Anesthesia Principles and Practice I: Lecture 8 - Renal Flashcards
(48 cards)
Kidney Anatomy
REVIEW
Left kidney vein is longer than right as has to go over aorta???
Renal Pyramid and Nephron
REVIEW!!!
Nephron Form and Function
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
Kidney Function Review
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.
Glomerular Filtration Rate
Stages of Kidney Disease
Once patient hits Stage 3, probably not going to get better
Prerenal Kidney Injury: Most Common
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.
Pre-renal Disease: Patient Population
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
NSAIDS and the Kidneys
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
Renal Azotemia
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
Post-Renal Azotemia
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.
What puts folks at risk for AKI?
Pre-existing disease
Old age
Sepsis
Trauma
Hypovolemia
Chronic Liver Disease
CHF
Anemia
Proteinuria
Burns
What do healthcare providers do that cause AKI?
Emergency Surgery
Major surgery, especially those requiring CPB
Inadequate Fluid Resuscitation
Sustained Hypotension
Delayed Tx of Sepsis
Admin of Nephrotoxic meds and Dyes
Complications of AKI
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.
Treatment of AKI
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.
Blood Flow- Lots
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
Things that impair the kidneys
Glomerular Dysfunction
Tubular dysfunction
Obstruction of the urinary tract
How do we measure kidney function?
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 much blood flow?
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
Hot Crossed BUNs
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
Serum Creatinine
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
Bun : Creatinine Ratio
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
Anesthetic Management: AKI
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.
Medication Implications
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