Seminal articles 2021 Flashcards
Ionized hypocalcemia in critically ill dogs. JVIM 2009. Holowaychuck
Main takeaway points (3)
- Incidence if ionized hypoCa = 16%
- Septic dogs w/ +ve culture more likely to have iHypoCa
- iHypoCa associated w/ longer ICU stay
Ionized hypocalcemia in critically ill dogs. JVIM 2009. Holowaychuck et al
Causes of iHCa in critically ill (6)
- Parathyroid gland dysfunction
- Cytokine-mediated suppression of PTH release
- Vit D deficiency of lack of vit D activation
- HypoMg
- Ca2+ chelation
- Accumulation of Ca2+ in tissue, body fluids nd cells
Effects of fluid therapy on total protein and its influence on calculated unmeasured anions in the anesthetized dog. JVECC 2008. Valverde et al
Main takeaway point
Degree of TP decr after 10 mL/kg of IVF did NOT affect unmeasured anions when compared to pre-fluids TP
-TP, Hgb, PCV and AG were decreased while K+ increased with IVF
Electrocardiographic assessment of hyperkalemia in dogs and cats. JVECC 2008. Tag et al
Main takeaway points (2)
- HyperK in critically ill dogs and cats don’t correlated well w/ ECG
- Strongest correlation when K>8.5 mEq/L
Electrocardiographic assessment of hyperkalemia in dogs and cats. JVECC 2008. Tag et al
How does hyperK affect cell membrane potential
- Resting [K+] determines resting membrane potential (RMP)
- K+channels are open @ rest
- Increased [K+] will reduce the conc gradient across the membrane –> less -ve RMP
- Although increasing K+ will make the RMP less negative, increasing K+ also inactivate the Na/K channels (=allows K+ efflux) therefore the cells actually much slower in reaching the threshold potential
- Decreased K+ permeability slows K+ efflux during phase 3
- Altered permeability ends when slow Ca channel closes and K+ influx returns RMP to the resting state
NET EFFECT: Depress upstroke velocity and prolongs duration of action potential
Electrocardiographic assessment of hyperkalemia in dogs and cats. JVECC 2008. Tag et al
Body protection vs hyperK (2)
- Intracellular shift of K+ - b2 receptors
- Renal excretion of K+ –> Direct effect of K+ on K channels in principall cells AND indirect effect of incr aldosterone release
Electrocardiographic assessment of hyperkalemia in dogs and cats. JVECC 2008. Tag et al
How does hyperK change ECG
5.5-6.5 mEq/L: Incr T wave
6.6-7 mEq/L: Decr R wave amplitude, prolonged QRS and PR interval, ST segment depression
7.1-8.5 mEq/L: Decr P wave amplitude and polonrged QT interval
8.6-10 mEq/L: No p waves (atrial standstill) and sinoventricular rhythm
>10 mEq/L: Widened QRS complex –> smooth biphasic waveform, ventricular flutter/vfib –> asystole
Arterial thromboembolism in 250 cats in
general practice. JVIM 2014. Borgeat et al
- prevalence ATP 0.3%
- 61.2% euth at presentation
- 70.1% of remaining served >24h after pres
- of these 44.1% survived for at least 7 d
- for cats that survived > 7d, MST 94 days
- 6 cats alive one year post-presentation
Indepen predictors of 24 hr death/euth:
- hypothermia
- management by clinic 2
Indepen predictors of > 24hr w/in 7d death/euth:
- hypothermia
- failure to receive aspirin, clopidogrel or both
TRISS trial
Lower versus higher hemoglobin threshold for transfusion in
septic shock. NEJM 2014
In patients w/ septic shock (ICU setting), transfusion threshold of 7g/dL compared to 9g/dL had NO difference in mortality (90d) and rates of ischemic events
- higher threshold had 50% fewer blood transfusion
- supports surviving sepsis guidelines
LIFENOX trial
Low-molecular-weight heparin and mortality in acutely ill medical patients. NEJM 2011
Enoxaparin + elastic stockings compared to placebo + elastic stockings did NOT reduce rate of death from any cause among hospitalized, acutely ill patients
Acute lung injury following blood transfusion: Expanding the definition. CCM 2008 Marik
definition of TRALI
bilateral alveolar infiltrates
PF ratio <300mmHg
clinical exclusion of CHF
no preexisting ALI before transfusion
onset of signs occur w/in 6 hours of transfusion
no temporal relationship to alternative ALI risk factors
Acute lung injury following blood transfusion: Expanding the definition. CCM 2008 Marik
theory for TRALI (2)
1 antibody-mediated rx (classic TRALI)
#2 interaction b/w biologically active mediators in banked blood products and the lungs - phenomenon of immunomodulation 2-hit theory (delayed TRALI)
1 antibody-mediated theory
Acute lung injury following blood transfusion: Expanding the definition. CCM 2008 Marik
- transfusion of anti-granulocyte antibodies (donor plasma) into patients w/ leukocytes that antigens
- > complement activation, pulmonary sequestration + activation of neutrophils, endothelial damage (capillary leak syndrome)
- multiparous female donors
2 biologically active mediators
Acute lung injury following blood transfusion: Expanding the definition. CCM 2008 Marik
Released by stored WBC: histamine, eosinophilic cationic protein, eosinopihlic protein X, myeloperoxidase, PAI-1
Released by stored RBC: IL-1, IL-6, IL-8, bactericidal permeability-increasing protein, PLA2, TNF-a
2 sequence of events
Acute lung injury following blood transfusion: Expanding the definition. CCM 2008 Marik
1st event: Pulmonary endothelial activation + neutrophil sequestration
2nd: Mediators activate adherent neuts –> endothelial damage, capillary leak, TRALI
Acute lung injury following blood transfusion: Expanding the definition. CCM 2008 Marik
TRALI histology
- early ARDS: interstitial and intraalveolar edema, neutrophil extravasation into interstitium + air space
- increased # of neuts w/in pulmonary capillary vasculature + small pulmonary vessels
Acute lung injury following blood transfusion: Expanding the definition. CCM 2008 Marik
delayed TRALI
- timing
- patient population
- characteristic
6-72 hrs after slow development risk factors: sepsis, trauma, burns, ICU patient, multiple units resolves slowly uncommon to have a fever
Clinical practice guideline: Red blood cell transfusion in adult trauma and critical care. CCM 2009
- use in hemorrhagic shock
- use in acute hemorrhage, hemodynamic instability/inadequate DO2
- Restrictive strategy (7 vs 10 g/dL) is effective in hemodynamically stable anemia
- Consider if Hgb<7g/dl and (1) requiring mechanical ventilation, (2) resuscitated ill trauma patients, (3) those w/ stable dz
- Not used as an absolute method to improve tissue O2 consumption
- assess septic patients individually
- avoid transfusion in those @ risk of ALI/ARDS
- RBC transfusion is an independent risk factor for MOF and SIRS
- RBC transfusions independently associated w. longer ICU + hospital stay, incr complications, incr mortality
Correlation of hematocrit, platelet concentration, and plasma coagulation factors with results of thromboelastometry in canine whole blood samples. AJVR 2012 Smith
2 main points
- Coagulation time is determined by coag factor concentration; other variables dependent on plt + fibrinogen concentration
- HCT affects tracing (RBC acts as a diluent for plasma coag factors): Anemia leads to artifactual hypercoagulability and vice versa
Decontamination of the digestive tract and oropharynx in ICU patients. NEJM 2009
Mortality decreased by 3.5% with selective digestive decontamination (SDD) and 2.9% with selective oropharyngeal decontamination (SOD)
SDD: IV and topcai ABX to prevent 2ry g-ve colonization
SOD: application of topical antibiotics in the
oropharynx only:
Refractometric total plasma protein measurement as a cage-side indicator of hypoalbuminemia and hypoproteinemia in hospitalized dogs. JVECC 2011 Hayes
2 main points
- Hypercholesterolemia and hyperglycemia falsely increased total plasma protein (TPP) readings
- Refractometric TPP<5.8 g/dL is strongly indicative of both serum hypoalbuminemia and hypoproteinemia, with high specificity
serum totl protein (g/L) = 0.3 +0.84 (refractometric TPP [g/L]
Red cell distribution width and all-cause mortality in critically ill patients. CCM 2013
What is RDW and why does it matter
mechanism of why it predicts mortality
red cell distribution (RDW) expression of the variation of the size of RBC
RDW = RBC / MCV
RDW is a strong predictor for all-cause mortality in people
Red cell distribution width and all-cause mortality in critically ill patients. CCM 2013
main findings (2)
RDW >=13% was a strong predictor for all-cause mortality and bloodstream infection
RDW-associated mortality is independent of anemia when RDW>14.7%
Red cell distribution width and all-cause mortality in critically ill patients. CCM 2013
mechanisms (3) of why RDW predicts mortality
inflammation
oxidative stress –> contribute to high RDW by reducing RBC survival + release of immature RBC
atrial underfilling and activation of RAAS –> accelerate erythrocytosis and incr RDW via macrocytosis