Flashcards in Renal/Heme Deck (90):
The dominant form of PKD is also associated with
intracranial aneurysms and mitral valve prolapse
___% of ESRD patients have DM
___% of ESRD patients have HTN
Patients going for surgery with ARF will always have an ASA designation of
Two types of dialysis
Continuous peritoneal dialysis
Wide spread systemic manifestations are seen from uremia when the GFR decreases below
Patients with a GFR < ____ rely on dialysis for survival
Continuous peritoneal dialysis involves _____ and may be better for those who _______
1) Diffusive solute transport across the peritoneal membrane
2) Those who do not tolerate rapid fluid shifts and those with poor vascular access
Dialysis is required in these conditions
Hyperkalemia (can cause fatal arrhythmia)
Severe acidosis (will inhibit proper enzyme activity)
Pericarditis (will help reduce the fluid around the heart)0
Refractory GI symptoms
An AV fistula involves the anastamosis of
The radial artery and cephalic vein
Emergency vascular access for dialysis can be obtained from
Femoral vein or internal jugular vein
Basic purpose of hemodialysis
Diffusion of solutes between the blood and the dialysis solution remove metabolic wastes and restore buffers to the blood
A weight gain of __-__% of body mass in 2 days is appropriate between dialysis treatments
These types of drugs are readily cleared by dialysis
Low-molecular weight, water soluble, non protein bound drugs
(Best to give scheduled drugs after dialysis)
S/S of uremic encephalopathy
What is disequilibrium syndrome?
Transient CNS disturbance after rapid decrease in ECF osmolality compared with ICF osmolality --> this is due to dialysis
Patients with a GFR < __ will generally have anemia
(Unless the patient is on aggressive EPO replacement therapy. Most ESRD patients will be on EPO to increase their hematocrit to 36-40%)
Why do ESRD patients usually tolerate their anemia well
Because they have acidosis and increased 2,3-DPG, both of which shift the hgb-oxygen disassociation curve to the right (facilitates the unloading of O2)
Why are most patients with ESRD anemic?
1) Decreased EPO (decreases RBC production)
2) Decreased RBC life-span
3) GI blood loss, hemodilution, bone marrow suppression
4) Excess PTH replaces bone marrow with fibrous tissue
When should you transfuse for someone with ESRD?
Transfuse only when absolutely indicated <6-7g/dL or significant intra-operative blood loss
What is an important cause of coagulation issues in someone with ESRD?
release of defective von Willebrand factor
What is autonomic neuropathy?
Autonomic neuropathy is a nerve disorder that affects involuntary body functions, including heart rate, blood pressure, perspiration and digestion.
It isn't a specific disease. Autonomic neuropathy refers to damage to the autonomic nerves. This damage disrupts signals between the brain and portions of the autonomic nervous system, such as the heart, blood vessels and sweat glands. This can cause decreased or abnormal performance of one or more involuntary body functions.
Autonomic neuropathy can be a complication of a number of diseases and conditions. And some medications can cause autonomic neuropathy as a side effect. Signs, symptoms and treatment of autonomic neuropathy vary depending on the cause, and on which nerves are affected.
May have dizziness and fainting, urinary problems, sexual difficulties, gastroparesis, sluggish pupils, or exercise intolerance.
Avoidance of high protein foods can be a subtle sign of
renal disease (contributing to azotemia)
Can an AV fistula revision be given class E status?
Yes, because E is necessary to save LIFE OR LIMB
Someone who can't tolerate large fluid shifts is more likely to be on (HD/peritoneal dialysis)
Continuous peritoneal dialysis
If someone's ESRD is progressing towards dialysis, we should place IVs on their (dominant/non-dominant arm)
Dominant, because if they have an AV fistula placed, this will be on their non-dominant.
When should someone have dialysis before surgery?
The day before or the morning of
Considerations for the patient who JUST had HD
May have low K+ (but remember, that their body is still equilibrating)
May be dry--BP can plummet
Neuro considerations in the renal patient
1) Peripheral neuropathies
2) Autonomic neuropathy
3) Uremic encephalopathy
Questions to ask renal patients for neuro
Ever feel confused? Slow thinking? Foggy?
Ever have seizures?
Numbness/tingling in your extremities?
Dizziness when you stand up? (ANS neuopathy)
Any involuntary movement? Shaking, etc.
Why do people in ESRD get anemia?
- Low production
Decreased RBC lifespan
Fluid overload (dilutional)
Excess PTH in circulation
- Bone marrow replaced with fibrous tissue
Why do most people in ESRD tolerate anemia well?
Acidosis and increased 2,3-DPG encourage off-loading.
However, person will not tolerate the anemia well if they also have CAD
Mortality rate for those on dialysis, and what do they die from?
25% die per year
1/2 from infection (use aseptic technique!!!!)
1/2 from CV disease
Are those with ESRD more or less likely to bleed?
- Impaired platelets (decreased plt factor III activity -> less adhesiveness and aggregation)
- defective vWF
- Dialysis causes hypocomplementemia
Affect of ESRD on CO
Increases it (d/t anemia)
Hypercalcemia in ESRD causes
Deposition on heart valves
People with inadequate dialysis can get this type of pericarditis
Can be asymptomatic, or cause:
- Chest pain
Are those with ESRD going to be fluid overloaded or dry?
Generally overloaded, but could be dry after HD
Effect of ESRD on the pulm system
1) Increased MV (to compensate for acidosis)
2) Pulm edema from fluid overload --> increased A-a gradient
3) Increased permeability of alveolar/capillary membrane (shows as butterfly wings on CXR)
Effect of ESRD on the endocrine system
1) Insulin resistance
2) Accumulation of PTH, insulin, glucagon, GH, LH, PL because we are not clearing them
Why do people with ESRD have accelerated atherosclerosis
LDL isn't cleared effectively
___-__ of ESRD patients will develop GI hemorrhage
This can be fatal
Effect of ESRD on the GI system
1) Hypersecretion of acid and delayed gastric emptying (autonomic neuropathy)--> GERD
3) GI hemorrhage
4) Incidence of Hep B&C d/t transfusions for amemia
5) Ascites from dialysis
Why do patients with ESRD have altered drug effects?
Low serum protein
Abnormal cell membrane activity
Less renal elimination
These drugs are eliminated unchanged by the kidneys, and are contraindicated in ESRD
Why is LMWH such a problem in those with ESRD?
Because it's excreted unchanged in the kidneys and not removed well by dialysis.
Will result in major bleeding problems.
Do we want to replace K+ if the level is below 3.5?
NOPE! If it is low, it's probably because the pt just had HD. Give it time to equilibrate.
___% of nephrons have to be lost before we see a change in GFR
A BUN > _____ is indicative of a decrease in GFR in patients with normal diets
Why might BUN be elevated in the absence of renal disease?
High protein diet
What is the most common cause of high BUN?
CHF secondary to the reabsorption of BUN
Creatinine levels won't increase until __-__ hours after a decrease in GFR
As the elderly age and thusly lose nephrons, why aren't their Cr levels elevated?
Less muscle mass.
Creatinine clearance test
24 hour collection (approximates GFR)
100-120 = normal
60-100 = decreased renal reserve
40-60 = mild impairment
25-40 = moderate insufficiency
<10 = ESRD
We will see these electrolyte abnormalities in renal failure
3) Acidosis with anion gap
4) Hypermagnesemia (affects muscles & relaxant choice)
5) Hypocalcemia (unclear why)
6) Hypoalbuminemia (esp with dialysis)
7) Hyperglycemia (insulin resistance)
At what point should we start worrying about K+ levels in ESRD?
Think about treating once it reaches 6-6.5.
Remember they are better at tolerating high K+ levels
Treatment for hyperkalemia (K+>6.5)
Calcium gluconate 10% (10-20mL)**** fastest - antagonizes the effects of K+ on heart muscle
Sodium bicarb (50-100mEq IV)--> moves K+ into the cell
Glucose (50mL of D50) + regular insulin (10 units)--> shifts K+ into the cells
Ion exchange resin
We want to avoid giving calcium gluconate to correct hyperkalemia if
the pt is receiving dig therapy
Are we concerned about bleeding if plt count is fine?
YES! Plts are present, but not functioning properly
When would we transfuse a pt in renal failure?
When absolutely indicated
- <6-7 g/dL
- significant intra-op blood loss
Factors: 1, 2, 5, 7, 10
Factors: 1, 2, 5, 7, 10 (same as PT)
PTT (plasma thromboplastin time)
Factors, 1, 2, 5, 8, 9, 10, 11, 12
Activated clotting time
Factors 1, 2, 5, 8, 9, 10, 11, 12 (same as PT)
Factors: 1 & 2
This test is the best screening measure to test for coagulation in ESRD
Bleeding time-- tells you plt function
How to reverse bleeding problems in ESRD
Desmopressin (.3-.4 mg/kg over 30min)
- increases release of vWF
Cryoprecipitate (10 units over 30 min)
Have blood ready to go
- T&C and blood warmer set up
Equation for calculating arterial oxygen content
FiO2(Hgb x 1.30) + (PaO2 x .003)
Goals if the patient is anemic
Keep CO2 high normal (acidotic side will favor release of O2 in tissues)
Keep the patient warm
Compensation for chronic anemia
Increase in CO
Decrease in SVR
Increase in plasma volume
Increase in 2,3-DPG
Increased extraction ratio in vascular beds
Redistribution of flow to organs with higher extraction ratios (heart, brain, and lungs)
Things to think about when deciding if we should transfuse
Is the anemia acute or chronic?
What caused the anemia?
What is their fluid status?
How urgent is the surgery?
What is the anticipated blood loss of the surgery?
Do they have co-existing disease that we don't want to reduce O2 in? (CAD, PVD, cerebrovascular disease, lung disease)
Will Hgb and Hct immediately reflect blood loss?
No, it takes about 3 days to reach a new plateau level
Trauma patient comes in with blood loss and hypotension. Should we manage with pressors or give blood?
Give blood! The patient is symptomatic. Also, giving pressors could make the condition worse by increasing O2 demand on the heart, but keeping O2 supply low.
Previous splenectomy may increase risk of post-op
In hemolytic anemia, EPO is prescribed for ___ days pre-op
In hemolytic anemia, acute drops below ___ and chronic levels below ___ should be considered for transfusion
Questions for someone with sickle cell disease
These people have 30% incidence of having complications. Complications include
- Pulm HTN
- Hepatic or splenic sequestration
- Renal failure
So ask to see if they've ever experienced any of these complications? Frequency and severity of occlusive crisis, etc?
Pre-op considerations for sickle cell disease
Transfuse if emergency surgery or no meetin 10/30.
Hydrate for 12 hours prior to surgery
Be wary of pre-op meds (decreased O2, and hypoventilationg causing acidosis can both result in sickling)
May be difficult to get IV access
How do we prevent a sickle crisis??
Avoid anything leading to
4) Stasis (positioning)
Complications of iron loading from chronic transfusions in thalassemia
Adrenal insufficiency (will have less response to pressors)
Liver dysfunction & coag abnormalities
Hypothyroidism and hypoparathyroidism
Arrhythmias (get EKG)
Heart failure (get ECHO)
How does thalassemia affect the airway
The compensatory increase in RBC production expands marrow, causing bones to expand, causing craniofacial deformities and overgrowth of the maxillae --> causing trouble with DVL
Things to consider with aplastic anemia
All 3 cell types are low--> think about implications
Often d/t autoimmune -> may be on steroids (need stress dose)
Aplastic anemia and induction
Avoid nasal intubation (bleeding)
Labile hemodynamic responses to induction
Regional anesthesia may or may not be OK - check coags
Caused by lack of enzyme in production of heme (which is a porphyrin), causing a build-up of precursors. Avoid meds that stimulate the RBC production pathway. Ask them what brings on their attacks like drugs and foods
S/S of porphyria attack
Life threatening muscle weakness (required intubation)
Severe abd pain
Meds that are unsafe in porphyria
Barbiturates***** (NO THIOPENTAL)
Nifedipine (probs avoid)
Ketorolac (Probs avoid)
What should we do if we have a patient with a hereditary bleeding disorder?
Get a hematologist consult
If your patient has DM or atherosclerosis, use this ratio to guide transfusion therapy