HYPERTENSION , CRF POST RT PATIENT FOR SURGERY

PRESENTOR : Dr.Kumar

MODERATOR : Dr.Suneela

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.”

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

Patho-Physiology Systemic Hypertension

1. Essential Hypertension – No identifiable cause is present

2. Secondary Hypertension-Cause is present

Essential Hypertension 95% of all cases of hypertensioncharacterized by a familial incidence

and inherited biochemical abnormalities.

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

Additional factorsGenetic factors1.Glucocorticoid remediable HTN: 2.Syndrome of apparent

mineralocorticoid excessAlcohol and tobacco use Obstructive sleep apneaPhysical activity

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

Chronic Condition

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

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

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.

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

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

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

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

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.

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

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

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

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

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.

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

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

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.

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

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%.

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

Causes <18 YEARSObstructive uropathyCong. AnomaliesCong.nephrotic

syndromeOxalosisInfantile PKDCortical necrosisHemolytic uremic

syndromeChr.glomerulo

nephritis

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

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

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.

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.

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 .

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 .

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).

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 .

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.

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.

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.

Peripheral neuropathy Demyelination of medullated fibres, long

fibres are involved earlier.

Sensory neuropathy: paraesthesia.

Motor neuropathy: foot drop.

Uremic autonomic neuropathy: postural hypotension, diarrhea.

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 .

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 .

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 .

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.

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

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.

Problems In Post Renal transplant

1. Persistent cardiovascular disease2. Bone disorders3. Electrolyte and acid base

imbalance4. Post transplant Diabetes Mellitus5. Malignancy6. Infection

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.

CARDIOVASCULAR DISEASE contd.

Risk factors – ConventionalSmokingHypertensionHyperlipidemia DM

Specific to transplant patients Anaemia Chronic fluid overload Hyperparathyroidism Immunosuppressants

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

CARDIOVASCULAR DISEASE contd.HYPERLIPIDEMIA

Causes ( GCS )-SteroidsSirolimus, Calcineurin inhibitors(CNI)

Rx-Lifestyle modification - Weight loss, exercise ↓ steroid dosageCyclosporine → tacrolimusStatins

2. BONE DISORDERS

Persistent hyperparathyroidismGout OsteonecrosisOsteoporosis

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

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

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

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

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

2. BONE DISORDERSOSTEOPOROSIS

Common bone disorder- parallel reduction in bone mineral and bone matrix→ Decreased bone mass

Maximum bone loss – first 6 month

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

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

ELECTROLYTE IMBALANCE contd.

HYPOPHOSPHATEMIADue to excess urinary excretion residual hyperparathyroidismGlucocorticoids low Vit D stateImplication – Profound respiratory muscle

weakness

ELECTROLYTE IMBALANCE contd.HYPERCALCEMIACauses – Persistent Hyperparathyroidism Co- administration of calcium and vit D

Implication – shortened Q-T interval and arrhythmias

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

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

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

POST TRANSPLANT DM (contd) RxSteroids minimizedTacrolimus avoidedOral hypoglycemic drugs and InsulinMetformin- most effective

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

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

INFECTIONS (contd.) 0-1 MONTH - ~ to those seen in non

transplant patients after surgery.UTI lung infections related to vascular cathetersBacterial> fungal

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)

-

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

INFECTIONS (contd.)Clinical implication – Minimizing infection should be the goalRequire meticulous surgical techniqueAntiviral prophylaxisAvoidance of excess immunosuppression

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)

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

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

Anesthetic challenges:preoperative assessment If on Hemodialysis

Hypovolemia: CVS instabilityHypokalemia: Arrhythmias, Susceptible to MR

Steroid- lympho proliferative disorder-airway obstruction

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

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

Premedication

Standard premedication may be used

BZP: duration & activity prolonged

Ranitidine: caution interaction with Cyclosporine

MonitoringPerioperative monitoring: risk/benefit

type of surgeryanesthesia plannedequipment available

CVP monitoring: Transplanted kidneys sensitive to

hypovolemiaDiuretic use: adequate intravascular volumeurine output

Technique General (balanced & TIVA) as well as

regional successfully used

General anaesthesiaNasal intubation better avoided

Use of LMA acceptable

Ketamine: cautious in HTN/CAD

Inhalation AgentsIsoflurane/desflurane :appropriate

Sevoflurane :safe

Enflurane : avoided--toxic fluoride metabolites

Muscle relaxantsAtracurium, Cisatracurium usually preffered

Vecuronium should be prevented –reno vasoconstriction

Delayed gastric emptying/RSI:Sch: K<5.5 meq/LRocuronium, miva

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

Regional anesthesiaAvoid:

uremic platelet dysfunctionSevere hypovolemia

Caution: Azathioprine, MMFUremic/diabetic peripheral neuropathy

Bupivacaine safe in clinical doses

POST OP CARE PAIN – Opioid based pain relief Morphine , pethidine – avoid if RFT

derangedParacetamol - in paediatric patientsNSAIDS to be avoidedEpidural analgesia

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