1. HYPERTENSION , CRF
POST RT PATIENT FOR
SURGERY
PRESENTOR : Dr.Kumar
MODERATOR :
Dr.Suneela

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. 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. Patho-Physiology
 Systemic Hypertension
1. Essential Hypertension – No identifiable
cause is present
2. Secondary Hypertension-Cause is present

5. Essential Hypertension
 95% of all cases of hypertension
 characterized by a familial incidence and
inherited biochemical abnormalities.

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. Additional factors
 Genetic factors
1.Glucocorticoid remediable HTN:
2.Syndrome of apparent
mineralocorticoid excess
 Alcohol and tobacco use
 Obstructive sleep apnea
 Physical activity

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. Chronic Condition

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. 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. 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.  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

16. 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

17. 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

18. 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

19. 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

20. 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

23. 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

24.  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

25.  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

26. 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

27. 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

28. 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

29.  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.

30. 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

31. 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%.

32. 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

33. Causes
<18 YEARS
 Obstructive uropathy
 Cong. Anomalies
 Cong.nephrotic syndrome
 Oxalosis
 Infantile PKD
 Cortical necrosis
 Hemolytic uremic
syndrome
 Chr.glomerulo nephritis

34. 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

35. 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

36. 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.

37. 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.

38. 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 .

39. 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 .

40. 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).

41. 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 .

42. 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.

44. 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.

45. 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.

46. Peripheral neuropathy
 Demyelination of medullated fibres, long fibres
are involved earlier.
 Sensory neuropathy: paraesthesia.
 Motor neuropathy: foot drop.
 Uremic autonomic neuropathy: postural
hypotension, diarrhea.

47. 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 .

48. 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 .

49. 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 .

50. 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.

51.  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

52. 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.

53. 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

54. 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.

55. CARDIOVASCULAR DISEASE
contd.
Risk factors –
 Conventional
 Smoking
 Hypertension
 Hyperlipidemia
 DM
 Specific to transplant patients
 Anaemia
 Chronic fluid overload
 Hyperparathyroidism
 Immunosuppressants

56. 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

57. CARDIOVASCULAR DISEASE contd.
HYPERLIPIDEMIA
Causes ( GCS )-
 Steroids
 Sirolimus, Calcineurin inhibitors(CNI)
Rx-
 Lifestyle modification - Weight loss, exercise
 ↓ steroid dosage
 Cyclosporine → tacrolimus
 Statins

58. 2. BONE DISORDERS
 Persistent hyperparathyroidism
 Gout
 Osteonecrosis
 Osteoporosis

59. 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

60. 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

61. 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

62. 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

63. 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

64. 2. BONE DISORDERS
OSTEOPOROSIS
 Common bone disorder- parallel reduction in bone
mineral and bone matrix→ Decreased bone mass
 Maximum bone loss – first 6 month

65. 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

66. 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

67. ELECTROLYTE IMBALANCE contd.
 HYPOPHOSPHATEMIA
 Due to excess urinary excretion
 residual hyperparathyroidism
 Glucocorticoids
 low Vit D state
Implication – Profound respiratory muscle weakness

68. ELECTROLYTE IMBALANCE contd.
 HYPERCALCEMIA
 Causes –
 Persistent Hyperparathyroidism
 Co- administration of calcium and vit D
Implication – shortened Q-T interval and
arrhythmias

69. 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

70. 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

71. 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

72. POST TRANSPLANT DM (contd)
Rx
 Steroids minimized
 Tacrolimus avoided
 Oral hypoglycemic drugs and Insulin
 Metformin- most effective

73. 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

74. 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

75. INFECTIONS (contd.)
 0-1 MONTH - ~ to those seen in non transplant
patients after surgery.
 UTI
 lung infections
 related to vascular catheters
 Bacterial> fungal

76. 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)
-

77. 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

78. INFECTIONS (contd.)
Clinical implication –
 Minimizing infection should be the goal
 Require meticulous surgical technique
 Antiviral prophylaxis
 Avoidance of excess immunosuppression

79. 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)

80. 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

81. 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

82. Anesthetic challenges:
preoperative assessment
 If on Hemodialysis
 Hypovolemia: CVS instability
 Hypokalemia: Arrhythmias, Susceptible to MR
 Steroid- lympho proliferative disorder-airway
obstruction

83. 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

84. 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

85. Premedication
 Standard premedication may be used
 BZP: duration & activity prolonged
 Ranitidine: caution interaction with Cyclosporine

86. 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

87. 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

88. Inhalation Agents
 Isoflurane/desflurane :appropriate
 Sevoflurane :safe
 Enflurane : avoided--toxic fluoride metabolites

89. Muscle relaxants
 Atracurium, Cisatracurium usually preffered
 Vecuronium should be prevented –reno
vasoconstriction
 Delayed gastric emptying/RSI:
 Sch: K<5.5 meq/L
 Rocuronium, miva

90. 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

91. Regional anesthesia
 Avoid:
 uremic platelet dysfunction
 Severe hypovolemia
 Caution:
 Azathioprine, MMF
 Uremic/diabetic peripheral neuropathy
 Bupivacaine safe in clinical doses

92. POST OP CARE
PAIN –
 Opioid based pain relief
 Morphine , pethidine – avoid if RFT deranged
 Paracetamol - in paediatric patients
 NSAIDS to be avoided
 Epidural analgesia

93. 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