Renal Flashcards
About how much of total body weight is water
~60%
varies with gender, age, body fat%
↑Muscle=↑Water
ECF is fluid outside of cells (______ & ______) = _____ volume of TBW
ECF is fluid outside of cells (ISF & Plasma) = < 1/2 volume of TBW
ECF is more immediately altered by kidneys
Osmolar Homeostasis is mainly mediated by which sensors located where
osmolarity sensors in the anterior hypothalamus
osmolar homestasis stimulates
stimulates thirst
pituitary release of vasopressin (ADH)
cardiac atria release ANP decreasing Na+/Water excretion
what mediates volume homeostasis
juxtaglomerular apparatus sense changes in volume
↓Vol @ JGA triggers Renin-Angiotensinogen-Aldosterone system (RAAS)→Na+/H20 reabsorption
normal Na+ level?
Na+ level okay for surgery?
135-145 mEq/L
≤125 or ≥ 155 mEq/L for elective surgery
signs of hypovolemia
Na+/H2O loss
-decreasd skin turgor, flat neck veins, dry mucous membranes, orthostatic hypotension, tachycardia, oliguria
renal or extrarenal losses
euvolemia causes of hyponatremia
Urine Na < 20: salt restricted diet
Urine Na > 20: glucocorticoid deficiency, hypothyroidism, high sympathetic drive, drugs, SIADH
signs of hypervolemia
peripheral edema, rales, ascites
example of renal losses leading to hypovolemia/hyponatremia
diuretics
mineralocorticoid deficiency
salt-losing nephritis
renal tubular acidosis
ketonuria
osmotic diuretic
Urine Na+ > 20
example of extrarenal losses leading to hypovolemia/hyponatremia
vomiting
diarrhea
3rd space losses
burns
pancreatitis
muscle trauma
Urine Na+ < 20
hypervolemia causing hyponatremia
Urine Na> 20: renal losses
-ARF, CKD
Urine Na< 20: avid sodium reabsorption
-nephrotic syndrome, cardiac failure, cirrihosis
most severe consequences of hyponatremia
seizure, coma, death
treatment of hyponatremia
treat underlying cause - look at volume status
*electroylte drinks
* normal saline
* diuretics
* hypertonic saline/3% NaCl
hypertonic saline/ 3% NaCl
80 ml/hr over 15 hours
Na+ correction should not exceed 1.5 mEq/L/hr
what can happen if Na+ correction of >6 mEq/L in 24 hours occurs
osmotic demyelination syndrome (can lead to permenent neuro demage)
common causes of hypernatremia (6)
excessive evaporation
poor oral intake (very old, very young, AMS)
overcorrection of hyponatremia
Diabetes Insipidus
GI losses
excessive sodium bicarb (treating acidosis)
hyponatremic seizures treatment
hyponatremic seizures= medical emergency
3-5mL/kg of 3% over 20 minutes until seizure resolves
renal water loss leading to hypernatremia hypovolemia
osmotic diuretic
loop diuretic
postrenal obstruction
intrinsic renal disease
profound glycosuria
euvolemia causes of hypernatremia
renal water loss:
Diabetes Inspidus: central, nephro, gestational
extrarenal water loss:
insensible losses- respiratory tract and skin
hypervolemia causing hypernatremia (8)
sodium gains
hyperaldosternosism
Cushings
Hypertonic Dialysis
IV Sodium Bicarb
Hyperalimentation
Hypertonic saline enemas
Salt water drownings
Urine Na > 20
extrarenal water loss leading to hypernatremia hypovolemia
diarrhea
GI fistulas
burns
sweating
s/s of hypernatremia
orthostasis
restlessness
lethargy
tremor/muscle twitching/spasticity
seizures
death
treatment for hypernatremia
root cause, assess volume status (VS, UOP< turgor, CVP)
hypovolemic: normal saline
euvolemic: water replacement (PO or D5W)
Hypervolemic: diuretics
Want Na+ reduction rate ≤____ mmol/L/hr and ≤ ____ mmol/L per day to avoid _____ _____, ____, and ______ damage.
Want Na+ reduction rate ≤0.5 mmol/L/hr and ≤ 10 mmol/L per day to avoid cerebral edema, seizures, and neurologic damage.
potassium
3.5-5 mmol/L
major ICF cation
<1.5% in ECF
what does serum K+ reflect
transmembrane K+ regulation more than total body K+
aldosterones effect on potassium
aldosterone causes the distal nephron to secrete K+ and reabsorb Na+
aldosterone inversely effects K+
renal failure and potassium
in renal failure, K+ excretion declines
excretions shifts toward the GI system
which is a slower process leading to buildup
hypokalemia common causes (7)
low PO intake
renal loss - diuretics, hyperaldosteronism
GI loss- N/V/D, malabsorption
intracellular shift - alkalosis, B-agonists, insulin
DKA (osmotic diuresis)
HCTZ
excessive licorice
additional causes of hypoK+
symptoms of hypoK+
cardiac and neuromuscular
* muscle cramps/weakness
* ileus
* dysrhytmias, U-wave
treatment of hypoK+
underlying cause
Potassium PO> IV (CVC) which may require days
IV K+ dose
10-20 mEq/L/hr IV
each 10 mEq IV K+ increases serum K+ by ~ 0.1 mmol/L
avoid what during hypoK+
excessive insulin
beta agonists
bicarb
hyperventilation
diuretics
hyperK+ causes (7)
renal failure
hypoaldosteronism
drugs that inhibit RAAS
drugs that inhibit K+ excretion
depolarizing NMB (succ increases K+ by .5-1 mEq/L)
acidosis (metabolic/respiratory)
cell death (trauma, tourniquet)
massive blood transfusion (storage and death of cells)
symptoms of HyperK+
chronic may be minimally symptomatic (malaise, GI upset)
skeletal muscle paralysis, decreased fine motor
cardiac dysrhtymias
EKG progression with HyperK+
Peaked T wave
P wave disappearance
prolonged QRS complex
sine waves
asystole
hyperK+ treatment
Calcium 1st inital treatment to stabilize the cell membrane
when should the pt be dialyzed before surgery
within 24 hrs
dialysis also initially causes hypovolemia, the day prior allows them to re-equillibrate
Fastest to slowest hyperK+ treatment
hyperventilation
*increasing the pH by 0.1 decreases K+ by 0.4-1.5 mmol/L
insulin +/- glucose
*10 units iV: 25g D50
*works in 10-20 min
bicarb
*drives K+ back into the cell
loop diuretics
kayexalate (hrs to days)
what to avoid during hyperK+ treatment
succinycholine
hypoventilation
LR and K+ containing fluids
presence of calcium in the body
1% in ECF
99% stored in bone
ionized Ca++ vs non ionized Ca++
only ionized Ca++ is physiologically active
nonionized Ca++ is protein bound to albumin (60%)
ionized ca++ level and influences
Normal iCa++ = 1.2-1.38 mmol/L
iCa++ is affected by albumin levels and pH
* alkalosis (increased pH) increases Ca++ binding to albumin decreasing iCa++
hormones that regulate Ca++
PTH stimulates release of Ca++ from bone into plasma
Calcitonin promotes calcium storage
vitamin D augments intestinal Ca++ absorption
causes of hypocalcemia
↓Parathyroid hormone (PTH) secretion
complication of thyroid/PT surgery - drop in Ca++ that leads to laryngospasm
Magnesium deficiency
Magnesium required for PTH production
Low Vit D or disorder of Vit D metabolism
Renal failure (kidneys not responding to PTH)
Massive blood transfusion (citrate preservative binds Ca++ rendering it inactive)
Check iCa++ after 4+ units of PRBCs may need to give Ca++
Normal Ca++ 9-11
hypercalcemia major causes
hyper-parathyroid or cancer
hyper-parathyroid serum Ca++<11
Cancer serum Ca++>13
Normal Ca++ 9-11
hypercalcemia less common causes
vitamin D intoxication
milk-alkali syndrome (excessive GI Ca++ absorption)
granulomatous disease (sarcoidosis)
s/s of hypocalcemia
parasthesias
irritability
hypotension
seziures
myocardial depression
prolonged QT-interval
post parathryoidectomy - hypocalcemia-induced laryngospasm
extra caution when extubating parathyroidectomy always have laryngospasm plan
s/s of hypercalcemia
confusion, lethargy
hypotonia, decreased DTR
ABD pain
N/V
Short QT-I
Chronic hypercalcemia - hypercalcuria & nephroliathiasis
hypomagnesemia
causes, symptoms, treatment
causes: low dietary intake or absorption; renal wasting
symptoms: muscle weakeness or excitation, seizures, ventricular dysrhythmia (torsades)
treatment: dependent on severity of symptoms, slower infusions for less severe
Torsades/seizures: 2g Mag Sulfate
hypermagnesemia
very uncommon
generally due to over-treatment
- pre-eclampsia
- pheochromocytoma
hyperMg++ symptoms
4-5 mEq/L: lethargy, N/V, flushing
>6 mEq/L: hypotension, decreased DTR
>10 mEq/L: paralysis, apnea, heart blocks, cardiac arrest
Check mag level at regular intervals if on gtt
hyperMg++ treatment
diuresis, IV calcium, dialysis
where are the kidneys located
located retroperitnoeal between T12-L4
right slightly caudal (lower) to the left to accomodate liver
nephron
strucutral/functional unit
1M per kidney
Consists of:
Glomerulus
Tubular system
Bowman capsule
Proximal Tubule (PCT)
Loop of Henle
Distal Tubule (DCT)
Collecting duct
what percent of the Cardiac output do the kidneys receive
20%
1-1.25L/min
which layer of the kidneys recieves 85-90% of renal blood flow
cortex = outer layer
medulla = inner layer is vulnerable to developnig necrosis in response to hypotension (decreased renal perfusion)
primary functions of the kidneys
Regulate EC volume, osmolarity, composition
Regulate BP (intermediately & Long-Term) *RAAS, ANP
Excrete toxins/metabolites
Maintain acid/base balance
Produce hormones (Renin, Erythropoietin, Calcitriol, Prostaglandins)
Blood glucose homeostasis
renal function labs
GFR (125-140 mL/min)
creatinine clearance (110-140 mL/min)
serum creatinine (0.6-1.3 mg/dL)
BUN (10-20 mg/dL)
BUN: creatinine ration (10:1)
Proteinuria (<150 mg/dL)
Specific gravity (1.001-1.035)
Lab values can be effected by factors outside of renal function
GFR best measures renal function over ______. heavily influcence by ______ ________
GFR best measures renal function over time. heavily influcence by hydration status
GFR is better for trending
normal GFR 125-140 mL/min
which renal function test is the most reliable measure of GFR
creatine clearance
serum creatinine can be influenced by what and used when?
influeneced by a high protein diet, supplements, muscle breakdown
good for acute monitoring, Serum creatinine is inversely related to GFR.
in acute case, doubled serum creatinine means a drop in GFR by 50%
Normal 0.6-1.3 mg/dL
blood urea nitrogen
urea is reabsorbed into the blood
affected by diet and intravsacular volume
lower BUN could mean malnourished or volume diluted
higher BUN could mean increased protein diet, dehydration, GI bleeding, trauma, muscle wasting
Normal 10-20 mg/dL
what is the BUN: creatinine ratio used for
hydration status
BUN (reabsorbed): Creatinine (not reabsorbed)
proteinuria
> 750 mg/day could suggest glomerular injury or UTI
*frothy bubbly urine (albumin)
Normal < 150 mg/dL
what does specific gravity test
the neprhons ability to concentrate urine
compares 1mL of urine to 1mL distilled water
Normal 1.001-1.035
assessing volume status
H&P
orthostatic pressure changes
decreased base excess
increased lactate
*drop in UOP is late sign
normal UOP
30 mL/hr; 0.5-1 mL/kg/hr
oliguria
<500 mL in 24hr
volume monitors
US to assess IVC collapse
CVP, RAP
LAP, PCWP (powerful stimuli for renal vasoconstriction)
PAP
SVV
Ultrasound assessment of IVC and hydration
> 50% collapse indicates fluid deficit
* consider passive leg raise to determine fluid resposiveness
SVV measurement
Compares inspiratory vs expiratory pressure
Assumes ventilated patient
Assumes sinus rhythm
AKI
failure to excrete nitrogenous waste products or maintain fluid/electrolyte homeostasis
*caused by hypotension, hypovolemia, and nephrotoxins (IV contrast)
azotemia
buildup of nitrogenous products (urea and creatinine)
hallmark of AKI
AKI with multisystem organ failure requiring dialysis carries what mortality rate
> 50% mortality rate
what percent of hospitalized and ICU patients have AKI
20% hospitalized pts
50% ICU patients
risk factors of AKI (9)
Pre-existing renal disease
Advanced age
CHF
PVD
Diabetes
Sepsis (hypotension)
Jaundice
Major operative procedures
IV Contrast
AKI diagnositc criteria
↑SCr by 0.3 mg/dL within 48 h
↑SCr by 50% within 7 days
↓Creatinine clearance by 50%
Abrupt oliguria *although not always seen in AKI
Physical sx:
Asymptomatic
Malaise
HypoTensioN
Hypovolemic or hypervolemic
pre-renal AKI causes (9)
hemorrhage
GI fluid loss
trauma
surgery
burns
cardiogenic shock
sepsis
aortic clamping
thromboembolism
Pre-renal= ↓ renal perfusion
intrarenal AKI causes (7)
acute gloemerulonephritis
vasculitis
intersitial nephritis
ATN
contrast dye
nephrotoxic drugs
myoglobinuria
Renal = direct nephron injury
postrenal AKI causes (4)
nephrolithiasis
BPH
clot rention
bladder carcinoma
Post Renal= outflow obstruction *easiest to treat
BUN: Creatinine ratio for all the forms of AKI
pre-renal BUN:Cr > 20:1
intrarenal BUN:Cr < 15:1
postrenal BUN:Cr varies
pre-renal azotemia
most common cause of AKI
1/2 of hospital aquired AKI are due to prerenal
aneshesia meds + volume and blood loss decrease RBF
*reversible
*treatment= restore RBF
BUN: Cr > 20:1
most common cause of acute tubular necrosis is
pre-renal AKI if not reversed will transition into renal AKI
drug treatmemt for pre-renal azotemia
fluids, mannitol, diuretics, maintain MAP, pressors
- volumize to restore renal flow but addding tone may increase RBF
renal azotemia
intrinsic renal disease
potentially reversible continuum
↓GFR (late symptom)
↓urea reabsorption in proximal tubule →↓BUN
↓Creatinine filtration→↑blood creatinine
BUN: Cr often < 15:1
post renal azotemia
outflow obstruction
↑Nephron tubular hydrostatic pressure
Renal ultrasonography useful
Reversibility is inversely related to duration
Tx- Remove obstruction if possible
Persistent obstruction damages the tubular epithelium
neuro complications of AKI
Related to protein/amino acids buildup in blood
Uremic Encephalopathy (Dialysis improves)
Mobility disorders
Neuropathies
Myopathies
Seizures
Stroke
CV complications of AKI
Systemic hypertension
Left ventricular hypertrophy
CHF
Pulmonary edema
Uremic cardiomyopathy
Arrhythmias
In order of incidence HTN→ LVH→ CHF→ ischemicheartdisease→ anemicheartfailure→ rhythm disturbances → pericarditis with or without effusion→cardiactamponade, uremic cardiomyopathy
hematological complications of AKI
Anemia
↓ EPO production
↓ red cell production
↓ red cell survival
Platelet dysfunction (plt function assay or TEG are valuable)
vWF disrupted by uremia
* Prophylactic DDAVP
* ↑VWF & Factor VIII to improve coagulation
* Can develop tachyphylaxis – give with anticipated blood loss
metabolic complications of AKI
Hyperkalemia
Water/sodium imbalances
Hypoalbuminemia (kidneys allowing albumin to escape)
Metabolic acidosis
Malnutrition
Hyperparathyroidism
* Parathyroid in overdrive to in attempt to stimulate the kidney to reabsorb Ca++
* Kidney receptor no longer responsive
AKI anesthesia implications
Correct fluid, electrolyte, acid/base status
Volume- NS preferred for renal (no K+)
Careful w/colloids
Albumin > synthetic colloids
MAP maintained (20% of baseline)
Vasopressors? (Vasopressin, Alpha-agonists)
Prophylactic sodium bicarb
* Decreases formation of free-radicals
* Prevents ATN from causing renal failure
why vasopressin during AKI
Vasopressin-preferentially constricts the Efferent arteriole, better than alpha agonists (constrict afferent arteriole) for maintaining RBF
anesthesia implications for AKI
Low threshold for invasive hemodynamic monitoring
Prefer preoperative dialysis
They may need post-op dialysis if they cannot clear drugs on their own
Recent labs, especially K+ within 1 hour of surgery
Want POC equipment available
Tailored drug dosing
Avoid drugs w/active metabolites
drugs to avoid with acute kidney injury
Avoid drugs w/active metabolites, drugs that ↓RBF, and renal toxins
Morphine/Demerol
leading cause of CKD
DM, HTN
what procedures do pts with CKD come to the OR for
dialysis access
DM, toe/foot debridement’s & amputations
Non-healing wounds
Often frequent flyers
stages of CKD
GFR decreases by 10 per decade starting from age 20
CKD CV effects
Systemic hypertension
Cause and consequence
Retention of sodium and water
Chronic activation of renin-angiotensin-aldosterone system
1st line-Thiazide Diuretics,
May need ACE-I/ARB
why ACE-Is, ARBs for CKD
↓systemic BP and glomerular pressure
↓proteinuria by reducing glomerular hyperfiltration
↓glomerulosclerosis
ACE-I/ARB anesthesia considerations
Want ACE-I/ARBs withheld on the day of surgery to ↓risk of profound hypotension.
Vasopressin, NE, and EPI may be needed if ACE-I or ARB is on board.
CKD and dyslipidemia
Dyslipidemia
Triglycerides often > 500
LDL often > 100
Predisposed to “Silent MI”
Peripheral & autonomic neuropathy, sensation may be blunted.
Which populations are high risk for silent MI? Women and Diabetics
CKD and anemia
Responsive to exogenous erythropoietin
Target Hbg 10
Platelet dysfunction
Transfusion -Risks vs benefits: excess hgb leads to sluggish circulation
inidications to consider dialysis
Volume overload
Severe hyperkalemia
Metabolic acidosis
Symptomatic uremia (neuro changes)
Failure to clear medications (active metabolites)
—————————————–
AEIOU
Acidosis
Electrolyte imbalance (K+)
Intoxication (active metabolites)
Overload - fluid
Uremia
HD or PD?
HD is more efficient than PD*
PD is slower, less dramatic volume shifts, may be more suitable to those that can’t tolerate fluid swings/vol shifts (i.e., pts w/poor cardiac function)
Hypotension is the most common SE
Infection leading Cause of death in dialysis pts (impaired immune system/healing)
anesthesia concerns with CKD
Assess the stability of ESRD
Body weight pre/post dialysis *within 24 h of surgery
Dose drugs on weight and GFR
Well-controlled BP, Meds continued?
Glucose management, A1C?
Aspiration precautions (DM, obesity)
Pressors
Anesthesia concerns for uremic bleeding
- normal platelet count/PT/PTT. Assess plt function.
- Cryo, F VIII, vWF
- Desmopressin
- Peak 2-4h; lasts 6-8h
- Tachyphylaxis
- Give preop
best NMB for CKD
cisatracurium
not dependent on renal elimination
Many anesthetic agents are _____-______ and ________ by renal tubular cells
Many anesthetic agents are lipid-soluble and
Reabsorbed by renal tubular cells
lipid insoluble drugs
eliminated unchanged in the urine, prolonged duration of action
*renal dosing - usually based on GFR
thiazides
Loop diuretics
Digoxin
many ABX
induction agents that use renal excretion
phenobarbital
thiopental
muscle relaxants that use renal excretion
pancuronium
vecuronium*
cholinesterase inhibitors excreted by kidneys
edrophonium
neostigmine*
CV drugs that use renal excretion
atropine
digoxin
glycropyrrolate
hydralazine
milrinone
antimicrobials excreted by the kidneys
aminoglycosides
cephalosporins
penicillins
vancomyocin
is sugammedex recommended for renal patients
sugammedex creates a covalent bond - theorectically not recommened for renal patients
how much of morphine is excreted through the urine
40%
*failure to clear leads to signficant active metabolites
*dialysis to clear metabolites
demerol
Analgesic and CNS effects
main adverse effect is neurotoxicity (nervousness, tremors, muscle twitches, seizures)
Multiple doses of meperidine result in the accumulation ofnormeperidinedue to its long elimination half-life (15-30 h) compared with meperidine (2-4 h)
preoperative concerns (6) for CKD
K+ < 5.5 mEq/L on elective surgery
Dialysis pts should be dialyzed within 24 hours preceding elective surgery
Aspiration prophylaxis, especially in DM
Anesthesia & Surgery decrease RBF & GFR
Blood loss activates baroreceptors→↑SNS outflow
* Catecholamines activate α1-Rs→↑afferent arteriole constriction→↓RBF
Longer periods of hypotension (cross-clamping, hemorrhage, sepsis) →↓RBF
