associated with _______ ________ ______, high catecholamines, and vascular _________; increased vasodilation, capillary leak due to tissue damage. excessive sympathetic activity; hypo-reactivity (blood vessels not responding to Norepi or Epi being released)
What are the hallmark effects of Sepsis? Low systemic vascular resistance, high cardiac output with tachycardia and hypotension
Give examples of where sepsis can cause multiple organ dysfunction Brain: altered mental status; Heart: tachycardia, hypotension, increase in lactate (heart not able to carry O2 so start anaerobic metabolsim); kidneys: AKI (acute oluguria or anuria, Increased serum creatinine, and metabolic acidosis
Other examples of organ dysfunction are seen in the blood (decreased platelets and protein C, increased D-Dimer, disseminated intravascular coagulation (DIC); what about damage to the liver? Jaundice, increased AST/ALT, decreased albumin, incerased INR >1.5, and acute liver failure
Organ dysfunction in the lungs? tachpnea, Hypoxia (PaO2 <70 mmHg, SaO2 <90%, acute respiratory distress syndrome (ARDS), PaO2/FiO2 </= 300
Using SOFA to define sepsis, what goes into the sepsis clinical criteria? INFECTION + Change in SOFA (greater than or equal to 2) Sepsis-related; organ; failure; assessment (consisting of decreased PaO2/FiO2; hypotension or vasopressors; decerase in platelets; decrease in glasgow coma scale, incerase in bilirubin, or increased creatinine oliguria
What is the main idea of the SOFA score? Idea is we're trying to measure how much organ failure is there. So the more organ failure you have--> the higher the score will be (so a +2 from your baseline)
What are the 2 most commonly used screening tools for the detection of sepsis or septic shock? SIRS (Systemic inflammatory response syndrome) qSOFI (Quick sequential Organ Failure Assessment)
SIRS criteria is considered positive if a pt meets 2 or more of the following: Temperature <36 C or 38 C (<96.8 F or > 100.4) Respiratory rate >20/min Heart rate >90 bpm WBC <4000 or >12000/mm^3 (leukopenia) or (Leukocytosis)
qSOFA is considered positive if a pt meets 2 or more of the following criteria: SBP < or = to 100mmHg RR > or = to 22/min Altered mental status (Glasgow coma scale (GCS) < 15)
Which of the screening tools is less specific but more sensitive? SIRS criteria (can give a lot of False (+))
Which of the screening tools is more specific but less sensitive? qSOFA (can give a lot of False (-))
Guidelines recommend against using _______ compared to SIRS, NEWS, or MEWS as a single screening tool for sepsis or septic shock qSOFA (study showed that only 24% of pts with infection had a qSOFA score of 2 or 3 giving tons of false (-) due to low sensitivity
What is the clinical criteria for Septic shock? Sepsis + Vasopressors to maintain MAP > or = to 65 mmHG AND Serum lactate level is greater than or equal to 2 IN THE ABSENSE OF HYPOVOLEMIA
Berman emphasized lactate levels in septic shock is really related to the body's inability to perfuse and get oxygenated blood to our organs so our body turns to (1)_______ _______ anaerobic metabolism to make energy and its all related more to PERFUSION
Goals of management of sepsis deals with: infectious disease management and hemodynamic management
Infectious disease management consists of: prompt initiation of antibiotics; aggressive abtibiotic dosing; source control; tailor regimen based on culture data; duration of therapy depends on infection and clinical response
Hemodynamic management consists of: early, aggressive resuscitation with BALANCED crystalloids; if hemodynamically unstable after fluid resuscitation--> initiate vasopressors and initiate steroids (if refractory)
Where can the main sources of infection come from for sepsis/septic shock? Pulmonary (40%) looking at CAP/VAP; Intra-abdominal (35%) looking at diverticulitis; Genitourinary (15%) UTI/ Pyleonephritis
Other sources of infection could come from? bacteremia, skin and soft tissue, CNS, miscellaneous
Who are the main causitive pathogens for sepsis infections? (*Be able to determine gram + or gram -) Gram (-) 44-59% consisting of E.Coli, Klebsiella, Proteus, Enterobaceter/P. Aeruginosa Gram (+) 37-52% consisting of S. aureus, S. pneumo, E. faecalis Fungi 4-10% consisting of C. Albicans Anaerobes 5% consisting of Bacteroides fragilis, C. Diff
First step is getting culture and rapidly starting antibiotics 1. obtain 2 sets of 🩸 cultures before antibiotic therapy (peripheral draw and from any invasive line) -obtain microbiologic culture (sputum, urine) to determine possible infection sources -obtain lactic acid w/in 1 HOUR of recognizing sepsis/septic shock and remeasure w/in 6 hours if >2mmol/L -if culture takes >45 min, DO NOT DELAY admin of abx
Berman: "if you are suspecting sepsis/septic shock-->obtain a lactic acid or a lactate and if elevated greater than 2, we need to reassess that every ____ hours to see how the body is perfusing; the exception is? 6h; If it takes too long for cultures such as 45 min--> then you should not delay the administration of antibiotics **hard stick--> give them abx and we'll get the cultures when we can"
Antibiotic timing: If sepsis is definite or probable and shock is present then we--> adminster abx immediately, ideally within 1 hour of recognition
Antibiotic timing: If sepsis is definite or probable and shock is absent then we--> adminster abx immediately, ideally within 1 hour of recognition
If sepsis is POSSIBLE and shock is present then we--> adminster abx immediately, ideally within 1 hour of recognition
If sepsis is possible and shock is absent--> rapid assessment of infectious vs non-infectious causes of acute illness; administer abx w/in 3 hours if concern for infection persists
Berman "if someone has that hypotension requiring vasopressors--> if that is present and you think sepsis is a possible cause, then we need to get abx started w/in __ _____ no matter what, even if you think there are other causes. 1 hour
If we dont have septic shock--> its a little heard to tell perhaps there are other causes of their clinical presentation, then we do a little work up and we have _____ 3 hours
When choosing antibiotic therapy. consider the suspected source of infection when choosing abx; Broad spectrum IV abs should be initiated that target: both gram + and gram - bacteria at minimum
If high risk for MDR (multi-drug resistant gram (-) organism, use ___ abx with gram (-) coverage 2
Risk factors for MRSA include: prior history of MRSA infection or colonization; recent IV abx w/in 90 days; history of recurrent skin infections or chronic wounds; presence of invasive devices (i.e. infusion port; HD; recent hospital admissions
Risk factors for MDR Gram (-) organisms consists of: proven infection or colonization w/ abx-resistant organism in the last year; local prevalence of abx-resistant organisms > or= 10%; Hospital acquired infection; broad spectrum abx use w/in 90 days; travel to hihgly endemic country w/in last 90 days; hospitalization abroad w/in 90 days
2 agents w/ gram (-) activity--> Name 2 combinations? 2 Beta lactams--> Cefepime or Piper/Tazo as one agent and other FQ or glycoside
Risk factors for candida-related sepsis Candida colonizations at multiple sites (urine, lungs); surrogate markers (B-D-glucan assay (neutropenia, immunosppuression, high severity of illness, long ICU stay); Central venous catheters, IV drug use, TPN, GI tract perforation; Emergency GI or hepatobiliary surgery; acute renal failure or HD, severe thermal injury
What are the principles of managing abx? 1. administer loading doses of abx 2. optimize PK/PD principles-> i.e prolonged infusion of B-lactam 3. Emergent source control
what should we consider when determining duration of antimicrobials in sepsis/septic shock? assess at least daily for ability to de-escalate (choose abx that are more narrow than what we originally chose and base on cultures we get back); use shortest effective duration over longer durations
What is the role of Procaclitonin (PCT) 1. undetectable in healthy states, but rises rapidly in pro-inflammatory states, especially bacterial infections 2. can be elevated in some non-infectious conditions including trauma, burns, certain cancers, cardiogenic shock, peritoneal dialysis and cirrhosis
Guidelines recommend _______ use of PCT for initiation of abx AGAINST
If optimal duration of therapy is unclear, consider use of PCT AND _______ _______ to decide when to discontinue antimicrobials clinical evaluation
Goal of earlu aggressive resuscitation is to: correct hypovolemia and increase perfusion; increase BP and normalize HR, MAP goal >/= to 65 mmHg; restore perfusion and normalize lactic acid
STEP 2: Fluid resuscitation with ISOTONIC crystalloids given as an IV bolus--> DOSE? at least 30 mL/kg (IBW) w/in 3 hours; Use ABW if obese (>/=30) *balanced crystalloids are preferred
Consider _______ if require substantial amounts of crystalloid to maintain adequate MAP Albumin *if we give them lots of fluids and pt is still having issues with Hyperkalemia, we can consider Albumin
Which fluids for resuscitation will we avoid using? Colloids such as Hetastarch and gelatin
What are the 2 types of IV fluids? Crystalloids (aqueous solution of salts and other water soluble molecules) and Colloids (large molecular weight solutions (>30,000 Da) these remain in the intravascular space for hours to days but are expensive.
Total body water consists of: Intracellular fluid (ICF) 2/3 Extracellular Fluid (ECF) 1/3
Extracellular fluid (ECF) 1/3 is divided further into Interstitial (75%) and Intravascular (25%). Which are we targeting for septic shock? Intravascular space *this is because we need to start perfusing the body better. so we want the fluid to be intravascular.
In septic shock, we are going to focus on these 2 fluids for resuscitation (so the fluids that are similar to our plasma and specifically want to use balanced fluids (ones that have BUFFERS),** which 2 are we needing to focus on for the exam? Lactated ringers and Plasmalyte (Normosol)
Why are we interested mainly in LR and Plasmalyte/Normosol? Na Content (130 and 140); they contain buffers (Lactate (28); Acetate (27) Gluconate (23); they are both isotonic and they are BALANCED
Why can't we use Dextrose 5%? we can't use hyotonic fluids since they won't stay in the intravascular space.
For exam purposes when choosing resusitation fluids, we need to know? Na+ content, because thats usually what controls the tonicity; Know if its isotonic or hypotonic; and if its a BALANCED fluid or not.
What is our most common colloid? What is the problem with it? Albumin; can cause volume overload b/c of these proteins that pull in a lot of fluid
Hydroxyethyl starch has what adverse effects? can cause renal dysfunction and increased mortality
Due to high cost and potential increased AE's, colloids are reserved for pts who have received _____ volumes of crystalloids and required _______ fluid resuscitation High; additional
What is the distribution of IV fluid for Isotonic fluids in the 1. Intracellular; 2. Interstitial; 3. Intravascular? *Based on 1 L 1. none 2. 750 mL 3. 250 mL
What is the distribution of IV fluid for Dextrose 5% in the 1. Intracellular; 2. Interstitial; 3. Intravascular? *Based on 1 L 1. 667 mL 2. 250 mL 3. 83 mL
What is the distribution of IV fluid for Albumin 5% in the 1. Intracellular; 2. Interstitial; 3. Intravascular? *Based on 1 L 1. none 2. none 3. 1000 mL (remember that albumni will get into the Intravascular space but again can cause VOLUME OVERLOAD
Many pts require > 30 mL/kg of fluids, continued resuscitation based on restoring ______ perfusion
What do we look for on a physical exam when pt is receiving fluid resuscitation? vital signs. CAPILLARY REFILL, pulse, skin tugor, and warmth, mental status, urine output (Goal >/= 0.5mL/kg/hr
What do we look for on lab findings when pt is receiving fluid resuscitation? LACTIC ACID, serum creatinine, AST/ALT
STEP 3: Vasopressor Therapy: we initiate when? and what agents do we use? initiate when Hypotension refractory to fluid resuscitation (MAP <65mmHg); Norepi (NE is first line vasopressor), Vasopressin if refractory to NE, Corticosteroids (last line if the above won't work
MAP formula: BP--> CO x SVR MAP--> 2/3 DPB + 1/3 SBP
Drug: NE: MOA and AE? a1 agonism, weak b agonism; AE: arrhythmias
Drug: Epi: MOA and AE? potent a1, and b agonism; AE: arrhythmias, splanchnic and cardiac ischemia, LACTIC ACIDOSIS, HYPERGLYCEMIA
Drug: Vasopressin: MOA and AE? stimulates V1 and V2 AE: DIGITAL AND MESENTERIC ISCHEMIA, cardiac ischemia, arrhythmias
Drug: Phenylephrine: MOA and AE? selective a1 agoinst; AE: splanchnic vasoconstriction; BRADYCARDIA
Drug: Dopamine: MOA and AE? D1 activity w/ low doses (1-4 mcg/kg/min); increased b1 w/ moderate doses (5-10 mcg/kg/min); Increased a1 and b1 with high doses (10-20 mcg/kg/min) AE: arrhythmias, CARDIAC ISCHEMIA, variable hemodynamic effects based on dose
Drug: Angiotensin II: MOA and AE? Vasoconstriction at AT1 receptors and release of aldosterone AE: THROMBOSIS, tachycardia, peripheral ischemia, thrombocytopenia
Drug: Dobutamine: MOA and AE? Primarily B agonism, minimum a1 AE: Arrhythmias, hypotension
All vasopressors are ________ and can cause tissue necrosis due to local vasoconstriction Vesicants
What is the preferred administration for Vasopressors? Central Venous Catheters (CVC-aka CENTRAL LINE)
Guidelines recommend starting _______ via ________ line when CVC not available Vasopressors; peripheral
What is the first line agent over other vasopressors? Norepinephrine
If inadequate MAP on NE, add this drug as an adjunct vasopressor instead of escalating NE dose; this is also the 2nd line vasopressor Vasopressin
This is a newer agent; may yse as adjucntive vasopressor after NE and Vasopressin, but it comes with increased risk of THROMBOSIS Angiotensin II
Consider this agent as an adjuct vasopressor after NE and Vasopressin; can use alone IF CARDIAC DYSFUNCTION SUSPECTED Epinephrine
This agent may be used with evidence of cardiac dysfunction despite adequate fluid resuscitation and use of vasopressors; use this agent in combination with NE Dobutamine
This agent is NOT PREFERRED--> it may be used in patients at low risk of tachyarrhythmias or with absolute or relative bradycardia Dopamine
This agent has no recommendation, not routinely used; may use in pts with tachyarrhythmias Phenylephrine
Step 4: Corticosteroids: Recommendation is for adults with spetic shock and an _________ requirement for vasopressor therapy and given IV ongoing
Which corticosteroid and what is the dose? IV hydrocortisone at 200 mg/day given as 50 mg IV q 6h
_________ infusion corticosteroids not recommended due to higher rates of hyperglycemia compared to intermittent dosing Continuous
Start corticosteroids when vasopressor doses exceed ___________ mcg/kg/min NE equivalents. Early admin of corticosteroids is associated with improved outcomes >/= 0.25
Created by: Xander635
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