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Questions and Answers
What is the primary concern when using Sevoflurane in patients with end-stage renal disease (ESRD)?
Which anesthetic technique is considered safe and effective for patients with chronic kidney disease (CKD)?
Which neuromuscular blockers are subjected to reduced clearance in patients with chronic kidney disease?
What is a key consideration before providing regional anesthesia in patients with uremic neuropathies?
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Why should neuromuscular blockade be avoided in patients with chronic kidney disease whenever possible?
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What is the role of erythropoietin in renal function?
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Which statement about Glomerular Filtration Rate (GFR) is accurate regarding normal values?
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In the context of renal tubular function, what does a fractional excretion of sodium (FENa) of less than 1% suggest?
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What is a common cause of acute kidney injury in hospitalized patients?
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Which of the following correctly describes the significance of creatinine clearance in kidney function assessment?
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Which anatomical feature relates to the position of the kidneys in the body?
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What is the impact of chronic renal disease on calcium absorption?
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How is the specific gravity of urine assessed, and what does it indicate?
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What physiological role does vitamin D play in renal function?
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Which mechanism increases renal blood flow during hypovolemia?
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Which of the following accurately describes prerenal disease in relation to acute kidney injury (AKI)?
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What is the primary goal in the treatment of acute kidney injury?
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Which of the following is NOT a common complication resulting from acute kidney injury?
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Which electrolyte imbalance is commonly seen with chronic kidney disease?
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In the context of acute kidney injury, which treatment has been shown to be ineffective?
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Which of the following conditions is most frequently a cause of postrenal disease?
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Which factor is a major risk for the development of chronic kidney disease?
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In patients with acute kidney injury, what initial urine output characteristic is concerning?
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Which drug or class should be avoided in patients with acute kidney injury?
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In which stage of chronic kidney disease is GFR at or below 15 mL/min?
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When managing a patient with acute kidney injury under anesthesia, which drug is advised to avoid due to potential hyperkalemia?
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Which clinical finding indicates a nephrotic pattern in intrinsic renal disease?
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What key aspect is monitored to evaluate fluid balance in a patient with chronic kidney disease?
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What potential cardiac complication can increase due to chronic kidney disease?
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Study Notes
Renal Anatomy
- Kidneys are retroperitoneal organs located between T12 and L4
- The right kidney is slightly lower than the left kidney
- The nephron is the functional unit of the kidney
- The kidneys receive innervation from the sympathetic and parasympathetic nervous systems
- Sympathetic innervation originates from T8-L1
- Parasympathetic innervation is provided by the vagus nerve (CN X) and the pudendal nerve (S2-S4)
- At least a T10 epidural or ESP is needed for a nephrectomy
Renal Functions
- The kidneys maintain extracellular fluid (ECF) composition by regulating ionic composition and osmolality
- Osmolality is the concentration of sodium
- Conserve non-ionic components like glucose and amino acids
- Excrete waste products
- Regulate arterial blood pressure
- Endocrine function includes the renin-angiotensin-aldosterone system (RAAS), erythropoietin production, and vitamin D activation
- Activated vitamin D increases calcium absorption from the gastrointestinal tract
- Erythropoietin stimulates red blood cell production
- Chronic renal disease can lead to anemia due to erythropoietin deficiency and hypocalcemia due to impaired calcium absorption
Assessment of Renal Function
- Glomerular filtration rate (GFR) is the best overall measure of renal function
- GFR is determined by the surface area for filtration (Kf), the difference in hydrostatic pressure across the membrane (ΔP), and the difference in osmotic pressure across the membrane (ΔΠ)
- Prerenal failure can decrease Kf and ΔP
- GFR typically mirrors cardiac output
- Normal GFR is 125-140 mL/min, decreasing by 8 mL/year after age 30
- GFR < 60 mL/min indicates chronic kidney disease (CKD)
- Creatinine is freely filtered and a good indicator of GFR
- Normal creatinine level is 0.6-1.3 mg/dL
- Creatinine clearance is the most reliable measure of GFR
- Normal creatinine clearance is 110-140 mL/min
- Creatinine clearance < 30 mL/min contraindicates drugs that rely on renal clearance (e.g., sugammadex)
- Blood urea nitrogen (BUN) is another indicator of renal function
- Normal BUN level is 10-20 mg/dL
- Proteinuria is an indicator of glomerular damage
- Normal protein excretion is < 150 mg/day
- Renal tubular function can be assessed using urine specific gravity, fractional excretion of sodium (FENa), and urinalysis
- Specific gravity should be < 1.018 in the absence of diuretics, glycosuria, or proteinuria
- FENa < 1% suggests prerenal disease
- FENa > 2% indicates tubular dysfunction
- Urinalysis can detect protein, blood, glucose, hemoglobin, leukocytes, and toxins
Acute Kidney Injury (AKI)
- AKI is a rapid deterioration of renal function over hours to days, leading to failure to excrete waste products and maintain fluid homeostasis
- Affects up to 20% of hospitalized patients and 50% of ICU patients
- Most common cause is hypotension and hypovolemia
- Symptoms can be asymptomatic, malaise, weight loss, orthostatic hypotension, volume overload, dyspnea
- Diagnosis based on creatinine increase (0.3 mg/dL in 48 hours or 1.5x baseline within 7 days) and decreased urine output (< 0.5 mL/kg/hr or < 500 mL/day)
- AKI can be oliguric or nonoliguric
Etiology of AKI
-
Prerenal AKI: caused by inadequate renal perfusion, often seen in CHF, liver dysfunction, or sepsis
- Most common type of AKI
- Rapidly reversible
- Induction of anesthesia or poor hemodialysis management can lead to prerenal AKI
-
Intrarenal AKI: caused by injury to the kidney itself, affecting the glomerulus, tubules, interstitium, or renal vasculature
- Can be caused by toxic drugs like aminoglycosides or vancomycin, NSAIDs
- Can have nephritic (hematuria) or nephrotic (proteinuria) patterns
-
Postrenal AKI: caused by obstruction of the urinary flow tract, often due to prostatic hypertrophy, stones, or tumor bulk
- Least common, but most easily reversible type
- Recovery potential is inversely related to the duration of obstruction
Complications of AKI
- Complications arise from impaired fluid balance and electrolyte homeostasis
- Volume overload is common
- Neurological complications include confusion, somnolence, and seizures
Risk Factors for AKI
- High-risk surgical procedures
- Advanced age
- Preexisting renal insufficiency
- CHF
- Diabetic neuropathy
- Liver failure
- Pregnancy-induced hypertension (preeclampsia)
- Sepsis/shock
Treatment of AKI
- Goal is to limit further renal injury and correct fluid, electrolyte, and acid-base imbalances
- Fluid resuscitation and vasopressor therapy are universal treatments
- Balanced salt solutions and Lactated Ringer's solution are preferred
- 0.9% NaCl can lead to hyperchloremic metabolic acidosis and hyperkalemia
- Norepinephrine and vasopressin are used to maintain mean arterial pressure (MAP) between 65-70 mmHg
- Dopamine use is not supported by literature to treat or prevent AKI
- Fenoldopam is a D1 agonist that increases renal perfusion but has no proven benefit in AKI treatment
- Loop diuretics can be used in hypervolemic, non-anuric AKI
- N-acetylcysteine and mannitol can decrease contrast dye-induced injury
- Blood glucose management is essential
- Continuous renal replacement therapy (CRRT) may be necessary
Pharmacology in AKI
- Ideal to select drugs that do not rely on renal excretion
- Drug doses rarely need alteration if creatinine clearance is > 30 mL/min
- Loading doses may not require adjustments unless volume status alters distribution
- Dosing intervals should be increased
- Avoid drugs with toxic or active metabolites
- Nephrotoxins like NSAIDs, aminoglycosides, vancomycin, and contrast dyes should be avoided
- Avoid drugs that decrease renal perfusion like ACE inhibitors, ARBs, NSAIDs, and diuretics
Anesthetic Management of AKI
- Only lifesaving surgery should be performed in patients with AKI due to high mortality and morbidity
- Anesthetic goals: maintain adequate systemic blood pressure and cardiac output, and avoid further renal insults
- Preoperative evaluation: EKG, blood chemistries, CBC, coagulation assessment, urine indices, chest radiograph if respiratory issues, preop dialysis for high-risk patients, DDAVP for platelet dysfunction
- Intraoperative management: large bore IVs (≥18g), avoid succinylcholine in hyperkalemia, correct anemia, maintain intravascular volume, avoid morphine, tramadol, and meperidine
Chronic Kidney Disease (CKD)
- Progressive, irreversible deterioration of renal function due to various diseases
- Leading causes are diabetes mellitus and hypertension
- Large racial disparity: ESRD rate in African Americans is 3.6x higher than Caucasians, Native Americans 1.8x higher
- ~15% of the US population has CKD
- Half of Americans will develop CKD in their lifetime
- Diagnosed when GFR < 60 mL/min for > 3 months
- GFR < 25 mL/min progresses to end-stage renal disease (ESRD) requiring dialysis or transplantation
- Stages of CKD are categorized by GFR and albuminuria excretion rate:
| Stage | GFR (mL/min) | Albuminuria Excretion Rate (mg/day) | Complications |
|---|---|---|---|
| G1 | > 90 | < 30 | Hyperkalemia, increased bleeding time, anemia, cardiovascular changes |
| G2 | 60-89 | 30-300 | Hypermagnesemia, platelet dysfunction |
| G3a | 45-59 | > 300 | Hyperphosphatemia, neurologic changes, increased cardiac output, CHF |
| G3b | 30-44 | > 300 | Hypocalcemia, autonomic dysfunction, O2-heme curve to right, dyslipidemia |
| G4 | 12-29 | > 300 | Metabolic acidosis, encephalopathy, renal osteodystrophy, systemic hypertension, pruritis |
| G5 | < 15 | > 300 | Unpredictable fluid volume, peripheral neuropathy |
Cardiovascular Effects of CKD
- Systemic hypertension increases the risk of left ventricular hypertrophy, CHF, CAD, and cerebrovascular disease
- Hypertension accelerates the progression of ESRD
Anesthetic Management of CKD
- Induction: patients often respond as if hypovolemic, requiring careful titration of induction drugs to prevent hemodynamic fluctuations
- RSI is often necessary
- Succinylcholine is safe in CKD, but rocuronium is often preferred
- Maintenance: general anesthesia with a balanced technique is safe and effective
- Use volatile agents sparingly, as they can lead to fluoride toxicity or compound A production
- TIVA with EEG monitoring is an option
- Cerebral oximetry can be useful in high-risk patients
- Hemodynamics are labile, so a defibrillator should be readily available
- Neuromuscular blockade should be avoided when possible
- Rocuronium and vecuronium have reduced clearance
- Laudanosine can cause seizures
- Neostigmine and edrophonium have reduced clearance, so risk of re-curarization is low
- Sugammadex is safe and effective in CKD with creatinine clearance > 30 mL/min
- Opioids can reduce the need for volatile anesthetics
- M6G can accumulate
- Regional anesthesia: brachial plexus block is useful for vascular access for hemodialysis
- Assess and document for uremic neuropathies before regional
- Neuraxial anesthesia is possible, with a T4-T10 sympathetic block potentially improving renal function
- All types of regional are possible, but consider vascular access location and future placement needs
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