Fluid management and Blood therapy Flashcards
1
Q
The daily fluid volume we require is?
A
25 to 35 mL/kg per day (~2–3 liters per day)
2
Q
What is the body Fluid distribution
A
Total body water 60% of lean body weight Intracellular water (ICV) 40% of body weight (2/3 TBW) Extracellular water (ECV) 20% of body weight (1/3 TBW) Plasma volume 4% Interstitial volume 16%
3
Q
The electrolyte composition of body fluid
A
Na K
ICF ..10 150
ECF 150 4.5
4
Q
etiology of hypokalemia
A
poor diet,Gi loss:vomit,diarhea,ngt suction,kayexalate
renal loss:Diuretics,metabolic alkalosis,Insulin,beta2 agonist
5
Q
Presentation of hypokalemia
A
Skeletal muscle cramp, weakness, paralysis,worsends digoxin toxicity
6
Q
Ekg hypokalemia
A
Short PR, long QT, Flat T-wave, U wave
7
Q
treatment Hypokalemia
A
Potassium supplementation
8
Q
What is the most important oncotically active constituent of ECF
A
Albumin
Because of its smaller molecular weight and higher concentration relative to other plasma proteins, albumin is the primary determinant of both capillary and interstitial oncotic pressures
9
Q
What parameters detects fluid movement
A
Osmotic Forces and Hydrostatic pressure
10
Q
Communication of plasma and ISF happens via?
A
Capillary pores
11
Q
Capillary Hydrostatic pressure is Affected by these factors
A
CO and Vascular tone, this is the intravascular blood pressure
12
Q
Interstitial fluid pressure is what kind of pressure
A
This is the hydrostatic pressure of the interstitial space
13
Q
Is the interstitial fluid pressure negative or positive
A
Its slightly negative,due to the lymphatic vessels contraction.
Rigid or encapsulated tissues of the kidneys, brain, bone marrow, and skeletal muscle have a slightly positive interstitial fluid pressure.
14
Q
Whats the plasma osmotic pressure
A
Plasma oncotic pressure (πp) is the osmotic force of colloidal proteins within the vascular space
15
Q
What is interstitial oncotic pressure
A
. Interstitial oncotic pressure is the osmotic force of colloidal proteins within the interstitial space
16
Q
Which parameters favors retention of fluid in the interstitial space
A
Increases in Capillary hydrostatic pressure and interstitial oncotic pressure favor filtration of fluid into the interstitial space
17
Q
Which parameters favors adsorption of fluid into the intravascular space
A
increases in interstitial fluid pressure and plasma oncotic pressure favor absorption of fluid into the intravascular space. (Nagelhout, 6th ed, 347-368)
18
Q
The rate of exchange between between the plasma and interstitial is affected by?
A
by the physical forces of hydrostatic and oncotic pressures and the permeability and surface area of the capillary membranes
19
Q
What are the forces that favor filtration from the capillary
A
The forces that favor filtration from the capillary are capillary hydrostatic pressure and interstitial oncotic pressure,
20
Q
What are the forces that oppose filtration form the capillary
A
are capillary oncotic pressure and interstitial hydrostatic pressure
21
Q
Whats the net filtration pressure
A
The forces that favor filtration from the capillary are capillary hydrostatic pressure and interstitial oncotic pressure, and the forces that oppose filtration are capillary oncotic pressure and interstitial hydrostatic pressure. The sum of their effects is known as net filtration pressure (NFP)
22
Q
What are the electrolytes that are the main determinant of osmotic pressures in the intracellular and extracellular
A
Osmotic forces dictate fluid movement
Na+ main determinant of extracellular osmotic pressure
K+ main determinant of intracellular osmotic pressure
23
Q
what is the function and mechanism of action of The Endothelial Glycocalyx
A
—- -a gel layer in capillary epithelium that creates a physiologically active barrier within vascular space
Creates a barrier between vessel and blood
It binds to circulating plasma albumin, preserving oncotic pressure and decreasing capillary permeability to water
Also contains inflammatory mediators, free radical scavenging, activation of anticoagulation factors
Hyperglycemia is a major risk factor for damage or destruction of the endothelial glycocalyx
Loss of endothelial glycocalyx integrity can lead to alterations in transcapillary fluid dynamics in the critically ill
matrix of glycoproteins, polysaccharides, and hyaluronic acid that bind to ionic side chains and plasma proteins to create a physiologically active barrier within the vascular space. ***This dynamic barrier ionically repels negatively charged polar compounds in addition to blood components, to create a zone of exclusion between the surface of the glycocalyx and the center of the vessel, aiding in the prevention of blood component adhesion to the vascular wall and augmenting laminar blood flow. By binding to circulating plasma albumin, the glycocalyx also helps to preserve capillary oncotic pressure and decrease capillary permeability to water
24
Q
Renin-angiotensin-aldosterone-system
Reabsorption of sodium (and water)
A
. In response to hypotension (as detected by intracardiac and renal afferent arteriole baroreceptors) and systemic sympathetic stimulation, the juxtaglomerular cells of the kidney release the enzyme renin. The interaction of circulating renin with the precursor angiotensinogen causes cleaving of angiotensinogen to the active substance angiotensin I. Angiotensin I exerts local vasoconstrictor activity, but its primary role is as a precursor for the more potent angiotensin II. This change occurs in the lungs as a result of angiotensin-converting enzyme (ACE) acting as a catalyst for the conversion of angiotensin I to angiotensin II. Angiotensin II is a potent vasoconstrictor and directly stimulates the renal tubules to reabsorb sodium and water. It also causes the adrenal cortex to release aldosterone, which further stimulates sodium and water retention by the kidneys
25
```
Antidiuretic hormone (ADH)
Reabsorption of water
```
. In response to even minute increases in serum osmolality (as detected by osmoreceptors in the hypothalamus), the posterior pituitary gland releases ADH, which causes aquaporin channels within the kidney to transiently reabsorb large quantities of water. This helps preserve circulating volume and contributes to a tremendous increase in urine concentration and osmolality. ADH also plays an important role in preserving blood pressure by acting as a potent arterial vasoconstrictor. Decreases in circulating blood volume (as detected by baroreceptors in the atria, carotid body, and aorta) stimulate this hormones release, although this mechanism is much less sensitive than osmolality-mediated secretion. The detection of increased serum osmolality also causes the hypothalamus to stimulate thirst
26
Atrial natriuretic peptide
Stimulated by stretch receptors in the atria
Stimulates kidneys to release sodium and water, thereby reducing intravascular volume
Inhibits renin and ADH
Stretch receptors within the cardiac atrial walls stimulate The release of ANP from cardiac myocytes as a result of increased-preload or hypervolemic states. This stimulates the kidney to release sodium and water, thus reducing circulating blood volume and offloading the heart. ANP also produces specific vasoactive responses in the afferent and efferent renal arterioles to increase the glomerular filtration rate, and it inhibits the release of renin and ADH. Conversely, during periods when preload is decreased, atrial receptors inhibit the release of ANP
27
the pre-op eval for fluid volume status are?
```
Skin turgor, mucous membrane, peripheral edema
Lung sounds
Vital signs
Urine output
HCT
Urine specific gravity
BUN/Creatinine
```
28
Effects of Acidosis
```
Increased P50
Decreased contractility
Increased SNS tone
Increased arrhythmias risk
Increased Cerebral blood flow
increased Icp
Increased Pvr
Hyperkalemia
```
29
Effects of Alkalosis
```
Decreased p50
Decreased coronary blood flow
Increased risk of dysrythmias
Decreased cerebral blood flow
Decreased ICP
Decreased PVR
Hypokalemia
Decreased ionised calcium
```
30
Intravenous fluid therapy
Hypotonic solutions
Replaces water loss
called maintenance fluids
examples: D5W
Isotonic solutions (Normal Osmolarity 285-295 mOsm/L)
Replaces water and electrolyte loss
called replacement fluids
examples: LR, NS
Hypertonic solutions
For hyponatremia or shock
examples: D5 1/2NS (405 mOsm/L), 3% NS (1026 mOsm/L
31
benefits of crys
. The use of crystalloids to replace active intravascular losses in the perioperative setting is beneficial for providing immediate restoration of circulating vascular volume, preservation of microcirculatory flow, decrease in hormone-mediated vasoconstriction, and correction of plasma hyperviscosity associated with acute hemorrhage
32
Disadvantages of crystalloids
Because isotonic crystalloids are distributed evenly throughout the extracellular space, their ability to expand plasma volume is transient. Because of their low molecular weight, crystalloid solutions contribute to hemodilution of plasma proteins and loss of capillary oncotic pressure. This favors filtration of approximately 75% to 80% of administered volumes into the interstitial space
33
Hypotonic solutions
1/2NS and D5W
34
Isotonic solutions
0.9NS,LR,Plamalyte A,Albumin 5%,Voluven 6%,Hespan 6%,
35
Hypertonic solutions
NAcl 3%,D5nacl 0.9%,D5 Nacl 0.45%,D5 Lr,Dextran 10%
36
Benefits of Plasmalyte-A, Normosol-R, and Isolyte S
because they do not contain calcium, these solutions are compatible with blood products.
These solutions have the most favorable acid-base profile compared to plasma; they preserve physiologic pH, renal perfusion, and overall renal function better than 0.9% saline. They also utilize sodium gluconate and sodium acetate as alkalinizing buffers rather than lactate.
37
adv and disadv of 0.9 Nacl in water
In large volumes, produces high Cl- content, which leads to dilutional hyperchloremic acidosis
The typical solution for diluting PRBCs (cannot use Ca++ containing crystalloids.
The presence of an extraordinarily high chloride load contributes to acid-base imbalances and the well-recognized tendency for 0.9% saline to contribute to dose-dependent hyperchloremic metabolic acidosis
Hyperchloremia may also have a significant impact on renal function. This is thought to be due in part to the impact of excess renal reabsorption of chloride on renal arteriolar vascular resistance, leading to a decrease in glomerular filtration rates. Hyperchloremia may also impair renal handling of bicarbonate
0.9% saline is the preferred fluid for patients at risk for cerebral edema. NS may also be indicated in fluid management of patients with anuria and end-stage renal disease who cannot excrete the potassium content of more balanced crystalloid solutions.
38
Adv and disadv of LR
Normal saline with electrolytes (K+, Ca++) and buffer (lactate)
273 mOsm/L, provides 100cc free water per liter of solution, tends to lower Na+
considered isotonic but actually slightly hypotonic
Lactate converted to bicarbonate (mild metabolic alkalosis)
Avoid large volume of LR in diabetics
byproducts of hepatic metabolism of lactate are gluconeogenic
Limit in ESRD as contains K+
Avoid mixing with PRBCs Ca++ binds to citrate
. LR is mildly hypotonic and may cause transient serum hypo-osmolality and associated cerebral edema. As a result, LR is contraindicated in patients with traumatic brain injury or other neurovascular insults.
39
Adv and disAdv of D5W
Hypotonic solution (260 mOsm/L)
Has little place perioperatively
Exception in neonates and DM who are receiving insulin
Even then typically D5 ½ NS is used.
Causes free water intoxication and hyponatremia
Provides 170-200 calories/1000cc for energy
Can cause hyperglycemia
40
Adv abd disadv of 3% and 5% Nacl
3% or 5% NaCl
3% has Na/ Cl 513 mEq; 5% has Na/ Cl 856 mEq
Used for low volume resuscitation (rarely)
Principle role is the treatment of hyponatremia
Risk of hyperchloremia, hypernatremia, and cellular dehydration.osmotic demyelination syndrome.
osmotic demyelination syndrome.
41
Adv and disadv of colloids
Osmotically active substances
High molecular weight
Administered in a volume equivalent to volume of fluid/ blood lost from intravascular volume
Half-life in circulation is 16 hours but can be 2-3 hours
Colloids are suspensions of high-molecular weight molecules in electrolyte solutions that produce intravascular volume expansion by directly increasing plasma oncotic pressure and interacting with the endothelial glycocalyx to decrease transcapillary filtration.
Colloid solutions are classified by molecular weight, concentration, and half-life.
42
Synthetic colloid: Dextran
```
Artificial colloid; high molecular weight
Use has been largely abandoned
Hyperosmolar, ½ life 6-12 hours
Side effects include
Acute renal failure
anaphylactoid reaction/ anaphylaxis
platelet inhibition; antithrombotic effects
noncardiac pulmonary edema
interference with crossmatching
```
43
Synthetic Colloid: Hetastarch(Hespan)
```
Synthetically derived from starchy plants (potatoes)
Classified by molecular weight
Allergenic potential
Coagulopathy
Severe Pruritis
Nephrotoxicity (BLACK BOX)
Max. dose: Limited to <20 mL/kg/day
```
Randomized controlled trials have demonstrated the risk of kidney injury, dialysis requirements, coagulopathy, and even increased mortality associated with HES
44
Adv and disadv of albumin
Colloid derived from pooled human plasma
Heat treated to eliminate risk of disease transmission
Does not contain coagulation factors or blood group antibodies
Available as 5% or 25% solution
Reduces complicatiomns assosciated with tissue edema
Anaphylaxis risk
45
Avoid colloid solutions if?
1.If patients have clinical conditions that are likely to precipitate endothelial injury such as hyperglycemia or sepsis.
46
Colloids benefits
Proponents of colloids say…
Prolonged increase in plasma volume by maintaining plasma oncotic pressure
Intravascular half life is 3-6 hours for colloid 20-30 minutes for crystalloid
Fluid of choice with hypoproteinemia
Less tissue edema
Less volume infused
47
Crystalloids benefits
Crystalloids equally effective as colloid in restoring intravascular volume if given in sufficient amounts
Support u/o better
Less likely to cause pulmonary edema, colloids associated with coagulation and antigenic problems
Inexpensive
48
Impact of surgery and anesthesia on vascular flow and
| organ perfusion
Stress activates hypothalamus-pituitary axis-release of cortisol
Cortisol stimulates protein catabolism, hepatic gluconeogenesis, glycogenolysis and release of plasma proteins
Release of catecholamines- increased HR, increased SVR, microcirculatory vasoconstriction, release of ADH, reabsorption of water, and potassium excretion
Stimulation of somatic and autonomic afferent nerves in the area of surgical incision triggers the activation of the hypothalamic-pituitary axis (HPA). As a result of this central nervous activation, the hypothalamus releases corticotropin-releasing hormone, prompting the anterior pituitary gland to secrete adrenocorticotropic hormone, which then elicits the creation and release of cortisol from the adrenal cortex. Cortisol stimulates protein catabolism, hepatic gluconeogenesis and glycogenolysis, and increased hepatic production and release of plasma proteins
increased interstitial oncotic pressure to help preserve intravascular volume.
hyperglycemia is a major risk factor for damage or destruction of the endothelial glycocalyx; it also impairs wound healing and contributes to osmotic diuresis.
49
Impact of surgery and anesthesia on vascular flow and
| organ perfusion
Surgical trauma and tissue injury leads to alterations in microcirculatory flow—vasodilation, tissue edema, intravascular loss, hypotension, and decreased organ perfusion.
Surgical trauma and tissue injury stimulate the local endothelial release of cytokines and other inflammatory mediators that contribute to hyperthermia, increased oxygen demands, and regional alterations in microcirculatory flow.
Unrestricted cytokines can contribute to vasodilation, endothelial damage, increased filtration, tissue edema, intravascular loss, hypotension, and decreased organ perfusion
promote inflammatory loss of gastrointestinal endothelial integrity leading to translocation of bacteria and systemic inflammatory responses.
cortisol is the profound anti-inflammatory effect it exerts by inhibiting the production, release, and vascular aggregation of inflammatory mediators.
.
The development of interstitial edema is a primary cause of tissue congestion, capillary collapse, loss of waste removal and nutrient exchange capabilities, decreased microcirculatory flow, and tissue ischemia
50
Intraoperative fluid requirements
Prophylactic volume administration in euvolemic patients is an antiquated practice with substantial risk of disrupting the endothelial glycocalyx and contributing to pathologic fluid overload”
Current evidence:
utilization of hemodynamic measures to evaluate fluid responsiveness in patients with active preoperative volume losses
Bowel preparations may cause excessive fluid losses
51
Sources to be considered for reason to give fluid replacement
1. Baseline maintenance fluid requirement- using LR in most cases
2. Fasting (NPO) deficit (maintenance rate x hours NPO for deficit)
3. Replacement of blood loss
(3:1 crystalloid replacement)
4. Evaporative losses
(based on invasiveness of surgery)
52
Fluid replacement Holliday Segar formular
Holliday-Segar formula: 4:2:1:
<10 kg- 4ml/kg
11-20kg: 40ml + next 10 kg @ 2ml/kg
>20 kg: 60ml + anything over 20 kg @1ml/kg
53
Fluid deficit replacement
The maintenance requirement multiplied by the number of hours patient NPO
If patient receiving maintenance IV fluids there is no NPO deficit but consider other losses
If baseline hypovolemia exists consider overall deficit larger than just NPO deficit
fluid should be replaced to restore mean arterial pressure, heart rate, and filling pressures prior to induction.
normal urine output is also desirable.
Fluid replacement approaching 75-100ml/kg may encounter dilutional coagulopathy
54
Npo deficit replacement
Replacement strategy
½ deficit replaced in 1st hour of surgery
¼ deficit replaced in 2nd hour of surgery
Remaining ¼ replaced in 3rd hour of surgery
Fluid deficit (75kg male) = 115ml/hr maintenance
8 hours NPO
115 x 8 = 920cc
Replacement
460cc in 1st hour
230cc in 2nd hour
230cc in 3rd hour
55
Monitoring blood loss parameters
Monitoring blood loss throughout cases is essential
Visual estimation
Floor and surgical drapes
Soaked gauze 4x4= 10cc of blood
Soaked laparotomy pads= 100-150cc of blood
Suction containers
56
whats the allowable blood loss
Determines how much blood you can lose to reach a particular hgb/hct
Helps estimate transfusion threshold
Decision to transfuse is always individualized and based on multiple factors including co-morbidities, rate of blood loss, and ability of surgeon to control ongoing blood loss
57
Evaporative fluid loss and 3rd space loss
Evaporative loss related directly to the surface area of surgical wound and duration of exposure
3rd space loss is due to fluid shifts and intravascular volume deficit caused by redistribution of fluids
Trauma, infection (sepsis), burns, ascites
• Superficial Trauma (orofacial): 1–2 mL/kg per hr
• Minimal Trauma (herniorrhaphy): 2–4 mL/kg per hr
• Moderate Trauma (major nonabdominal or laparoscopic abdominal surgery): 4–6 mL/kg
per hr
• Severe Trauma (major open abdominal surgery): 6–8 mL/kg per hr
58
Blood loss replacement
Blood loss
replace 3:1 - 3 cc crystalloid for 1 cc blood loss
replace 1:1 - blood, colloid
59
ERAS and Goal-directed Fluid Therapy (GDFT)
ERAS Enhanced Recovery After Surgery
Aim: “utilize individualized hemodynamic end-points to support oxygen transport balance by minimizing oxygen demand and optimizing CO, tissue oxygenation, capillary and macrovascular flow, oxygen and nutrient delivery, and end-organ perfusion”
Mostly questioning science behind replacement of third space losses
MAP, CVP, and urine output do not have good predictive value at measuring fluid responsiveness
60
FRank starling Curve mechanism
The basis of the Frank-Starling mechanism is the relationship between left ventricular end diastolic volume (LVEDV) and myocardial contractility (as measured by SV). An increase in left ventricular preload will, to an extent, increase myocardial contractility by stretching cardiac sarcomeres and optimizing the overlap of actin and myosin filaments to generate greater myocardial force. This allows the myocardium to compensate for increases in ventricular preload. The Frank–Starling mechanism is highly effective until the point at which the sarcomere cannot generate additional force; further increases in preload after this point will generate no further increases in SV
61
What is the gold standard for direct evaluation of cardiac function and volume status
Esophageal Doppler/ Echo
| TEE
62
lImitations to noninvasive hemodynamic monitoring with pulse contour analysis.
```
Inaccurate readings with the following:
Spontaneous ventilation
Small tidal volumes
Open chest
Sustained Arrhythmias
High levels of PEEP
Right heart dysfunction
```
63
what are the goal-directed fluid protocol
Pre-op: limiting NPO times
Intra-op: Baseline assessment of target hemodynamic measures
Small fluid boluses (200-250 mL) to assess responsiveness
Vasoactive or inotropic support as needed
Post-op: Fluid management within the ERAS protocol is continued when the patient transitions to the postoperative phase. Early discontinuation of intravenous fluid therapy and initiation of oral intake is encouraged
64
What is a primary cellular injury?
Direct surgical trauma from the incision, heating elements such as cautery, retraction of internal organs and so on, can lead to primary cellular injury.
Primary cellular injury can impair oxygen and nutrient delivery to vital organs resulting from global and local perfusion changes.
65
what is a secondary cellular injury
Secondary cellular injury is a process that is caused by the stress response associated with surgery that results in the release of local inflammatory mediators or the systemic effects of cytokines, inflammatory mediators, or hormones.
66
The two fundamental elements that affect post-surgical outcomes are attributed to
fluid therapy and effective pain management
67
whats the outcome of both pri/sec cellular injury
The combination of both primary and secondary injury at the cellular level has been attributed to delayed wound healing, gut dysfunction, and may lead to post-surgical complications.
68
What's the indication for blood transfuse
```
Expand intravascular volume
Increase oxygen-carrying capacity
Hemoglobin and hematocrit
Clinical judgment based on certain factors
Cardiovascular status
Age
Anticipated blood loss
Arterial oxygenation
Cardiac output and blood volume
```
69
Guidelines and transfusion threshold
ASA guidelines 2006 state the following recommendations regarding blood transfusion
Rarely indicated if HBG >10g/dl and almost always indicated if HGB< 6g/dl
If HGB is between 6-10g/dl transfusion is based on the patient’s risk for complications and inadequate oxygenation
Use of a transfusion trigger of HGB is not recommended
Where appropriate use autologous blood, cell saver or normovolemic dilution
Indications for transfusion more liberal for autologous vs blood bank blood
70
Standards for PRBC transfusion
SCREEN: Type specific ABO and Rh factor and antibodies (99.94% rate of compatibility)
CROSSMATCH: Further testing with the actual unit to be administered
Mixes patient blood with unit to test for agglutination
1 unit PRBC (200 ml)
increase hgb ~ 1gm/dL/ hct ~2-3%
hct 65- 70% per unit
Citrate toxicity occurs with multiple units
Hypocalcemia
Monitor ionized calcium
Leukocyte-reduced blood decreases rates of complications
71
UNIVERsal donor blood type is?
Group O,
| because their RBCs are devoid of any of the ABO antigens, but have both A and B antibodies in the plasma.
72
Universal recipient blood type is?
Group AB
| AB blood possess both A and B antigens on the RBCs, and lack anti-A and anti-B antibodies
73
what's the most important blood compatibility test
The most important tests of blood compatibility are those used to determine ABO and Rh (also known as type D ) blood groupings.
Transfusion of ABO or Rh incompatible blood can result in serious hemolysis. Patients who may need a transfusion and banked blood stored for transfusion are typed to determine ABO and Rh status.
74
The ratio of infusion and resultant values of of h/h is?
PRBC infusions are generally administered in a ratio of 1 mL for each 2 mL of blood loss (along with crystalloids or colloids for volume). The 1 to 2 ratio is the result of the higher Hct of PRBC. A common assumption is one unit of PRBCs increases Hgb 1 g/dL and Hct 2% to 3%.
75
What are the blood storage complications
Time-related; >14 days begin to show changes
Depletion of 2,3-diphosphoglycerate (DPG)
Depletion of ATP (adenosine triphosphate)
Oxidative damage
Increased adhesion to human vascular endothelium
Acidosis
Altered morphology of red blood cells (change in shape, decreased flexibility, membrane loss)
Accumulation of microaggregates
Hyperkalemia (as high as 17.2 mEq/L)
Absence of viable platelets (after 2 days of refrigerated storage)
Absence of factors V and VIII
Hemolysis
Accumulation of proinflammatory metabolic and breakdown products
76
Whats Autologous blood?
Pts blood given back to pt.nit of packed red blood cells
Complications of autologous transfusion include
anemia
pre-op myocardial ischemia from the anemia
administration of the wrong unit (1:100,000)
need for more frequent blood transfusion
febrile and allergic reaction
77
whats cell Cell saver blood?
Salvage of blood from the surgical site
Blood processed- is washed and separated
Red cells are transfused back
Contraindications to cell salvage
Surgery with wounds contaminated with bacteria, amniotic fluid, malignant cells or patients with sepsis, chemical contaminants
Large volume cell saver transfusion: dilution of clotting factors and thrombocytopenia
Jehovah’s Witness: may accept cell saver
78
Contraindications to cell saver blood are?
Contraindications to cell salvage include surgery with wounds contaminated by bacteria, sepsis, bowel contents, amniotic fluid, or malignant cells. Cell-washing devices can provide a volume equivalent to 10 units of blood per hour for transfusion in cases of massive blood loss. Prolonged use of cell salvage for large volume autotransfusion may be associated with dilution of clotting factors and thrombocytopenia, and regular laboratory or point of care monitoring is required. Cell salvage should be considered in all cases where significant blood loss, greater than 1000 mL, is anticipated
Use cell salvage in combo with leukocyte depletion filter..this is safe!
79
Whats is acute normovolemic hemodilution(ANH)
Remove blood from patient
Replace blood volume lost with crystalloid or colloids
After surgical blood loss has slowed or stopped, the patient’s blood transfused back to the patient
80
Platelet transfusion
Multi-donor pooling (6 to 10) vs. single donor apheresis units
Uses include
thrombocytopenia
dysfunctional platelets
active bleeding
platelet count <50,000 for low, moderate risk surgery
Platelet count <100,000 for high risk surgery
5 day shelf life; stored at room temp
One unit increases platelet count 7,000-10,000 one hour after transfusion
HIGH Bacterial contamination risk in 1: 12000
Contamination of platelets is of particular concern. Platelets are stored for a maximum of 5
days at room temperature, and carry a risk of bacterial contamination of 1 in 12,000
81
FFP transfusion
Contains clotting factors and plasma proteins (no platelets)
Stored FROZEN for up to 1 year
VOLUME 200-250CC
MUST BE ABO Compatible
Uses
Urgent reversal of warfarin
Known coagulation factor deficiencies
Correction of microvascular bleeding in the presence of increased PT or PTT
Correction of microvascular bleeding in the patient transfused with more than one blood volume when PT and PTT cannot be obtained in a timely fashion
FFP is contraindicated for augmentation of plasma volume or albumin concentration
FFP is usually administered in doses of 5 to 8 mL/kg for reversal of warfarin, and 10 to 20 mL/kg for all other purposes, and it increases coagulation levels by 20% to 30%.
82
Cryoprecipitate transfusion
```
Derived from precipitate remaining after FFP is thawed
Contains:
Factor VIII (minimum 80 IU)
XIII
fibrinogen (minimum 150 mg)
von Willebrand factor
plasma
fibronectin
Used in the treatment of
von Willebrand’s disease
fibrinogen deficiencies (massive transfusions)
ABO compatible
Administer through a filter rapidly (200ml/h) and complete within 6 hours
```
83
what are the risk of transfusion
Human immunodeficiency virus (HIV) 1 : 1,500,000–1 : 2,000,000
Hepatitis B virus (HBV) 1 : 200,000–1 : 360,000
Hepatitis C virus (HCV) 1 : 1,000,000–1 : 2,000,000
Bacteria (All) 1 : 28,000–1 : 143,000
Acute hemolytic TR 1 : 625,000
Delayed hemolytic TR 1 : 400,000
Alloimmunization 1 : 1600
Immunosuppression (TRIM) 1 : 1
Transfusion-related acute lung injury 1 : 8000
All RBC mistransfusions 1 : 14,000–1 : 18,000
Anaphylactoid reactions 1 : 150,000
Fatalities 1 : 600,000
