Post obstructive diuresis (POD) is a condition characterized by excessive urination following the relief of a urinary tract obstruction, resulting in risks such as dehydration and electrolyte imbalances. It can manifest as physiological or pathological diuresis and requires careful monitoring and management of fluid and electrolyte replacement based on urine output. The prognosis depends on various factors like the duration and degree of obstruction, infections, and overall kidney function recovery.

1. POST OBSTRUCTIVE
DIURESIS

2. DEFINITION
• Post obstructive diuresis is a polyuric state in which copious amounts of
salt and water are eliminated after the relief of a urinary tract obstruction.
• Urine production exceeding 200ml/hr in consecutive 2 hours or greater
than 3L/ day.

3. INTRODUCTION
It’s potentially life-threatening polyuria that can develop after the release of the
obstruction in various ways
• Insertion of Foley catheter for obstructed bladder
•Percutaneous nephrostomy
• Double-J stent in patients with B/L ureteric obstruction or U/L ureteric
obstruction in a solitary functioning kidney

4. PATHOPHYSIOLOGY
• DIURESIS is a normal physiological response to eliminate excess
volume and solutes accumulated during the obstruction
• Diuresis will resolve once the kidneys normalize the volume
and solute status - homeostasis
• Elimination of solute and water even after homeostasis-
PATHOLOGICAL .
• These patients are at risk of severe dehydration, electrolyte
imbalances, hypovolemic shock, and even death if fluid and
electrolyte replacement is not initiated.

5. TYPES
• Physiological diuresis
• Pathological diuresis
• Urea diuresis (Uosm>250)
• Sodium diuresis(Uosm>250)
• Water diuresis(Uosm<150)

6. •TYPES
Urea diuresis :
• MC
• Self limiting, lasts 24-48 hours
• Increased fluid intake suffices
Sodium diuresis:
• second mc
• Self-limiting with potential for longer durations(>72 hrs)
• Treat electrolyte imbalances
Water diuresis :
• Rare
• Temporary Nephrogenic DI, secondary to impaired renal tubular response to
ADH

7. Mechanism
Pathologic post obstructive diuresis :
• characterized by :
• Inappropriate renal handling of water and/or solutes
• Disruption of the medullary interstitial solute gradient and profound diuresis
and natriuresis.
• Precipitating Factors :
• Downregulation of sodium transport channels
• downregulation of AQP channels
• poor responsiveness of the collecting duct to vasopressin,
• and altered regulation of ANP

8. 3 main factors
1. TUBULOPATHY
• Impairment of dilution and concentration capacity
• decrease in sodium reabsorption
• leakage of potassium , magnesium and phosphorus
• insensitive to ADH.
• Decrease in H+ ions secretion in urine

9. 2.PHYSIOPATHOLOGICAL STATE CAUSED BY ACUTE RENAL FAILURE
• hyperurecemia
• hypercreatininaemia
• hyperkalemia and metabolic acidosis
• Dilutional hyponatremia
• Sodium overload

10. 3.BIOCHEMICAL AND IMMUNOLOGICAL
• Action of atrial natriuretic factor
• Prostaglandins, prostacyclins, thromboxane A2, endothelins
• Macrophage infiltrate of an obstructed kidney
• elevation of PAF and cytokines

11. Derangement of urinary concentrating ability
• Normal urine concentrating ability requires a hypertonic medullary interstitial
gradient
• Active salt reabsorption from the thick ascending loop of Henle
• Urea back flux from the inner medullary collecting duct and Water permeability
of the collecting duct mediated by VASOPRESSIN and AQUAPORIN water channels
• Obstructive nephropathy can disrupt some or all of theses mechanisms and leads
to deficits in urinary concentration

12. Accumulation of ANP
An accumulation of vasoactive substances in BUO that could contribute to
significant post obstructive natriuresis
ANP:
• Increases afford to arteriolar dilation
• Efferent arteriolar vasoconstriction, thus increasing PGC
• Decreases the sensitivity of tubuloglomerular feedback
• Inhibits release of renin
• Increases Filtration coefficient(kf)
• Secreted ANP - profound diuresis and natriuresis

13. •Risk factor for developing POD
• High serum creatinine level
• High sodium bicarbonate level
• Urinary retention
•Renal insufficiency
• Heart failure
• Dizziness
• CNS depression
Others -
•Lower urinary tract symptoms, prostate disease, long- standing diabetes,
recurrent catheterization, fecal impaction, and the use of anticholinergic
medications
Independent RF
Substantial RF

14. Diagnosis
• Clinical : Urine output
• Dehydration : thirst, tachycardia, orthostatic hypotension
• Urinary sodium and potassium levels
• Urine osmolality : to know solute or urea-type of diuresis
• Urea diuresis : generally self-limiting
• Solute diuresis : can convert to pathologic POD & requires careful
monitoring
• Spot urine sodium levels >40 mEq/L suggests tubular injury

15. Monitoring
• Polyuria lasts for 48hrs
• Hourly monitoring of urine specimens obtained for volume, osmolality, Na &
urea
• Clinical observation of weight every 8 hours
• Repeat blood studies at least every 24 hours
• Look for postural hypotension or tachycardia
• Continuous monitoring of BP& HR

16. TREATMENT
Aims :
• Complete relief of urinary tract obstruction
• Replacement of electrolytes
• Correction of intravascular volume
• Appropriate patient monitoring

17. 1) Normovolemic patient :
• Regularly quantify volume & urinary electrolytes every 3 hrs,
compensate 100% in initial 24 hrs
• Urine output compensation will be reduced to 75% on 2nd
day; to 50%
on the third day, and so forth until compensation interruption in a few
days

18. 2) Patient with Na overload :
• The principle of compensation can be applied in minimal proportions (75, 50 or even
30% on the first day) as the initial output is already positive
• Polyuria that follows POD allows to decrease sodium overload
3) Patient in dehydration :
• Increase compensation (125% or 150% on first day)
• Polyuria, if not compensated >100%, will aggravate dehydration

19. Management of POD has two major risks.
• Hydroelectrolytic compensation insufficiency with risk of extra or
intracellular dehydration.
1.Insufficient or irregular supervision with underestimation of output.
2. The presence of another cause of dehydration: vomiting,
hemorrhage.
3. Inadequate intake with overvaluation of oral intake.
• Excess of hydroelectrolytic compensation with risk of maintaining
polyuria.
1. Lack of supervision with overvaluation of output.
2. Underestimation of oral intake.

20. FLUID MANAGEMENT
• In the first 24 hours, urine output should be checked hourly.
• If it's over 200 mL/hour, then 80% of the hourly output should
be replaced intravenously with 0.45% saline.
• After 24 hours of persistent diuresis,
• Total fluids infused should be about 1 L less (or <75%) than the
previous day's output, provided the patient is hemodynamically
stable.
• Once the urine output </= 3 L per day, oral fluids should suffice.

21. • If there are signs of hypovolemia, then total fluids replaced should be
about 0.5 L less, instead of 1 L, than the last 24 hours' output.
• Replacement of electrolytes, e.g. potassium and magnesium, may be
necessary and should be guided by the levels.

22. PROGNOSIS
Recovery of renal function depends upon:
• Duration of obstruction
• Degree of obstruction
• Unilateral or bilateral
• Concomitant infection
• Replacement volume: does not exceed 2/3 of daily urine output, to avoid
iatrogenic extracellular volume expansion

23. EXPERIMENTAL MODULATION
• Ureteral obstruction induces expression of COX-2 in collecting duct
cells and downregulation of AQP2 receptors is mediated by COX-2
• COX-2 INHIBITORS prevented the downregulation of AQP2 and
significantly diminished postobstructive diuresis.
• cGMP pathway has been demonstrated in both in vitro and in vivo
models to allow membrane insertion of AQP2.
• SILDANEFIL CITRATE elevate intracellular cGMP and facilitate
collecting duct accumulation of AQP2.

24. Thank you