GUT

1. Genito-urinary
Surgery And
Anesthesia

2. BASIC FUNCTIONS OF THE KIDNEY
 Glomerulus –
• filtration and subsequent excretion of nitrogenous wastes.
 Tubules – Selective reabsorption or secretion of
• water and ions to maintain fluid balance
• hydrogen ions to maintain acid–base homeostasis.
 Endocrine –
• The production of renin
• the release of prostaglandins
• activation of both erythropoietin and vitamin D.

3. Main Functions Of The Kidneys
A WET BED
• Acid-Base Balance
• Water Balance
• Electrolyte Balance
• Toxin Removal
• Blood pressure Control
• Erythropoietin Production
• Vitamin D Metabolism

4. Effects of Anesthesia on Normal Renal Function
• General anesthesia is associated with a decrease of renal
blood flow, GFR, urinary flow, and electrolyte excretion
• Anesthesia may alter renal function by direct or indirect
effects
• Drugs associated with catecholamine release lead to
vasoconstriction, an increase in renal vascular resistance,
a decrease in renal blood flow, and a decrease in renal
function (indirect effects)

5. • High levels of spinal or epidural anesthesia can impair
venous return, diminish cardiac output, and reduce renal
perfusion.
• In most cases, changes in renal function are transient and
reversible.
• If they persist into the postoperative period, the cause is
often a combination of factors such as preexisting renal or
cardiovascular disease, or severe fluid imbalance, and the
importance of the anesthetic effects is decreased
Effects of Anesthesia on Normal Renal Function

6. VOLATILE ANESTHETICS AND RENAL FUNCTIONS
• Volatile anesthetics cause a decrease in GFR by
decreasing renal perfusion pressure either by
decreasing systemic vascular resistance (isoflurane
or sevoflurane) or cardiac output (halothane).
• This decrease in GFR is exacerbated by hypovolemia
and the release of catecholamines and antidiuretic
hormone as a response to painful stimulation
during surgery

7. SEVOFLURANE AND ITS RENAL EFFECTS (THEORETICAL)
• Sevoflurane is degraded in basic carbon dioxide
absorbents (Barium Hydroxide and Soda lime) into a
vinyl ether called compound A.
• Compound A has been implicated to cause renal injury
through fluoride toxicity (animal studies).
• High intra-renal fluoride concentrations impair the
concentrating ability of the kidney and may theoretically
lead to non-oliguric renal failure

8. Methoxyflurane And Its Effects On Kidneys
• Methoxyflurane causes vasopressin-resistant
polyuria, serum hyperosmolality, hypernatremia,
increased concentrations of serum urea nitrogen
and inorganic fluoride, and decreased urinary
potassium, sodium, osmolality, and urea nitrogen
concentrations.
• Therefore, clinically it is no longer used

9. VOLATILE ANESTHETICS AND RENAL FUNCTIONS

10. OPIOIDS AND ITS RENAL EFFECTS
• Opioid are may decrease renal blood flow, GFR and
urine output which is minimal and transient.
• Remifentanil pharmacokinetics are unaffected by
renal functions due to rapid ester hydrolysis.
• With the exception of morphine and meperidine,
significant accumulation of active metabolites do not
occur.

11. OPIOIDS AND ITS RENAL EFFECTS
• The renal toxicity appears in the context of inappropriate use:-
either higher than needed doses, in the presence of other
toxins, chronic use of opioids (accumulation of metabolites),
deranged renal functions or with pre-existing dehydration.
• The accumulation of morphine metabolite (morphine-6-
glucuronide) and meperidine metabolite(normeperidine) has
been reported to prolong respiratory depression in patients
with kidney failure.
• Increased level of normeperidine has been associated with
seizures.

12. EFFECTS OF MUSCLE RELAXANT ON RENAL FUNCTIONS
• Upon administering histamine releasing muscle relaxants
(mivacurium, atracurium, succinylcholine, d-tubocurarine),
there is transient fall in blood pressure, renal blood flow
and cardiac output.
• Based on clinical and experimental data, it appears that
muscle relaxants have only a modest impact on RBF and no
meaningful adverse influence on postoperative Renal
functions when Blood Pressure and Cardiac Output are
adequately maintained

13. Effect Of Positive Pressure Ventilation On Kidneys
• Positive-pressure ventilation used during general
anesthesia can decrease venous return, cardiac output,
renal blood flow, and GFR.
• Decreased cardiac output leads to release of
catecholamines, ADH, renin, and angiotensin II with
the activation of the sympathoadrenal system and
resultant decrease in renal blood flow

14. EFFECT OF REGIONAL ANAESTHESIA ON KIDNEYS
• Spinal and epidural anesthesia only slightly decrease GFR
and RBF in proportion to the decrease in mean arterial
pressure.
• The preexisting intravascular volume and the quantity of
intravenous fluids given strongly influence the renal
response to spinal and epidural anesthesia.
• There is also decreased diuresis and a marked fall in sodium
excretion.
• These trends are gradually reversed during recovery.

15. EFFECTS OF POSITIONING ON KIDNEYS?
Kidney Rest Position
Trendelenburg
Position
Lithotomy Position

16. EFFECTS OF POSITIONING ON KIDNEYS?
• Open procedures on kidney are carried out in ‘kidney
rest position’ – lateral flexed position.
• Dependant leg is flexed and the other is extended.
• Axillary roll – placed under dependant upper chect.
• Operating table is extended to achieve maximal
separation between iliac crest and costal margin.
• Kidney rest is elevated to raise the non dependant
iliac crest higher and increase surgical exposure.

17. EFFECTS OF POSITIONING ON KIDNEYS?
• This position is associated with adverse respiratory and
circulatory effects.
• It can significantly decrease the venous return to heart by
compressing the inferior vena cava.
• Also, the venous pooling in the legs potentiates anesthesia
induced vasodilation.
• Lithotomy and Trendelenburg position:-
• Elevation of leg drain blood into central circulation acutely,
mean BP and CO are increased
• Conversely, rapid lowering of legs from these positions acutely
decreases venous return and can result in hypotension.

18. Acute Kidney Injury And Acute Tubular Necrosis
• Acute kidney injury (AKI) is an acute decline in renal
function sufficient to result in the retention of
nitrogenous end-products of metabolism
• Causes :
• Pre-renal – Inadequate perfusion – 40%–70%
• Renal – Intrinsic renal disease – 10%–50%
• Post-renal – Obstructive uropathy – 10%

19. PREVENTION OF ACUTE TUBULAR NECROSIS (ATN)
 PREOPERATIVE ASSESSMENT
• Factors known to be associated with increased risk for
AKI should be known and managed
 PERIOPERATIVE MANAGEMENT
o Prevention of new AKI by:
• Maintain oxygenation
• Maintain normocarbia
• Optimize intravascular volume and cardiac output

20. ASSESSMENT OF RENAL FUNCTIONS
• Why is assessment of renal function important?
1. Preoperative renal dysfunction is associated with
greater risk of postoperative complications.
2. Certain well-defined risk factors for new AKI or
deterioration in renal function are detectable
preoperatively

21. Conditions
Associated With
Increased Risk Of
Perioperative
Acute
Kidney Injury
(AKI) OR (ATN)
1. Preoperative renal disease
2. Diabetes mellitus
3. Hypertension 4. Cardiac failure
5. Preoperative ‘shock’ states
6. Cirrhosis 7. Sepsis
8. Biliary obstruction
9. Multiple system trauma
10. Multiple organ failure
11. Extracellular fluid volume deficit
12. Elderly patients
13. Aortorenal vascular disease

22. HISTORY AND EXAMINATION
• SYMPTOMS
• In the early stages of renal disease there may be no symptoms.
• When symptoms do occur, they include:
• Fatigue, general malaise, headaches
• Nausea, weight loss, loss of appetite
• Pruritus, dry skin • Polyuria
• Polydypsia • Dysuria

23. • SIGNS
• Hypertension of long-standing
• Hypervolemia (e.g. edema, dyspnea)
• Hypovolemia (e.g. decreased skin turgor, tachycardia, hypotension)
• MEDICATION
• Diuretics • Antihypertensive therapy
• Potassium supplements
• Immunosuppressive agents
HISTORY AND EXAMINATION

24. INVESTIGATIONS
1- PLASMA
 Electrolytes are increased early
oSodium, potassium, chloride and bicarbonate The changes in
their levels will exacerbate dysrhythmias and compromise
resuscitation
 Frank renal failure results in hypocalcemia, hyperphosphatemia
and hypermagnesemia

25. INVESTIGATIONS
1- PLASMA
 Urea and nitrogen
• Urea is produced by protein catabolism in the liver
 Creatinine is a by-product of muscle metabolism and
production is related to muscle mass
• Serum creatinine is an insensitive indicator of renal
function – the value may be normal even if GFR is reduced
by 50%.

26. INVESTIGATIONS
2- URINE
 APPEARANCE
• Gross – bleeding, infection
• Microscopic – casts, bacteria, cells
 pH: Normally urine is acidic
 SPECIFIC GRAVITY (SG)
• SG refers to the concentration of
solutes in urine; the ability to
concentrate is a measure of
tubular function. This is, however,
nonspecific .
Substances/conditions affecting SG
Protein
Glucose
Mannitol
Diuretics
Extremes of age
Antibiotics (carbenicillin)
Temperature
Hormonal imbalance (pituitary,
adrenal and thyroid disease)

27.  OSMOLALITY
•The number of osmotically active particles per unit solvent (mOsm/L).
•Osmolality is more specific than SG:
• Oliguria + Osmolality > 500 suggests prerenal azotemia
• Oliguria + osmolality < 350 likely to be acute tubular necrosis
 PROTEIN
• <150 mg/24 h: normal excretion (exercise and standing can increase
this)
• >750 mg/24 h: indicator of renal parenchymal disease
• Massive: glomerular damage
INVESTIGATIONS
2- URINE

28. INVESTIGATIONS
3- CREATININE CLEARANCE
 Measures the glomerular filtration of creatinine (Cr) which approximates GFR
 eGFR = 141 × min(Scr/κ, 1)α × max(Scr/κ, 1)-1.209 × 0.993Age × 1.018 [if female] × 1.159 [if black]
o Abbreviations / Units
• eGFR (estimated glomerular filtration rate) = mL/min/1.73 m2
• SCr (standardized serum creatinine) = mg/dL
• κ = 0.7 (females) or 0.9 (males)
• α = -0.329 (females) or -0.411 (males)
• min = indicates the minimum of SCr/κ or 1
• max = indicates the maximum of SCr/κ or 1
• age = years

29. INVESTIGATIONS
4- OTHER TESTS
 Advanced renal disease affects most organ systems.
 Additional tests that may be useful in patients with advanced renal
disease include
• chest radiography
• electrocardiography
• complete blood count, serum electrolytes, and acid-base studies

30. ANESTHETIC MANAGEMENT OF PATIENTS
WITH ADVANCED RENAL DISEASE
• PREMEDICATION
• The effects of premedication with sedative drugs and opioids are
unpredictable due to decrease plasma proteins and the effect of
altered blood pH
• Agents to reduce gastric acidity and volume.
• Antihypertensives should generally be continued in the
perioperative

31.  INDUCTION
• The pharmocokinetics of propofol are usually unaltered
• Thiopental has an increased volume of distribution and decreased
plasma protein binding resulting in an increase in free drug
concentration
• Avoid suxamethonium if the serum potassium level is greater than
5mmol/L
• Atracurium, cisatracurium and mivacurium are the neuromuscular
blocking agents of choice because of their rapid elimination and
independence of renal metabolism and excretion
ANESTHETIC MANAGEMENT OF PATIENTS
WITH ADVANCED RENAL DISEASE

32.  MAINTENANCE:
1-Monitoring:
• Standard Monitoring
• CVP monitoring or transesophageal Doppler is a useful guide to
volume status and systemic blood pressure.
• Urine output should be monitored.
• Invasive Monitoring if required only
ANESTHETIC MANAGEMENT OF PATIENTS
WITH ADVANCED RENAL DISEASE

33. 2- General Anesthesia:
 Response to IV anesthetic is unpredicted due to
(1) volume of distribution (which is often increased)
(2) protein binding (which may be decreased)
(3) low pH
(4) dependence on renal excretion for the parent drug or metabolites.
 Ketamine and benzodiazepines are less heavily protein bound,
but metabolites of ketamine depend on renal excretion
 Propofol is accepted for both induction and maintenance
ANESTHETIC MANAGEMENT OF PATIENTS
WITH ADVANCED RENAL DISEASE

34.  Inhalational Anesthetic:
• Isoflurane and desflurane are effective inhalational agents, with
minimal metabolism.
• Enflurane use is controversial due to the potential accumulation of
fluoride ions
 Opioids:
• Patients with kidney disease can develop high levels of morphine-
6-glucuronide and resultant respiratory failure
• Remifentanil does not accumulate in CKD
• Meperidine metabolites can cause convulsions when present in
high concentrations, and cannot be removed by dialysis, and
should be avoided.

35. Technique Advantages Disadvantages
Regional •Minimal changes in renal
hemodynamics
•May shorten hospital stays
•Allows for earlier detection of
capsular tears and bladder
perforation
•Lower incidence of postoperative
nausea and vomiting
•Reduced amount of operative
blood loss and the incidence of
deep vein thrombosis with
transurethral resection of prostate
•Presence of peripheral
neuropathy
•Tendency for bleeding
•Patient anxiety
•Less suitable for
prolonged procedures
•Hypotension with
sympathetic block; may
cause reluctance to
expand volume

36. Technique Advantages Disadvantages
Intravenous
anesthetics
• Hemodynamic stability • Unpredictable response
Hypertension
• Greater need for N 2 O
and neuromuscular
blockers
Volatile
anesthetics
•Good airway control
•Blood pressure control
•Duration not dependent on
urinary excretion
•Less neuromuscular blocking with
drugs required
•Fi o 2 can be increased because
N 2 O not necessary
•Alterations in renal
hemodynamics
•Decreased cardiac output
•Hypotension
•Increased incidence of
postoperative nausea and
vomiting

37. POSTOPERATIVE MANAGEMENT
• Consider admission to HDU after major surgery or if
significant comorbidities exist.
• Reevaluate fluid balance and hydration regularly using
clinical assessment, CVP and urine output (if any).
• Give supplemental oxygen.
• Measure serum electrolytes regularly.
• Thromboembolic prophylaxis is important.