Lecture 5: AKI and CKD Flashcards
glomerulus
selective filtration water and solutes from blood
filtration of blood - 125 mL/min is excreted as urine
tubular system
reabsorption of essential minerals; excretion of non essential ones
can everything get thry glomerulus
Nephrons work very efficiently
Not everything can get thru glomerulus: proteins, large RBC cant get thru
In a healthy, functioning kidney, these things should not get thru
can glucose affect filtration
Glucose levels are elevated can affect the filtration - that’s why if we see things we shouldn’t in urine this is a bad thing
how does the capillary network around nephrons
There is a rly rly dense capillary network around nephrons - without reabsorption couldn’t occur. Semi permeable nephron to be reabsorbed back into bloodstream.
what is the functional unit of the kidneys
nephrons
what stims filtration
hydrostatic pressure
what causes hydrostatic pressure
Arteries can cause this hydrostatic pressure, water, fluid volume, blood pressure (if you don’t have adequate pressure you won’t have adequate filtration)
proximal tubule
Reabsorbs sodium, k, etc. into blood stream
Loop of Henle
specific concentrating and conservation of water (loop diuretics affect this)
Distal tubules
change to be permeable or impermeable to have this final concentration (antidiuretic hormones) more antidiuretic hormone - the more permeable the nephrons are. Also affects acid-base balance because it excretes acid.
collecting duct
all comes together and excreted thru urine
bowman’s capsule
helps filter blood to start process of making urine
cardiac output + kidneys
the kidneys are highly vascular and receive up to 20% of the cardiac output - about 1L to 1.2 L/min of blood flow
what does the renal artery divide into
artery divides into arterial branches that become progressively smaller vessels ending w afferent arterioles
afferent arterioles
single afferent arteriole supplies blood to each glomerulus
When we have decreased pressure in filtration, we have dilation in our afferent arteriole
efferent arterioles
blood exits glomerulus by efferent arterioles
Increase pressure - some constriction to afferent, makes it easier to go out, hard to get in
urine formation 3 processes
- glomerular filtration
- tubular reabsorption
- tubular secretion
functions of the kidneys
- elimination of metabolic wastes
- bp reg
- erythrocyte production
- vit D activation
- prostaglandin synthesis
- acid-base balance
if someone is in resp distress
O2 levels increase, going to develop resp acidosis, to try and offset that we try and breathe better. Kidneys help with this.
true/false many pts w CKD are anemic
true
what do our kidneys do to control bp
We have control of bp - low volume of kidneys, they sense that releasing renin, doing angiotensin to angiotensin 1, then to angiotensin 2. main effects of angiotensin 2 - cause constriction bc trying to raise bp. RAAS sys raises bp. This is released when gets signal there’s low volume.
describe fluid retention and the kidneys
Do fluid retention - work on adrenal cortex and releases aldosterone. Reserves volume. To increase bp.
why will pts w kidney disease be on vit d and calcium supplements
Vitamin D we absorb is not in active form so kidneys activate this. This facilitates calcium. So someone w kidney disease, they will be on vit d and calcium supp bc we know these things are compromised. Important bc cholecalciferol - this is inactive form. If they need the active form - calcitrol. (if kidney damaged)
vit d helps body absorb calcium + healthy kidneys convert vit D into its active form.
describe prostaglandin synthesis
Prostaglandin synthesis - has impact on stim renin, also has RAAS sys impact. Affects constriction and dilation of this.
how much GFR can be lost without obvious symptoms
Up to 80% of GFR can be lost without obvious symptoms.
describe what lab work to look at for kidney disease + assessment
Kidney disease can be partial or complete.
We can look at lab work: GFR, creatinine, urea.
Edema can be a sign of fluid retention - can be related to kidney function.
Monitor urine output - if they can’t get rid of fluid.
Need to know pt baseline
overview of CKD
- presence of kidney damage or decreased function for a period greater than 3 mo
- develops slowly over mo to yrs
criteria for CKD
one or both:
1. decreased kidney function - GFR of less than 60 mL/min/1.73 m2
2. kidney damage - urinary albumin excretion of greater or equal to 30 mg/day or equivalent
CKD GFR
<60 mL/min/1.73 m2 accompanied by urine sediment or abnormal results of imaging tests
what helps diagnose w CKF
kidney biopsy w documented abnormalities
AKI definition + diagnosis
- sudden decline in renal function
- develops over hrs or days
- increased BUN and Cr
- oliguria <400 mL/24 hrs
- hyperkalemia and Na retention
Look at urea and creatinine
Unable to get rid of these electrolytes
Kidney wants to help w perfusion, so multiple comorbidities - their oral intake decrease, this can cause hypotension, and damage to kidneys
Giving them an IV bolus, or ringer’s, etc. 100/hour or something.
Or can be quite severe and need dialysis.
Can be a wide range.
common recent history for AKI
- SOB, change in cognitive function, mental status
- rapid fluid volume gains
- wt gains of more than 2 pounds per day
- sleeping on additional pillows and/or sitting in a chair to sleep
- nutritional-metabolic pattern
signs suggesting extracellular fluid depletion for AKI
thirst, decreased skin turgor, lethargy
signs suggesting intravascular fluid volume overload for AKI
pulmonary congestion, increasing HF, rising bp
predisposing factors for AKI
use of over-the counter medicines, recent infections needing antibiotics, antihypertensive medicines, any diagnostic procedures
AKI is usually secondary to…
dehydration, hypotension, infection, etc
ongoing assessment portions for AKI
- wt monitoring
- daily
- flux in wt over 1-2 lbs/day indicating fluid gains + losses
- consider pts dry wt - intake and output monitoring
- neuro findings - change to LOC
- hemodynamic monitoring
Dry wt: wt b4 they started retaining fluids.
Should be voiding every 3-4 hours at most
Check urine output
30 mls/hr is minimum
describe blood urea nitrogen (BUN)
3.6-7.1 mmol/L
- by product of protein and amino acid metabolism
- elevated with decrease in glomerular filtration rate (GFR) and resulting decrease in urea excretion
- decrease w volume overload, liver damage, severe malnutrition (from depleted protein stores), use of phenothiazines, or preg
Can trend whether it has gotten worse just for this admission, or whether this has happened many times.
Kidneys not working - blood isn’t turning into urine, your urea is elevated
describe creatinine
male: 53-106 mmol/L
female: 44-97 mcmol/L
- by product of muscle and normal cell metabolism
- completely excreted when kidney function is normal
- even small increases in serum creatinine rep a significant decrease in GFR
describe estimation of GFR
- normal 90-120 ml/min/1.73 m^2
- estimation based on creatinine level, age and sex
- GFR is defined as amount of blood filtered by glomeruli in a given time
hemoglobin + hematocrit for AKI/CKD
- can indicate increases and decreases in intravascular fluid volume
- an increase in hematocrit value often indicates fluid volume deficit, resulting in hemoconcentration
- decreased hematocrit value can indicate fluid volume excess because of the dilutional effect of the extra fluid load
CKD prob anemic
Not testing on anion gap - just know there is impact on gases if affected and things can be done to know about this
albumin
- primarily responsible for maintenance of colloid osmotic pressure
- decreased albumin levels in the vascular space resulting in a fluid shift from plasma to interstitium, creating peripheral edema
acidosis
- acidosis (pH less than 7.35) is one of the trademarks of severe acute kidney insult
- metabolic acidosis occurs as a result of the accumulation of unexcreted waste products
what can happen to electrolytes w CKD/AKI
imbalance w renal failure
BUN to creatinine ratio
- usual ratio of BUN to creatinine is 10 to 1
- BUN and creatinine levels are elevated and maintained at a 10:1 ratio, the disorder is intrarenal, or affecting tubules of kidneys
- greater than 10:1 the cause is most likely prerenal
creatinine clearance
85-135 ml/min
- amount of creatinine in excreted urine and the amount of creatinine in the blood over 24 hrs
- renal failure - decrease in urine, increase in blood
osmolality
1. elevated osmolality
2. decreased osmolality
- an elevated osmolality indicates hemoconcentration or dehydration
- a decreased osmolality indicates hemodilution or volume overload
blood gases - anion gap
- an increased anion gap level usually reflects overproduction or decreased excretion of acid products and indicates metabolic acidosis;
- a decreased anion gap indicates metabolic alkalosis
what should u not find in urine
Should not have glucose in urine - the process that reabsorbs glucose only goes so far
should not have protein
shouldn’t really have ketones either
urine drug screen (UDS)
- used to find ALOC
- detects: alcohol, illegal drugs, prescription + nonprescription meds, other substances
AKI diagnostic procedures
- ultrasound
- physiologic traits, masses or cysts, renal artery stenosis, obstruction - CT -kidneys, ureters, bladder (CT KUD)
- urolithiasis (kidney stones) - x ray
- masses, fluid collections, obstructions - bladder scan
- contrast/radiopaque dye
- potentially nephrotoxic
- require adequate hydration pre and post
- may need to hold certain meds ex: metformin - kidney biopsy
- diagnosis of kidney disease
CKD risk factors
- HTN
- DM
- cardiovascular disease
- glomerulopathies
- interstitial nephritis
- hereditary renal disease
- obstructive uropathy
- developmental or congenital disorder
- obesity
- age >65 yrs
- heredity and ethnicity
- dyslipidemia
- systemic lupus erythematosus
- scleroderma
- primary amyloidosis
- hep B or C
- multiple myeloma
- exposure to nephrotoxic substances
- excessive K and Na intake
stage 1 of CKD
> 90 (normal or increased GFR)
normal renal function, with proteinuria
stage 2 CKD
60-89
mild loss of kidney function with proteinuria
stage 3 CKD
30-59
mild to moderate loss of kidney function, with proteinuria
stage 4 CKD
15-29
severe loss of kidney function
with proteinuria
stage 5 CKD
<15
end stage renal disease w proteinuria
the onset of ESRD results in…
a constellation of s/s referred to as uremia
CKD goals of care
- prevention or slowing of disease
- early identification
*prepare pts for RRT - refer to nephrologist
prevention of CKD
- avoid meds w nephrotoxic side effects in pts w AKI or CKD
- NSAIDS for pain relief are avoided in pts w elevated creatinine levels
- use of intravascular contrast dye is preferably delayed until the pt is fully rehydrated
what are reversible causes CKD
- decreased renal perfusion
- administration of nephrotoxic meds
- urinary tract obstruction
early stage of CKD manifestation
- Polyuria
- results from inability of kidneys to concentrate urine
- urine production > 2.5-3 L over 24 hrs
- occurs most often at night
- decreased renal concentrating ability
late stage of CKD manifestation
- oliguria
- < 400 ml/24 hrs : occurs as CKD worsens - anuria
- urine output <40 mL per 24 hrs
CKD clinical manifestations resp sys
- kussmaul respiration (deep + labored)
- dyspnea
- PE
- uremic pleuritis
- pleural effusion
- predisposition to resp infection
to manage fluid overload for CKD what is the dietary sodium restriction
<2g/day
for fluid overload describe diuretic therapy
1. the type of diuretic
2. in moderate cases
3. in more severe cases
4. in oliguric AKI
- loop diuretics (furosemide/lasix)
- in moderate CKD (GFR >30 mL/min/1.73m2) - 80 mg of furosemide
- in more severe CKD - 200 mg of furosemide
- doses may be adjusted upward to as much as 500 mg of IV furosemide
CKD manifestations in CVS
- HTN
- HF
- L ventricular hypertrophy
- peripheral edema
- dysrhythmias
- uremic pericarditis
2 antihypertensive drugs to treat CKD and protect kidneys
- ACE inhibitors (ramapril [altace], enalapril [vasotec])
- ARB agents (losartan [cozaar])
3 drugs for fluid overload
loop diuretics, SGLT2 inhibitors, thiazide diuretics
for a non diabetic where do we want bp
less than 130-140/90 mm Hg
for a diabetic where do we want bp
less than 125-130/80 mm Hg
what is the waste product accumulation + s/s associated w that of CKD
- as GFR decreases, BUN increases, and serum creatinine levels increase
- n/v, lethargy, fatigue, impaired thought processes, headache may occur
how does CKD alter carb metabolism
caused by impaired glucose use
- from cellular insensitivity to the normal action of insulin
how does CKD cause elevated triglycerides
- hyperinsulinemia stim hepatic production of triglycerides
- altered lipid metabolism:
1. decreased levels of enzyme lipoprotein lipase which are important for breakdown of lipoproteins
how can CKD cause metabolic acidosis
- due to increasing tendency to retain hydrogen ions
- defective reabsorption/regeneration of bicarbonate
how do we provide care for CKD metabolic acidosis
- can be treated w bicarbonate supplements (sodium bicarb) - requires careful monitoring of volume status
- decreased protein intake - diminishes acid and sulfate generation
- increased fruit intake - provides citrate that is converted to bicarb, fruits can be high in K
what can CKD hyperkalemia cause
fatal dysrhythmias
what can sodium imbalance do in CKD
- low or norm
- hyponatremia - water shifts into cells-swelling
what can low calcium levels do in CKD
Low calcium levels our parathyroid hormone can demineralize bones which is not great for bone health obviously - can also increase phosphate levels
how does CKD manifest in magnesium imbalance
how does metabolic acidosis in CKD result
- inability of kidneys to excrete acid load (primarily ammonia)
- defective reabsorption/regeneration of bicarb
when do we treat hyperkalemia non pharmacologically what numbers
<5.5 mmol/L
when do we treat hyperkalemia pharmacologically what numbers
> 5.5 mmol/L
for hyperkalemia whats considered a low potassium diet
<2 g/day
what can we give for hyperkalemia
- calcium gluconate
- removal of K from body using: diuretics, GI cation exchanges (ex kayexalate), dialysis
what main thing do we give for hyperkalemia + what does this cause risk for
If at risk for developing dysrhythmia
Give calcium gluconate to stabilize heart muscle
why does CKD cause anemia
- due to decreased production of erythropoietin
- resulting in decreased erythropoiesis by bone marrow
- from decrease in functioning renal tubular cells - deficient iron stores
- folic acid - removed w dialysis
why is there bleeding tendencies w CKD
uremic bleeding
bc of defect in platelet function
why is there infection risk w CKD
- changes in leukocyte function
- altered immune response and function
- diminished inflammatory response
how do we treat CKD anemia (3) dont describe just state
- erythropoietin (Epogen, darbepoetin)
- iron supplements
- folic acid supplements
what does erythropoietin do to help anemia
(epogen, darbepoetin)
- erythropoiesis-stim agents (ESAs) - administered IV or SQ
- increased hemoglobin and hematocrit in 2-3 wks
- side effect: HTN
iron supplements side effects
gastric irritation, constipation, dark stools
why are folic acid supplements helpful for anemia
- needed from RBC maturation
- removed by dialysis
why are ppl w CKD at risk for mineral and bone disorder
- abnormalities of calcium, phosphorus, PTH, Vit D metabolism
- abnormalities in bone turnover, mineralization, volume, linear growth, or strength (renal osteodystrophy)
- vascular or other soft tissue calcification
- results in skeletal and extra skeletal complications
to prevent mineral + bone disorder in CKD what should phosphate intake be restricted too
<1g/day
to prevent mineral + bone disorder in CKD what phosphate binders should be taken w meals
- calcium carbonate (caltrate, tums)
- calcium acetate (PhosLO): binds w phosphate in bowel and excretes
to prevent mineral + bone disorder in CKD what shuold be supplemented
supplement w vit d
- calcitriol (rocaltrol)
- serum phosphate level must be lowered before calcium or vit d is administered
how to help w dyslipidemia for pts w CKD
admin statins for pts w stages 1-3 of CKD
describe the CKD uremic state, s/s, and what they may need
1.Due to an increased waste of blood
2. manifestations: anorexia, n/v, pericarditis, peripheral neuropathy, CNS abnorms
3. may require kidney replacement therapy: hemodialysis, peritoneal dialysis, kidney transplantation
what is stomatitis
inflammation of tongue and lips
what is uremic fetor
urinous odour of breath
CKD clinical manifestations GI
- every part affected
- inflammation of mucosa due to excessive urea
- mucosal ulcerations
- stomatitis
- uremic fetor
- GI bleeding
- anorexia, n/v
- constipation
neuro clinical manifestations of CKD
- restless legs syndrome
- muscle twitching
- irritability
- decreased ability to concentrate
- peripheral neuropathy
- seizures (uncommon)
- coma (more common)
2 clinical manifestations for integ of CKD
- pruritus
- uremic frost (rare)
AKI stage 1
increase in serum creatinine to 1.5-1.9x baseline, OR increase in serum creatinine by greater or equal to 0.3 mg/dL, OR reduction in u/o to <0.5 mL/kg/hr for 6-12 hrs
AKI stage 2
increase in serum creatinine to 2-2.9x baseline, OR reduction of u/o t <0.5 mL/kg/hr for more or equal to 12 hours
AKI stage 3
increase in serum creatinine to 3x baseline, OR increase in serum creatinine to more or equal to 4 mg/dL, or reduction in u/o to <0.3 mL/kg/hr for more than or equal to 24 hours, or anuria for greater or equal to 12 hours, or the initiation of kidney replacement therapy, or in pts <18 yrs, decrease in eGFR to <35 mL/min/1.73m^2
what does RIFLE stand for
risk
injury
failure
loss
ESRD
describe the risk category of RIFLE criteria
Sert criteria: increased creatinine x1.5
U/O criteria: UO<0.5mL/kg/h x6hr
high sensitivity
describe the injury category of RIFLE criteria
Sert criteria: increased creatinine x2
U/O criteria: UO<0.5mL/kg/h x12hr
describe the failure category of RIFLE criteria
Sert criteria: increased creatinine x3 or creatinine greater or equal to 4mg/dl (acute rise of greater or equal to 0.5 mg/dl)
U/O criteria: UO<0.3mL/kg/h x24hr or anuria x12hrs
high specificity
describe the loss category of RIFLE criteria
persistent ARF** = complete loss of renal function > 4 wks
describe the ESRD category of RIFLE criteria
end stage renal disease
what does 4 mg/dl = ___________ mmol/L
= 354 mmol/L
prerenal AKI injury
(55-60%)
- any condition that decreases blood flow, bp, or kidney perfusion before arterial blood reaches the renal artery
- arterial hypoperfusion due to low cardiac output, hemorrhage, vasodilation, thrombosis, or other cause reduces the blood flow to kidney, glomerular filtration decreases, u/o decreases
intrarenal AKI injury
(35-40%)
- condition produces an ischemic or toxic insult directly at parenchymal nephron tissues
- most common cause: acute tubular necrosis (ATN) from ischemia, nephrotoxin exposure, sepsis
postrenal AKI injury
(5%)
- any obstruction that hinders flow of urine beyond the kidney to remainder of urinary tract
clinical course of AKI: initiation phase (3)
- increased creatinine and BUN
- decreased u/o
- lasts hrs to days
clinical course of AKI: maintenance phase length
days to wks
clinical course of AKI: recovery phase
return to BUN, creatinine and GFR toward normal
clinical course of AKI maintenance phase urinary changes (3)
- oliguria <400 mL/day
- anuria <50 mL/day
- urinalysis: casts, RBC, WBC, and SG around 1.010. proteinuria if failure related to glomerular membrane dysfunction
clinical course of AKI maintenance phase fluid volume excess
when output decreases fluid retention occurs
clinical course of AKI maintenance phase metabolic acidosis
- kidneys cannot synthesize ammonia - needed for hydrogen ion metabolism or to excrete acid products of metabolism
- defective reabsorption and regeneration of bicarbonate
clinical course of AKI maintenance phase sodium balance
damage tubules cannot conserve Na
clinical course of AKI maintenance phase potassium excess
kidneys excrete 80-90% of potassium
clinical course of AKI maintenance phase waste product accumulation
- kidneys unable to excrete BUN and Cr
clinical course of AKI maintenance phase hematological disorders
- anemia due to impaired erythropoietin
- uremia decreased platelet adhesiveness
- WBCs altered - immunodeficiency
clinical course of AKI maintenance phase calcium deficit/phosphate excess
kidneys cannot activate vit d
clinical course of AKI maintenance phase neuro changes
- accumulation of nitrogenous waste in brain and other nervous tissue
clinical course of AKI recovery phase (4)
- begins when urine output gradually increase
- ends w acid-base, electrolytes, BUN, and Cr normalizing
- lasts several mo to a yr
- some scar tissue
name 3 age related concerns for AKI
- decreased # of functioning nephrons
- impaired function of other organs
- kidney less able to compensate for changes in fluid volume, solute overload, and cardiac output
common causes of AKI for older ppl
- dehydration
- hypotension
- diuretic therapy
- aminoglycoside therapy
- obstructive disorders (ex: prostatic hyperplasia)
- surgery
- infection
- radiocontrast agents
what are some interventions we do for AKI fluid overload (3 things don’t go into specifics)
- diuretics
- fluid restriction
- RRT
describe 3 diuretics for fluid overload in AKI
- loop diuretics (80-200 mg IV furosemide [lasix])
- dose adequately is u/o >200 mL within 2 hours - thiazide diuretics (hydrochlorothiazide)
- osmotic diuretic (mannitol)
describe fluid restriction criteria for fluid overload in AKI
- 600 mL + 24 hr output
- include diarrhea, emesis, urine, drainage
for fluid depletion what are 3 things we do in AKI
- fluid depletion
- crystalloids (usually 1st choice) and colloids
- may require additional fluids (burns)
describe fluid depletion objectives
objectives of volume replacement are to replace fluid + electrolyte losses and to prevent ongoing loss
describe crystalloids and colloids
crystalloids (1st choice)
- crystalloids - 0.9 NaCl, 0.45 NaCl
- colloids - albumin, pentaspan, hetastarch
- initially 1-3 L of fluid, assessment to pt’s response critical
how do we treat hyperkalemia for AKI
- stop supplements
- low K diet (<2g/day)
- insulin w glucose
- calcium gluconate
- removal of K from body: diuretics, GI cation exchangers (ex: kayexalate), dialysis (K>6.5)
how do we treat metabolic acidosis for AKI
- RRT (pH<7.1)
- bicarbonate administration considered
hypertension vs hypotension collaborative care for AKI
when assessing for uremia what s/s r we looking for
anorexia, n/v, metallic taste, ALOC
renally cleared drugs
metformin, gabapentin, cefepime, morphine
nephrotoxin drugs
aminoglycoside antibiotics, amphotericin, tenofovir, nephrotoxic chemotherapy
what do we do for hypocalcemia w AKI
- treat hyperphosphatemia first
- symptomatic - IV calcium
what do we do for hyperphosphatemia for AKI
- phosphate-binding agents (calcium carbonate)
- restrict dietary phosphorous (<2g/day)
- RRT
what do we do for hypomagnesemia for AKI
IV or PO supplements
what do we do for hypermagnesemia for AKI
- limit intake (meds and nutrition)
- diuretics
- RRT
for AKI what is the recommended energy intake and protein
energy intake is 25-35 kcal/kg/day w 1.5-2.5g/kg/day of protein
what is dialysis
- movement of fluid and molecules across semi-permeable membrane from 1 compartment to another
- correction of fluid and electrolyte imbalances and to remove waste products
what 3 things help dialysis do its role
- diffusion
- osmosis
- ultrafiltrate
what is diffusion
movement of solutes from an area of greater concentration to an area of lesser concentration
what is osmosis
movement of fluid from an area of lesser to an area of greater concentration of solute (only for water)
what is ultrafiltrate
(water and fluid removal)
- results when there is a osmotic gradient or pressure gradient across the membrane
what are 3 renal replacement therapy indications
- volume overload resulting in compromised cardiac or pulmonary status, or both
- elevated K levels
- metabolic acidosis (serum bicarb level <15 mmol/L)
- BUN > 43 mmol/L, GFR <15, creatinine>
- significant change in mental status
- acute poisoning
- signs of uremia
what is peritoneal dialysis
- Composition of fluid dictates what happens
- by process of osmosis, diffusion, ultrafiltration, excess fluid and solutes travel from peritoneal capillary fluid through the capillary walls, through the peritoneal membrane, and into the dialyzing fluid.
- after a selected period, fluid is drained out of abdomen by gravity
- process repeated at regular prescribed intervals
- dwell time will affect the amount of fluid removed
how long after insertion of peritoneal dialysis port can it be used
immediately, but ideally 10-14 days
what type of membrane is the peritoneum
semipermeable
what are the 2 types of PD just state them
- automated peritoneal dialysis (APD)
- continuous ambulatory peritoneal dialysis (CAPD)
describe automated peritoneal dialysis (APD)
- continuous cycling peritoneal dialysis
- done while pt sleeps
- usually leaves fluid in the abdomen during the day
describe continuous ambulatory peritoneal dialysis (CAPD)
- during the day
- dialysis fluid is always in the peritoneal cavity
what is the biggest concern for PD
Infection is biggest complication not good.
Not getting tested on the cycles
what are 5 contraindications for PD
- history of multiple abdominal surgery or severe abdo condition
- recurrent abdo wall or inguinal hernias
- excessive obesity w large abdo wall and fat deposits
- pre-existing vertebral disease (ex: chronic back problems)
- severe obstructive pulmonary disease
if membrane for PD is scarred what happens
won’t be semi-permeable anymore
describe some PD complications (a lot)
- exit site infections **
- peritonitis
- abdo pain
- outflow problems
- hernias
- lower back problems
- bleeding
- pulmonary complications
- protein loss
- carbohydrate and lipid abnormalities
- effectiveness
what are things we need to know before pt goes to hemodialysis, and during, and after (assessment wise)
- VS assessment (q30-60 min)
- fluid status assessment
- peripheral edema
- lung and heart sounds
- pre and post wt
- treatment usually 3-5 hrs at least 3x per week
Takes their blood filters it and puts it back in
Assess vital signs basically the whole procedure
Can potentially become hypotensive
Removing blood, cleaning it, then returning it
3 types of hemodialysis just state
- AVF - arteriovenous fistula
- AVG - arteriovenous graft
- tunnelled hemodialysis catheter
describe AVF - arteriovenous fistula
Takes months to mature, so can’t use it right away. Once fistula can mature, then you can use dialysis. Goes access into the vein - so we want to make it a stringer vessel with increased blood flow and can withstand the increase pressure. So they anastomose them, and then pumps pressure by the arterial flow to cause it to get thicker and stronger. Less likely to develop clots.
- surgically connecting vein and artery usually in forearm
describe AVG - arteriovenous graft
if the veins aren’t appropriate they put a synthetic graft which is what they access. Some arterial blood flows into this loop. More likely to develop clots and infection - which is why its not 1st option.
- synthetic graft attached to artery and vein (2 wks)
- not suitable for AVF
describe tunnelled hemodialysis catheter
can be in the neck, can be femoral - Moreso for convenience and decreased risk of infection usually the neck. Can be temporary or permanent.
internal jugular or femoral vein
6 nursing care for hemodialysis
- SIGN - on kardex and above bed. no BP, venipuncture, IV in arm
- do not access catheter
- EPO and folic acid given in renal unit post HD
- no IMs or invasive procedure 4-6 hrs post
- check for thrill and bruit
- most meds are given post dialysis
what is on palpation for fistula norm/abnorm
- thrill: palpable vibration - normal
- pulse - abnorm
what is norm on auscultation of fistula
bruit - low pitched, soft, machinery-like rumbling sound - norm
name hemodialysis complications
- hypotension
- muscle cramps - from removal of sodium
- loss of blood
- hepatitis
- infections/sepsis
- disequilibrium syndrome
advantages of PD
- ease of travelling
- do well clinically
- fewer dietary restrictions
- if poor vascular access
- diabetics do well
- less technically challenging
treatment of choice for EDRD
- kidney transplant
dialysis vs treatment
- lack of donated organs
- some pts are physically and/or mentally unstable for transplant
- some pts do not want transplants
- transplant not discussed
