NA 731 Renal.pdf

# NA 731 Pathophysiology for Nurse Anesthesia II Fall 2022 ## Renal Pathophysiology ### Content Outline - Physiology review - Assessment of kidney function - Acute kidney injury - Chronic kidney disease - Renal transplant ### Renal Anatomy - Retroperitoneal → T12 - L4 w right slightly lower tha...

# NA 731 Pathophysiology for Nurse Anesthesia II Fall 2022 ## Renal Pathophysiology ### Content Outline - Physiology review - Assessment of kidney function - Acute kidney injury - Chronic kidney disease - Renal transplant ### Renal Anatomy - Retroperitoneal → T12 - L4 w right slightly lower than left - Functional unit: nephron - Complex tubule system with interaction with vascular system - Innervation - SNS: Preganglionics from T8-L1 - PSNS: CN X (vagus) to kidney and pudenal nerve (S2, S3, S4) to the ureters - Nociception = afferent SNS fibers from T10-L1 - Need at least a T10 epidural or ESP for a nephrectomy ### Renal Functions - Functions - Maintain ECF composition via regulation of ionic composition and osmolality (osmolality = Na concentration) - Conserve non-ionic components: glucose, amino acids, etc - Excretion of waste products - Regulates arterial blood pressure - Endocrine function → RASS, erythropoietin, vitamin D - vitamin D: when activated, will increase Ca2+ absorption from Gl tract - erythropoietin: stimulates red blood cell production - Chronic renal disease: anemia 2/2 deficiency of erythropoietin; hypocalcemia 2/2 impaired Ca2+ absorption ### Assessment of Renal Function: Diagnostic Data #### Glomerular Filtration Rate (GFR) - Glomerular filtration rate - the best overall measure of renal function - GFR = & × (ΔΡ – ΔΠ) - Kf: surface area for filtration - AP: difference in hydrostatic forces across the membrane - AΠ: difference in osmotic pressures across the membrane - In prerenal failure, progressing disease will cause a decrease in the surface area for filtration (Kf) - In prerenal failure, hypovolemia will cause a decrease in the hydrostatic force differential (AP) - GFR typically mirrors cardiac output - Normal GFR = 125-140mL/min → decreases 8 mL/yr after 30 YO - GFR < 60 mL/min indicates CKD - Evaluated by assessing: - Creatinine: 0.6-1.3 mg/dL → freely filtered - Creatinine clearance: 110-140mL/min → the most reliable measure of GFR - Creatinine clearance < 30: do not administer drugs that rely on renal clearance (ex: sugammadex) - Blood urea nitrogen: 10-20 mg/dL - Protein: < 150mg/day #### Renal Tubular Function - Specific gravity of urine (specific gravity is the concentration of fluid when compared to water; the closer to 1, the more dilute the fluid) - In the absence of diuretics, glycosuria, proteinuria this should be < 1.018 - Fractional excretion of sodium: measure of the percentage of filtered sodium excreted in urine - The most useful differentiation between prerenal and renal disease - FENa < 1%: normally functioning tubules are conserving sodium → suggestive of prerenal disease - FENa > 2%: tubules unable to conserve sodium → consistent with tubular dysfunction - Urinalysis: analysis for pH, spec gravity, microscopy - Presence of protein, blood, glucose, hemoglobin, leukocytes, and toxins can indicate pathological state ### Acute Kidney Injury - Characterized by deterioration of renal function over a period of hours to days → results in failure of kidney to excrete wastes and maintain fluid homeostasis - Affects up to 20% of hospitalized patients and 50% of ICU patients - Most common cause: hypotension and hypovolemia - Symptoms: asymptomatic, malaise, weight loss, orthostatic hypotension, volume overloaded (cirrhosis), dyspneic. Dx: - Creatinine increase 0.3mg/dL in 48hrs, or 1.5X baseline within 7 days - Abrupt decrease in urine output to < 0.5 mL/kg/hr or < 500 mL/day - Can be oliguric or nonoliguric ### Etiology of AKI #### Prerenal disease - Caused by inadequate renal perfusion - Often due to CHF, liver dysfunction, or sepsis - Most common form of AK - Rapidly reversible - Induction of anesthesia or poor HD management during an anesthetic can lead to prerenal disease - Urine indices are often normal - Blood and urine specimens must be analyzed to determine cause, before treatment #### Intra/Intrinsic Renal Disease - Caused by injury to A/P of kidney - Can be due to injury to glomerulus, tubules, interstitium, or renal vasculature - Can be due to toxic drug effects → ABX (most often aminoglycosides or vancomycin) and NSAIDs - Can have nephritic (hematuria) or nephrotic pattern (proteinuria) #### Postrenal Disease - Caused by obstruction of urinary flow tract - Often due to prostatic hypertrophy, stones, tumor bulk - Least common but most easily reversible type of AKI - Potential for recovery is inversely related to the duration of obstruction Dx: often with U/S ### Complications of AKI - Most result from impaired fluid balance and/or electrolyte homeostasis - Volume overloading is common - Neuro: confusion, somnolence, seizures ### Risk Factors for AKI | Pathophysiologies | High-risk surgical procedures | Advanced age | Preexisting renal insufficiency | CHF | Diabetic neuropathy | Liver failure | Pregnancy-induc ed HTN (preeclampsia) | Sepsis/shock | |---|---|---|---|---|---|---|---|---| | due to the accumulation of protein and amino acids in blood and fluid overload | | | | | | | | | | CV/pulmo: HTN, CHF, pulmonary edema | | | | | | | | | | Due to sodium and, thus, fluid retention | | | | | | | | | | EKG: arrhythmias with peaked T waves, wide QRS | | | | | | | | | | Due to hyperkalemia | | | | | | | | | | Hematologic: anemia, decreased vitamin D function, uremia-induced platelet dysfunction | | | | | | | | | | Decreased EPO can lead to Hct between 20-30% | | | | | | | | | | Decreased vitamin D function can cause hypocalcemia → deficiency in Ca2+ (clotting factor 4) → increased bleeding risk | | | | | | | | | | Metabolic: hyperkalemia, hyperphosphatemia, hypocalcemia, hypermagnesemia, hyponatremia, hypoalbuminemia, metabolic acidosis | | | | | | | | | | GI: anorexia, nausea, vomiting, ileus, and upper GI bleeding | | | | | | | | | | Infection risk increases | | | | | | | | | ### Treatment of AKI - GOAL: limit further renal injury while correcting fluid, electrolyte, and acid-based arrangements - Fluid resuscitation and vasopressor therapy are universal treatments for prevention and management of AKI Balanced salt solutions and LR can be used →0.9% NS has been associated with hyperchloremic metabolic acidosis, with hyperkalemia - Norepinephrine and vasopressin are used to maintain MAP between 65-70mmHg - Dopamine use is not supported by literature to treat or prevent AKI → can also lead to tachycardia | Dosage | Receptor | Effects | |---|---|---| | 0.5-2 mcg/kg/min | D1 | increased renal and mesenteric blood flow | | 2-10 cg/kg/min | B1 | increased inotropy, increased CO | | > 5 mcg/kg/min | | increased NE release (indirect action) | | 10-20 mcg/kg/min | A1 and B1 (mostly A1) | vasoconstriction | - Fenoldopam - D1 agonist that increases renal perfusion/blood flow → clinical trials show no true benefit in treatment of AKI - Loop diuretics can be used with hypervolemic, non-anuric AKI - N-acetylcysteine and mannitol can decrease injury related to radiopaque dyes - Manage blood glucose - CRRT ### Pharmacology in AKI - Selection of drugs that do not depend on kidney for excretion is ideal, but not always possible - As long as creatinine clearance is > 30 mL/min, drug doses rarely must be altered - Loading doses will require no alteration, unless the patients VD has changed due to fluid overload - This can affect water soluble agents - Dosing intervals will increase - Drugs with toxic and/or active metabolites should be avoided altogether - Nephrotoxins should be avoided → includes NSAIDs, some ABX (aminoglycosides and vancomycin), contrast dyes - Avoid drugs that decrease renal perfusion: ACEIs, ARBS, NSAIDs, diuretics ### Anesthetic Management of AKI - Only lifesaving surgery should be performed in patients with AKI due to high mortality and morbidity among this population - Goals - Maintain adequate systemic BP and cardiac output - Avoid other renal insults → drug injury, hypovolemia, hypoxia - Preoperative evaluation: EKG, blood chemistries, CBC, coagulation assessment, urine indices - With any respiratory issues a chest radiograph is ordered - Preop dialysis in those at high-risk - DDAVP for platelet dysfunction in those undergoing higher-risk procedures - Intraoperative: - Large bore IVs (≥18g) - Avoid succinylcholine with hyperkalemia - Correct anemia - Properly maintain intravascular volume - Avoid morphine, tramadol, and meperidine since they reduce GFR and have toxic metabolites ### Chronic Kidney Disease - Progressive, irreversible deterioration of renal function resulting from a wide variety of diseases - Leading cause is diabetes mellitus, followed closely by hypertension - Large racial disparity → ESRD rate in AA patients is 3.6X Caucasians; Native American rate is 1.8X - Most often this is due to untreated hypertension - ~15% of American population has CKD - Half of Americans will develop CKD in their lifetime - Diagnosed when GFR < 60mL/min for > 3 months - Decrease in GFR to less than 25mL/min will progress to ESRD requiring dialysis and transplantation | Stages of CKD | GFR | Stage | Electrolyte imbalances | Uremic coagulopathy | |---|---|---|---|---| | G1 | > 90 | 1 | Hyperkalemia | Increased bleeding time | | G2 | 60-89 | 2 | Hypermagnesemia | Platelet dysfunction | | G3a | 45-59 | 3 | Hyperphosphatemia | Neurologic changes | | G3b | 30-44 | 3 | Hypocalcemia | Autonomic dysfunction | | G4 | 12-29 | 4 | Metabolic acidosis | Encephalopathy | | G5 | <15 | 5 | Unpredictable fluid volume | Peripheral neuropathy | | Albuminuria Stage | Albumin Excretion Rate | | Anemia | Cardiovascular changes | | A1 | <30 mg/day | | | | | A2 | 30-300 mg/day | | | | | A3 | > 300 mg/day | | Increased cardiac output | CHF | | | | | O2-heme curve to right | Dyslipidemia | | | | | Renal osteodystrophy | Systemic HTN | | | | | Pruritis | | ### Cardiovascular Effects of Chronic Kidney Disease - Systemic HTN increases left ventricular hypertrophy, CHF, CAD, and cerebrovascular disease - Also speeds the development of ESRD ### Anesthetic Management of CKD: Induction - Most often, ESRD patients respond to induction of anesthesia as if they were hypovolemic or "volume contracted" - Hypotension is most likely → risk is increased when the patient is uremic or on anti-HTN - Induction drugs should be titrated to effect to prevent hemodynamic fluctuation - RSI is often necessary - Succinylcholine: OK to use even with K < 5.5mEq/dL → response is not exaggerated in patients with CKD - Rocuronium: may be the best option, but is sugammadex a possibility? - Since SNS activity is impaired, which comes with the ability to compensate, then even small changes to management can lead to significant decrease in systemic blood pressure ### Anesthetic Management of CKD: Maintenance - General anesthesia with a balanced technique is a safe and effective plan - volatile anesthetics are not dependent on renal function - Sevoflurane might be avoided because it can lead to fluoride toxicity and/or production of compound A → patients with ESRD are at increased risk of dysfunction - TIVA is an option and EEG monitoring can help titrate medications - Cerebral oximetry may be useful in high-risk patients - Hemodynamics are expected to be labile, and defibrillator must be available - Neuromuscular blockade should be avoided if possible - Rocuronium and vecuronium are subject to reduced clearance - Laudanosine can lead to seizure activity - Neostigmine and edrophonium are subject to reduced clearance, so the risk of re-curarization is not very great. - Sugammadex appears safe and effective with CKD with creatinine clearance > 30mL/min - Opioids lack serious cardiac depressant effects and when used can reduce need for VA - M6G can accumulate ### Anesthetic Management of CKD: Regional & Positioning - Brachial plexus block (supraclavicular, infraclavicular, axillary are all appropriate) is useful for placing vascular access for chronic hemodialysis - The presence of uremic neuropathies should be assessed and documented prior to provision of regional anesthesia - Neuraxial anesthesia is possible - A T4-T10 sympathetic block may improve renal function by attenuating vasoconstriction and suppressing surgical stress - All types of regional are possible, but you must consider where the vascular access is and consider for future placement. - Protect hemodialysis access ### Positioning - Consider poor nutritional status and effects on skin integrity ### Renal Transplantation - Transplant patients live typically 4 years longer than a dialysis patient - Living donors are preferred over deceased donors - Donor kidney is transplanted into the lower abdomen and received vascular supply from iliac vessels, then the ureter is anastomosed directly to the bladder - Management - can be regional or general, but SNS blockade can block control of systemic pressure - Most receive antirejection drugs and steroid prior - Renal function is not affected by choice of anesthetic - Traditional management called for aggressive crystalloid infusion by targeting specific blood pressure and central venous pressure - Dobutamine is the most appropriate inotrope - Cardiac arrest has been reported when the clamp is removed due to entrapment of renal preservative solution