PERIOPERATIVE MANAGEMENT OF URAEMIC SYNDROME

DEFINITION :

Uremia is a clinical syndrome associated with fluid, electrolyte, and hormone imbalances and metabolic abnormalities, which develop in parallel with deterioration of renal function.

PATHOPHYSIOLOGY : 

Kidney site of hormone production , secretion, acid-base homeostasis, fluid and electrolyte regulation, and waste-product elimination.

Renal failure metabolic abnormalities such as anemia, acidemia, hyperkalemia, hyperparathyroidism, malnutrition, and hypertension, uremia can occur.

Uremia usually develops only after clearance falls to less than 10 mL/min

The features of uremia identified in patients with ESRD may be present to a lesser degree in people with a glomerular filtration rate (GFR) that is barely below 50% of the normal rate.

SIGN & SYMPTOMS OF UREMIA

SIGN & SYMPTOMS OF UREMIA

ANEMIA

In the setting of CRF, anemia may be due to : iron deficiency , vitamin deficiencies (eg, folate,

vitamin B-12), hyperparathyroidism, hypothyroidism, and decreased red blood cell survival

Iron deficiency, which may occur as a result of occult GI bleeding

Elevated PTH levels are thought to be associated with marrow calcification, which may suppress red blood cell production and lead to a hypoproliferative anemia

Usually not transfused unless the hemoglobin < 6-7 g/dL or expectant large blood loss

COAGULOPATHY

Bleeding diatheses are characteristic findings in patients with end-stage renal disease (ESRD)

remic bleeding tendency is related to multiple dysfunctions of the platelets

Alterations of platelet adhesion and aggregation are caused by uremic toxins

ACIDOSIS

Metabolic acid-base regulation is controlled primarily by tubular cells located in the kidney

Failure to secrete hydrogen ions and impaired excretion of ammonium may initially contribute to metabolic acidosis

Metabolic acidemia may contribute to other clinical abnormalities, such as hyperventilation, anorexia, stupor, decreased cardiac response (congestive heart failure), and muscle weakness.

HYPERKALEMIA

A potassium level of greater than 6.5 mEq/L is a clinical emergency.

Renal function declines, the nephron is unable to excrete a normal potassium load, which can lead to hyperkalemia if dietary intake remains constant.

Acidemia or type IV renal tubular acidosis, may contribute to decreased potassium excretion

Hyperkalemia is common when drugs, such as potassium-sparing diuretics (eg, spironolactone, amiloride, triamterene), ACE inhibitors, angiotensin-receptor blockers, beta-blockers, or nonsteroidal anti-inflammatory drugs are used in the setting of renal insufficiency or renal failure

CALCIUM, PARATHYROID, AND VITAMIN D ABNORMALITIES

vitamin D-3 is produced in the skin liver for hydroxylation (25[OH] vitamin D-3) transported to the kidney second hydroxylation occurs 1,25(OH)2 vitamin D-3 is formed is responsible for GI absorption of calcium and phosphorus and suppression of PTH.

Reduced insulin clearance and increased insulin secretion can lead to increased episodes of hypoglycemia and normalization of hyperglycemia in diabetic patients

Levels of thyroid hormones, such as thyroxine, may become depressed, while reverse triiodothyronine levels may increase because of impaired conversion of triiodothyronine to thyroxine.

CARDIOVASCULAR ABNORMALITIES

Cardiovascular abnormalities, including uremic pericarditis, pericardial effusions, calcium and phosphate deposition–associated worsening of underlying valvular disorders

Uremic suppression of myocardial contractility, are common in patients with CRF

Patients are at increased risk for cardiac arrhythmias due to underlying electrolyte and acid-base abnormalities

Renal dysfunction may contribute to associated fluid retention, which may lead to uncontrolled hypertension and congestive heart failure.

MALNUTRITION

Malnutrition usually occurs as renal failure progresses and is manifested by anorexia, weight loss, loss of muscle mass, low cholesterol levels, low BUN levels in the setting of an elevated creatinine level, low serum transferrin levels, and hypoalbuminemia.

Decreased serum albumin concentration is a very strong and independent predictor of mortality among dialysis patients

PREOPERATIVE MANAGMENT

Conduct a thorough history and physical (uraemia syndrome).

Obtain information on the following during the history and physical examination:

Blood pressure and and sugar trends

Radiocontrast exposure

Presence of anemia Bleeding tendencie

Prior surgical experience nephrotoxic drugs

Allergie Significant history of cardiac disease or peripheral arterial disease (PAD)

Nutritional and volume status Functional capacity

Presence of comorbid disease

OTHER IMPORTANT HISTORY PATIENT WITH CKD:

Stable or unstable angina, history of myocardial infarction

Arrhythmias (atrial fibrillation)Comorbid disease (eg, pulmonary

disease, history of stroke, transient ischemic attacks

the patient's history of previous surgeries, which helps to determine the effects of general anesthesia and the presence of allergies to medications

LABORATORY STUDIES AND OTHER TESTS Perform a CBC, particularly to investigate for the presence of

anemia of CKD, Study the patient's serum chemistry results, including

potassium, magnesium, and phosphate concentrations, to establish the level of renal function and electrolyte concentrations. Also, obtain digoxin and other levels.

ECG to investigate for arrhythmias, conduction system abnormalities (eg, left bundle-branch block), evidence of silent MI or ischemia, electrolyte abnormalities (eg, hypokalemia, hyperkalemia), and hypocalcemia or hypercalcem

ABG will help asses hypoxemia and acid base status BUN/Cr: help asses the adequacy of dialysis Glucose levels help assess for the need of intraoperative

insulin needs preoperative dialysis on the day of surgery or previous day of surgery is usually recommended

Chest X-ray

In light of the high prevalence of cardiovascular disease and increased perioperative morbidity in patients with CKD, a thorough cardiovascular risk assessment is indicated and should be performed in accordance with the ACC/AHA guidelines

Clinical predictors of preoperative cardiovascular risk (eg, MI, congestive heart failure [CHF]) can be described as major, intermediate, or minor risk factors.

Patients with major clinical predictor should have their procedures postponed until their medical management is optimized.

CLINICAL PREDICTORS OF PREOPERATIVE CARDIOVASCULAR RISK

Major Intermediet Minor

Unstable coronary syndromes

Mild angina pectoris Advanced age

Recent MI based on clinical symptoms or the results of noninvasive testing

Prior MI with pathological Q waves

Abnormal ECG findings

unstable or severe angina

Compensated or prior CHF

Rhythm other than sinus (eg, atrial fibrillation)

Decompensated CHF

Diabetes mellitus Low functional capacity

Significant arrhythmias

History of stroke

Severe valvular disease

Uncontrolled systemic hypertension

INDUCTION OF ANESTHESIA

patients with nausea, vomiting or GI bleeding should be induced with rapid sequence intubation with cricoid pressure

Slow injection of induction drugs to minimize decreases systemic BP.

Anesthetic induction drug uremia-induced disruption of Blood-brain barrier. decreased protein binding of drugs more unbound drugs to reseptor sites.

MAINTANANCE OF ANETHESIA

In pateints not dependent on HD maintain with N2O combined isoflurane, desflurane, or short-acting opioids. Sevoflurane may avoided because of fluoride nephro toxicity and production of coumpond A.

In patients ESRD recommended : total i.v anesthesia with remifentanyl, propofol and cis atracurium.

Potent volatile anesthetic useful for : contolling intra operative systemic hypertension, decreases doses NMBA needed. hazard execive depression BP.

OPIOID

Opioid decreased cardiovascular depreesion, avoid hepatotoxicity and nephrotoxicity.

Not reliable in control intraop. BP elevation.

In anephric patients small doses opioid prolonged sedation and depression of ventilation

Pharmacology : active metabolite of opioid accumulate in the circulation and LCS

MUSCLE RELAXANT

renal diseases slow exertion of vecuronium and rocuronium

clearence independent of renal function : mivacurium, atracurium cisatracurium.

renal failure delay clearence laudanosine

Diagnosis of residual neuromuscular blocade after reversal NMBA should be considered in anephric patient who manifest mucle weakness.

FLUID

Fluid management and urine out Patients with : -severe renal disfunction

but not requiring HD may benefit from preoperative hydration with administrative salt solutions.

RL solutions (k= 4mEq) and other potasium containing should not be administered to anuric patient.

Recommended : salt solution (3-5 ml/kg/hour i.v) to maintain acceptable urine output, (500 ml iv) to restore circulating volume in hypovolemia

MONITORING

If invasive monitoring required : Venous Pressure monitoring : necessarry. CVP or PAOP monitoring by the presence of

underliying dissease or pulmonary edema. Must be remembered : (1) the catheter must

be accessed asepticaly. (2)the catheter if left heparinized and must be aspirated before conecting to an intravenous line or pressure tranducer. (3) if it is to be disconnected at the end of the procedure, it must be re heparinized and sealed aseptically again.

REGIONAL ANESTHESIA

Brachial plexus block useful for placing vascular shunts for HD.

Before perform : Adequacy of coagulation should be considered and the presence of uremic neuropathies excluded.

Co-existing metabolic acidosis may decrease the seizure threshold for local anesthetic.

POSTOPERATIVE MANAGMENT

Inadequate reversal NMBA should be considered in anephric patients.

In the use of parenteral opioid for post operative analgesia potential for CNS depression and hypoventilation administration of naloxone.

EKG continue for detecting dysrhytmia in hiperkalemia.

O2 supplemental especially if anemia