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CCP 226 Immune πŸ› Flashcards

1
Q

target UO in sepsis

A
  1. > 0.5mL/kg/hr

this is based on KDIGO definition of AKI being Urine output less than 0.5 mL/kg/h for 6 hours

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2
Q

SIRS Criteria (β‰₯ 2 meets SIRS definition)

A
  1. Temp >38Β°C (100.4Β°F) or < 36Β°C (96.8Β°F)
  2. Heart rate > 90
  3. Respiratory rate > 20 or PaCOβ‚‚ < 32 mm Hg
  4. WBC > 12,000/mmΒ³, < 4,000/mmΒ³, or > 10% bands
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3
Q

qSOFA (Quick SOFA) Score for Sepsis

A
  1. Altered mental status GCS <15
  2. Respiratory rate β‰₯22
  3. Systolic BP ≀100
  4. qSOFA Scores 2-3 are associated with a 3- to 14-fold increase in in-hospital mortality
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4
Q

risk factors for sepsis

A
  1. Advancing age of patients
  2. Immunosuppression (diabetes, cancer, steroids, etc)
  3. Multi drug resistant infection
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5
Q

definition of sepsis

A
  1. Life threatening organ dysfunction caused by a dysregulated host response to infection
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6
Q

definition of septic shock

A
  1. Despite adequate fluid resuscitation, requires vasopressors to maintain a MAP >65 mmHg
    with a lactate >2mmol/L
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7
Q

qSOFA

A
  1. Respiratory rate > 22 per minute
  2. Altered mental status (GCS <15)
  3. Systolic blood pressure < 100 mmHg
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8
Q

most common sources of infection in sepsis

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A 
Meningitis
Pneumonia
Intra-abdominal
Genitourinary
Skin and soft tissue
Endocarditis
Lines/Tubes
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9
Q

% increase in mortality for each hour delay in ABX in septic shock

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A

8% per hour

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10
Q

results of VAAST trial (vasopressin in septic shock)

A
  1. can add vasopressin to NE to achieve MAP goal

2. can add vasopressin to NE to decrease NE dose

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11
Q

Type A lactic acidosis

A

Type A = Tissue Hypoxia

1. Shock: septic, hypovolemic, cardiogenic,
obstructive
2. Acute mesenteric ischemia
3. Acute limb ischemia
4. Carbon monoxide poisoning
5. Cocaine use
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12
Q

Type B lactic acidosis

A

Type B = Independent of Tissue Hypoxia

Seizure
DKA
Thiamine deficiency

Drugs; metformin, isoniazid, beta 2
agonists, epinephrine, Propofol,
salicylates

Inborn errors of metabolism
Malignancy (e.g. lymphoma)

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13
Q

most common type of bacteria in lung infection

A
  1. Gram Positive Streptococcus pneumoniae, which is responsible for almost 50% of cases
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14
Q

most common type of bacteria in abdominal infection

A
  1. Gram Negative

2. Anerobes

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15
Q

most common type of bacteria in renal infection

A
  1. Gram Negative E coli and Klebsiella pneumoniae
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16
Q

Sepsis treatment pathway

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. Cultures and source control (ie. drain abscess)
  2. Early Antibiotics
  3. Restore Perfusion (fluid loading)
  4. Adjuncts (ie. vasopressors, steroids)
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17
Q

sepsis MAP goal in early resuscitation

A

MAP β‰₯ 65 (based on original EGDT data)

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18
Q

A higher MAP goal (ie. 80) may be beneficial in what septic populations?

A
  1. History of CKD

2. History of chronic HTN

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19
Q

As norepinephrine doses rise, what adjunct should be considered?

A
  1. Vasopressin

2. dose 0.03 - 0.04 units/min

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20
Q

What are two pitfalls of epinephrine infusion in sepsis?

A
  1. Causes rise in skeletal lactate production, which skews lactate-clearance trending.
  2. More arrhythmogenic than other pressors.
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21
Q

common gram positive infections

A
  1. MRSA.
  2. Streptococcus .
  3. Staphylococcus.
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22
Q

PCADS mnemonic in sepsis

A
  1. Perfusion
  2. Cultures
  3. Antibiotics
  4. Diagnose
  5. Source control
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23
Q

Osteomyelitis definition

A

bone infection

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24
Q

myositis definition

A

Skeletal muscle infection

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25
Q

pathophysiological process of fluid extravasation in sepsis

A
  1. Microbe elicits an innate immune response in host
  2. Inflammatory response is produced by IL 1, 6, and TNF-a
  3. Inflammation spreads the membrane-like wall of the vasculature, allowing for fluid to escape into the interstitium.
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26
Q

pathophysiological process of septic cardiomyopathy

A
  1. inflammatory mediators such as IL 1, 6, and TNF-a cause disruption of cardiac myocyte activity
  2. leads to troponin elevation, myocardial depression, and some ECG changes
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27
Q

initial recommended fluid loading in sepsis

A

30mL/kg based on The Current Surviving Sepsis Campaign β€œSepsis 3.0” guidelines

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28
Q

passive leg raise test

A
  1. Elevate the legs to 45 degrees for 40-60 seconds
  2. watch for increase in Arterial BP (MAP) or decrease in HR

Indicates volume responsiveness

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29
Q

oxygen delivery equation

A

DO2 = CO x CaO2

CaO2 = (1.34 x Hgb x SaO2) + (0.003 x PaO2)

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30
Q

oxygen consumption equation

A

VO2 = CO x (CaO2 - CvO2)

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31
Q

oxygen extraction ratio

A

O2ER = (CaO2 - CvO2) / CaO2

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32
Q

Normal serum calcium levels

A
  1. Serum Ionized = between 1.15 and 1.30 mmol/L (anything over 1.0 is ok)
  2. Serum Total = 2.2 to 2.7 mmol/L

serum ionized calcium is the only one that is really important because that is the amount of β€œuseful” calcium you have in your serum.

ionized is the Ca++ content measured on your EPOC

33
Q

Components of the 1 hour sepsis bundle

A

1) Measure lactate
2) Obtain cultures
3) Begin broad-spectrum ABx
4) Isotonic 30mL/kg bolus if MAP < 65 or Lactate > 4
5) Vasopressor if MAP <65 (following fluid admin)

this is based on american β€œCMS Core Measures” protocol for centre for medicare and Medicaid services guidelines

34
Q

refractory septic shock treatment pathway

A

1) Optimize DO2 (Preload, afterload, contractility)
2) Source control (remove infected lines)
3) Correct profound metabolic acidosis (pH <7.0)
4) Correct hypocalcemia (serum ionized Ca++ < 1.0)
5) Adjunctive therapies (corticosteroids)

35
Q

What are some examples of non-infectious aetiologies that can cause SIRS?

A

Trauma, burns, pancreatitis, transfusion reactions

36
Q

What is the definition of septic shock as per sepsis 3?

A

1) Vasopressors required after sufficient fluid resuscitation to maintain map > 65mmHg
2) Lactate greater than 2 And a diagnosis of sepsis

37
Q

define sepsis

A

Life threatening organ dysfunction cause by a dysregulated host response to infection

38
Q

most common type of bacteria in skin infection

A

Gram positive, generally group A streptococcus (i.e., Streptococcus pyogenes), followed by methicillin-sensitive Staphylococcus aureus

39
Q

most common type of gram positive organisms

A
  1. Step
  2. Staph
  3. MRSA
40
Q

most common type of gram negatives organisms

A
  1. salmonella
  2. e. coli
  3. space bugs πŸ›
41
Q

what is the role of measuring serum lactate in sepsis resuscitation?

A
  1. serum lactate Identifies and can help quantify decreased tissue perfusion
  2. Trending lactate helps inform resuscitative efforts.
  3. important to recognize that the use of epinephrine or concomitant liver failure can confound lactate measurements
42
Q

how do the Organisms found in sepsis cause direct injury that can provoke hemodynamic collapse

A

excreted toxins cause direct vessel injury which opens endothelial tight junctions leading to vascular collapse

43
Q

how does host immune response result in endothelial injury and hemodynamic collapse in sepsis

A
  1. pathogen-excreted toxins activate the innate immune response and results in vasodilatory cytokine release
  2. the host immune system continues to release pro-inflammatory chemokines that promote ongoing inflammation and endothelial derangement
44
Q

how can pulse pressure variation on a-line be used to assess fluid responsiveness in sepsis?

A
  1. PPV of >10%-15% is an accurate predictor of fluid responsiveness
  2. patient must be in sinus rhythm
  3. patient must be mechanically ventilated with no spontaneous breaths
  4. patient must have normal lung compliance and abdominal compartment pressures
  5. patient must have an arterial line

PPV % = PPmax – PPmin Γ— 100

45
Q

Early Goal Directed Therapy (EGDT) definition

A
  1. The Rivers trial (2001) randomized patients with severe sepsis or septic shock to early goal-directed therapy (EGDT) vs. standard therapy
  2. EGDT used aggressive management of 5 key parameters to specified targets to optimise oxygen delivery to tissues in sepsis
46
Q

Early Goal Directed Therapy (EGDT) cocktail

A

Target Parameters:

  1. CVP 8-12 mmHg
  2. MAP 65 – 90 mmHg
  3. Urine output >0.5 ml/kg/hr
  4. Mixed venous oxygen saturation >65% / ScvO2 >70%
  5. Haematocrit >30%

Target Interventions

  1. Reduce work of breathing by early use of mechanical ventilation
  2. Large-volume fluid resuscitation
  3. Use of vasoactive agents: noradrenaline, dobutamine
  4. Transfusion
47
Q

why is normal saline a poor resuscitative fluid

A
  1. Normal saline increases systemic inflammation and multiorgan system dysfunction via hyperchloremia and worsened metabolic acidosis
48
Q

when are Adjunctive corticosteroids recommended in sepsis?

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. shock that are refractory to catecholamines and volume resuscitation
  2. defined as IV fluids to the limit of volume responsiveness and requires two vasopressors to reach a MAP goal >65 mmHg
49
Q

sepsis initial treatment pathway

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. Early investigations to determine infectious source
  2. Early source control with appropriate antibiotics
  3. Ongoing crystalloid resuscitation (Plasmalyte or LR preferred) as long as fluid responsive
  4. First line vasopressor NORepinephrine 2 to 200 mcg/min for MAP goal of 65 mmHg
  5. consider EPInephrine 2 to 50mcg/min if bradycardic
  6. consider vasopressin 0.03-0.04 units/min when NORepinephrine >15mcg/min
  7. foley/central line/invasive arterial monitoring
  8. trend lactate and fluid responsiveness
  9. If lactate fails to improve on subsequent readings consider septic-induced cardiomyopathy or other source of hyperlactatemia
  10. adjunctive agents such as corticosteroids if refractory shock
50
Q

common reasons why sepsis is missed as an inpatient diagnosis

A
  1. Lack of knowledge of sepsis risk factors, signs, symptoms
  2. Observations performed infrequently in certain patients
  3. Failure of sepsis screening processes
  4. Rationalize that fever is disease related
  5. β€œit can’t be sepsis because there is no fever”
  6. Staff do not give high priority to watching for sepsis due to workload and/or lack of knowledge
  7. Failure to communicate sepsis risk/symptoms in clinical handover
  8. Not testing lactate when appropriate
  9. Anchoring on current diagnosis, sepsis not considered
51
Q

clinical exam findings for sepsis based on source of infection

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. Cough/sputum/chest pain/shortness of breath (lungs)
  2. Abdominal pain/distension/vomiting/diarrhea (abdomen)
  3. Dysuria/frequency/indwelling catheter (kidneys)
  4. Skin or joint (pain/swelling/redness) (skin)
  5. Central line present (line sepsis)
  6. Mottled skin, cold extremities (shock)
  7. Fever/headache/nuchal rigidity (meningitic)
52
Q

clinical exam findings for lungs as a primary source of infection (identify source/source control)

A
  1. Cough
  2. sputum
  3. chest pain
  4. shortness of breath
53
Q

clinical exam findings for abdomen as a primary source of infection (identify source/source control)

A
  1. Abdominal pain
  2. distension
  3. N/V/D
54
Q

clinical exam findings for GU/kidneys as a primary source of infection (identify source/source control)

A
  1. Dysuria/frequency
  2. presence of indwelling catheter
  3. cloudy/foul smelling urine
55
Q

clinical exam findings for skin as a primary source of infection (identify source/source control)

A
  1. heat (Calor)
  2. pain (dolor)
  3. redness (rubor)
  4. swelling (tumor)
56
Q

STAT labs in a patient with suspected sepsis

A
  1. Serum Lactate (Repeat q2h if initial lactate >2 mmol/L)
  2. CBC and differential (looking for WBC count >12,000 or <4000 or bands >10%)
  3. INR, PTT, electrolytes, BUN, creatinine, glucose, LFT, lipase, troponin
  4. Blood cultures X 2 sets BEFORE antibiotics (include culture from central line, if present)
  5. Urinalysis and urine C&S
  6. Sputum for C&S
57
Q

STAT investigations in a patient with suspected sepsis

A
  1. Labs
  2. CXR
  3. ECG
58
Q

initial broad-spectrum ABX coverage for sepsis at any site

A
  1. vancomycin + piperacillin-tazobactam
59
Q

initial broad-spectrum ABX coverage for CNS infection (meningitis)

A
  1. vancomycin + cefTRIAXone + acyclovir
60
Q

initial broad-spectrum ABX coverage for GI/GU infection

A
  1. piperacillin-tazobactam
61
Q

initial broad-spectrum ABX coverage for skin infection

A
  1. vancomycin
62
Q

initial broad-spectrum ABX coverage for Community Acquired Pneumonia (CAP) infection

A
  1. cefTRIAXone

2. azithroMYCIN

63
Q

Comprehensive Head to toe assessment for infection source

A
  1. Diagnostic imaging (XR/CT)
  2. Urine microscopy/culture
  3. Sputum culture
  4. Faeces for C.difficile if diarrhoea
  5. Wound swab for culture
  6. Nasopharyngeal swabs
  7. Lumbar puncture (if indicated)
64
Q

goal for timing of ABX in sepsis

A
  1. Administer after blood cultures drawn and within 1 hour of presentation
65
Q

high risk patient cohorts for sepsis

A
  1. Looks unwell (homeless/poor baseline health status)
  2. Age > 65
  3. Recent surgery
  4. Immunocompromised (AIDS; chemotherapy;
    neutropenia; asplenia; transplant; chronic steroids)
  5. Chronic illness (diabetes; renal failure; hepatic failure;
    cancer; alcoholism; IV drug use)
66
Q

common sites for culturing in working up sepsis

A

blood, urine, cerebrospinal fluid [CSF], ascites fluid

67
Q

preferred vasopressors in order of administration in sepsis

A
  1. Norepinephrine 0.01-3.0 ΞΌg/kg/min
  2. Vasopressin 0.03 units/min (Addition of vasopressin generally utilized once norepinephrine dose is β‰₯15 ΞΌg/min)
  3. Epinephrine 0.01-2 ΞΌg/kg/min
68
Q

steroid dosing in refractory septic shock

A

Hydrocortisone 50 mg IV q6h for shock refractory to catecholamines and volume resuscitation

69
Q

what is the role of Methylene blue in refractory septic shock

A

Can counteract vasoplegia in distributive shock, but benefits to tissue oxygen delivery or mortality have not been demonstrated

last ditch hail mary

70
Q

discuss β€œsource control” and how to Find and control the source of infection in sepsis

A
  1. Remove old indwelling catheters as soon as possible. (The risk of a line-associated bloodstream infection is dependent on the duration and type of access)
  2. Physical exam requires full exposure and inspection to assess for CNS, odontogenic, sinus, respiratory, GI, GU, and soft tissue infections.
  3. CXR, Bedside U/S of the heart, lungs, abdominal right upper quadrant, kidneys, and bladder, CT scans as indicated by patient presentation
71
Q

discuss the approach to ongoing Monitoring for organ dysfunction and inadequate perfusion in Sepsis/critical illness

A
  1. Serial exams to evaluate Vital signs, mental status, cardiopulmonary exam, capillary refill, peripheral pulse, and skin
  2. Urine output (Normal urine output is at least 0.5 mL/kg/h)
  3. Chem-7/BMP (optimize acid/base status and electrolytes while monitoring renal function and maintaining relative euglycemia)
  4. Lactate (Identifies and quantifies decreased tissue perfusion. Trending lactate helps inform resuscitative efforts. confounded by epinephrine or liver failure)
  5. Blood gas (early detection of critical acid-base disturbances and ARDS)
72
Q

Sepsis definition (sepsis-3)

A

β€œlife-threatening organ dysfunction due to a dysregulated host response to infection.”

73
Q

Sequential Organ Failure Assessment (SOFA) Score

A
  1. SOFA Score is a mortality prediction score that is based on the degree of dysfunction of six organ systems
  2. score is calculated on ICU admission and q24 hours until discharge using the worst parameters measured during the prior 24 hours
74
Q

give some examples of why a septic patient may not meet SIRS criteria (ie, why does SIRS have shitty sensitivity for sepsis)

A
  1. elderly patients not mounting a febrile response
  2. current beta blocker use
  3. diagnostic futility of the WBC
75
Q

discuss the use of vasopressin in sepsis

A
  1. Adding low-dose vasopressin (0.01-0.04 units/min) as a catecholamine-sparing agent in patients responding appropriately to norepinephrine infusion offers no survival advantage
  2. Vasopressin infused at 4 units/h (0.07 units/min) may decrease dysrhythmias and increase cardiac index measurements compared with norepinephrine alone. However, it also increases total bilirubin measurements, should be used with caution in patients with mesenteric ischemia due to its strong effects on splanchnic vasculature, and is generally not recommended
76
Q

describe the role of ProCESS, ARISE, and ProMISe trials in current best practice guidelines for management of sepsis, and their impact on our understanding of EGDT

A
  1. In the initial study of early goal-directed therapy for sepsis, the treatment arm of the study received the majority of its fluid resuscitation early, while the control arm received the same volume but had it administered later, in violation of the treatment protocol.
  2. When repeated in the ProCESS, ARISE, and ProMISe trials, in which the treatment and control arms all received fluid resuscitation and antibiotics in the same way, the additional measures recommended in Rivers’s Early Goal-Directed Therapy protocol (central venous pressure of 8-12 mm Hg, red blood cell transfusion and dobutamine for central venous oxygen saturation <70%, vasodilators for MAP >90 mm Hg) made no difference in ultimate mortality
77
Q

Patients at highest risk of fungemia

A

the chronically ill with multiple comorbidities
recent antibiotic exposure
a CVC in situ
known Candida colonization

78
Q

the addition of antifungal therapy should be considered in which cohorts of patients with sepsis?

A

patients on TPN, with neutropenia or other immunosuppression, or with peritonitis or another breach of bowel wall integrity

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