Sirolimus – so used in recipients who develops cancer
Hypertension , crf post renal transplant patient for surgery
HYPERTENSION , CRF
POST RT PATIENT FOR
PRESENTOR : Dr.Kumar
“An adult is considered to be
hypertensive when systemic BP>140/90
mm Hg or more on atleast two
occasions measured at least 1or2
CATEGORY SYSTOLIC in
Normal <120 <80
Pre-hypertension 120-139 80-89
Stage 1 HTN
Stage 2 HTN
1. Essential Hypertension – No identifiable
cause is present
2. Secondary Hypertension-Cause is present
95% of all cases of hypertension
characterized by a familial incidence and
inherited biochemical abnormalities.
Factors causing Genesis
increased sympathetic nervous system activity in
response to stress
overproduction of sodium-retaining hormones and
high sodium intake
inadequate dietary intake of potassium and
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
1.Glucocorticoid remediable HTN:
2.Syndrome of apparent
Alcohol and tobacco use
Obstructive sleep apnea
JNC VII Causes of Secondary HypertensionJNC VII Causes of Secondary Hypertension
Thyroid or parathyroid disease
Chronic steroid therapy
Chronic kidney disease
Cocaine or amphetamines
Ephedra, mu huang, bitter orange
Cyclosporine or tacrolimus
Chobanian AV et al. JAMA. 2003;289:2560-2572
NSAIDS=Non-steroidal anti-inflammatory drugs
Isolated systolic Hypertension
Aging with associated aortic rigidity
c. Aortic regurgitation
Decreased peripheral vascular resistance
a. Arteriovenous shunts
b. Paget's disease
Treatment of Essential
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.
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
-Patients with concomitant risk factors
(hypercholesterolemia, diabetes mellitus, tobacco
abuse, family history, age older than 60 years)
-evidence of target organ damage are most likely
to benefit from pharmacologic antihypertensive
Treatment of Secondary
1. correction of renal artery stenosis via
angioplasty or direct repair and
2. adrenalectomy for adrenal adenoma or
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 crises typically present with a blood
pressure of higher than 180/120
1. hypertensive urgency
2. hypertensive emergency
based on the presence or absence of impending
or progressive target organ damage
evidence of acute or ongoing target organ damage
2. intracerebral hemorrhage,
3. acute left ventricular failure with pulmonary edema
4. unstable angina,
5. dissecting aortic aneurysm
6. acute myocardial infarction,
8. microangiopathic hemolytic anemia,
9. renal insufficiency
require prompt pharmacologic intervention to
lower the systemic blood pressure
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
Typically, mean arterial pressure is reduced by about
20% within the first 60 minutes and then more
Thereafter, the blood pressure can be reduced to
160/110 over the next 2 to 6 hours as tolerated by the
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
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
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
ARBs increases the potential for hypotension during
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 Anesthesia
Hypotension during induction in patients continuing
ACE inhibitor or ARB therapy.
Direct laryngoscopy and tracheal intubation can
produce significant hypertension in patients with
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
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.
1. Intraoperative hypertension
2. 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
no evidence that a specific neuromuscular blocker is
best for patients with hypertension
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
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
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
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
Stage Description GFR
1 Kidney Damage with
2 Kidney Damage with
mild fall in GFR
3 Moderate fall in GFR 30-59
4 Severe fall in GFR 15-29
5 Kidney Failure <15
ESRD AGE >18Yrs
Type 1 D.M.
Type 2 D.M.
Ig A Nephropathy
Hyper tension develops in approximately 80%
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
Atherosclerosis and vascular calcification (high
Uremic pericarditis if untreated leads to cardiac
tamponade & later constrictive pericarditis.
Dysrhythmias due to Hyperkalemia and
Due to decreased erythropoietin production,
Diminished erythrocyte survival,
Diminished production of R.B.C’s due to fibrosis of
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.
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
Severe anaemia affects the blood-gas partition
coefficient so onset & recovery is faster .
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 .
Electrolyte and fluid
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 .
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.
Several abnormalities of coagulation factors like(dec plat
F III, platelet dysfn).
Pletelet FIII decreased because of accumulation of toxic
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 system
Features of uremia are initially malaise & reduced
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.
Demyelination of medullated fibres, long fibres
are involved earlier.
Sensory neuropathy: paraesthesia.
Motor neuropathy: foot drop.
Uremic autonomic neuropathy: postural
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
Presents with anorexia,nausea &vomiting,GI bleed &
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 .
Uremia impairs normal immune mechanisms .
It is obtunded further by giving
As a result sepsis remains a major prob.
So strict aseptic technique is followed .
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
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
The excretion of anticholinesterases and anticholinergic
agents will be prolonged as they are highly ionised and
POST TRANSPLANT STATE
A chronic kidney disease - continued organ
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.
Problems In Post Renal transplant
1. Persistent cardiovascular disease
2. Bone disorders
3. Electrolyte and acid base
4. Post transplant Diabetes Mellitus
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.
2. BONE DISORDERS
Very common in 1st post transplant
Risk factors –
Degree of pre- transplant disease
Duration of dialysis
Deficiency of vitamin D
Poor allograft function
BONE DISORDERS –
Symptoms – mostly asymptomatic
Dx – increased plasma Ca
decreased plasma phosphate
Rx – vitamin D analogs (stopped if S
- phosphate supplements
BONE DISORDERS - HYPERPARATHYROIDISM
Surgery – indications –
1) severe symptomatic hypercalemia in early post
2) persistent moderately severe hypercalcemia for
> one year post transplantation
Surgery done – subtotal parathyroidectomy
2. BONE DISORDERS
Cyclosporine – most
Impairs renal uric acid
High dose steroids
Synthesis inhibitor i.e.
Allopurinol ( dec. dose of
NSAIDS – Avoid
ELECTROLYTE IMBALANCE contd.
Due to excess urinary excretion
low Vit D state
Implication – Profound respiratory muscle weakness
ELECTROLYTE IMBALANCE contd.
Co- administration of calcium and vit D
Implication – shortened Q-T interval and
ELECTROLYTE IMBALANCE contd.
Cause - CNI induced
Rx – magnesium supplements if plasma Mg levels <
Clinical implication - ↑ risk of perioperative
arrhythmias, impaired respiratory muscle power
ACID BASE IMBALANCE
Distal (hyperchloremic) renal tubular acidosis -
occurs due to:
Clinical Implication - intraoperative electrolyte
prolonged NM blockade
interference with drug PK
4. POST TRANSPLANT DIABETES
New onset DM –
Increased CV risk
Risk factors –
Positive hepatitis C
Episodes of acute
POST TRANSPLANT DM (contd)
Oral hypoglycemic drugs and Insulin
Metformin- most effective
Causes of ↑ cancer incidence –
Immunosuppressants → inhibit normal tumor
of oncogenic viruses
Factors related to primary renal disease ( analgesic
abuse, HBV , HCV, certain herbal preparations)
Renal cystic disease
↓ the dose of immunosuppression
Sirolimus – increasing evidence of
Post Transplant Lymphoproliferative Disorder
Cause- Infection and transformation of B cell by
0-1 MONTH - ~ to those seen in non transplant
patients after surgery.
related to vascular catheters
> 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
-need long term SMX- TMP prophylaxis
Clinical implication –
Minimizing infection should be the goal
Require meticulous surgical technique
Avoidance of excess immunosuppression
Common surgical indications
First 48 hrs of transplant:
Rexploration for bleeding/reduced urine/thrombosis
Graft failure: Redo surgery
Uncontrolled hypertension-- Nephrectomy
Lymphoceles, Wound infections
Joint replacements (renal osteodystrophy,
GI bleed, CABG, dental (gum hyperplasia)
Anesthetic challenges &
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
Atracurium, Cisatracurium usually preffered
Vecuronium should be prevented –reno
Delayed gastric emptying/RSI:
Sch: K<5.5 meq/L
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:
Non specific tissue and plasma esterases
POST OP CARE
Opioid based pain relief
Morphine , pethidine – avoid if RFT deranged
Paracetamol - in paediatric patients
NSAIDS to be avoided
POST OP CARE
Cardiovascular collapses have occured upto 2
days post op.
All monitoring should be continued till 2nd post op
In patients with CV disease :
Perioperative beta blockers – can be considered
Haematocrit > 30%