Dialysis Flashcards
How is a fistula made
Artery attached to vein. High pressure arterial blood -> vein enlarges and thickened wall, allows two large bore cannulas to be placed on a regular basis
Why is fistula preferred for haemodialysis
Lower infection risk that neck line
how often do you have haemodialysis
4 hours 3 x a week
Types of RRT
Intermittent haemodialysis
Continuous haemofiltration
Continusous haemodialysis
Peritoneal dialysis
What is continious therapy used for
AKI when improved benefits over intermittent therapy - improved tolerability as result slower removal of solute and water
How does haemodialysis work
Blood -> dialysis machine which has a membrane so solutes diffuse between dialysate fluid and blood
How long does it take for an AV fistula to become usable
6-8 weeks
Complications of haemodialysis
Access related - bactaraemia -> endocarditis, discitis
Venous stenosis
Access failure
Haemodynamic instability
N+V
Headahce
Cramps, esp leg
Reactions to dialysis membranes
How does peritoneal dialyisis
Diasylate fluid -> abdominal cavity,filtration across peritoneal membrane, after several hours used fluid drained
What patients are not suitable for peritoneal dialysis
Functional peritoneal membrane
eg no prev intra abdominal pathology - prev peritonitis, surgery, adhesions
What is Continuous ambulatory peritoneal dialysis (CAPD)
Manual dialysate exchanges are typically performed 3-5 x a day
20-40 minutes per exchange
Automated dialysis what is
machine performs exchanges overnight
12 hours
Complications of peritoneal dialysis
Bacterial/fungal peritonitis
Catheter problems: infection, blockage, kinking, leaks, displacement (more likely if patient becomes constipated)
Weight gain
Worsening glycaemic control in patients w diabetes
failure of peritoneal membrane requiring switch to haemodialysis
Encapsulating peritoneal sclerosis
Cloudy peritonitis peritoneal fluid means
Peritonitis
Intraperitoneal disease - appendicitis, cholecystis, bowel ischaemia
Retroperitoneal disease - pancreatitis, renal cell carcinoma
Drugs - vancomycin, amphotericin B
Allergic reaction - increased eosinophils
Bloody haemodialysis drained fluid
Coagulopathy
Retrograde menstruation
Ovulation
Strenous exercise
Ovarian cyst rupture
Adhesions
Catheter ass trauma
Chylous peritoneal fluid drainage (White)
High triglycerides
Lymphatic obstruction
Trauma
Abdominal lymphomes
Pancreatitis
Drugs - CCB
Gold standard for RRT
Renal transplant
How does renal transplant work
Old kidneys left in place
L or R iliac fossa
Benefits of transplantation
obviates the
need for dialysis, can ameliorate anaemia and renal bone disease
and improves quality of life and long-term survival.
Contraindications to transplantation
Active or recent malignancy
Active infection
Significant comorbidity
Complications of renal transplantation
Operative comps
Stenosis of graft artery or ureter
Side effects from immunosupressive therapy Opportunisitic CMV
Malignancy
Recurrence of OG disease
Hyperacute graft rejection
Acute graft rejection
Chronic allograft rejection
Malignancy from renal transplantation
Epstein Barr virus -> non hodgkin B cell lymphomas, non melanoma skin cancers (squamous and basal)
Side effects of immunosupressive therapy
(nephrotoxicity + HPTN secondary to tacrolimus or ciclosporin)
hyeracute graft rejection
untreatable and should not occur if
appropriate cross-matching has been performed
How does acute graft present
Creatinine rise in 1st week to 3 months
Diagnosed by graft biopsy
Initial treat - IV steroids
All have some level of acute rejection
How does a chronic allograft nephropathy present
Multiple reasons
Doesn’t normally respond to increased immunosupression
Peritonitis signs
Abdominal pain varying severeity
Cloudy effluent
Vomitting, nausea, paralytic ileus, sometime bowel perforation
TREAT - intra peritoneal anitbiotics
When considered for transplant
eGFR <15%
Within 6 months of dialysis
Medically fit
All tests done
Basics of drug metabolism
Absorption
Distribution
Metabolism
Excretion
Why is oral absorption reduced in kidney disease
Nephrotic/fluid overload -> oedema in gut
Uraemia - N+V
Reduced gut motility
Increased gut pH
Concurrent medication
Phosphate binders eg calcium acetate
Gut motility in diabetes
Reduced - drugs stay in stomach longer
Role of phosphate binders in kidnye disease
Distribution of drugs how effected in kidney imapriemnt
Oedema - larger volume of distribution into water soluble compartment
Changes in hydration status
Long term malnutrition and muscle mass
What are patients with CKD on long term dialysis more at risk of that effects drug distribution
Malnutrition -> reduced muscle mass -> reduced protein binding, reduced tissue bindinG OF DRUGS
What drugs is metabolism slower for in CKD
Vitamin D
Insulin
What is the problem with excretion in renal impairemnt?
Any drug predominantly excreted by the kidney will accumulate
What does accumulation from impaired excretion of drugs cause?
Increased side effects
Increased toxic effects
Increased therapeutic effects
What are aminoglycosides toxic to?
Tubular cells
What drugs can directly cause acute intersitial nephritis
Trimethoprin, penicillins, vancomycin, NSAIDs
What renal damage can immune modulators cause
Nehropathies
Tubular damage
Acute intersitial nephritis
What drugs are indirectly renotoxic and why
Drugs that cause altered haemodynamics compromising renal perfusion eg ACEi/ARB, diuretics, vasodilators
Ideal drugs for renally impaired
Not metabolised or excreted by kidneys
Wide therapeutic index
Few/benign side effects
Doesnt interact with other drugs
Not affected by hydration status
Low protein binding
Low Na content (will cause more oedema if not)
Low infusion volume
Drugs to absolutely avoid in renal impairemnt
Preominantly renally excreted
Nephrotoxic
Serious dose related adverse effects
Narrow TI
not possible to monitor levels
Theoretical eGFR for Different dialysis (function of kidney assumed)
150-200 druing, 0 in between (overall average <10)
5-10 peritoneal dialysis
15-25 - CVVH
30-40 CVVHDF
CVVH mechanism of action
Continious - works by convection
CKD supportive medications
Renal anaemia
Bone chemistry
Acid/base balance
Analgesia
Antidepressants
Extra vitamins
Laxatives
Who is laxatives with CKD particuarly important in?
Peritoneal dialysis
What drugs could be used for bone chemistry
Alfacalcidol, phosphate binders, cincalcet, etelcalcitide
What medication used for acid base balance in CKD
Na bicarbonate
What is renavit used in
Extra vitamins for haemodialysis intermittent patients
What is the active form of vitamin D
Alfacalcidol - drug unaffected by dialysis
statin risks with CKD on ITU
Risk of accumulation therefore increased risk of myopathy
Why is calcium acetate required in dilaysis patients?
Phosphate is not removed in dialysis so needs to be removed seperately
What happens if patient vitamin D intake is too high?
Hypercalcemia and hyperphosphatemia
What happens to EPO dose on dialysis
Needs to be increased as less functioning kidney to produce hormone
What can ACEi cause that is dangerous in a renal patient?
Hyperkalemia - less ability to be removed through kidneys, solely relying on dialysis
Why are patients told to eat a low potassium diet if renal impairment on ACEis
ACEis can cause hyperkalemia
Why is oxycodone used over morphine for pain relief in renal impairment
active metabolites of oxycodone less renotoxic than morphine
Still reduce dose if renal impairment worse
Why can sodium bicarbonate be discontinued on dialysis
Given through dialysis machine rather than oral
Drug factors in dialysis
Molecular weight
Protein binding
Water solubility
Absorption of drug molecule onto dialysis membrane (membrane or drug charged)
Dialysis factors in drug dosing in RRT
Duration of dialysis
Flow rate - blood and dialysate
Type of membrane used - permeability
How use creatinine clearnace on dialysis
don’t calculate on dialysis as not accurate - dose as if <10
What consider when prescribing for every renal patient
Choice, starting dose, frequency (lower dose, less frequent as rule of thumb)
Adjust dose according to response
Monitor for toxicity
Back up dosage pescriptions with serum drug level monitoring where possible
Hyperacute liver failure what is it
Jaudniced encephalopathy less than or = to one week after incident
Biochemical picture in hyperacute liver failure
Significantly elevated PT
Low to mod rise in bilirubin
Marked increase INR
Rapid progression