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Assessment Of Anuria &
Management Of Post
Obstructive Diuresis
BY
DR. AHMAD JUNAID
POST GRADUATE RESIDENT
DEPARTMENT OF UROLOGY & RENAL TRANSPLANT
ALLIED HOSPITAL FAISALABAD.
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
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
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
AETIOLOGY OF ANURIA
 REDUCED BLOOD FLOW
 HYPOXIA
 SEPSIS
 OBSTRUCTION
TYPES OF ANURIA
 PRERENAL
 RENAL
 POSTRENAL (OBSTRUCTIVE)
PRERENAL ANURIA
HYPOVOLUMIA:
 DEHYDRATION
o PROLONGED VOMITING
o DIARRHOEA
o BURNS
 BLOOD LOSS
 SEPSIS (GRAM NEGATIVE SEPTICEMIA)
 CARDIOGENIC SHOCK
RENAL ANURIA
 DRUGS
 POISONS
 CONTRAST MEDIA
 ECLAMPSIA
 INCOMPATIBLE BLOOD TRANSFUSION
 DISSEMINATED INTRAVASCULAR COAGULATION
POST RENAL
/OBSTRUCTIVE ANURIA
 Bilateral PUJ obstruction by stone.
 Unilateral PUJ obstruction by stone with contralateral ureteric
obstruction.
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
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
EVALUATION
 HISTORY
 CLINICAL EXAMINATION
 INVESTIGATIONS
HISTORY:
 Urge to void
 Duration
 Pain, hematuria, stone passage
 Symptoms of uremia
 Any precipitating event
CLINICAL EXAM
 Bladder not palpable
 Confirmed by catheter
 Signs of uremia
INVESTIGATIONS
 XRAY KUB
 ULTRASOUND SCAN
URINARY TRACT
 SERUM UREA
 SERUM CREATININE
 SERUM ELECTRTOLYTES
 BLOOD CP
 IUV usually contraindicated
 Retrograde Urography
 CT scan
 RENAL SCAN
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
Management
 REMOVE THE OBSTRUCTION
 CIRCUMVENT / BYPASS THE OBSTRUCTION
 DEFINITE SOLUTION
POSSIBLE OPTIONS
 URETERIC STENTING
 PERCUTANEOUS NEPHROSTOMY
 DEFINITE SURGERY
o STONE REMOVAL
o URETERIC REIMPLANTATION
INDICATIONS FOR DIALYSIS
 HYPERKALEMIA (K > 7 mmol/L)
 METABOLIC ACIDOSIS (HCO3 < 12 mmol/L)
 PULMONARY OEDEMA
 PERICARDIAL EFFUSION
 CNS CHANGES
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.
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
TYPES
Post obstructive Diuresis is of 2 types:
o Physiological Diuresis
o Pathological Diuresis
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.
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.
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
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
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.
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
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
There are few complications noted in literatures of
untreated post obstructive diuresis
 Volume depletion
 Hyponatremia or hypernatremia
 Hypokalemia
 Hypomagenesemia
 Metabolic acidosis
 Shock
 Death
THANK YOU

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Assessment of anuria & management of post obstructive diuresis

  • 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)
  • 7.
  • 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
  • 21.
  • 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