What are the lab tests that evaluate for glomerular function?

GFR

BUN

Serum Creatinine

Creatinine Clearance

GFR

normal ~125mL/min

What is a potentially misleading test of renal function? Why?

According to Ron, regardless of other possible causes, if the BUN is above ___ then renal issues exist.

BUN

Can be elevated by reasons other than renal failure such as:

high protein diet

GI bleeding

dehydration

exercise

increased catabolism

steroids

BUN above 50

(usually reflect decr GFR)

How is creatinine produced?

How is it filtered?

produced at a relatively steady rate by hepatic conversion of skeletal muscle creatine

freely filtered at the glomerulus

What are the normal values of serum creatinine for females & males?

What happens this level in the elderly?

The serum creatinine is slow or fast to reflect acute changes in GFR.

female: 0.6-1.0mg/dl

male: 0.8-1.3mg/dl

elderly: decreased secondary to decr muscle mass

*so even slight elevations in the elderly can be an issue

slow to reflect acute changes in GFR

*How is creatinine clearance calculated?

What units ?

creatinine clearance (ml/min)=

[(140-age) X LBM (kg)] / [plasma creatinine (mg/dl) X 72]

(LBM=lean body mass)

creatinine clearance (mg/ml)=

{[Urinary Creatinine (mg/100ml)]/[Plasma Creatinine (mg/100mL)}    

X    

Urine Volume (ml/min)

What are the normal values for creatinine clearance for females and males?

What happens to it as we age?

female: 85-125ml/min

male: 95-140ml/min

decreases with age

What is urine specific gravity an assessment of?

Normal specific gravity of plasma and urine?

What if both of the above are the same?

assessment of urine concentrating ability

plasma: 1.010 (290 mOsm/kg)

urine specific gravity: > 1.018

implies adequate concentrating ability

If they are the same, there is a problem...kidneys are not concentrating at all.

What is the normal for proteinuria?

Causes of incr proteinuria?

normal ≤150mg/day

Causes:

glomerular damage

failure of reabsorption

excessive plasma proteins

orthostatic proteinuria (common in teenagers - benign finding)

microalbuminuria (early indicator of diabetic nephropathy)

urine specific gravity

proteinuria

urinary sodium

glycosuria

Urinalysis

CBC

Electrolytes

pH

EKG

 protein

 glucose

 blood

 leukocytes

 pH

 specific gravity

 presence of casts

 crystals

 microorganisms

CBC

Anemia is secondary to _______ ________

Kidneys required to excrete_______acids

Inability to excrete an _____ urine from renal insufficiency results in increased _____ ph  and decreased _____ ph.

Kidneys required to excrete non-volatile acids

(the only volatile acid in the body is CO2 and can be excreted via exhalation, all other acids in the body, like lactic acid, are non-volatile or fixed meaning they have to be excreted through the kidneys)

Inability to excrete an acidic urine from renal insufficiency results in increased urine pH and decreased serum pH

changes associated with hyperkalemia:

peaked T waves

prolonged PR interval and QRS

AV conduction delay

loss of P waves

V-Fib

asystole

Neurohormonal Reglulation

How does the body protect against hypovolemia & hypotension?

What are 3 mechanisms?

Protect against hypovolemia and hypotension through:

vasoconstriction and salt and water retention

Sympathoadrenal Axis

Renin-Angiotensin-Aldosterone

Arginine-Vasopression (ADH)

What do the "vasoconstrictor systems" do to the following:

 RBF

 GFR

 Urine flow

Na excretion

decreases them all:

decr RBF

decr GFR

decr Urine flow

decr Na excretion

Neurohormonal Reglulation

How does the body protect against hypervolemia and hypertension?

What are 3 mediators of this?

Protect against hypervolemia and hypertension through:

vasodilation and salt & water excretion

BradyKinins

Atrial Natiuretic Peptide (ANP)

Prostaglandins

KAP

What effects do the "vasodilator systems" have on the following:

RBF

GFR

Urine flow

Na excretion

 Increase in all:

incr RBF

incr GFR

incr Urine flow

incr Na excretion

*How does surgery and trauma affect the neurohormonal regualtion systems?

How long does this last?

T/F anesthesia in and of itself will not necessarily cause damage to someones kidneys, rather the surgical trauma causes potential for more issues?

surgery and trauma may produce significant vasoconstriction and salt and water retention

lasting for several days

True; per Ron 

Surgery & trauma lead to vasoconstriction and salt & water retention that lasts for several days.

What can this lead to?

Vasoconstriction predisposes the kidneys to additional _______.

Leads to postop oliguria & edema

Vasoconstriction predisposes the kidneys to additional injury

Sympathoadrenal axis

What senses decreased BP? Where are these receptors located? 

What does this result in?

decreased BP sensed by baroreceptors

in aortic arch/carotid sinus

results in increased adrenergic output

Sympathoadrenal axis

Where are the G-protein receptors involved in the SNS mechanism located? (2)

What do these mediate/cause r/t the sympathoadrenal axis?

What stimulates these G-protien receptors?

vascular smooth muscle and mesangium

mediate vasoconstriction

 adrenergic stimulation, as well as:

Angiotension II

vasopression

leukotrienes

and others

 What are the predominantlly a-adrenergic effects of sympathoadrenal stimulation?

What are 4 a-adrenergic agonists?

 results in vasoconstriction

NE

epi

 phenylephrine

 high-dose dopamine 

(Dopamine >10 mg/kg/min: alpha effects predominate; arterial vasoconstriction & BP ensue)

What are the B-adrenergic effects of sympathoadrenal stimulation?

What are the intrinsic renal effects d/t B-adrenergic stimulation?

 Name 2 B-agonists

 increase RBF secondary to increased CO

intrinsic renal effects unclear

Isoproterenol

 Dobutamine

(Dopamine 5-10 m g/kg/min: B₂ effects predominate; cardiac contractility & HR)

What are the renal effects of sympathoadrenal stimulation with Dopaminergic agonists?

Name 3 dopaminergic agonists

selectivey increase RBF

may oppose a-adrenergic induced vasoconstriction

Dopexamine

fenoldopam,

low-dose dopamine 

(Dopamine <5 mg/kg/min predominantly stimulates DA₁ & DA₂ receptors in renal, mesenteric & coronary beds; = vasodilatation)

Where is Aldosterone released from?

in response to?

see slide 15 for RAAS

released from adrenal cortex in response to:

Angiotensin II

Hyponatremia

Hyperkalemia

increases blood volume by:

active Na absorption

passive H2O absorption

Why is Aldosterone's effect delayed?

How long does it take to start working?

acts via mRNA transcription, so effect is not immediate but delayed 1-2 hours

(mRNA transcription in tubule cells causes increased activity of the NaK pump and formation of ENaC channels)

What does Arginine Vasopressin regulate?

Where is it synthesized and stored?

regulates urine volume & osmolality

synthesized in hypothalamus

stored in pituitary

What is AVP released in response to?

Per Ron which is the most potent stimulator of AVP release?

increasing plasma osmolality (osmoreceptors)

decreased intravascular volume & arterial

hypotension (stress)

angio II

Aldosterone

Arterial hypotension

How does AVP help maintain adequate glomerular filtration?

look at slide 18 about stimulus for AVP secretion

constriction of efferent arterioles

little to no effect on afferent arterioles

promote renal vasodilation

maintain intrarenal hemodynamics

enhance sodium and water excretion

stimulate PLA2

act as vasodilators enhancing the action of prostaglandins

In addition to kinins, what can stimulate PLA2? 

see slide 20

hypotension

ischemia

angiotensin II

norepi

AVP

HI ANA

Where is ANP released from?

In response to what?

It ____ vascular smooth muscle via formation of _____?

released from atrial myocytes in response to increased atrial volume & subsequent wall stretch

It dilates vascular smooth muscle via formation of cGMP

ANP at the ___ receptor

competitively blocks ____

non-competitvely blocks ___

ANP at the PLC receptor

competitively blocks NE

non-competitively blocks angiotensin II

renin secretion

aldosterone release

AVP secretion

How may dopamine produce renal protection?

Why is effectiveness limited?

What is the interpatient variability?

Bottom Line?

DA1 effects - increased RBF

B-adrenergic effects - increased CO & renal perfusion

Effectiveness limited by its mixed adrenergic effects

Significant (30-fold) interpatient variability in plasma levels

bottom line: useful as an inotropic agent when oliguria persists despite adequate intravascular volume 

(no good evidence that it helps renal, but it is still used)

What is Dopexamine?

What disease process is it useful in? Why?

Dopaminergic agonist

synthetic analog of dopamine

has found use in CHF producing:

afterload reduction

increased RBF

What is Fenoldopam and what is it approved for? 

At _____ mcg/kg/min produces a _____ increase in ___ and ____?

Dopaminergic agonist

selective DA1 receptor agonist

approved for short-term treatment of severe hypertension, particularly renovascular

At 0.03-0.3 mcg/kg/min produces a dose-related increase in RBF and natriuresis

Prostaglandins & renal protection:

counteract?

maintain perfusion of?

Synthetic PGE1 has been shown to prevent ____-induced ____ in animal models?

counteract the vasoconstrictive effects of NE and angiotension II

maintain perfusion of the inner cortex

Synthetic PGE1 has been shown to prevent ischemia-induced ARF in an animal model

 Ca channel blockers & renal protection:

increase?

interference?

increase RBF & GFR & induce natriuresis in HTN patients

interference with renal autoregulation may worsen renal function if accompanied by hypotension

Atrial natriuretic peptide

animal studies show significant improvement in ___ and ___, with reduction in _______ when given in ATN of both ischemic and nephrotoxic etiology

Atrial natriuretic peptide

mixed results in humans following multiple multicenter RCTs, varying from marked _____ in survival to _____

-may potentially worsen outcome in ____, as opposed to _____ acute renal failure

mixed results in humans following multiple multicenter RCTs, varying from marked improvement in survival to no effect

-may potentially worsen outcome in non-oliguric, as opposed to oliguric acute renal failure

1. decreased renal reserve

2. renal insufficiency

3. end-stage renal disease (ESRD)

What is the GFR in decreased renal reserve?

Symptoms?

GFR 60-75% of normal

asymptomatic and often without abnormal lab

What is the GFR in renal insufficiency?

symptoms?

GFR 25-40% of normal

elevated creatinine and BUN, but nocturia may be the only symptom - variable

What is the GFR in ESRD?

symptoms?

GFR< 25% of normal

multiple organ dysfunction, fatal without dialysis

What is the most severe form of chronic renal failure?

GFR in in this stage?

Uremic Syndrome

GFR< 10% of normal

Regulatory - extracellular volume and composition

Excretory - elimination of waste products

Secretory

Systemic Hypertension

Uremic Pericarditis

In CRF, what does systemic HTN represent?

Retention of Na and water leading to expansion of intravascular volume

Activation of the RAAS

How do we manage retention of Na & water in CRF?

How do we manage activation of the RAAS in CRF?

-managed with diuretics and/or dialysis to remove volume

RAAS: managed w/ ACEI/ARBs

CHF

coronary artery disease

cerebrovascular disease

What is normocytic, normochromic anemia due to in CRF?

How is it treated?

inadequate production of erythropoietin

effectively treated with human recombinant erythropoietin

desmopressin, cryoprecipitate, conjugated estrogens

What test correlates best w/ tendency to bleed?

Are platelet count, PT & PTT always abnormal in CRF?

What 3 thing can be out of whack w/ incr bleeding and CRF?

Bleeding time

No, platelet count, PT, and PTT may remain normal

1. decreased platelet factor 3

2. abnormal platelet aggregation & adhesiveness

3. impaired prothrombin consumption

What are the neurologic symtpoms in CRF?

When will some symptoms improve? Especially which one?

 D/t the distal motor weakness seen in many of these pts and their decreased bone mass they have an increased risk for ____ and ____.

see slide 35 r/t renal osteodystrophy

Wide variation in symptoms ranging from insomnia and irritability to seizures, uremic encephalopathy, and coma

Also may see a symmetrical, distal, sensory & motor neuropathy (may be superimposed on DM neuropathy)

some symptoms will improve with dialysis particularly uremic encephalopathy

Breaks and falls

What are the pulmonary changes seen in CRF?

What do these respond to?

-low press. pulmonary edema secondary to increased permeability of alveolar capillary membranes

-peripheral vascular congestion appearing as butterfly wing distribution on chest film

responds to dialysis

aggresive management of hypertension:

ACEI

ARB

B-blockers

What are other treatments of CRF besides management of HTN and diabetes?

dietary protein restriction ≤0.6g/kg/day

treatment of anemia w/ erythropoietin

ultimately dialysis or transplant

1. maintain renal blood flow with adequate perfusion pressure

2. suppress vasoconstricting, salt retaining response to surgical stimulation & pain

3. avoid or minimize nephrotoxic insults

Effectively suppresses the sympathoadrenal stress response and release of:

catecholamines

renin

AVP

RA & the kidney

RBF and GFR remain adequate as long as...

Do all GA techniques affect GFR and UOP?

What about RBF & FF? Why?

Renal autoregulation with GA?

all tend to reduce both GFR & UOP but minimal compared to surgical effects per Ron

RBF reduced, but FF maintained or increased likely due to angiotension-induced efferent arteriolar constriction

renal autoregulation typically preserved

How do IAs affect RBF & GFR?

How do we decrease this effect?

mild to moderate reductions in RBF and GFR

attenuated by fluid loading

How do high dose opioid GA techniques affect RBF and GFR?

How do they compare to IAs in suppressing the SNS response to surgery?

minimal effect on RBF and GFR

more effective than volatile in suppressing the vasoconstricting, salt retaining effects of releasing: catecholamines, angiotensin, aldosterone, AVP

How do IV induction agents affect RBF?

Exception?

How does this agent affect RBF & UOP?

produce small decreases in RBF

with the exception of Ketamine which:

increases RBF, decreases UOP likely via sympathetic activation

How can IA produce nephrotoxicity?

What fluroide levels produce injury?

____ μm/l rarely induce injury

___ μm/l high incidence of injury

metabolic breakdown to free flouride ions, producing a tubular lesion resulting in loss of concentrating ability

Peak flouride levels:

<50μm/l rarely induce injury

>150μm/l high incidence of injury

What are the fluroide levels of:

Methoxyflurane

Enflurane

Isoflurane

Desflurane

Methoxyflurane can produce >100μm/l

(no longer available)

Enflurane rarely exceeds 25μm/l

Isoflurane <4μm/l

Desflurane minimal

Does Sevo or Enflurance produce more flouride ions?

Is this clinically signifiant?

greater flouride ion prodution with Sevo than enflurane

 but:CLINICALLY SIGNIFICANT FLOURIDE-INDUCED NEPHROTOXICITY NOT PRODUCED WITH SEVO

What is Compound A produced from?

Is this clincally significant?

Degradation of sevo during low flow states through CO2 absorbents

-shown to produce renal injury in animal models 

-CLINICALLY SIGNIFICANT RENAL INJURY FOLLOWING LOW-FLOW SEVO NOT REPORTED IN HUMANS

What may positive pressure ventilation & PEEP decrease? 

What does the effect correlate with?

RBF

GFR

Na excretion

UOP

effect correlates with level of airway pressure

Mechanism for renal effects of PPV and PEEP

Transmission of ______ pressure to _____ space leading to: decreased __, ____, & __

Decreased CO leads to _______ increase in symapthetic tone with renal _____ & ____ conservation.

Decreased filling volume reduces ___ secretion with subsequent increases in ______, ______ and ____activity

transmission of intrapleural pressure to intravascular space leading to:

decreased VR, filling pressure, and CO

decreased CO leads to baroreceptor-mediated increase in symapthetic tone with renal vasoconstriction and Na/water conservation

decreased filling volume reduces ANP secretion with subsequent increases in sympathetic tone, renin activation and AVP activity

 Nipride

-reduces RBF the most

Nitroglycerin

- produces less reduction in RBF than Nipride

DECREASED BP

How does Nipride affect the renal system?

Per lec what are the 2 major concerns/risks with deliberate hypotension?

decreases renal vascular resistance, but shunts blood away from the kidneys

produces significant RAAS activation and catecholamine release

1. Periop vision loss
2. decrease RBF

preexisting renal dysfunction

periop hemodynamic instability

What is the incidence of ARF in AAA repair?

overall

elective

ruptured

Which of the above has highest incidence? Why?

overall: 12%

elective: 4%

ruptured: 26%

Ruptured AAA repair has highest incidence of ARF b/c they were HD unstable to begin with

With a suprarenal or infrarenal aortic cross-clamp, what happens to RBF?

What is seen immediately following release? Despite the above what is the GFR at 2 and 24hrs post release compared to control?

What if clamp times are longer than 50-60 minutes?

RBF decreased to ~50% of normal

following release:

RBF increases to supranormal levels (reflex hyperemia)

at 2 hours GFR remains ~1/3 of control values

at 24 hours GFR still only ~2/3 of control values

clamp times longer than 50-60 minutes may produce prolonged decrease in GFR

Is there evidence that some drugs may provide renal protection during cross-clamp?

*Is there evidence to support the use of mannitol or low dose dopamine to prevent renal injury with aortic cross-clamping?

What intervention is more important to attenuate the residual decreased in GFR following release of cross-clamp?

controversy exists

little evidence to support the use of mannitol or low dose dopamine to prevent renal injury with aortic cross-clamping

FLUID LOADING

Is there renal dysfuntion and/or acute renal failure associated with procedures involving CPB?

If so what is incidence?

YES

7% renal dysfunction

2% Acute Renal Failure

Mannitol

Dopamine

no, little evidence that outcome are improved

postop cardiac dysfunction

preop serum creatinine >1.9mg/dl

What patients are particularly susceptible to renal dysfunction

Renal dysfunction or failure may occur in up to _____ of patients following liver transplant

Obstructive jaundice is indicated by...

hepatic failure/obstructive jaundice

renal dysfunction or failure may occur in up to 2/3 of patients following liver transplant

bilirubin levels of 35mg/dl (clog up kidneys)

How can you prevent renal dysfunction in patients with Hepatic Failure/obstructive jaundice? (2)

Which method has better evidence to support it?

preoperative hydration

low-dose dopamine

 low dose dopamine has shown no advantage over preop hydration

What is the typical presentation of nephrotoxic ARF?

Nephrotoxic kidney failure means the kidneys are failing b/c of _____ not just decreased perfusion.

non-oliguric with decreased concentrating ability

some toxic substance

What is Aminoglycosides nephrotoxicity directly related to?

How can this be reduced?

directly related to high trough levels

may be reduced by once daily dosing

during stress, impaired prostaglandin activity due to NSAIDs results in failure of their protective activity, with subsequent decrease in RBF & GFR

(stress activates SNS & vasoconstriction, prostaglandins can help oppose those some - this protective mechanism blocked w NSAID use)

When is Cyclosporine used and what is it?

How can it cause a nephrotoxic insult?

Concurrent _________ may allow a dosage reduction & reduce incidence of ATN.

immunosuppressive agent used extensively following organ transplant

induces SNS hyperreactivity, hypertension, and renal vasoconstriction

Concurrent calcium channel blockade may allow a dosage reduction & reduce incidence of ATN

microvascular obstruction

direct tubular toxicity

When can nephrotoxic insult risks be markedly increased with the use of radiocontrast dyes?

 Is it ok to procede w/ surgery during this time?

in diabetic RI, hypovolemia, CHF

and/or

with a secondary insult (surgery) in the first 3-5 days following radiocontrast

-elective surgery should be postponed during this time period

N-Acetylcysteine

Fenoldopam

Rhabdomyalysis

hemolysis

Jaundice

How does Rhabdomyalysis produce a pigment nephropathy?

How can hemolysis cause renal damage?

(fyi no star for this slide =-)

myoglobin transformed to ferrihematin and precipitates in the proximal tubules

secondary to RBC stroma deposition

at conjugated bilirubin >8mg/dl, bile salt excretion ceases and portal septicemia occurs

circulating endotoxins induce renal vasoconstriction

1. Maintain renal blood flow with adequate perfusion pressure

2. Suppress the vasoconstricting, salt retaining response to surgical stimulation & pain

3. Avoid or minimize nephrotoxic insults

List the concerns that should be considered for preoperative evaluation of a renal pt.

*print or review table on slide 57

Anemia

Blood volume status

Coagulopathy

Continue antihypertensives

Blood glucose

Last dialysis

(best within 24hrs of surgery)

Serum K

ABCC BLS

usual indications (pt just ate a big mac)

delayed gastric emptying d/t uremia

diabetic gastroparesis

During induction, it is important to _____!!!

What is uremia?

Uremia and/or antihypertensive use by the pt will cause them to have a _____ responsive SNS. What do you need to watch out for d/t this?

TITRATE INDUCTION SLOWLY

uremia is a term used to loosely describe the illness accompanying kidney failure, in particular the increased nitrogenous waste products associated with the failure of this organ.

Less responsive SNS so watch out for bigger drops in BP with induction then normal

PPV

position changes

blood loss

drug-incuded myocardial depression

What VIA should be avoided with renal disease?

List 2 Advantages and Disadvantages of VIA with renal disease?

avoid Sevo (risk for Compound A)

Advantages:

easily titratable (great for breakthrough HTN)

allows reduction in dose of MR which might have prolonged duration with renal disease

Disadvantages:

high incidence of concurrent hepatic disease with renal pts 

risk of depression of CO by VIA

What are the advantages of opioids for maintenance of anesthesia?

Disadvantages?

Which opioid is very titratable?

T/F multiple anesthestic routes are okay?

List an example of TIVA technique

Advantages

less myocardial depression

avoid concerns over hepato- & nephrotoxicity

Disadvantages

less able to control BP elevations

not as titratable (as VIAs)

Remifentanyl

TRUE

TIVA: Propofol + Remi + Cisatracurium

What MR are renally excreted?

What about reversal agents?

T/F prolongation of both MR & reversal agent is similar, so no real increase in risk for re-curarization with renal disease?

Vecuronium

Rocuronium

Pancuronium

Neostigmine, Edrophonium, Pyridostigmine

true per lec

Mivacurium

Atracurium

Cisatracurium

MAC

Succs is safe to use with renal patients...

2 exceptions?

Extensive neuropathy

High or high-normal serum K+

What antihypertensives are unaffected by impaired renal function? (4)

*said in class to just read over this...

Propranolol

Labetalol

Esmolol

Calcium Channel Blockers

What antihypertensives are affected by impaired renal function? (4)

*said in class to just read over this...

Furosemide

Thiazide diruectics

Methyldopa

Guanethidine

What changes are seen with antihypertensive drugs used for deliberate hypotensive anesthesia technique with renal pts?

*in class said just to read this.......

Trimethaphan - unchanged

Nitroglycerin - unchanged

Nitroprusside - potential for thiocyanate toxicity

Hydralazine - prolonged

Esmolol - unchanged

What vasopressors can be used for hypotension but has the greatest negative impact on the renal vasculature?

What vasopressors are preferred with renal pts?What is the risk with these?

Phenylephrine is effective but has

greatest negative impact on renal vasculature so it would not be your first choice.

B-adrenergic agonists - preferable,

but may increase myocardial irritability

What is the ideal way to correct hypotension?

What if this doesn't work, then what?

ideally blood volume expansion

but if unsuccessful:

B-adrenergic agonists

Dopamine

What fluids should be avoided for fluid management/UOP of renal pts?

What is typically course of action with severe renal dysfunction, but not ESRD?

Avoid K containing fluids (LR)

preop hydration may be helpful

typically NS is used, sometimes 1/2 NS

What is the most likely etiology of decreased UOP?

How can you correct this?

most likely etiology is inadequate circulating fluid volume

likely to respond to fluid bolus

assure adequate intravascular fluid replacement prior to using mannitol or lasix to stimulate output

What is not predictive of postop renal function?

What condition narrows the margin of safety for a fluid challenge?

Intraop UOP is not predictive

ESRD - tend to be more restrictive with fluids

some people suggest avoiding the radial and ulnar arteries due to potential need for an AV fistula in the future

pressures & gases will be inaccurate if placed in same arm as their fistula

Why should you use strict asepsis when placing a central line?

What should are 2 options for monitoring volume status intraop?

renal pts are extremely prone to infection

CVP vs PA cath

decide which based on underlying disease processes

What may be used, but is not ideal if IV access is difficult?

What should you be aware of when accessing these ports/caths?

portocath or temporary dialysis catheter

strict asepsis

must aspirate left heparin before use

re-heparinized line when done using it

What should you be aware of/concerned with when positioning a renal patient?

Poor nutrition = fragile skin

Fistulas must be protected and well padded

May want access to fistula for periodic palpation

ideal surgical conditions secondary to vasodilation

good postop analgesia

avoids many of the concerns with GETA

1. must assure adequate coagulation

2. possible presence of preexisting diabetic or

    uremic neuropathies

       (document if present so it will be evident that they weren't caused by block)

3. metabolic acidosis lowers seizure threshold  

    following an intravasuclar injection

4. duration may be shorter? Ron has never seen this

What are the considerations for postop management?

Inadequate reversal of MR if weakness is apparent

Smaller doses of narcs, particularly: Morphine & Demerol (M3/M6 & Normeperidine metabolites)

Continuous EKG monitoring

Continued supplemental oxygen, particularly if anemic

When do they next need dialysis?

diabetes mellitis

glomerulonephritis

polycystic kidney disease

systemic hypertension

Where is a donor kidney placed?

How does it receive blood supply?

placed in lower abdomen

blood supply from iliac vessels

ureter anastomosed to bladder

What drug selection is ideal for a renal transplant?

What are the 2 critical aspects of anesthetic management with renal transplant?

What monitor is usually used to help evaluate fluid status?

drug selection as previously described for all renal issues

maintenance of euvolemia & adequate perfusion pressure is critical

CVP monitoring is usually helpful

osmotic diuresis with mannitol facilitates urine formation by transplanted kidney without relying on renal tubular mechanisms

(the transplant takes a little while to start functioning once placed)

What substances are released when vascular clamps are released after a renal transplant?

What does this cause and how do you treat it?

release of K & acid metabolites (vasodilating) into circulation

Hypotension d/t:

1. Vasodilating substances released(transient)

2. Addition of ~300mL new capacity of intravascular space within new kidney

hypotension usually responds to fluid bolus

How should a patient with a transplanted kidney presenting for surgery be managed?

What 4 aspects should be considered?

Should be managed as described for a patient with chronic renal insufficiency/failure

1. appropriate drug selection
2. maintenance of fluid volume & perfusion 
3. strict asepsis d/t immunosuppression
4. consideration of coexisting disease (ie DM, CV disease)

In ARF, a deterioration of renal funciton occurs over _____ or ______.

ARF results in inability of kidneys to? (2)

hours or days

inability to maintain fluid & electrolyte homeostasis

inability to excrete nitrogenous wastes

increase in serum creatinine >0.5mg/dl

50% decrease in creatinine clearance

decreased function resulting in need for dialysis

Oliguric <400ml/day

Non-oliguric >400ml/day

The mortality rate of severe ARF has not improved significantly in past 50 years, due to ____, ____ patient population

If ARF is associated with ________ failure & severe ________ or ________ failure mortality is close to 50%.

If ______ is required, mortality exceeds 50%.

The mortality rate of severe ARF has not improved significantly in past 50 years for severe ARF, due to older, sicker patient population

If ARF is associated with multiorgan failure and severe hypotension or respiratory failure mortality is close to 50%.

If dialysis required, mortality exceeds 50%

What are the 3 classifications of ARF?

Prerenal 

Renal

Postrenal

What is prerenal failure?

What causes renal failure?

caused by primary or secondary renal disease, toxins, or pigments

obstruction of the urinary tract

*chart on slide 77 but Ron said dont worry about it too much---but do causes of ARF on slide 78.

limit further renal damage

correct H2O, electrolyte, acid-base imbalance

hypovolemia

hypotension

sepsis

What fluids should be used for fluid resuscitation of ARF, which one is contraindicated?

Is Norepi a good choice for ARF hypotension?

Dopamine?

crystalloid vs colloid

probably not HESPAN

(it may increase the risk of ARF in septic pts or pts w/ transplanted kidney)

Yes, Norepinephrine increases GFR more than other vasopressors per lec.

Dopamine - not bad but no definitive evidence that it decreases risk for ARF or really helps a lot per Ron.

In general, attempts to convert oliguric to non-oliguric renal failure with diuretics are unsuccessful and potentially harmful

KEY IS VOLUME!!

post-transfusion ATN decreased inpatients who recieve mannitol in addition to adequate hydration

forced alkaline diuresis with mannitol useful in preventing ATN following renal crush injury

N-acetylcysteine

Fenoldopam

Diuretics

N-acetylcysteine/Fenoldopam

Dialysis

What is imparied in sepsis regarding the kidneys?

What is vasomotor nephropathy that occurs with sepsis?

renal autoregulation

renal vasoconstriction in the presence of increased CI

INCREASED:

sympathoadrenal stimulation

RAA stimulation

thromboxane

leukotrienes

PGF2

DECREASED:

renal blood flow

GFR

sodium excretion

UOP

further renal vasoconstriction

 What is U63557A?

How does it protect the kidneys during sepsis?

selective thromboxane synthetase inhibitor

protective effect against deterioration of creatinine clearance in animal sepsis model

Is high-dose methylprednisolone effective for renal protection in sepsis?

Is supranormal oxygen supplementation protective to the kidneys in sepsis?

Is low-dose Dopamine beneficial for renal protection in sepsis?

Unclear

Renal DO2 & VO2 not tied to systemic values

↓renal DO2 doesn't appear to cause tubular injury

High dose inotropes may worsen injury

Widely used, but controversial as to its benefit:

combined with phenylephrine, it increases RBF in non-specific patients, but not in sepsis

Large study looked at Dopamine 2mcg/kg/min vs placebo in sepsis & found no difference in serum creatinine, need for dialysis, ICU stay, or mortality

What patients may benefit from Norepinephrine in sepsis?

Goal of BP with this treatment?

Benefits of NE? (3)

patients with septick shock, hypotension, & oliguria may benefit from addition of NE

to maintain MAP >60mmHg

Benefits:

increased SV

decreased HR

increased GFR

*remember NE causes positive inotropy and vasoconstrictor but only has a transient increase in HR  

for patients whom high-dose Dopamine can be weaned off by substitution with NE

*Dopamine = much larger inc. in HR

patients in vasodilatory shock

hypotension, increased CI, decreased SVR

excessive baroreceptor-mediated release following sustained hypotension

(stores in posterior pituitary get used up)

Is an infusion of AVP beneficial in sepsis?

How does it work?

In one study, infusion of AVP at 2.4U/hr increased systolic BP from 92-146mmHg and allowed discontinuation of catecholamine infusions

additional effect on vascular smooth muscle K+ ATP channels restoring their sensitivity to norepinephrine