Hypertension , crf post renal transplant patient for surgery
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Transcript of Hypertension , crf post renal transplant patient for surgery
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HYPERTENSION , CRF POST RT PATIENT FOR SURGERY
PRESENTOR : Dr.Kumar
MODERATOR : Dr.Suneela
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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.”
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Classification:
CATEGORY SYSTOLIC in mmHg
DIASTOLIC in mmHg
Normal <120 <80
Pre-hypertension 120-139 80-89
Stage 1 HTNStage 2 HTN
140-159>160
90-99>100
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Patho-Physiology Systemic Hypertension
1. Essential Hypertension – No identifiable cause is present
2. Secondary Hypertension-Cause is present
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Essential Hypertension 95% of all cases of hypertensioncharacterized by a familial incidence
and inherited biochemical abnormalities.
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Factors causing Genesisincreased sympathetic nervous system activity
in response to stressoverproduction of sodium-retaining hormones
and vasoconstrictorshigh sodium intakeinadequate dietary intake of potassium and
calciumincreased renin secretiondeficiencies of endogenous vasodilators such as
prostaglandins and nitric oxide (NO) the presence of medical diseases such as
diabetes mellitus and obesity
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Additional factorsGenetic factors1.Glucocorticoid remediable HTN: 2.Syndrome of apparent
mineralocorticoid excessAlcohol and tobacco use Obstructive sleep apneaPhysical activity
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poorly controlled essential hypertension
ischemic heart disease angina pectoris left ventricular hypertrophy congestive heart failure cerebrovascular diseaseStrokeperipheral vascular disease renal insufficiency suggests end-organ disease due to
chronic,poorly controlled essential hypertension
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Chronic Condition
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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
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Isolated systolic HypertensionAging with associated aortic rigidity Increased cardiacoutput a. Thyrotoxicosis b. Anemia c. Aortic regurgitation Decreased peripheral vascular
resistance a. Arteriovenous shunts b. Paget's disease
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Treatment of Essential Hypertension
GOALSto 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.
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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
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Treatment of Secondary HypertensionSurgical 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
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Hypertensive CrisesDefinition:Hypertensive crises typically present with a
blood pressure of higher than 180/120 categorized as 1. hypertensive urgency 2. hypertensive emergencybased on the presence or absence of
impending or progressive target organ damage
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Hypertensive Emergencyevidence of acute or ongoing target organ damage1. encephalopathy, 2. intracerebral hemorrhage, 3. acute left ventricular failure with pulmonary edema4. unstable angina, 5. dissecting aortic aneurysm6. acute myocardial infarction,7. eclampsia,8. microangiopathic hemolytic anemia,9. renal insufficiency require prompt pharmacologic intervention to
lower the systemic blood pressure
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Treatmentgoal 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 absence of symptomatic hypoperfusion of target organs.
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Hypertensive UrgencyHypertensive 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
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Management of Anesthesia in Patients with Essential HypertensionPre 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
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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
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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
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Induction of AnesthesiaHypotension 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 changes.
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Maintenance of Anesthesiato 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 hypertension2. Intraoperative hypotension
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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
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Intraoperative HypotensionHypotension 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.
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Postoperative ManagementPostoperative 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
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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%.
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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
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Causes <18 YEARSObstructive uropathyCong. AnomaliesCong.nephrotic
syndromeOxalosisInfantile PKDCortical necrosisHemolytic uremic
syndromeChr.glomerulo
nephritis
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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
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Pathophysiologic consequences
CardiovascularHyper 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
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CardiovascularAtherosclerosis and vascular calcification
(high calcium&phosphate product).
Uremic pericarditis if untreated leads to cardiac tamponade & later constrictive pericarditis.
Dysrhythmias due to Hyperkalemia and hypocalcaemia.
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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 capillariesQualitative dysfunction of platelets due to
decreased platelet factor III activity. Aluminium toxicity & iron,folate,vitB6,B12.
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Haematological effectsAbsence 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 .
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Respiratory systemPulmonary 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 .
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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).
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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 .
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Endocrine Secondary
hyperparathyroidismosteomalacia, 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.
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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.
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Central nervous systemFeatures 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.
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Peripheral neuropathy Demyelination of medullated fibres, long
fibres are involved earlier.
Sensory neuropathy: paraesthesia.
Motor neuropathy: foot drop.
Uremic autonomic neuropathy: postural hypotension, diarrhea.
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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 .
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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 .
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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 .
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altered drug handling in CRFvolume of distribution is usually decreased, but
may be increased if there is fluid retentionHypoalbuminaemia 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.
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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
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POST TRANSPLANT STATE A chronic kidney disease - continued organ
dysfunctionPost transplant surgery frequency is ~
41%Surgery unrelated to transplant ~ 6%Incidence and urgency of surgery does not
vary with the source of donor kidneyMortality related to the degree of
immunosuppression and not additional operation.
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Problems In Post Renal transplant
1. Persistent cardiovascular disease2. Bone disorders3. Electrolyte and acid base
imbalance4. Post transplant Diabetes Mellitus5. Malignancy6. Infection
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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.
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CARDIOVASCULAR DISEASE contd.
Risk factors – ConventionalSmokingHypertensionHyperlipidemia DM
Specific to transplant patients Anaemia Chronic fluid overload Hyperparathyroidism Immunosuppressants
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CARDIOVASCULAR DISEASE contd.HYPERTENSION
Causes – Native kidney diseaseCNIs (60-80%
prevalence) Weight gain
Target BP - <120/80 (JNC VII)
Allograft dysfunctionSteroids Transplant renal
artery stenosis
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CARDIOVASCULAR DISEASE contd.HYPERLIPIDEMIA
Causes ( GCS )-SteroidsSirolimus, Calcineurin inhibitors(CNI)
Rx-Lifestyle modification - Weight loss, exercise ↓ steroid dosageCyclosporine → tacrolimusStatins
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2. BONE DISORDERS
Persistent hyperparathyroidismGout OsteonecrosisOsteoporosis
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2. BONE DISORDERSHYPERPARATHYROIDISM
Very common in 1st post transplant year
Risk factors – Degree of pre- transplant
diseaseDuration of dialysis
Contributing factors-Deficiency of vitamin DPoor allograft function
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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
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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
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2. BONE DISORDERSGOUT
Cyclosporine – most
important causeImpairs renal uric acid
clearanceRx – Colchicine High dose steroids Synthesis inhibitor i.e.
Allopurinol ( dec. dose of azathioprine)
NSAIDS – Avoid Switch to Tacrolimus
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2.BONE DISORDERS OSTEONECROSIS (AVASCULAR NECROSIS)
Cause - High dose steroidsSites - humeral head, femoral condyles,
proximal tibia, vertebraeSymptom – mainly pain Rx – resting the joint , decompression ,
joint replacement
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2. BONE DISORDERSOSTEOPOROSIS
Common bone disorder- parallel reduction in bone mineral and bone matrix→ Decreased bone mass
Maximum bone loss – first 6 month
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BONE DISORDERS – OSTEOPOROSIS contd.
CausesSteroidsOngoing hyperparathyroidism Vit D def /resistance Phosphate depletion RxWeight bearing exerciseSteroid minimizationElemental calcium and calcitriol
Clinical implication – Increased risk of fracture
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3.ELECTROLYTE ACID BASE IMBALANCE
HYPERKALEMIA Causes:CNI induced impairment of tubule
potassium secretionPoor graft functionExcessive intakeACE-I, SMX-TMP
Clinical implication – muscle weakness, ECG changes
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ELECTROLYTE IMBALANCE contd.
HYPOPHOSPHATEMIADue to excess urinary excretion residual hyperparathyroidismGlucocorticoids low Vit D stateImplication – Profound respiratory muscle
weakness
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ELECTROLYTE IMBALANCE contd.HYPERCALCEMIACauses – Persistent Hyperparathyroidism Co- administration of calcium and vit D
Implication – shortened Q-T interval and arrhythmias
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ELECTROLYTE IMBALANCE contd.
HYPOMAGNESEMIACause - CNI inducedAsymptomaticRx – magnesium supplements if plasma Mg
levels < 1.5mg/dl Clinical implication - ↑ risk of perioperative
arrhythmias, impaired respiratory muscle power
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ACID BASE IMBALANCE
METABOLIC ACIDOSIS CausesDistal (hyperchloremic) renal tubular acidosis -
occurs due to: CNI Rejection Residual hyperparathyroidism Clinical Implication - intraoperative electrolyte imbalance prolonged NM blockade interference with drug PK
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4. POST TRANSPLANT DIABETES MELLITUS New onset DM –
CommonIncreased CV riskRisk factors – Older ageObesityPositive hepatitis C
antibody statusFamily history
Deceased donor allograft
SteroidsCNI Episodes of acute
rejection
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POST TRANSPLANT DM (contd) RxSteroids minimizedTacrolimus avoidedOral hypoglycemic drugs and InsulinMetformin- most effective
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5.MALIGNANCYCauses 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
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MALIGNANCY contd. Treatment↓ the dose of immunosuppression Sirolimus – increasing evidence of antineoplastic
effects
Post Transplant Lymphoproliferative Disorder (PTLD)
1-2% incidenceFeared complicationCause- Infection and transformation of B cell by
EBV
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INFECTIONS (contd.) 0-1 MONTH - ~ to those seen in non
transplant patients after surgery.UTI lung infections related to vascular cathetersBacterial> fungal
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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)
-
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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
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INFECTIONS (contd.)Clinical implication – Minimizing infection should be the goalRequire meticulous surgical techniqueAntiviral prophylaxisAvoidance of excess immunosuppression
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Common surgical indicationsFirst 48 hrs of transplant:
Rexploration for bleeding/reduced urine/thrombosis of graft
Late presentations:Graft failure: Redo surgeryUncontrolled hypertension-- NephrectomyLymphoceles, Wound infectionsJoint replacements (renal osteodystrophy,
steroid)Cesarean SectionsGI bleed, CABG, dental (gum hyperplasia)
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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 rejectionBU, S.Cr, SE (Na,K,Ca,Mg)Avoid nephrotoxic drugs
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Anesthetic challenges:preoperative assessment Assess Rejection
Azotemia, proteinuria, hypertensionPruritis, lethargy, nausea, skin pigmentation
Care for co-morbidities: HTN, CAD, DM,CHFStress testingCoronary angiography
Hyperlipidemia:Increases perioperative CVS
morbidity/mortality
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Anesthetic challenges:preoperative assessment If on Hemodialysis
Hypovolemia: CVS instabilityHypokalemia: Arrhythmias, Susceptible to MR
Steroid- lympho proliferative disorder-airway obstruction
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Anesthetic challenges: Drugs
Immunosuppressants Double edged swordContinue perioperatively in adequate dosesOral dose of CSA : 4-7 hrs before surgery“Stress-coverage” steroids: if recently withdrawn
Affect the choice of anesthesia
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Immunosuppressants Agent Type Side effect
Cyclosporine A calcineurin inhibitor
1) Expensive 2) Nephrotoxic3) Gastric atony4) Hirsutism5) HTN/lipidemia
Prolongs effects of muscle relaxants,Delayed gastric emptying
Tacrolimus (PK 506) calcineurin inhibitor
1) Hyperglycemia
2) Increases viral replication
Avoid in diabeticsAvoid in HCV/HIV
Mycophenolate MofetilMMF
nucleoside synthesis inhibitor
ThrombocytopeniaAnemia
Avoid Regi0nal
Intravenous globulins (OKT3)
Antithymocyte/lymphocyte
Cytokine releaseThrombocytopeni
a
Non cardiogenic pulmonary edema
Azathioprine nucleoside synthesis inhibitor
Thrombocytopenia
Cannot prevent long term rejection
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Premedication
Standard premedication may be used
BZP: duration & activity prolonged
Ranitidine: caution interaction with Cyclosporine
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MonitoringPerioperative monitoring: risk/benefit
type of surgeryanesthesia plannedequipment available
CVP monitoring: Transplanted kidneys sensitive to
hypovolemiaDiuretic use: adequate intravascular volumeurine output
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Technique General (balanced & TIVA) as well as
regional successfully used
General anaesthesiaNasal intubation better avoided
Use of LMA acceptable
Ketamine: cautious in HTN/CAD
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Inhalation AgentsIsoflurane/desflurane :appropriate
Sevoflurane :safe
Enflurane : avoided--toxic fluoride metabolites
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Muscle relaxantsAtracurium, Cisatracurium usually preffered
Vecuronium should be prevented –reno vasoconstriction
Delayed gastric emptying/RSI:Sch: K<5.5 meq/LRocuronium, miva
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Analgesia Avoid NSAIDS:
GI Hmge, nephrotoxicityAugment Cyclosporine A nephrotoxicity
Opiate analgesics often usedMeperidine,M3G and M6G: prolonged
sedationRemifentanyl@ 0.1-0.5 mics/kg/min:
short actingNon specific tissue and plasma esterases
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Regional anesthesiaAvoid:
uremic platelet dysfunctionSevere hypovolemia
Caution: Azathioprine, MMFUremic/diabetic peripheral neuropathy
Bupivacaine safe in clinical doses
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POST OP CARE PAIN – Opioid based pain relief Morphine , pethidine – avoid if RFT
derangedParacetamol - in paediatric patientsNSAIDS to be avoidedEpidural analgesia
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POST OP CARECardiovascular 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
consideredMaintain normothermiaHaematocrit > 30%Adequate analgesia