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Hypertension , crf post renal transplant patient for surgery

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Hypertension , crf post renal transplant patient for surgery

  1. 1. HYPERTENSION , CRF POST RT PATIENT FOR SURGERY PRESENTOR : Dr.Kumar MODERATOR : Dr.Suneela
  2. 2. HYPERTENSION  Defintion : “An adult is considered to be hypertensive when systemic BP>140/90 mm Hg or more on atleast two occasions measured at least 1or2 weeks apart.”
  3. 3. Classification: CATEGORY SYSTOLIC in mmHg DIASTOLIC in mmHg Normal <120 <80 Pre-hypertension 120-139 80-89 Stage 1 HTN Stage 2 HTN 140-159 >160 90-99 >100
  4. 4. Patho-Physiology  Systemic Hypertension 1. Essential Hypertension – No identifiable cause is present 2. Secondary Hypertension-Cause is present
  5. 5. Essential Hypertension  95% of all cases of hypertension  characterized by a familial incidence and inherited biochemical abnormalities.
  6. 6. Factors causing Genesis  increased sympathetic nervous system activity in response to stress  overproduction of sodium-retaining hormones and vasoconstrictors  high sodium intake  inadequate dietary intake of potassium and calcium  increased renin secretion  deficiencies of endogenous vasodilators such as prostaglandins and nitric oxide (NO)  the presence of medical diseases such as diabetes mellitus and obesity
  7. 7. Additional factors  Genetic factors 1.Glucocorticoid remediable HTN: 2.Syndrome of apparent mineralocorticoid excess  Alcohol and tobacco use  Obstructive sleep apnea  Physical activity
  8. 8. poorly controlled essential hypertension  ischemic heart disease  angina pectoris  left ventricular hypertrophy  congestive heart failure  cerebrovascular disease  Stroke  peripheral vascular disease  renal insufficiency suggests end-organ disease due to chronic,poorly controlled essential hypertension
  9. 9. Chronic Condition
  10. 10. 2.Secondary Hypertension 37 JNC VII Causes of Secondary HypertensionJNC VII Causes of Secondary Hypertension Medical Conditions Sleep apnea Thyroid or parathyroid disease Aortic coarctation Pheochromocytoma Cushing’s syndrome Chronic steroid therapy Renovascular disease Primary hyperaldosteronism Chronic kidney disease Drugs Alcohol Cocaine or amphetamines Ephedra, mu huang, bitter orange Erythropoietin Cyclosporine or tacrolimus Sympathomimetics Adrenal steroids Oral contraceptives NSAIDS Chobanian AV et al. JAMA. 2003;289:2560-2572 NSAIDS=Non-steroidal anti-inflammatory drugs
  11. 11. Isolated systolic Hypertension  Aging with associated aortic rigidity  Increased cardiacoutput a. Thyrotoxicosis b. Anemia c. Aortic regurgitation  Decreased peripheral vascular resistance a. Arteriovenous shunts b. Paget's disease
  12. 12. Treatment of Essential Hypertension  GOALS  to decrease systemic blood pressure to lower than 140/90 mm Hg, but in the presence of diabetes mellitus or renal disease, the goal is lower than 130/80 mm Hg  decreasing the incidence of cerebrovascular accidents  decreases the morbidity and mortality associated with ischemic heart disease  prevents progression to a more severe stage of hypertension and decreases the risk of congestive heart failure and renal failure.
  13. 13.  LIFE STYLE MODIFICATION- Patients who do not manifest clinical evidence of cardiovascular disease or target organ damage may benefit from a trial of lifestyle modification  PHARMACOLOGICAL THERAPY -Patients with concomitant risk factors (hypercholesterolemia, diabetes mellitus, tobacco abuse, family history, age older than 60 years) and -evidence of target organ damage are most likely to benefit from pharmacologic antihypertensive therapy
  14. 14. Treatment of Secondary Hypertension  Surgical Therapy: 1. correction of renal artery stenosis via angioplasty or direct repair and 2. adrenalectomy for adrenal adenoma or pheochromocytoma  Pharmacologic Therapy:  renal artery revascularization is not possible  blood pressure control with ACE inhibitors alone or in combination with diuretics.  Renal function and serum potassium concentration must be carefully monitored
  15. 15. Hypertensive Crises  Definition:  Hypertensive crises typically present with a blood pressure of higher than 180/120  categorized as 1. hypertensive urgency 2. hypertensive emergency  based on the presence or absence of impending or progressive target organ damage
  16. 16. Hypertensive Emergency  evidence of acute or ongoing target organ damage 1. encephalopathy, 2. intracerebral hemorrhage, 3. acute left ventricular failure with pulmonary edema 4. unstable angina, 5. dissecting aortic aneurysm 6. acute myocardial infarction, 7. eclampsia, 8. microangiopathic hemolytic anemia, 9. renal insufficiency require prompt pharmacologic intervention to lower the systemic blood pressure
  17. 17. Treatment  goal of treatment to decrease the diastolic blood pressure promptly but gradually  A precipitous decrease in blood pressure to normotensive levels may provoke coronary or cerebral ischemia  Typically, mean arterial pressure is reduced by about 20% within the first 60 minutes and then more gradually.  Thereafter, the blood pressure can be reduced to 160/110 over the next 2 to 6 hours as tolerated by the
  18. 18. Hypertensive Urgency  Hypertensive urgencies are situations in which BP is severely elevated, but the patient is not exhibiting evidence of target organ damage.  These patients can present with headache, epistaxis, or anxiety.  Selected patients may benefit from oral antihypertensive therapy
  19. 19. Management of Anesthesia in Patients with Essential Hypertension  Pre operative evaluation: 1. Determine adequacy of blood pressure control 2. Review pharmacology of drugs being administered to control blood pressure 3. Evaluate for evidence of end-organ damage 4. Continue drugs used for control of blood pressure
  20. 20.  review the pharmacology and potential side effects of the drugs being used for antihypertensive therapy  hemodynamic instability and hypotension will occur during anesthesia in patients receiving ACE inhibitors  discontinue ACE inhibitors 24 to 48 hours preoperatively in patients at high risk of intraoperative hypovolemia and hypotension.  ARBs increases the potential for hypotension during anesthesia.  necessitating use of vasopressin or one of its analogues
  21. 21.  risk of rebound hypertension should certain drugs, especially β-adrenergic antagonists and clonidine, be abruptly discontinued.  Hypokalemia (<3.5 mEq/L) despite potassium supplementation is a common preoperative finding in patients being treated with diuretics.  Hyperkalemia can be seen patients being treated with ACE inhibitors
  22. 22. Induction of Anesthesia  Hypotension during induction in patients continuing ACE inhibitor or ARB therapy.  Direct laryngoscopy and tracheal intubation can produce significant hypertension in patients with essential hypertension  deep inhalation anesthesia or injection of an opioid, lidocaine, β-blocker, or vasodilator protect from MI  Direct laryngoscopy that does not exceed 15 seconds in duration helps minimize blood pressure
  23. 23. Maintenance of Anesthesia  to minimize wide fluctuations in blood pressure.  Management of intraoperative blood pressure lability is as important as preoperative control of hypertension in these patients. Problems 1. Intraoperative hypertension 2. Intraoperative hypotension
  24. 24. 1. Intraoperative hypertension  produced by painful stimulation, i.e., light anesthesia  A nitrous oxide–opioid technique can be used for maintenance of anesthesia  Antihypertensive medication by bolus or by continuous infusion is an alternative to the use of a volatile anesthetic for blood pressure control intraoperatively  no evidence that a specific neuromuscular blocker is best for patients with hypertension
  25. 25.  Intraoperative Hypotension  Hypotension during maintenance of anesthesia may be treated by decreasing the depth of anesthesia and/or by increasing fluid infusion rates.  Cardiac rhythm disturbances that result in loss of sequential atrioventricular contraction such as junctional rhythm and atrial fibrillation can also create hypotension  ephedrine or phenylephrine may be necessary to restore vital organ perfusion pressures  patients treated with ACE inhibitors or ARBs is responsive to administration of i.v fluids or vasopressin.
  26. 26. Postoperative Management  Postoperative hypertension is common in patients with essential hypertension.  assessment and treatment to decrease the risk of myocardial ischemia, cardiac dysrhythmias, congestive heart failure, stroke, and bleeding.  conversion can be made to the patient's usual regimen of oral antihypertensive medication
  27. 27. Chronic Renal Failure  CRF occurs where GFR has been reduced to 10% (20ml/min) of normal function and ESRD when GFR falls below 5% (10ml/min).  The relationship between serum creatinine and GFR is not linear (figure 1) and serum creatinine does not rise until GFR has fallen below 50%.
  28. 28. Stages of Chronic Kidney Disease (NKF,2003) Stage Description GFR 1 Kidney Damage with normal GFR >/=90 2 Kidney Damage with mild fall in GFR 60-89 3 Moderate fall in GFR 30-59 4 Severe fall in GFR 15-29 5 Kidney Failure <15
  29. 29. Causes <18 YEARS  Obstructive uropathy  Cong. Anomalies  Cong.nephrotic syndrome  Oxalosis  Infantile PKD  Cortical necrosis  Hemolytic uremic syndrome  Chr.glomerulo nephritis
  30. 30. ESRD AGE >18Yrs  Type 1 D.M.  Chr. G.N.  Type 2 D.M.  Hypertensive N.S.  MPGN  Obstructive uropathy  Ig A Nephropathy  SLE  Others 21.6
  31. 31. Pathophysiologic consequences Cardiovascular  Hyper tension develops in approximately 80% patients  Sodium and water retention, hyper secretion of renin – high conc. of renin, angiotensin-‫װ‬ and aldosterone with LVH, hypertensive cardiomyopathy, hypertensive crises  Ischemic heart disease
  32. 32. Cardiovascular  Atherosclerosis and vascular calcification (high calcium&phosphate product).  Uremic pericarditis if untreated leads to cardiac tamponade & later constrictive pericarditis.  Dysrhythmias due to Hyperkalemia and hypocalcaemia.
  33. 33. Haematological effects Anaemia  Due to decreased erythropoietin production,  Diminished erythrocyte survival,  Diminished production of R.B.C’s due to fibrosis of bonemarrow.  Reduced dietary intake and absorption of iron.  Fragility of capillaries  Qualitative dysfunction of platelets due to decreased platelet factor III activity.  Aluminium toxicity & iron,folate,vitB6,B12.
  34. 34. Haematological effects  Absence of correction of the anaemia,there are compensatory mechanisms for the reduction in oxygen carrying capacity .  increase in cardiac output & an increase in the 2,3DPG.  Severe anaemia affects the blood-gas partition coefficient so onset & recovery is faster .
  35. 35. Respiratory system  Pulmonary congestion & edema are seen with resultant hypoxaemia & hypocapnia .  Intra peritoneal fluid causes diaphragmatic splinting with basal atelectasis & shunting.  Uremia can cause pleuritis.  Immunosuppressed patients are more susceptable to pulmonary infections .
  36. 36. Electrolyte and fluid disturbances  Impaired ability to excrete water,electrolytes & free acids.  Hyperkalemia  Hypocalcaemia (osteodystrophy, osteoporosis, pathologic #)  Hypermagnesemia (hypotension, potentiation of depolarizing muscle relaxants, coma)  Hypervolemia (CHF, pulmonary edema, pleural effusion, hypertension).
  37. 37. Electrolyte and fluid disturbances  Uremic patients tolerate hyperkalaemia & it is safe to administer anaesthesia in the presence of higher K levels,unless there are ECG changes.  Methods for preoperative correction include glucose-insulin,sodium bicarbonate ,10ml of 10% of calcium gluconate,hyperventilation ,furosemide or dialysis & kayexilate .
  38. 38. Endocrine  Secondary hyperparathyroidismosteomalacia, renal osteodystrophy (bone pain, fractures),  Insulin half life is prolonged in CRF, due to decreased tubular metabolism of insulin.  However there is post receptor defect in insulin action, and relative insulin resistance.  Hyperprolactinaemia – loss of libido in both sexes, amenorrhea in women.
  39. 39. Coagulation  Several abnormalities of coagulation factors like(dec plat F III, platelet dysfn).  Pletelet FIII decreased because of accumulation of toxic waste products,  These products are removed by dialysis.  Other methods  platelet , cryoprecipitate & desmopressin acetate .  Desmopressin acetate increase the activity of factors VIII,XII,von willebrand factor.
  40. 40. Central nervous system  Features of uremia are initially malaise & reduced mental ability.  Others are seizures,coma & death .  Dialysis associated with dysequilibrium syndrome.  Due to sudden changes in extracellular volume,electrolytes & cerebral edema.  Presents as dehydration,weakness, vomiting,hypotension ,convulsions & coma.
  41. 41. Peripheral neuropathy  Demyelination of medullated fibres, long fibres are involved earlier.  Sensory neuropathy: paraesthesia.  Motor neuropathy: foot drop.  Uremic autonomic neuropathy: postural hypotension, diarrhea.
  42. 42. Myopathy  A combination of poor nutrition, hyperparathyroidism, Vit.D deficiency and disorders of electrolyte metabolism.  Muscle cramps are common & quinine sulphate will be helpful.  Restless leg syndrome  patients legs are jumpy during the night which is improved by clonazepam .
  43. 43. Gastrointestinal tract  Presents with anorexia,nausea &vomiting,GI bleed & diarrhoea .  Delayed gastric emptying,increase in acidity & gastric volume .  Pt benefits from administration of histamine H2 receptor antagonist as a premedication .  Ascites is a rare but important complications .
  44. 44. Immune system  Uremia impairs normal immune mechanisms .  It is obtunded further by giving immunosuppresant therapy  As a result sepsis remains a major prob.  So strict aseptic technique is followed .
  45. 45. altered drug handling in CRF  volume of distribution is usually decreased, but may be increased if there is fluid retention  Hypoalbuminaemia and acidosis increase the free drug availability of highly protein bound drugs  The doses of benzodiazepines and thiopentone may need to be reduced by 30% - 50%  The elimination of highly ionised, water soluble drugs such as atropine are partially or completely dependent on renal excretion and may be markedly reduced.
  46. 46.  The elimination of volatile anaesthetic agents is not dependent on renal function and their activity is unaffected by CRF.  The hepatic metabolism of both enflurane and sevoflurane will produce nephrotoxic fluoride ions and their use should be discouraged for prolonged durations  Atracurium and cisatracurium are obvious choices for muscle relaxation.  The excretion of anticholinesterases and anticholinergic agents will be prolonged as they are highly ionised and water soluble.  Avoid NSAIDS
  47. 47. POST TRANSPLANT STATE  A chronic kidney disease - continued organ dysfunction  Post transplant surgery frequency is ~ 41%  Surgery unrelated to transplant ~ 6%  Incidence and urgency of surgery does not vary with the source of donor kidney  Mortality related to the degree of immunosuppression and not additional operation.
  48. 48. Problems In Post Renal transplant 1. Persistent cardiovascular disease 2. Bone disorders 3. Electrolyte and acid base imbalance 4. Post transplant Diabetes Mellitus 5. Malignancy 6. Infection
  49. 49. 1. CARDIOVASCULAR DISEASE  Most common cause of mortality in those with functional grafts – 30-40%  Increased incidence of : coronary heart disease, CHF, ventricular hypertrophy, hypertension, cerebrovascular disease, peripheral vascular disease.
  50. 50. CARDIOVASCULAR DISEASE contd. Risk factors –  Conventional  Smoking  Hypertension  Hyperlipidemia  DM  Specific to transplant patients  Anaemia  Chronic fluid overload  Hyperparathyroidism  Immunosuppressants
  51. 51. CARDIOVASCULAR DISEASE contd. HYPERTENSION  Causes –  Native kidney disease  CNIs (60-80% prevalence)  Weight gain  Target BP - <120/80 (JNC VII)  Allograft dysfunction  Steroids  Transplant renal artery stenosis
  52. 52. CARDIOVASCULAR DISEASE contd. HYPERLIPIDEMIA Causes ( GCS )-  Steroids  Sirolimus, Calcineurin inhibitors(CNI) Rx-  Lifestyle modification - Weight loss, exercise  ↓ steroid dosage  Cyclosporine → tacrolimus  Statins
  53. 53. 2. BONE DISORDERS  Persistent hyperparathyroidism  Gout  Osteonecrosis  Osteoporosis
  54. 54. 2. BONE DISORDERS HYPERPARATHYROIDISM  Very common in 1st post transplant year  Risk factors –  Degree of pre- transplant disease  Duration of dialysis  Contributing factors-  Deficiency of vitamin D  Poor allograft function
  55. 55. BONE DISORDERS – HYPERPARATHYROIDISM contd.  Symptoms – mostly asymptomatic  Dx – increased plasma Ca decreased plasma phosphate  Rx – vitamin D analogs (stopped if S Ca.>11mg/dl ) - phosphate supplements
  56. 56. BONE DISORDERS - HYPERPARATHYROIDISM contd.  Surgery – indications – 1) severe symptomatic hypercalemia in early post transplant period 2) persistent moderately severe hypercalcemia for > one year post transplantation  Surgery done – subtotal parathyroidectomy
  57. 57. 2. BONE DISORDERS GOUT  Cyclosporine – most important cause  Impairs renal uric acid clearance  Rx –  Colchicine  High dose steroids  Synthesis inhibitor i.e. Allopurinol ( dec. dose of azathioprine)  NSAIDS – Avoid
  58. 58. 2.BONE DISORDERS OSTEONECROSIS (AVASCULAR NECROSIS)  Cause - High dose steroids  Sites - humeral head, femoral condyles, proximal tibia, vertebrae  Symptom – mainly pain  Rx – resting the joint , decompression , joint replacement
  59. 59. 2. BONE DISORDERS OSTEOPOROSIS  Common bone disorder- parallel reduction in bone mineral and bone matrix→ Decreased bone mass  Maximum bone loss – first 6 month
  60. 60. BONE DISORDERS – OSTEOPOROSIS contd. Causes  Steroids  Ongoing hyperparathyroidism  Vit D def /resistance  Phosphate depletion Rx  Weight bearing exercise  Steroid minimization  Elemental calcium and calcitriol Clinical implication – Increased risk of fracture
  61. 61. 3.ELECTROLYTE ACID BASE IMBALANCE HYPERKALEMIA Causes:  CNI induced impairment of tubule potassium secretion  Poor graft function  Excessive intake  ACE-I, SMX-TMP Clinical implication – muscle weakness, ECG changes
  62. 62. ELECTROLYTE IMBALANCE contd.  HYPOPHOSPHATEMIA  Due to excess urinary excretion  residual hyperparathyroidism  Glucocorticoids  low Vit D state Implication – Profound respiratory muscle weakness
  63. 63. ELECTROLYTE IMBALANCE contd.  HYPERCALCEMIA  Causes –  Persistent Hyperparathyroidism  Co- administration of calcium and vit D Implication – shortened Q-T interval and arrhythmias
  64. 64. ELECTROLYTE IMBALANCE contd. HYPOMAGNESEMIA  Cause - CNI induced  Asymptomatic  Rx – magnesium supplements if plasma Mg levels < 1.5mg/dl Clinical implication - ↑ risk of perioperative arrhythmias, impaired respiratory muscle power
  65. 65. ACID BASE IMBALANCE METABOLIC ACIDOSIS Causes  Distal (hyperchloremic) renal tubular acidosis - occurs due to:  CNI  Rejection  Residual hyperparathyroidism Clinical Implication - intraoperative electrolyte imbalance prolonged NM blockade interference with drug PK
  66. 66. 4. POST TRANSPLANT DIABETES MELLITUS  New onset DM – Common  Increased CV risk  Risk factors –  Older age  Obesity  Positive hepatitis C antibody status  Family history  Deceased donor allograft  Steroids  CNI  Episodes of acute rejection
  67. 67. POST TRANSPLANT DM (contd) Rx  Steroids minimized  Tacrolimus avoided  Oral hypoglycemic drugs and Insulin  Metformin- most effective
  68. 68. 5.MALIGNANCY  Causes of ↑ cancer incidence –  Immunosuppressants → inhibit normal tumor ↓ surveillance mechanisms uncontrolled proliferation of oncogenic viruses  Factors related to primary renal disease ( analgesic abuse, HBV , HCV, certain herbal preparations)  Renal cystic disease
  69. 69. MALIGNANCY contd. Treatment  ↓ the dose of immunosuppression  Sirolimus – increasing evidence of antineoplastic effects Post Transplant Lymphoproliferative Disorder (PTLD)  1-2% incidence  Feared complication  Cause- Infection and transformation of B cell by EBV
  70. 70. INFECTIONS (contd.)  0-1 MONTH - ~ to those seen in non transplant patients after surgery.  UTI  lung infections  related to vascular catheters  Bacterial> fungal
  71. 71. INFECTIONS (contd.)  1-6 MONTHS – Oppurtunistic infections  CMV, EBV, listeria, pneumocystis carini, nocardia  Prevention – Antiviral prophylaxis (3-6 months)  SMX-TMP prophylaxis (6 to 12 months) -
  72. 72. INFECTIONS (contd.) > 6 MONTHS – risk of infection decreases  can be divided into 2 groups – 1) Good graft function, no need of late supplemental immunosuppression – infection risk similar to general population 2) Poor graft function, received large cumulative doses of immunosuppression – remain at risk of oppurtunistic infection -need long term SMX- TMP prophylaxis
  73. 73. INFECTIONS (contd.) Clinical implication –  Minimizing infection should be the goal  Require meticulous surgical technique  Antiviral prophylaxis  Avoidance of excess immunosuppression
  74. 74. Common surgical indications  First 48 hrs of transplant:  Rexploration for bleeding/reduced urine/thrombosis of graft  Late presentations:  Graft failure: Redo surgery  Uncontrolled hypertension-- Nephrectomy  Lymphoceles, Wound infections  Joint replacements (renal osteodystrophy, steroid)  Cesarean Sections  GI bleed, CABG, dental (gum hyperplasia)
  75. 75. Anesthetic challenges & preoperative assessment  Avoidance of infection: Maintain sterility  Signs of intra-abdominal sepsis..often absent  fever, leukocytosis, peritonitis signs absent  Assess/Preserve graft function:  previous episodes of rejection  BU, S.Cr, SE (Na,K,Ca,Mg)  Avoid nephrotoxic drugs
  76. 76. Anesthetic challenges: preoperative assessment  Assess Rejection  Azotemia, proteinuria, hypertension  Pruritis, lethargy, nausea, skin pigmentation  Care for co-morbidities: HTN, CAD, DM,CHF  Stress testing  Coronary angiography  Hyperlipidemia:  Increases perioperative CVS morbidity/mortality
  77. 77. Anesthetic challenges: preoperative assessment  If on Hemodialysis  Hypovolemia: CVS instability  Hypokalemia: Arrhythmias, Susceptible to MR  Steroid- lympho proliferative disorder-airway obstruction
  78. 78. Anesthetic challenges: Drugs  Immunosuppressants  Double edged sword  Continue perioperatively in adequate doses  Oral dose of CSA : 4-7 hrs before surgery  “Stress-coverage” steroids: if recently withdrawn Affect the choice of anesthesia
  79. 79. Immunosuppressants Agent Type Side effect Cyclosporine A calcineurin inhibitor 1) Expensive 2) Nephrotoxic 3) Gastric atony 4) Hirsutism 5) HTN/lipidemia Prolongs effects of muscle relaxants, Delayed gastric emptying Tacrolimus (PK 506) calcineurin inhibitor 1) Hyperglycemia 2) Increases viral replication Avoid in diabetics Avoid in HCV/HIV Mycophenolate Mofetil MMF nucleoside synthesis inhibitor Thrombocytopenia Anemia Avoid Regi0nal Intravenous globulins (OKT3) Antithymocyte/lymp hocyte Cytokine release Thrombocytopenia Non cardiogenic pulmonary edema Azathioprine nucleoside synthesis inhibitor Thrombocytopenia Cannot prevent long term rejection
  80. 80. Premedication  Standard premedication may be used  BZP: duration & activity prolonged  Ranitidine: caution interaction with Cyclosporine
  81. 81. Monitoring  Perioperative monitoring: risk/benefit  type of surgery  anesthesia planned  equipment available  CVP monitoring:  Transplanted kidneys sensitive to hypovolemia  Diuretic use: adequate intravascular volume  urine output
  82. 82. Technique  General (balanced & TIVA) as well as regional successfully used  General anaesthesia  Nasal intubation better avoided  Use of LMA acceptable  Ketamine: cautious in HTN/CAD
  83. 83. Inhalation Agents  Isoflurane/desflurane :appropriate  Sevoflurane :safe  Enflurane : avoided--toxic fluoride metabolites
  84. 84. Muscle relaxants  Atracurium, Cisatracurium usually preffered  Vecuronium should be prevented –reno vasoconstriction  Delayed gastric emptying/RSI:  Sch: K<5.5 meq/L  Rocuronium, miva
  85. 85. Analgesia  Avoid NSAIDS:  GI Hmge, nephrotoxicity  Augment Cyclosporine A nephrotoxicity  Opiate analgesics often used  Meperidine,M3G and M6G: prolonged sedation  Remifentanyl@ 0.1-0.5 mics/kg/min:  short acting  Non specific tissue and plasma esterases
  86. 86. Regional anesthesia  Avoid:  uremic platelet dysfunction  Severe hypovolemia  Caution:  Azathioprine, MMF  Uremic/diabetic peripheral neuropathy  Bupivacaine safe in clinical doses
  87. 87. POST OP CARE PAIN –  Opioid based pain relief  Morphine , pethidine – avoid if RFT deranged  Paracetamol - in paediatric patients  NSAIDS to be avoided  Epidural analgesia
  88. 88. POST OP CARE  Cardiovascular collapses have occured upto 2 days post op.  All monitoring should be continued till 2nd post op day.  In patients with CV disease :  Perioperative beta blockers – can be considered  Maintain normothermia  Haematocrit > 30%  Adequate analgesia

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