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Critical Care Literature Flashcards

1
Q

Can COP be affected by general anesthesia?

A

YES, • COP in healthy dogs under GA decreased by 5mmHg (not predicted by IVF volume given or concurrent TS measurement)

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2
Q

How do axillary and rectal temps compare?

A

• Axillary and rectal temp are correlated but large gradient 3-4 degree F
○ Axillary and auricular are much less stressful!

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3
Q

Is a low refractometric TPP a good prediction of hypoAlb?

A

Not great
suboptimal for prediction of hypoalbuminemia (high proportion of false negatives)
○ Refractometric TPP

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4
Q

During hospitalization, what was seen with ascorbic acid?

A

It increased in dogs

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5
Q

What was the effect of IV dextrose (similar to parenteral nutrition) in healthy dogs on coagulation?

A

mildly interfere with coagulation but NOT clinically significant
○ MA lower, higher D-dimers, prolonged PT/PTT

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6
Q

Can you perform BMBT in cats?

A

YES
• 55 sedated cats for BMBT (primary hemostasis): Reference values of 34-105 sec
○ Consecutive readings in cats can vary up to 87sec!

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7
Q

Can the Anticoagulant Rodenticide Test detect second generations rodenticides (brodifacoum, bromethalin)?

A

No, Only detects warfarin

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8
Q

When should you consider vWD in cats?

A

• VWD has been reported in a few cats!!! Consider when platelet count and coags are normal

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9
Q

What was a major determinant of thrombin generation in healthy dogs?

A

Canine platelet membrane derived microparticles

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10
Q

In ex vivo models, does HES affect platelets?

A

YES, longer closure times - suggesting platelet dysfunction

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11
Q

What is see in dogs with trhombosis?

A

Normo and hypercoag state are common

Activated Protein C resistance is common

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12
Q

Based on TEG, what is predictive of survival in sepsis?

A

Higher Protein C and AT, and hypercoag for survival in sepsis (elevated MA)

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13
Q

What happens to PT/PTT in citrated blood that sits out?

A

• Stored citrated whole blood at room temp for 24 and 48 hrs did not significantly alter PT but it significantly shorted PTT - meaning that samples can be sent out to measure PT BUT NOT for PTT

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14
Q

What is seen with hemoabdomen in cats?

A

Evenly distribution of neoplasia (46%, most HAS of spleen) and non-neoplasia (54%)
○ Anemia, prolonged PT/PTT, most hypovolemic
○ Poor prognosis

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15
Q

What factor def should be considered in a dog that has excessive bleeding but normal coags?

A

Factor 13

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16
Q

What is the prognosis of dogs with hemophilia A?

A 
Hemophilia A (Factor VIII def) - Had a good long term prognosis
		○ Severity of FVIII:C activity did NOT predict CS, transfusion needs, or long term prognosis
		○ Mixed breed, GSD, Labs most common (most
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17
Q

Is severity of FVIII:C activity predict CS, transfusion needs, or outcome?

A

NO :)

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18
Q

After trauma in dogs, what is poor prognostic indicator regarding coag?

A

hypocoaguable were more likely NOT to survive

○ Prolonged PTT correlated with nonsurival (also with APPLE score, lactate, and base excess)

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19
Q

What is seen on coag panel in healthy BMD?

A

Healthy Bernese Mountain Dogs have prolonged PTT - May be related to high lupus anticoagulants and antiphospholipid antibodies in these dogs (importance = unknown)

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20
Q

What is true regarding Antithrombin Activity

A

Increased mortality risk, which progressively increased as ATA decreased (sen: 58%, Spec 85% = 85% not sole factor)
○ Low AT: IMHA, pancreatitis, hepatopathy, neoplasia

More dogs had Leukocytosis, hemostatic changes, hypoalbuminemia, hyperbilirubinemia

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21
Q

What happened to feline monocytes after exposure to LPS?

A

• Surface expressed and intracellular TF can be measured in feline monocytes
○ Treatment with LPS induced dose dependent TF expression on feline monocytes
§ Response was inhibited by giving fetal bovine serum

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22
Q

How do NSAIDs affect platelet function?

A

• Common NSAIDs did NOT significantly affect platelet function (aspirin (at anti-infalmmatory, 10mg/kg q12hrs), carprofen, meloxicam), HOWEVER, deracoxib had a mild decrease in platelet aggregation
○ No changes in plasma thromboxane or prostanglandins noted

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23
Q

What is post trauma coagulopathy?

A

• Post-trauma coagulopathy resulting in hemorrhage leadings to preventable deaths within 24 hrs
Resulting from endothelial dysfunction and inflammation - systemic hypocoag and hyperfibrinolysis!! = BLEEDING

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24
Q

What are platelet inhibitors that result in thrombocytopathia during hepatobiliary disease?

A

Bile and FDPs (they accumulate)

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25
Q

How does hepatobiliary disease affect primary and secondary hemostatsis?

A

○ Primary hemostasis:
§ Thrombocytopenia: GI bleeding, thrombosis, DIC consumption, hypersplenism from portal hypertension, decreased thrombopoeitin
□ Exception in hepatoceullar carcinomas if tumor makes TPO
§ Thrombocytopathia: Changes in platelet membrane, decreased thromboxane synthesis, storage pool defects in ATP and seronotin, circulating ihibitors - bile acids and FDPs (not cleared by liver)
§ Effects on vasculature: Esp with portal hypertension - increased shear stress that then leads to endothelial cell dysfunction (hypocoag, esp with NO and increased endotoxin)
○ Secondary Hemostasis
§ Coag defs (esp Vit K) and changes in anticoagulants
§ Chronic hepatitis: Decreased fibrinogen

DIC looks the same as changes with liver dz, in humans they look at platelets and Factor VIII then

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26
Q

In acute and chronic hepatitis what is the prognosis with prolonged PT/PTT?

A

Worse prognosis

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27
Q

IN aflatoxin and cycad seed ingestion what is predictive of nonsurvival?

A

Prolonged PT/PTT and low protein C and AT

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28
Q

What are the 3 main imbalances that occur in coagulation with hepatobiliary disease?

A 
Impaired hemostasis (low plt, dysfunctional plts, decreased coag factors, decreased vit K, dysfibrinogenemia)
Promote hypercoag (increased vWF, portal hypertension, decreased protein C,S, AT, abnormal endothelial function)
Promote fibrinolysis (increased tPA, decreased TAFI)
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29
Q

What is seen on TEM when hetastarch is added?

A

hypocoagubility - Effects appear to be related to dose dependent alternation in fibrinogen and inhibition of platelet function

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30
Q

What effect did venipuncture trauma have on TEG?

A

• Mild to moderate venipuncture trauma had little effect on TEG overall (R significantly affected = shorter) - More rapid initation of clot formation

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31
Q

What is true regarding monitoring heparin with TEG?

A

Progressive changes in TEG tracing (prolonged R and decreased angle and MA); maximal change at 3-5 hrs after dosing
○ Extensive prolongation of R (even with little heparin (0.075U/ml) may indicate that TEG is too sensitive to be used to monitor heparin
§ This is below lower limit of AntiXa Activity

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32
Q

Why should we do cautious about using protamine to reverse heparin?

A

• Protamine in healthy dogs: Prolonged clot formation time and decreased overall clot strength based on TEG in dose dependent manner (Hypocoag state)

May need to cautious about using to reverse effect of heparin

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33
Q

What affects did pred have on TEG?

A

• Prednisone (2mg/kg/day for 7 days) +/- with aspirin (0.5mg/kg/day) resulted in increased clot strength (increased MA) and decreased clot lysis in healthy dogs

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34
Q

What are the 3 main effects of pred on coag?

A

increased MA, elevated fibrinogen, and decreased AT levels)
○ When low dose aspirin given with steroids no effect on TEG results
○ Lots of variation when used in clinical cases

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35
Q

If you have a low HCT what happens to TEG?

A

HYPERcoag

Thought that normally RBCs act as a dilute for plasma coag factors, so then they are gone = hyper

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36
Q

Did sedation affect TEG in cats?

A

Yes!shorter clotting time, and greater alpha angle, BUT no difference in MA (unlikely to be clinical significant)

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37
Q

Is TEG good screening for dogs given LPS endotoxin?

A

NO! D-dimers was the earliest indication of coag changes

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38
Q

Do dogs with antiphospholipid antibodies play a role in thrombosis?

A

NO! • Antiphosphosolipid Antibodies do NOT play strong role in thrombosis in dogs (spontaneous thrombosis, HAC, and IMHA dogs)
○ No dogs had lupus anticoagulants

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39
Q

What happens to platelets at very HIGH doses of cyclosporine?

A

alter platelet plasma membranes (flow P-selectin and phosphatidylserine, COX expression) AND increased thromboxane production in dogs at immmunosuppressive dose (19 mg/kg PO q12hrs)
○ Suggesting that hypercoagulability is possible at this dose

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40
Q

What should cats with renal infarcts be screened for?

A

Need to be screened for occult cardiomyopathy
○ If renal infarcts: More likely to have HCM (4.5X) and have distal aortic thrombi (8X); Less likely to have neoplasia (0.7X)

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41
Q

In cats with renal infarcts what is the role of hyperT4?

A

None, no association noted

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42
Q

In acutely paralyzed dogs and cats what is an accurate diagnostic marker of acute ATE?

A

• ΔGlucose and %Δglucose (from peripheral to central venus) are accurate diagnostic marker of acute ATE in acutely paralyzed dogs and cats
○ Δglu cutt offs: 30 mg/dl (cats); 16 mg/dl (dogs)
§ Sen: 100%, Spec 90% (cats), 100% (dogs)
○ Compared to controls with ortho/neuro dz resulting in acute limb paralysis

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43
Q

What is known about TEGs in ITP patients?

A

At start all dogs were hypocoaguable based on TEG but over the treatment all dogs had TEG tracing suggestive of hypercoagubility (unknown clinical risk of thrombosis)

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44
Q

What do dogs with PLN have besides hypercoag?

A

High protein C

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45
Q

What is the prognosis of dogs with aortic thrombosis?

A

MST significantly longer in dogs with chronic disease compared to acute disease (chronic MST 30 days, 0-959 vs acute MST 1.5 days, 0-120)
§ Overall poor outcomes, but protracted periods
§ Acute (45%), chronic (48%)
§ Weak pulses (19%), Absent pulses (55%)

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46
Q

What concurrent diseases are see with aortic thrombi in dogs?

A

Neoplasia. Steroids, renal dx, cardiac dz

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47
Q

What concurrent diseases are see with splenic thrombi in dogs?

A

Neoplasia (54% - LSA), steroids (43%), SIRS (26%), DIC (20%), pancreatitis (18%), IM (16% - IMHA)
§ PLN or HAC
§ Concurrent splenic infarct in 33%

48
Q

What % of dogs with splenic thrombi have portal v thrombi too?

A

18%

49
Q

What is the most common disease in dogs with port vein thrombosis?

A

Hepatic disease

50
Q

How many PVT dogs were on steroids?

A

42%!!!

51
Q

When should you consider a PVT?

A

Dogs with abdominal pain, ascites, and thrombocytopenia

52
Q

What is the prognosis of PVT in dogs?

A

§ 42% survived to d/c: Better survival if on anticoagulants; worse if multiple thrombi or SIRS

53
Q

What is known about D-dimers and PTE?

A

○ D-dimers

54
Q

What corrected prolonged BMBT in dogs on aspirin and should be considered if aspirin induced coagulopathy in dogs?

A

IV DDAVP (desmopressin)

55
Q

What are Eptifibatide and abciximab? What did they show in cats?

A

• Glycoprotein IIb/IIIa antagonists in cats: Eptifibatide causes significant reduction in platelet aggregation in vitro, BUT no antiplatelet effect noted with abciximab

56
Q

In dogs on low dose aspirin, how many responded?

A

1/3 had platelet inhibition, BUT 2/3 had aspirin resistance!!! Not related to COX expression
Another study: 30% failed to respond

57
Q

Is Anti10a good to monitor Dalteparin in dogs or Enoxparin in cats?

A

• Dogs getting Dalteparin: Inconsistent dose adjustments using Ant-Xa
○ Dogs with high G values on TEG may require closer monitoring and greater dose adjustments to get target AntiXa levels
○ Bleeding complications in 3/38 (rare)
○ IMHA, PLE, PLN, Neoplasia

• Enoxaparin (LMWH, 1mg/kg SQ q12hrs) in cats had antithrombotic effects in a venous status model in healthy cats (significant at 4hrs, reduction but NOT significant at 12 hrs)
	○ Anti-Xa activity was poorly correlated with thrombus formation = POOR predictor of enoxaparin's antithrombotic effects
58
Q

What is true regarding fibrinolysis in dogs compared to humans?

A

• Dogs are hyperfibrinolytic compared to humans and likely will need HIGHER doses of anti-fibrinolytics
○ Tranexamic acid needed to inhibit (dogs 144.7 vs humans 14.7)
○ E-Aminocaproic acid needed to inhibit (dogs 511.7 vs humans 122)

59
Q

What should greyhound get prior to amputation and why/

A

• E-Aminocaproic acid should be administer prior to limb amputation in greyhounds, since it reduced the frequency of bleeding (controlling for dogs that also got FFP) - 5.7 X more likely to bleed if they did not get EACA!!
○ 28% had delayed post-op bleeding 48-72 hrs after surgery

60
Q

What is the MOA of E-Aminocaproic acid?

A

Prevents activation of plasmin by binding to lysine binding site on plasminogen = BLOCKs activation of plasminogento to plasmin by plasminogen activator

61
Q

What is the prevalence of VetALI with transfusions of blood or plasma?

A

• VetALI (PaO2: FiO2

62
Q

In which cat blood type may you get discordant results?

A

Phenotype B

63
Q

What can be used in hypotensive cats to increased SAP?

A
  • Bovine Hemoglobin Glutamer-200 (Hb-200) can be used in hypotensive cats to increase SAP (increased >80 mmHg in 75% cats)
    • Adverse effects: resp, vomiting, pigmented serum (30)
    • Given as bolus or CRI
64
Q

In cats, what resulted in significantly greater increased in PCV after transfusion?

A

type specific, cross matched pRBCs results in significantly greater increase in post-transfusion PCV compared to typed, NOT cross matched PCV transfusions

65
Q

Which cytokine is increased in stored canine pRBCs that could be proinflammatory? How can it be reduced?

A

○ Marked, storage-time dependent accumulation of IL-8 noted in canine pRBCs = Pro-inflammatory effects of transfusion in stored RBCs

This was attenuated when leukoreduction was performed

66
Q

What is seen in healthy dogs that get a transfusion and how can this be lessened?

A

○ Profound inflammation in response to transfusion in normal dogs
§ Increased WBC (esp Neutrophils), increased fibringogen, and CRP

When pRBCs underwent leukoreduction it eliminated this inflammatory response

67
Q

What are the components of ADCAS in anemic dogs?

A

ADCAS: Anemic Dog Clinical Assessment Score: MM color, Pulse quality, HR

68
Q

What happened to various parameters in dogs with anemia after transfusion?

A

§ All ADCAS variables decreased after transfusion

§ Hgb concentration, HCT, CvO2 increases significantly, lactate decreased significantly after the transfusion

69
Q

Did pRBC storage time affect survival in dogs?

A

NO, unless dogs with hemolysis (90% with IMHA): Longer duration pRBC storage was a negative risk factor for survival
□ Every 7 days increase in storage = 0.79 lesser odds of 30 day survival!!

70
Q

In general what was pRBC storage time associated with in dogs?

A

longer duration of storage associated with development of new or progressive coagulation failure and TED
□ No association with pRBC storage and survival in all dogs
□ NOTE: It was close with MODS (p=0.053) and DIC (p=0.061)
□ NOTE: Oldest transfusions were close to having effect as well (p=0.053)

71
Q

Did dogs getting other non pRBC transfusions affect their chances of having a complication?

A

YES

Also higher pretransfusion HCT and larger dose of pRBCS = risk of nonsurvival

72
Q

What is true regarding the delivery of canine and feline pRBCs?

A

○ Delivery of canine pRBCs via mechanical systems (volumetric pump or syringe pump) was associated with HIGH risk of early loss of transfused cells (via labeled RBCs assess by flow cytometry)
§ RBCs delivered by gravity flow had more “survive” in 24 hrs
○ In feline pRBCs there is NOT a difference with delivery method (gravity vs pump) in the short or long term

Average T1/2 transfused RBCs: 23 days

73
Q

Can you use refridgerated plasma instead of frozen?

A

Yes!
○ It takes about 35 mins to thaw FFP (WOW that is a long time) - Refrigerated plasma is a faster option that did have significant decreased in activity of all clotting factors but it was minor (no values outside RR)

74
Q

What happens to plasma when it is left at room temp?

A

○ Standard that FFP is produced by freezing plasma from blood within 8 hrs of collection, BUT when plasma was stored at ambient temp for 8, 12, and 24 hrs there was NOT change in therapeutic coagulation factor and hemostatic protein content!!!
§ Frozen plasma after 24 hrs had significantly HIGHER FVIII and FX (compared to prep’ed at 8hrs)

75
Q

Why should Greyhounds not be FFP donors?

A

significantly LOWER Factor X, fibrinogen, and vWF = Should NOT be used on FFP donors!

76
Q

What is true regarding plasma that has been froxen for 5 years?

A

○ FFP loses factor V and VII after 1 year and then becomes frozen plasma - HOWEVER canine frozen plasma (stored for 5 years) resulted in hypercoagubility (TEG) and Factor VIII and X activity was lower but still present
§ Need to check it this can be clinically used (this would save a ton of money)

77
Q

Can you refreeze FFP within 1 hr of thawing?

A

YES! ○ Refreezing FFP within 1 hr after initial thawing did NOT affect hemostatic protein activity or content (similar to FFP without refreezing)

78
Q

What is the main use of FFP now?

A

○ FFP mostly used for coagulopathies now (not really used for hypoalbuminemia or pancreatitis)
§ FFP resulted in reduction in PT/PTT
§ FFP did not significantly increase albumin (15-18 ml/kg)

79
Q

Are canine blood donors iron def?

A

○ Canine blood donors did NOT have iron deficiency (high serum iron concentrations than controls, higher % transferrin saturation, lower unsaturated iron binding capacity)
§ Freq donors (14 consecutive blood donations every 8 wks) developed mild iron def (still within RR) = Decreased % transferrin saturation and increased unsaturated iron-binding capacity, and total iron binding capacity

80
Q

How quickly do blood donors regenerate their RBCs?

A

restored depleted RBCs within 10 days after donation and MAINTAINED iron status

81
Q

What was seen in VBG of cats with Aelurostrongylus abstrusus?

A

Hypoventilation (likely related to parasite obstructing airways) and respiratory acidosis
○ Normalized with tx

82
Q

In which patients is HH blood gas the worst?

A

With hypoalbuminemia patients

83
Q

What results in a decreased in ScVO2?

A
  1. Decreased O2 tissue delivery (low CO, decreased PaO2, anemia)
  2. Increased O2 tissue uptake (sepsis, shivering, seizures, fever)
84
Q

What is a STRONG predictor of mortality in critically ill patients and how can it be used?

A
  • Central venous oxygen saturation (ScVo2) is a strong predictor of mortality in critically ill dogs
    • Each 10% drop in ScvO2 below 68% = 68% Odds of non-survival increase by 2.66X
85
Q

What is the use of N-acetylcystein in critically ill dogs?

A

• Randomized, blinded, placebo control: N-acetylcysteine vs placebo in critically ill dogs
○ Ill dogs experience oxidative stress (lower Vit , elevated urine 8-isoprostane/creatinine ratio, lower glutathionine) = BUT giving NAC within first 48 hrs did NOT impact illness severity or survival
§ If did maintain glutathione levels (which dropped in placebo) and increased plasma cysteine

86
Q

What are risk factors of nosocomial infections?

A

• 16.3% dogs, 12% cats during hospitalization

○ Risk Factors: Longer hospital stays, placement of U cath, sx, antiulcer meds, ABX

87
Q

What can be used to differentiate sepsis from SIRS? What disease does this not work well for?

A

• NT-pCNP can be used to differentiate sepsis from SIRS and normal animals (mainly expressed in endothelium and MPs)
○ NOT great with septic peritonitis!!! (75% had false negative!)
○ Cutoff: 10.1pmol/L (sepc 89%, sen 25% but w/o septic abdomen sen 92%)

88
Q

What is the MOA of hypocalcemia in sepsis?

A

• Cross-over study: Hypocalcemia (tCa and iCa) that occurs with endotoxin (injection of LPS) is associated with hypovitaminosis D (increased PTH level results)
○ Urinary tCa is below limit of detection in septic dogs

No change in iMg noted

89
Q

What is true about urine protein in SIRS dogs?

A

Evidence of glomerular and tubular dysfunction
• SIRS alters urine protein excretion in dogs: SIRS dogs had higher UPC, urine albumin to creatinine, and urinary retinol-binding protein: creatinine than controls
○ Urine electrophoresis revealed 11 bands compared to 3 in controls
§ Mainly LMW (58%, 80kDa)
○ Indicates both glomerular and tubular dysfunction!

90
Q

In cats what is more likely with sepsis than SIRS?

A

High band neutrophils and hypoalbuminemia seen in sepsis compared to nSIRS
○ IL-1B and IL-6, Chloride (low) = Prognostic biomarker of nonsurvival in cats with sepsis

91
Q

What are Prognostic biomarker of nonsurvival in cats with sepsis?

A

IL-1B and IL-6, Chloride (low)

92
Q

What are the 3 models of MODS?

A

• Models:
○ “One Hit”: Organ failure develops as direct results of massive initial insult (sepsis, polytrauma, burn)
○ “Two Hit”: Priming insult which followed by subsequent insult (can be small like catheter infection)
○ “Sustained Hit”: Continuous insult (ventilator-associated pneumonia)

93
Q

In dogs with sepsis how often do we see MODS? And what is the prognosis?

A

• 114 dogs with sepsis: 78% had 1 organ dysfunction, 50% had MODS (dysfunction of at least 2 organ systems)
○ Mortality rate increased as # dysfunctional organ systems increased
○ Mortality rate in MODS 70% compared to non-MODS 25%

94
Q

What is APPLE?

A

• APPLE: Acute Patient Physiologic and Laboratory Evaluation Score - Validated in dogs and cats
○ DOGS (810)
§ 10 variables: Creatinine, WBC count, albumin, SpO2, total bilirubin, mentation score, RR, age, lactate, free fluid in body cavity
§ 5 variables: Glucose, albumin, mentation score, platelet count, and lactate
○ CATS (600) - 8 variable predicts outcome significantly better than 5 variable
§ 8 variable: Mentation score, temp, MAP, lactate, PCV, BUN, chloride, body cavity fluid score

5 variables: Mentation score, temp, MAP, lactate, PCV

95
Q

What % of dogs that undergo CRP are discharged?

A

About 5%

96
Q

Is there an advantage of vasopressin over EPI in CPR?

A

NO

97
Q

What is an early prognostic indicator of successful weaning of dogs off PPV?

A

• PaO2/FiO2 is a early prognostic indicator of successful weaning of dogs off PPV (cutoff: 252 mmHg)

98
Q

What is true about giving LRS and its effects on lactate?

A

• LRS rapidly given to healthy dogs significantly increase plasma lactate concentration within 10 mins and returned to baseline within 60 mins after stopping fluid (2-4)
○ Need to consider this when using lactate to assess prognosis in dogs on being resuscitated with LRS

99
Q

What is true regarding giving IVF boluses to hypotensive dogs and does it affect prognosis?

A

• Hypotension in dogs: IVF boluses resulted in increased SAP but did NOT reliably decreased HR
○ Dogs that normalized BP within first hour more likely to be d/c alive!

100
Q

When fluid resuscitating dogs, what results in the fastest effects?

A

• Dogs with limited fluid volume resuscitation with hypertonic saline and HES achieved stabilization significantly faster than with conventional with large volumes of crystalloids

101
Q

What are the numbers on colloids? 6% Hetastarch 650/0.7.13.4:1

A 
6% Hetastarch 650/0.7.13.4:1
Concentration
Name of HES
MW (kDa)
Molar Substitution
C2:C6 Ratio
102
Q

What are the major factors that affect coagulation when HES is given?

A

Decreased plt adhesion
Decreased circulating vWF
Decreased FVIII
Increased fibrinolysis

103
Q

What is true regarding COP measures in plasma vs whole blood in dogs and cats?

A

• Plasma and whole blood COP differ but are still within RR (21-25 mmHg) - Recommend that use the same sample type for comparisons in a patient
○ Same significant result NOT seen in cat’s COP measurements - Still do it in on the same sample type for comparison

104
Q

What is the effect of 5% Lyophilized canine specific albumin (14 dogs with septic peritonitis)?

A

Increase in albumin, COP, and BP (increase in albumin lasted 24 hrs)
○ 1 dog died of resp signs (120 hrs) after transfusion

105
Q

Is 5% Human Serum albumin safe in critically ill dogs?

A

• 5% Human Serum Albumin: 20 ml/kg/day until albumin 20g/L
○ Dogs: 4 days; Cats: 3 days
○ Safe in large number critically ill (418 dogs and 170 cats) with hypoalbuminemia
○ NO control group (CAUTION)

106
Q

Is there a difference in complication rates btwn NE vs NG tubes?

A

NO

107
Q

Did septic complication with TPN affect survivals?

A

No

108
Q

What are the major components of plasma?

A 
Coag factors
Albumin
Alpha 2 marcoglobulin
Igs
AT
109
Q

What makes the endothelial glycocalyx happy?

A

Plasma

MAD with colloids and crystalloids

110
Q

Is FFP helpful in pancreatitis?

A

NO! Mortality was high in FFP group

111
Q

What is the Dal blood type in dogs?

A

Dalmatians do NOT have it, so if you give blood to them it sensitizes them

112
Q

What cat is exclusively Type A?

A

Simaese

113
Q

What do you do if you have an anemic Type B cat and no B blood?

A

Give dog blood

But short life span

114
Q

What is the free water def?

A

0.6 x current BW x [(current Na/desired Na)-1]

Strictly free water loss when free water def = change in BW

115
Q

How do you correct Na for hyperglycemia?

A

1.6 X increase glucose over 100 (first 400), then 2.4 x increase glucose

Critical Care (2 decks)

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