Hand out

1. Part- Anesthesia and urinary
system
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2. Common renal pathophysiololgy
• Diseases affecting the kidneys are often grouped into
syndromes based on common clinical and laboratory
findings.
-nephrotic syndrome
-acute renal failure
-chronic renal failure
-nephritis
-nephrolithiasis
-urinary tract obstruction and infection.
The anesthetic care of patients is based on the status of their
preoperative renal function rather than by syndrome.
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3. Renal failure
• When the renal dysfunctional state becomes
decompensated.
• Depending on the progress of dysfunction it
can be:
1. acute renal failure
2. chronic renal failure
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4. Acute renal failure
• The sudden inability of the kidneys to vary urine
volume and content appropriately in response to
homeostatic needs.
• Results in:
- accumulation of urea in the blood (uremia) and
creatinine
- reduced urine production
• Mortality rate for isolated ARF is less than 10%.
• Critically ill surgical patients with ARF mortality is
up to 90%.
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5. Cnt…
• The course of acute renal failure varies widely
• Depending on the predominant etiologic antecedents
ARF can be:
1. Prerenal azotemia
2. Intrinsic ARF
3. Postrenal azotemia (obstructive uropathy)
• In 50% of patients, ARF is 2° to ischemia; in 35% of
patients, ARF is due to nephrotoxic causes; and in the
remaining 15%, patients have acute tubular interstitial
nephritis or acute glomerular nephritis.
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6. ARF cnt…
Prerenal azotemia
• Caused by acute circulatory problems that impair
renal perfusion
• It is an increase in blood urea nitrogen (BUN)
associated with renal hypoperfusion or ischemia.
• Metabolically active cells of the loop of Henle are
especially vulnerable to hypoxic damage 2° to
hypoperfusion.
• Depending on severity and duration it can result
in acute tubular necrosis.
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7. Cnt…
• Necrosis of tubular cells release debris into
tubules, causing flow obstruction, increased
tubular pressure and back leak of tubular
fluid.
• Decreased perfusion pressure is associated
with the release of norepinephrine,
angiotensin II, AVP, and endothelin.
• Prerenal failure is usually reversible if the
circulatory status is promptly improved.
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8. Cnt…
Prerenal Causes of Oliguria:
• Hypovolemia
• Dehydration
• Hypotension like in septic shock
• Low cardiac output states
• Aortic/renal artery clamping
• Thromboembolic phenomena
• Hemorrhage
• Transfusion reaction
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9. ARF cnt…
Intrinsic acute renal failure
• “Intrinsic” implies to renal etiology of ARF, ischemia,
toxins, and renal parenchymal diseases.
• Cortical necrosis – a massive renovascular insult such
as prolonged suprarenal aortic clamping or renal artery
embolism.
• Nephrotoxins damage renal tubules or
microvasculature.
• Renal parenchymal diseases may affect glomerulus or
interstitium, and frequently immune mediated or part
of more systemic disorder that targets the kidney.
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10. Cnt…
Renal Causes of Oliguria
• Ischemic injury from shock
• Nephrotoxins
- Antibiotics
- Chemotherapeutic agents
- Radiocontrast dyes
- Free hemoglobin and myoglobin
• Cellular debris
• Acute interstitial nephritis
• Hypersensitivity reactions
• Acute glomerulonephritis
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11. Cnt…
• ARF secondary to primary renal disease is the
most serious of the three types.
• The most commonly implicated nephrotoxins;
I. Exogenous nephrotoxins:
Aminoglycosides, amphotericin B, radiographic
contrast dyes, cyclosporine, and cisplatin.
II. Endogenous nephrotoxins:
- Hemoglobin (intravascular hemolysis)
- myoglobin (rhabdomyolysis).
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12. ARF cnt…
Post renal azotemia
• Downstream obstruction of the urinary tract accounts
<5% for ARF cases.
• The obstruction may occur at any point from the renal
pelvis to the distal urethra.
• Complete obstruction eventually develops into ARF,
whereas prolonged partial obstruction leads to chronic
renal impairment
• Intraluminal pressure then rises and eventually
transmitted back to the glomerulus, there by reducing
the filtration pressure.
• Reversible when the obstruction is removed.
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13. Cnt…
Postrenal Causes of Oliguria
• Calculi
• Tumors
• Clot retention
• Surgical ligation
• Edema
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14. Cnt…
Obstruction: 1. may be suggested by
- physical examination (distended bladder)
- a plain abdominal x-ray (revealing bilateral
renal calculi).
2. confirmed by demonstrating dilation of the
urinary tract proximal to the site of obstruction.
Treatment: 1. bladder outlet - catheterization
- suprapubic cystostomy.
2. ureteral obstruction - nephrostomy or ureteral
stents.
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15. • Acute renal failure also is classified according to
urine flow rates;
-oliguric
-nonoliguric and
-polyuric renal failure.
• Acute oliguric renal failure: when creatinine and
BUN concentrations progressively increase while
urine flow remains less than 20 ml/hr in an
adequately hydrated patient who has stable
blood pressure and a patent urinary outflow
tract.
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16. • Nonoliguric and Polyuric acute renal failure:
- Ps may have normal or high urine flow rates,
but they have biochemical abnormalities that
are similar to the abnormalities occurring in
patients with low urine output.
-Their management is less complex than that of
oliguric patients.
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17. Intraoperative oligurea
• Intraoperative oliguria is a normal response to
the stress of surgery and ongoing blood and fluid
losses.
• Urine flow rate has traditionally been used as a
measure of renal well being for intraoperative
and critical care.
• Urine flow rate <0.5ml/kg/hr may be a useful sign
of renal hypoperfusion with other objective signs.
• In what situation farther fluid administration is
indicated in case of oligurea?
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18. Cnt…
• If oligurea persists and signs of heart failure or
volume overload appear, the patient’s
hemodynamic profile should be farther assessed
to optimize cardiac output and systemic oxygen
delivery and to improve renal perfusion.
• Hypotension – the most common intraoperative
cause secondary to systemic vasodilatation like in
sepsis, hypovolemia, and depressed myocardial
contractility.
• can be corrected with vigorous fluid resuscitation
in combination of inotropic-vasopressor agents
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19. Treatment of ARF
• In nonoliguric patients diuretics and mannitol
may be used.
• Standard treatment for oliguric and anuric
patients - restriction of fluid, sodium,
potassium, and phosphorus.
• Dialysis - to treat or prevent uremic
complications
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20. Chronic renal failure (CRF)
• progressive and irreversible decline in renal function
over the course of at least 3–6 months.
• CRF: when GFR has been reduced to 10% (20ml/min)
of normal function.
• End stage renal disease (ESRD): when GFR falls below
5% (10ml/min).
-dependant on renal replacement therapy (RRT) to
survive.
The main causes:
• Diabetes mellitus and hypertension remain important
factors may cause up to 65 % of ESRD.
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21. CRF cnt…
• Interstitial nephritis, secondary to renal stones,
obstruction of the urinary tract, tuberculosis and
various nephrotoxins, are responsible for up to 20% of
ESRD
• Glomerulonephritis is the main cause of ESRD
worldwide (11%– 49%).
- Proliferative glomerulonephritis 2° to endemic
infections like streptococcus, schistosomiasis, and
malaria.
- Focal segmental glomerulonephritis
- Autoimmune nephropathy
- IgA nephropathy .
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22. cnt…
• serum creatinine does not rise until GFR has
fallen below 50%.
• Uremia: refers to the effects resulting from
the inability to excrete products of the
metabolism of proteins and amino acids
normally carried out by the kidney.
• Some of toxic products amino acids listed
bellow;
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23. Cnt…
Table 1 Major identified uraemic toxins
Guanidine Benzoates
Methlguanidine Creatine
Phenols Creatinine
Guanidinosuccinic acid Tryptophan
Tyrosine Aliphatic amines
Myoinositol Glucuronoconjugates
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24. Effects of CRF on
1. Fluid and electrolyte balance;
• Total-body contents of Na++ and H2O are increased in
chronic renal failure (CRF)….hypervolemia.
• Sodium balance, most patients have a mild degree of
sodium and water retention.
• Potassium, it tends to be elevated and may be
worsened by some drugs (betablockers, potassium
sparing diuretics (spironolactone), angiotensin
antagonists, non-steroidal anti-inflammatory agents
and nephrotoxins).
-In acute acidosis the serum potassium will rise
0.5mmol/l for each 0.1 unit decrease in pH.
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25. Cnt…
• Calcium: Total plasma calcium concentration is
reduced.
• Hyperphosphataemia when GFR < 20ml/min.
• Acidemia: In early stages of CRF acidemia is well
compensated.
-Chronic metabolic acidosis is common in ESRD.
It is because of inability
I. to secrete protons and buffers such as phosphate
II. to regenerate bicarbonate
limits the clearance of hydrogen ions.
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26. Cnt…
2. Cardiac and Pulmonary Manifestations:
- Hypertension
- left ventricular hypertrophy
- Accelerated atherosclerosis
- Pericarditis
- pulmonary congestion and edema
3. Hematologic Manifestations
- anemia which is normochromic, normocytic
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27. Diabetic Nephropathy
• Thickening of glomerular basement
membrane due to high filtration pressure
from Diabetes, deposition of sugar, protein,
lipid or other wasteful products.
• Is a syndrome, where the ‘kidney is damaged’
due to long-term complications of diabetes.
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28. Pathophysiology
• Hypertension and hyperglycemia induced morphological
and functional changes in kidney.
• In DN there will be hemodynamic changes in the
glomerulus.
- increased filtration & hyperperfusion
=microalbuminuria
- increased vasodilatation of afferent arteriole due to
dysfunction of vasoconstrictive authoregulation.
- this results in increased intraglomerular pressure associated
with morphological changes in the mesangial cells
(hypetrophy)
-hypertrophy ………...decreased GFR
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29. Cnt…
• Thickening of glomerular basement
membrane leads to glomerular sclerosis.
• All of this changes in the glomerular
hemodynamics if left untreated results in RF.
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30. Stages of Diabetic Nephropathy
Stage 1: GFR is higher than normal
Stage 2: thickening of glomerular basilar membrane
and mesangial proliferation
Stage 3: Urine albumin excretion rate at 20-
200ug/min (diagnosis of Diabetic Nephropathy)
and blood pressure begins to rise.
Stage 4: Diabetic Nephropathy-clinical proteinuria
stage
Stage 5: end stage renal failure.
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31. Signs and symptoms
As the disease advances;
• Frequent urination
• Presence of excess serum protein in urine
• Poor appetite (anorexia)
• Ill feeling (malaise) and fatigue
• Generalized itching
• Blood in urine (Discolored reddish urine)
• Increased blood pressure
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32. Cnt…
• Edema due to reduced plasma oncotic
pressure.
• Unintentional weight gain
Laboratory tests: -positive microalbuminuria
-too much protein in
the urine (proteinuria)
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33. Treatment of diabetic
nephropathy
It involves the following:
• Controlling the blood sugar levels
• Treating hypertension
• Restriction in protein intake
• Lowering of serum lipids
• Recommending angiotensin converting enzyme
inhibitors
• If it is left untreated, it leads to chronic renal
failure and the definitive management will be
dialysis or kidney transplant.
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34. Nephrotic Syndrome
• A nonspecific disorder in which the kidneys are
damaged, causing them to leak large amounts of
protein.
• Characterized by:
- proteinuria at least 3.5 grams per day and
subsequently hypoalbuminemia; ≤2.5 g/dl
- Hyperlipidaemia
- Edema
• It can be primary nephrotic syndrome or secondary
nephrotic syndrome.
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35. Glomerulonephritis
• A renal disease characterized by inflammation of the
glomeruli, or smaller blood vessels in the kidneys.
• Characterized by leakage of protein and red blood cells
into urine while toxins are retained in the body.
• Can be caused by:
- prior streptococcal infection
- Autoimmune disease like in SLE.
- Antibody-mediated such as IgA nephropathy
• Acute or chronic
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36. Pyelonephritis
• It is a retrograde urinary tract infection that
involves the pelvis of the kidney.
• When it becomes sever, results in;
- pyonephrosis (pus accumulation around the
kidney),
- urosepsis (a systemic inflammatory response
of the body to infection),
- kidney failure and even death.
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37. Pyelonephritis Cnt…
• Signs and symptoms:
- painful urination
- abdominal pain radiating to the back
- nausea
- tenderness at the costovertebral angle
- fever
- tachyarrhythmia
If the pt develops urosepsis, septic shock, rapid
breathing, violent shivering, and delirium will
occurred.
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38. Pyelonephritis Cnt…
• Urinalysis on urine test strip may reveal white
blood cells and nitrite.
• Mostly treated by antibiotic therapy and
sometimes it needs surgical intervention like
- percutaneous nephrolithotomy
- percutaneous nephrostomy
- ureteroscopy
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39. Revising questions as a summery
Say true or false and reason out if you say false for QNo
1 - 4.
1. In a pt with adequate urine out put, there will not be
any consideration for acute renal failure.
2. We can diagnose ARF by intraoperative oligurea.
3. In CRF serum creatinine rises as the GFR starts to
decrease.
4. Micturation reflex is entirely controlled by spinal
nerves only.
5. Discuss abnormalities of urine output associated with
acute renal failure.
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40. Cnt…
6. Discuss the effects of CRF on:
I. fluid & electrolyte balance.
II. Cardiac and Pulmonary Manifestations
III. Hematologic Manifestations
7. What is the most common cause of intraoperative
oligurea?
8. What are the three phase process for urine formation?
9. How can you explain metabolic acidosis?
10. What information can we get from Increased urine
osmolality about renal tubular function?
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41. Cnt…
11.Discuss about renal authoregulation:
I. At high arterial blood pressure.
II. At low arterial blood pressure.
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