This document discusses anuria, its causes and management. It defines anuria as a complete absence of urine production for 24 hours. Anuria can be prerenal, renal, or postrenal/obstructive. Postrenal or obstructive anuria is caused by bilateral or unilateral urinary tract obstruction. After relief of obstruction, some patients experience post obstructive diuresis, defined as urine output exceeding 200 ml/hr. Management of post obstructive diuresis involves monitoring urine output and electrolytes, fluid replacement, and hemodialysis if needed to correct fluid imbalance. Complications of untreated post obstructive diuresis can include volume depletion, electrolyte imbalances, metabolic acidosis, shock and death

1. Assessment Of Anuria &
Management Of Post
Obstructive Diuresis
BY
DR. AHMAD JUNAID
POST GRADUATE RESIDENT
DEPARTMENT OF UROLOGY & RENAL TRANSPLANT
ALLIED HOSPITAL FAISALABAD.

2. ANURIA
DEFINITION:
COMPLETE ABSENCE OF URINE PRODUCTION FOR
24 HOURS
The patient has not passed the urine & the bladder is
also empty even on catheterisation

3. DIFFERENTIAL DIAGNOSIS
Urinary Retention:
When patient, despite an urge to void, is unable to push urine out of
bladder due to either infra vesical obstruction or inability to generate
effective detrusor contractions.
Correct catheterization yields urine relieving symptoms.
Extravasation:
Leakage of urine into tissues / body cavity Peritoneum Bladder rupture /
perforation

4. DIFFERENTIAL DIAGNOSIS
Oliguria:
<300 ml urine / 24 hrs
Renal failure:
When kidneys no longer able to maintain
renal functions
 Acute: sudden, potentiality reversible
Sudden rise of S creatinine by 1
 Chronic: insidious, progressive.
nonreversible

5. AETIOLOGY OF ANURIA
 REDUCED BLOOD FLOW
 HYPOXIA
 SEPSIS
 OBSTRUCTION

6. TYPES OF ANURIA
 PRERENAL
 RENAL
 POSTRENAL (OBSTRUCTIVE)

8. PRERENAL ANURIA
HYPOVOLUMIA:
 DEHYDRATION
o PROLONGED VOMITING
o DIARRHOEA
o BURNS
 BLOOD LOSS
 SEPSIS (GRAM NEGATIVE SEPTICEMIA)
 CARDIOGENIC SHOCK

9. RENAL ANURIA
 DRUGS
 POISONS
 CONTRAST MEDIA
 ECLAMPSIA
 INCOMPATIBLE BLOOD TRANSFUSION
 DISSEMINATED INTRAVASCULAR COAGULATION

10. POST RENAL
/OBSTRUCTIVE ANURIA
 Bilateral PUJ obstruction by stone.
 Unilateral PUJ obstruction by stone with contralateral ureteric
obstruction.

11. OBSTRUCTIVE ANURIA
 Bilateral Ureteric Obstruction:
Extramural:
o Tumors of cervix, ovary, uterous, vagina, urinary bladder,
prostate, rectum, colon, caecum & lymphomas
o Idiopathic retroperitoneal fibrosis
o Retrocaval ureter, pararenal cysts, aberent vessels, ligatures
Intraluminal:
o Calculus, sloughed papilla, clot, ureteric malignancy,
crystaluria

12. OBSTRUCTIVE ANURIA
Intramural:
o Congenital PUJ obstruction or stenosis
o Ureterocele and congenital small ureteric orifice
o Strictures ( stone, repair, tuberculosis, schistosomiasis)
o Ureteric / vecsical malignanncy
o Kinks & adhesions ( sec to VUR)
Unilateral PUJ or ureteric obstruction in case of
o Contralateral nephrectomy
o Already obstructed or nonfunctional
o Congenitally absent

13. EVALUATION
 HISTORY
 CLINICAL EXAMINATION
 INVESTIGATIONS

14. HISTORY:
 Urge to void
 Duration
 Pain, hematuria, stone passage
 Symptoms of uremia
 Any precipitating event

15. CLINICAL EXAM
 Bladder not palpable
 Confirmed by catheter
 Signs of uremia

16. INVESTIGATIONS
 XRAY KUB
 ULTRASOUND SCAN
URINARY TRACT
 SERUM UREA
 SERUM CREATININE
 SERUM ELECTRTOLYTES
 BLOOD CP
 IUV usually contraindicated
 Retrograde Urography
 CT scan
 RENAL SCAN

17. MANAGEMENT
 Catheterise the patient
 Restore circulatory volume deficit in a dehydrated patient
o Iv fluids
o Cvp 7-9 cm h2 o
o Dopamine, mannitol
o Frusemide 80 mg iv
 Correct hypoxia
 Iv antibiotics if patient is having sepsis
 Nutritional support
 Consider dialysis

18. Management
 REMOVE THE OBSTRUCTION
 CIRCUMVENT / BYPASS THE OBSTRUCTION
 DEFINITE SOLUTION

19. POSSIBLE OPTIONS
 URETERIC STENTING
 PERCUTANEOUS NEPHROSTOMY
 DEFINITE SURGERY
o STONE REMOVAL
o URETERIC REIMPLANTATION

20. INDICATIONS FOR DIALYSIS
 HYPERKALEMIA (K > 7 mmol/L)
 METABOLIC ACIDOSIS (HCO3 < 12 mmol/L)
 PULMONARY OEDEMA
 PERICARDIAL EFFUSION
 CNS CHANGES

22. POST OBSTRUCTIVE
DIURESIS
High urine output exceeding (>200ml/hr) 0.5-1 L per
hour after the obstruction is relieved.
Patients with edema, hypertension and azotemia are most
likely to exhibit this condition.

23. o Accumulation of total body water, Sodium and urea.
o Impairment of Tubular re-absorptive capabilities.
True incidence of Post obstructive diuresis (POD) is not
known
Clinically significant POD:
occurs only in the setting of
Prior bilateral ureteral obstruction (BUO) or unilateral
obstruction of a solitary functioning kidney
Appears uncommon following UUO due to compensation by
normally functioning contra-lateral kidney.
FACTORS NECESSARY ARE

24. TYPES
Post obstructive Diuresis is of 2 types:
o Physiological Diuresis
o Pathological Diuresis

25. Physiological Diuresis:
Self limiting – As a response to solute (Sodium , Urea ) and water
overload. Stops after return to euvolumeic state.
Pathological Diuresis:
Inappropriate diuresis of water beyond euvolemic state.
Due to insensitivity of collecting tubule to ADH.
Other defects in urinary concentrating ability of the kidney and
tubular reabsorption of solutes.

26. PATHOPHYSIOLOGY
Numerous mechanisms have been proposed to describe the
pathophysiology of Post Obstructive Diuresis
o Progressive reduction in the medullary concentration gradient secondary
to vascular washout and down-regulation of sodium transporters in the
thick ascending loop of Henle.
o Reduction in glomerular filtration rate, which leads to ischemia and loss
of juxtamedullary nephrons.
o Reduced response of the collecting duct to circulating antidiuretic
hormone, leading to nephrogenic diabetes insipidus.

27. Obstruction
PhysiologicDiuresis
Relief ofObstruction
Release of Solute Retention andVolumeExpansion
Continue > 48hrs
Urine production >200ml/hr in 2 consecutive hrs Urine production
> 3-4L/day
Pathologic Diuresis
PATHOPHYSIOLOGY

28. Release of Natriuretic Peptide
Decrease reabsorption of Sodium (NaCl) in tubule
Loss of medullary gradient
Reduced response of cortical duct toAnti Diuretic Hormone
Impairment ofTubuloGlomerularFeedback
Water cannot be taken out from the tubule

29. MANAGEMENT
Treatment of POD should be directed toward
o Complete relief of urinary tract obstruction
o Replacement of electrolytes,
o Correction of intravascular volume, and appropriate patient monitoring.
o In signs of urosepsis draw appropriate blood and urine cultures
before administering broad-spectrum intravenous antibiotics.

30. Obstruction Relieve
Instatement of Urine
Collection Instruments
Mental Status Impairment
Edema
Congestive Heart Failure
Hypertension Azotemia
Folley Catheter
Condom Catheter
Assess Hydration status and
Post-Obstructive Diuresis Risk
PostObstructive Diuresis
POD Management Discharge
Yes No
MANAGEMENT

31. POD Management
Monitoring
Urine volume every hr in first 24 hr
Vital signs every 6 to 8 hr
Serum electrolyte levels every 12 to 24 hr
Urea and creatinine levels every 12 to 24 hr
Weight every 24hr
Physiologic Pathologic
Subside within 48
hrs
Persistent after 48hrs
Fluid Management,TightMonitoring,
and ReEvaluation
IV fluid replacement
Frequent monitoring of urine
and serum electrolyte levels
Repeat imaging to rule out
persistent obstruction
Discharge
Hemodialysis If fluid correction cannot be
achieved

32. There are few complications noted in literatures of
untreated post obstructive diuresis
 Volume depletion
 Hyponatremia or hypernatremia
 Hypokalemia
 Hypomagenesemia
 Metabolic acidosis
 Shock
 Death

33. THANK YOU