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Anesthetic Concerns For The Patient With Renal and Hepatic Disease
Anesthetic Concerns For The Patient With Renal and Hepatic Disease
R4
Imply abnormal handling of anesthetic drugs, multiorgan dysfunction, general debility, and specific problem associated with replacement therapy and transplantation.
- A challenge to anesthegiologists.
Electrolyte imbalance
Extracellular potassium
Maintained in narrow range(3.5 to 5.0 mEq/l). Active intracellular transport by a sodium ATP pump at the cell membrane. Clinical and ECG manifestations of hyperkalemia(or hypokalemia) depend on potassium flux rather than the serum concentration. Catabolic stress, acidosis, potassium-sparing diuretics, erythrocyte transfusion Rapid, life-threatening hyperkalemia.
Hypermagnesemia
Muscle weakness, susceptibility to muscle relaxants.
Hypomagnesemia
Associated with hypokalemia, ventricular irritability.
Hyperphosphatemia
Increased bone deposition of calcium hypocalcemia. Decreased renal synthesis of vitamin D. and
Hypocalcemia
Secondary hyperparathyroidism and bone resorption. The syndrome of renal osteodystrophy. Treatment : vitamin D, calcium salts, phosphate binders(aluminium hydroxide), dietary phosphate restriction.
Cardiovascular problems
Systemic hypertension LVH(concentric or asymmetric) Hyperlipidemia
a high prevalence of accelerated atherosclerosis.
Pulmonary problems
Increased minute ventilation
to compensate chronic metabolic acidosis.
serum muscle
atelectasis,
CAPD
abdominal distension compromises ventilation capacity(FVC). and forced vital
Impaired hematopoiesis
Normochromic, normocytic anemia Hct. between 25 and 28%. Decreased erythrpoietin production by the kidney. Bone marrow depression(uremia, aluminum toxicity), decreased RBC survival, chronic blood loss from GI tract or laboratory studies.
Uremic coagulopathy
Abnormal platelet function(thrombocytopathy) occurs when BUN exceeds 60 to 80 mg/dl. Bleeding time prolonged(> 15 minutes). Impaired platelet aggregation.
d/t defective endothelial release of von Willebrand factor-factor VIII complex.
Peptic ulcer
up to 25% in CRF patients.
Hepatitis B and C
high incidence in patients hemodialysis. often anicteric or in a carrier state. on chronic
Neurologic dysfunction
Depend on the acuity of uremia. Personality changes, drowsiness, asterexis, myoclonus, seizures. Major surgery, gastrointestinal bleeding, infection
precipitate acute encephalopathy.
Ascites
elevates diaphragm, decreases FRC. increase intraabdominal pressure, decreases venous return and renal blood flow. Spontaneous bacterial peritonitis(10% of patients). resistance to loop diuretics. exacervate intravascular hypovolemia and hypokalemia, worsen hepatic perfusion. spironolactone(specific aldosteron antagonist): choice.
Metabolic alkalosis
worsens hepatic encephalopathy. Extracellular hydrogen ion concentration , ammonium(NH4+) is converted to ammonia(NH3), crosses lipid membrane(nonionic diffusion trapping). Treatment potassium chloride with careful volume repletion. Refractory alkalosis corrected by central venous infusion of dilute(0.1N) hydrochloric acid.
Gastrointestinal dysfunction
Potential for active viral hepatitis(A,C,D). Delayed gastric emptying
risk of regurgitation and aspiration during induction.
Hepatorenal syndrome
Any degree of renal insufficiency that occurs in the presence of liver failure. A specific form of vasomotor nephropathy
severe prerenal oliguria, low urine sodium(10mEq/l), progressive azotemia.
Hyperdynamic circulation
A fixed low systemic vascular resistance.
countless tiny arteriovenous shunts in the skin(spider nevi, palmar erythema), GI tract and lung.
Respiratory failure
Hepatopulmonary syndrome
hypoxemia refractory to increased inspired oxygen fraction in patients with advanced liver disease. By intrapulmonary shunting through the arteriovenous anstomoses. Reactive or fixed pulmonary hypertension.
Aspiration risk(in hepatic encephalopathy). High risk for perioperative pulmonary complications.
Hematologic abnormalities.
Factor VII deficiency
Impaired hepatic synthesis, impaired vitamin absorption. Prolongation of prothrombin time. marker of hepatic synthetic dysfunction. K
Thrombocytopenia
platelet count 50,000 to 75,000/mm3. Hypersplenism in portal hypertension, bleeding or DIC. acute GI
Factor V deficiency
a sensitive marker of acute liver dysfunction. used after liver transplantation. Dysfibrinogenemia(in advanced liver disease).
Anemia
acute or chronic blood loss, malnutrition, bone marrow suppression. Chronic alcoholism : macrocytic anemia.
Nutritional-metabolic problems
Loss of glycogenesis(hepatic synthesis) glycogen
Poikiloglycemic(regulated by exogenous administration) Hypoglycemia(blood glucose<100mg/dl) acute liver failure or end stage liver disease.
Neurologic complications
Hepatic encephalopathy
elevated arterial ammonia merely a marker of disordered protein mechanism. caused by various peptides, mercaptans, and false or depressive neurotransmitters(octopamine, tryptophan). grade 1 = confabulation, construction apraxia; grade 2 = drowsiness, asterexis, confusion; grade 3 = stupor; grade 4 = coma. Breakdown of the blood-brain barrier result in acute cerebral edema. precipitating factors hypovolemia, GI bleeding, surgery, infection, hypokalemic metabolic alkalosis. alcohol-induced encephalopathy(thiamine deficiency), Wernicke encephalopathy(oculomotor palsy, cerebellar ataxia), Korsakoff psychosis(amnesia, confabulation).
Drugs
unbound
fraction
in
Drugs
predominantly biotransformation.
dependent
on
hepatic
Lidocaine, all benzodiazepines, all opioids, many nondepolarizing muscle relaxants(except atracurium, cisacurium). Drugs with metabolism that depends on the cytochrome oxidase(CP450) system(diazepam, midazolam). - more sensitive to liver dysfunction than simple glucuronide conjugation(lorazepam, propofol). Lidocaine primary metabolite, methylglycinexylydide. sensitive indicator of liver function and reserve.
Enflurane
Renal injury only in the presence of nephrotoxins, hepatotoxins, or enzyme inducers.
Substantial amount of the fluoride causing nephrotoxicity stems from local production(in the kidney), not correlate with serum concentrations.
Compound A
a metabolite produced by the interaction of sevoflurane with outdated sodalime when fresh gas flows are less than 2 L/min. use sevoflurane with fresh gas flow greater than 2 L/min, avoid in patients at risk for perioperative renal injury.
Hepatotoxic effects
Related to the extent of hepatic metabolism. Mild hepatotoxicity
1 in 700 cases. related to injury caused by reductive metabolites, formed in an hypoxic milieu.
Perioperative Management
Preoperative preparation
Hemodialysis
controls the manifestations of ARF(fluid overload, acidosis, hyperkalemia, acute uremia). Does not completely correct thrombocytopathy or not reverse osteodystrophy and neuropathy. Adverse effects hypovolemia, hypotension, MI, electrolyte imbalance. best scheduled the day before surgery.
Peritoneal dialysis
provides hemodynamic stability but not effective in hypermetabolic states. Abdominal distension compromise perioperative pulmonary function.
Operative preparation
Sedative or opiod premedication
minimized or avoided.
Aspiration prophylaxis
anticholinergic agents, H2 blockers, metoclopramide, sodium bicitrate.
BP cuffs or arterial catheters should be avoided on the arm with an AV fistula or shunt. Do not place a urinary catheter in anuric or oliguric patients(ascending infection). Fracture and joint injury in patient with renal osteodystrophy. Active warming devices(prevent hypothermia).
General anesthesia
At induction : aspiration precautions, preoxygenation, preinduction fluid load(250 to 1000 ml). Succinylcholine Not contraindicated if serum potassium < 5.0 mEq/l, had dialysis within 24 hours. nondepolarizing agents pancuronium and pipecuronium Should be avoided. mivacurium and and cisatracurium Metabolized independent of renal elimination. vecuronium and rocuronium ok.
Increase mechanical minute ventilation Compensate chronic metabolic acidosis. In anuric patients, Maintenance fluid kept in minimal, fluid losses must be fully replaced.
Postoperative care
Emergence may be delayed, complicated by vomiting, aspiration, hypertension, persistent neuromuscular blockade, respiratory depression, pulmonary edema. In patient with chronic metabolic acidosis,
opioid-induced respiratory depression Cause a decrease in ph and acute hyperkalemia. A short period of postoperative mechanical ventilation Controlled emergence, avoids reversal agents, fascilitates evaluation of neurologic and ventilatory function before extubation.
Liver disease
Preoperative evaluation
Child-Pugh classification Most widely used tool for assessment of risk in patient with cirrhosis. Prothrombin time Prolonged > 3 seconds above control, not corrected with vitamin K.
Preoperative preparation
Hepatic failure
Drain tense ascites before surgery. Performed with caution because of the hypovolemia, hypotension, and liver injury. risk of
spironolactone(aldosterone antagonist)
Exacerbate hyperkalemia in the presence of ARF. Should be discontinued 3 to 4 days before surgery.
Treatment of encephalopathy
Protein restriction, lactulose, neomycin.
Drug handling
pharmacokinetics. Large volume of distribution and impaired hepatic elimination. Loading dose requirement may be high, but emergence is delayed. Doses of all sedative drugs should be decreased. Cisatracurium Metabolism is independent of liver function. Neuromuscular blocker of choice
Volatile anesthetics Decrease hepatic blood flow Overcome by appropriate hemodynamic management. Opioids(except remifentanil) Accumulate, delayed emergence. Propofol A relatively short-acting drug in patients with cirrhosis. Myocardial depression, inhibition of reflex tachycardia, vasodilation. Intraoperative hypoxemia(ascites, intrapulmonary shunting), bleeding(coagulopathy), oliguria(vasomotor nephropathy).
Postoperative care
Emergence may be delayed, complicated by vomiting, aspiration, hypotension, respiratory depression, acute respiratory failure.
extubate only when the patient is fully awake. A short period of postoperative mechanical ventilation.