Anesthesia Principles and Practice I: Lecture 8 - Renal Flashcards

(48 cards)

1
Q

Kidney Anatomy

A

REVIEW

Left kidney vein is longer than right as has to go over aorta???

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Renal Pyramid and Nephron

A

REVIEW!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Nephron Form and Function

A

At the glomerulus, small solutes are forced out of the blood by pressure.

The PCT site of action of osmotic diuretics (mannitol) and carbonic anhydrase inhibitors (acetazolamide).

Water passes

Thick Ascending Loop of Henle- Furosemide (Lasix) act here.

DCT- Where thiazide diuretics act (hydrochlorothiazide)

Collecting Duct- K+ Sparing diuretics (spironolactone)

KNOW WHICH ONES ARE POTASSIUM SPARING!!!???

Glomerulus is in cortex of kidney, Loop of Henle and collecting duct is in the medulla. Furosemide blocks the absorption of Na+, K+, 2Cl- co-transporter going into medulla decreasing osmolality to less water excreted into medulla by descending limb to more water excreted as water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Kidney Function Review

A

Important filters for removing waste and water
Glomerular Filtration

Balance the electrolytes in the body
Na+, K+, Ca++, HCO3- (Bicarbonate- acid-base balance)

Has a big role in Blood Pressure

Kidney also has important endocrine functions
Erythropoietin- Stimulates RBC production (Kidney function goes down hill, less RBCs are made)
Calcitriol- Responds to hypocalcemia by ↑Ca++ absorption
Renin (Enzyme)- Renin-Angiotensin System helps regulate BP

Loop of Henle has groups of cells called macula densa which contact afferent arterioles called juxtaglomerular cells. This combo makes up the juxtaglomerular complex (JGC) which secretes renin and erythropoietin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Glomerular Filtration Rate

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Stages of Kidney Disease

A

Once patient hits Stage 3, probably not going to get better

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Prerenal Kidney Injury: Most Common

A

3 Major criteria
↑ in creatinine (Cr) > 0.3 mg/dl in 48 hrs
↑ of creatinine > 1.5 x baseline (presumed in previous week)
↓ in urine = or < 0.5 ml/kg/hr (Oliguria definition)

Due to an imbalance in delivery of nutrition and O2 during times of increased demand. Potential causes
Intravascular Volume Depletion
Hypotension
Sepsis
Shock
Over-Diuresis
Heart Failure
Cirrhosis
Aortic/Renal Artery Clamping
Drugs impairing autoregulation
NSAIDS, ACE inhibitors, ARBs
Thromboembolism
Hepatic Failure

Azotemia- condition marked by abnormally high serum concentrations of nitrogen-containing compounds like BUN and Creatinine.
Oliguria criteria (<0.5 ml/kg/hr) is least reliable. Pre-renal Kidney failure is improved with volume.

Pre-renal azotemia- rapidly reversible if underlying cause is corrected.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Pre-renal Disease: Patient Population

A

The Elderly- high risk group
Predisposed to poor fluid intake
Greater chance of polypharmacy (including nephrotoxins)
Higher incidence of co-morbidities
… doesn’t hurt to give them some “pressors” early to be ahead of it

Among Hospitalized Patients
Oft due to CHF
Liver dysfunction
Septic Shock

Perioperative
Anesthetic drugs reduce blood flow and therefore perfusion pressure
Surgical Blood Loss and hypovolemia will exacerbate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

NSAIDS and the Kidneys

A

We always hear that NSAIDS damage the kidneys, but how?

↓ Renal plasma flow caused by a decrease in prostaglandins.
Prostaglandins regulate vasodilation at the glomerular level
NSAIDs disrupt the signal to vasodilate in response to vasoconstrictor hormone release by the body.
This results in hypoperfusion/ischemia of the kidney

Basically, you block the ability for your body to respond to changes in fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Renal Azotemia

A

Acute glomerulonephritis
Acute interstitial nephritis
Acute tubular necrosis
Ischemia
Nephrotoxic Drugs (aminoglycosides, NSAIDS)
Solvents (ethylene glycol, carbon tetrachloride)
Heavy Metals (mercury, cisplatin)
Radiographic contrast dyes
Myoglobinuria (from Rhabdomyolysis)
Intratubular obstruction (crystals, paraproteinemia)

Almost ¾ of of cases of acute interstitial nephritis are attributable to medications, usually antibiotics and NSAIDSs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Post-Renal Azotemia

A

Nephrolithiasis
Benign Prostatic Hyperplasia
Clot retention
Malignancy
Bladder Obstruction
Least common and most easily reversible type of AKI
Percutaneous nephrostomy can relieve obstruction and improve function.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What puts folks at risk for AKI?

A

Pre-existing disease
Old age
Sepsis
Trauma
Hypovolemia
Chronic Liver Disease
CHF
Anemia
Proteinuria
Burns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What do healthcare providers do that cause AKI?

A

Emergency Surgery
Major surgery, especially those requiring CPB
Inadequate Fluid Resuscitation
Sustained Hypotension
Delayed Tx of Sepsis
Admin of Nephrotoxic meds and Dyes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Complications of AKI

A

Retained fluid and electrolyte balance
Results in multiorgan dysfunction
Infection likely and large cause of M&M

Neurologic complications
Confusion, somnolence, seizure, and polyneuropathy

Cardiovascular and Pulmonary Complications
Systemic HTN
CHF
Pulmonary Edema

Hematology
Anemia
↓ Vit D Activation
Coagulopathy
↓ EPO production

CHF/Pulmonary Edema may indicate diuretic therapy.
Coagulopathy is a result of platelet function inhibition from uremia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Treatment of AKI

A

Renal Failure
Severe Metabolic acidosis
Electrolyte abnormalities (esp hyperkalemia) may require dialysis
Recombinant EPO for anemia
Kidney Transplant

Maintain Glucose <180 mg/dL
Fluid Resuscitation and vasopressor therapy are paramount to return perfusion
Maintain a MAP of 65-70 mmHg in Sepsis, Norepi first line pressor. Vaso 2nd.
Diet control
Meds for BP
Vitamin D, Calcium Supplements

Rhabdomyolysis is rare, but giving NaHCO3 may help solubilize myoglobin. Rhabdo is a downstream effect of MH. Presentation is coca cola looking urine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Blood Flow- Lots

A

20-25% of Cardiac Output

80% Cortical, 10-15% juxtamedullary nephrons

O2 Consumption is determined by Renal Blood Flow

Oxygen tension 50mmHg cortical, 15 mmHg medullary

Redistribution from sympathetic stimulation, catecholamines, angiotensin II, heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Things that impair the kidneys

A

Glomerular Dysfunction
Tubular dysfunction
Obstruction of the urinary tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How do we measure kidney function?

A

Glomerular Filtration Rate (GFR, first and foremost)
BUN
Creatinine (Bun and Creatinine are both nitrogenous waste products measured as a proxy)
Tubular Function (Like the Ninja Turtles)
Protein- Not supposed to be in urine
Glucose- Diabetics have microvascular damage impairing function
Imaging Studies Hydronephrosis is a swelling of the kidney occurring when urine cannot drain. Blocking of the ureter or other outflow obstruction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How much blood flow?

A

Clearance- volume of plasma cleared of a substance by unit of time. ↑Clearance = more plasma cleared of a substance

Renal Blood Flow- 600-1200 ml/min

GFR- 20% of Renal blood flow
Males- 120+/- 25 ml/min
Females- 95 +/- 20 ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Hot Crossed BUNs

A

10-20 mg/dL
>50 mg/dL is associated with renal impairment

Liver- Catabolizes ammonia into urea. When impaired, NH3 accumulates causing lethargy, slurred speech, cerebral edema, and asterixis

Directly related to protein catabolism and inversely related to glomerular function

40-50% Reabsorbed by renal Tubules

Asterixis- inability to sustain posture, associated with sudden brief, shock0like involuntary movements

21
Q

Serum Creatinine

A

Males 20-25 mg/kg, Females 15-20 mg/kg

Serum- 0.8-1.3/ 0.6-1 mg/dL

Downstream product of muscle metabolism

Inversely proportional to GFR

GFR ↓ 5% per decade after age 20
Serum Cr stays constant

22
Q

Bun : Creatinine Ratio

A

Usual Ratio between 10:1 - 20:1
↑Ratio reflects decrease in Renal Blood Flow
An increase in Tubular flow results in increased urea reabsorption
Urea and creatinine are nitrogenous end products of metabolism
Urea comes from dietary protein and tissue protein turnover
Creatinine comes from skeletal muscle catabolism

23
Q

Anesthetic Management: AKI

A

Preop Plans
ECG, Serum Chemistries, Complete Blood Count, Coagulation Panel.
Adequate Peripheral Venous Access- consider second IV.
Preop Dialysis may be needed- Severe Electrolyte abnormalities
Correct anemia- Fe, EPO, or PRBC depending on timeframe
Maintenance and restoration of intravascular fluid volume.
NSAIDS, aminoglycosides, radiocontrast, Proton Pump inhibitors should be used judiciously.
Careful with drug that can lead to Prerenal Injury- Diuretics, ACE Inhibitors, ARBs

Desmopressin (DDAVP) can be given preop to those with platelet dysfunction to ↑vWF/Factor VIII and improve coagulation.

24
Q

Medication Implications

A

Morphine- Can accumulate Morphine-6-Glucoronide

Meperidine (Demerol ®)- Makes Normeperidine-Seizures

Tramadol- O-desmethyltramadol

Succinylcholine- May further exacerbate hyperkalemia, do not give if K+ is >5.5 mEq/L

25
Chronic Kidney Disease (CKD)
Chronic and progressive deterioration of renal function. Estimated GFR <60 ml/min A Decrease to <25 mL/min eventually progresses to end stage-renal disease (ESRD) Diabetes Mellitus and Undiagnosed Hypertension are biggest Risk Factors ~15% of Americans have CKD Approximately ½ our population will develop it at some point. Racial Disparities in CKD Risk is 3.6x higher for Black/African Americans 1.8x higher in Native American population 1.5x higher risk for Hispanics ## Footnote Genetic variables and disparity in access to healthcare is thought to underlie these differences in prevalence
26
CKD
Symptoms are often undetectable due to all the back up in the kidneys Renal reserve function may hide CKD until function is <10% of normal Renal ultrasound may help rule out obstructive disease/polycystic kidney disease CT- Gold standard for diagnosis of nephrolithiasis
27
Adaptation to CKD
Increase is Creatinine and Urea Not proportional to level of impairment Cr levels may remain within normal limits until 50%↓ in GFR Serum K+ concentration WNL until GFR approaches 10%... wont see till the kidneys are essentially failing Sodium Sodium levels remain intact until function is severely limited ## Footnote WNL = within normal limits
28
Multi-Organ Issues
Cardiovascular Mortality from cardiac causes is 10X higher in CKD versus non-CKD patient Acute MI- 2-year mortality >70% in Dialysis Patients Hypotension non-responsive to volume replacement should be worked up for Cardiac Tamponade Immunologic- Infection is second leading cause after CV disease. Pulmonary/UTI common. Anemia- chronic anemia can lead to ↑Cardiac Output, Left Ventricle Hypertrophy, LV Dilation Uremic Bleeding- from impaired platelet function. Treatment includes DDAVP, conjugated estrogen, and Cryoprecipitate. Neurologic Mild issues include impaired abstract thinking, insomnia, irritability. Severe seizures, obtundation, uremic encephalopathy, coma
29
Hemodialysis
Patients that are hypertensive and hypervolemic despite diuretics/salt restriction Hemodialysis- Diffusion of solutes between blood and dialysis solution Removes metabolic waste Replenishes buffers Blood is heparinized to prevent clotting Countercurrent of dialysate flows across semi-permeable membrane. ~65% reduction in BUN Takes around 4 hours Annual mortality rate ~16%
30
Peritoneal Dialysis
<10% of all Dialysis Patients Plastic Catheter is anchored in the peritoneal cavity May be better for patients that cannot handle huge fluid shifts CHF Unstable Angina Peritonitis is a common and Serious complication Hospitalization rates are high than hemodialysis.
31
Complications of Hemodialysis
Hypotension- Most common side effect d/t ↓intravascular volume. Hypotension may Also be d/t Myocardial stunning/Ischemia Cardiac Dysrhythmias Pericardial Tamponade Air Embolism Antihypertensive medication Most hypotensive events can be managed by: Slowing ultrafiltration Reposition patient into T-berg ↑Venous return Admin of small saline boluses Exposure of Blood to foreign substances Dialysis reactions including anaphylaxis/anaphylactoid reactions Use of ACE inhibitors can predispose to these things ## Footnote Anaphylaxis is not dose dependent; Anaphylactoid is dose dependent (LOOK UP WHAT IG EACH ARE!!!)
32
Malnutrition and Metabolic
Protein Energy Wasting Catabolism and anorexia beget lean muscle loss Fluid retention can mask this weight loss Dietary consultation and supplementation may be necessary ESRD Patient’s used to living with a higher potassium, so they can tolerate a higher potassium till signs are seen Cardiac and neuromuscular responses to hyperkalemia are less than in patient’s with normal renal function Infection a common cause of M&M
33
Anesthetic Management of Patients with CKD
Make sure patient is optimized for surgery with timing of dialysis Prevent further kidney injury Common comorbidities in dialysis patients: Angina 17% Hx of MI 12% TIA/Stroke 11% Smoking 15% Diabetes 9% Malignancy 13% Anesthesia Meds That Require Significant Elimination by the Kidney: Thiopental (leathal injection) Pancuronium (Peds hearts) Atropine/Glycopyrrolate Edrophonium and Neostigmine Inotropes Hydralazine/Inotropes, Milrinone Aminoglycosides Cephalosporins Codeine, Meperidine, Morphine ## Footnote METs <4 (Walking a flight of stairs) should prompt cardiac workup
34
Preop: CKD
BP must be under control NO ACE/ARB on Day of Surgery Target glucose <180 mg/dL >5.5 mEq/L may result in delay of surgery Expect metabolic acidosis from persistently low bicarbonate levels Preop coagulopathy should be treated with DDAVP Ponder Gastric Aspiration Prophy, def with Diabetics H2 blockers are renally eliminated, adjust dose ## Footnote 1 unit of insulin drops blood glucose by 25 mg/dL
35
Monitoring: CKD
Arterial Access can help predict fluid response TEE may be needed to monitor hemodynamics Do not start PIV on limb with AV Fistula Avoid IV in nondominant arm if possible Avoid upper arm of dominant arm The vessels may ne needed for future AV grafts Femoral lines carry infection risk Dorsalis Pedis/Posterior Tibialis arterial access May be inconvenient with patient positioning Edema/Poor tissue perfusion may be an issue Arterial pressure and gases will NOT be accurate if placed in same limb as AV Fistula ## Footnote Not a good call to use Dialysis access catheters for fluid admin, may need to be used in a pinch. ALWAYS ASPIRATE HEPARIN out of these lines and reintroduce when discontinued
36
Induction of Anesthesia: CKD
Hypotension on induction is very common RSI with sux if needed and K is <5.5 mg/dL Roc will have a very increased DOA ↓ Sympathetic Nervous System Activity impairs peripheral vasoconstriction Small volume changes, PPV, abrupt positioning changes, and med related depression of heart function can have marked effects This means you may have to treat hypotension very aggressively Do not be afraid to use stronger meds if Neo is "refractory" (Vasopressin/Levophed etc), maintaining end organ perfusion is your main focus ## Footnote I am quick to prepare a backup phenylephrine infusion for these patients.
37
Anesthesia Maintenance: CKD
Processed EEG (BIS etc) may assist in dosing maintenance infusions/volatile: You may be able to get away with less anesthesia but need to confirm patient is not aware. Hemodynamic instability is the norm Consider presurgery placement of defibrillator pads in high-risk patients Avoid or underdose NMBs: Slow excretion of vec and roc Atracurium and Cisatracurium do not depend on renal excretion Laudanosine is a product of Benzylisoquinolinium metabolism- potentially toxic systemic effects Renal Excretion ~50% for Neostigmine Sugammadex appears safe in CKD with creatinine clearance> 30 ml/min No current data under that level of kidney function Opioids can reduce VA dose and therefore their myocardial depressant tendencies. Remifentanil can be used safely ## Footnote Laudanosine can cross BBB and may cause excitement/seizures. Has effects at GABA, opioid, and nicotinic acetylcholine receptors
38
Fluids and Urine Output
Patients with severe renal dysfunction w/o hemodialysis may benefit from preop hydration ~500 ml to increase urine output Risk of hyperchloremic metabolic acidosis w/ hyperkalemia with large NS resuscitation It is not recommended to use mannitol or Lasix to stim urine output if they are already hypovolumic May further damage kidneys Blood transfusions as needed to deliver oxygen carrying capacity
39
Anesthesia for Vascular Access
Brachial plexus blocks are useful Produces Vasodilation that may help surgical process Be Cognizant of the chance of platelet dysfunction and residual heparin effects if considering neuraxial anesthesia TAP/ESP blocks may help control post-op pain after abdominal surgery/kidney transplant and nephrectomy
40
Patient Positioning and Perioperative Hemodialysis
Poor nutritional status makes these patient’s skin very prone to damage and bruising. These means pad boney prominences very well. Protect fistulas 100 percent Optimal positioning would allow for Fistula palpation to confirm patency Patient’s with ESRD should have dialysis within 24 hours of elective surgery Patients on peritoneal dialysis and having abdominal surgery undergo hemodialysis postop.
41
Post-Op Management: CKD
CKD Patient’s are high risk for periop MI, continuous post-op ECG is recommended. Hemodialysis 24 hours postop, after fluid shifts have settled. Multimodal analgesia is beneficial
42
Renal Transplantation
Those who receive a transplant outlive those that remain on the transplant list by about 4 years. CV Disease and infection are most likely killers Live Donor Kidney- is preferred to deceased-donor kidneys. Kidney from Cadaver can be preserved up to 48 hours. Donor Kidney received perfusion from Iliac vessels Ureter is anastomosed to bladder.
43
Management of Anesthesia for Renal Transplant
Thymoglobulin- Antirejection drug admin over several hours. Side effects include chills, headache, abdominal pain Premed with Tylenol, corticosteroids, +/- antihistamines Methylprednisolone 7 mg/kg max 500 mg- usually given in the OR Prednisone Taper post op Tacrolimus rejection maintenance- usually started POD 1 General Anesthesia usually preferred to Epidural to control ventilation Surgical Retraction near the diaphragm can make breathing mechanics difficult. Mannitol admin is common after new kidney- prevents acute tubular necrosis by decreasing excess tissue and intravascular fluid. Upon release of renal vessel clamps- Hypotension is a possibility as vasodilators are released from that new kidney ”Renal Dose Dopamine”- Has largely been refuted. Dobutamine may be more appropriate Arterial lines are common to monitor global perfusion. ## Footnote Metabolic by products like lactate, etc.
44
Postop Issues: Renal Transplant
Acute Immunologic Rejection- Can occur almost immediately after blood supply to the kidney is restored. Treatment- removal of kidney, definitely in the face of DIC Continue immunosuppressive therapy postop Tacrolimus- Calcineurin inhibitor Corticosteroid Hematoma formation- May arise in graft postop, potential for it to obstruct vessels. Opportunistic Infections- prolonged immunosuppression Frequency of Cancer- 30-100x higher in transplant recipients.
45
Nephrolithiasis (Kidney Stones)
Most Stones are Calcium Oxalate (75%) can be d/t hyperparathyroidism. Stones in Renal Pelvis are usually painless Unless Infection or Obstruction is present Renal Stone passing into Ureter cause extreme flank pain, N/V, and hematuria. Obstruction of the ureter by a stone can cause renal failure How do we get them out? Extracorporeal Shock Wave Lithotripsy- brings risk of cardiac dysrhythmias d/t R on T Phenomenon. Ureteroscopy- Most common approach requiring Anesthesia ## Footnote Percutaneous removal of kidney stones may be necessary for stones >20mm and Staghorn (branching) calculus. This is carried out in the prone position.
46
Hepatorenal Syndrome
Presents as acute oliguria in patients with decompensated cirrhosis. Occurs in 25-30% of patients in acute liver disease Treatment- re-establishing splachnic circulation with pressors (levophed/albumin etc) Albumin bolus 1g/kg up to 100g may be administered. Midodrine- alpha agonist given PO Octreotide- Somatostatin analogue This is a diagnosis of exclusion in chronic liver failure patients ## Footnote Liver failure, the kidneys start failing even with no structural damage
47
Benign Prostatic Hyperplasia
Presenting Symptom is generally disruption of urine flow Treatment- alpha adrenergic antagonists like terazosin, doxazosin, tamsulosin May cause orthostatic hypotension in some TURP- has been gold standard of treatment for many years, new technologies are presenting Photoselective Vaporization and Laser Enucleation Less blood loss, reduced irrigant needs, ↓hospital stay, ↓post-op catheter
48
TURP Syndrome
Large volumes of nonconductive irrigation solution (glycine, mannitol, sorbitol) are used to remove tissue and prevent conduction of electrocautery to cause thermal injury Resorption of large volumes of fluid can cause hyponatremia Long resection time and height of irrigating fluids can ↑risk Shoulder pain during TURP under spinal may indicate surgeon has perforated the bladder ## Footnote If the bladder is perforated the patient may experience referred shoulder pain from diaphragmatic irritation.