Eko Indra P
 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.(1)
 The Basic Parameter is variable between one journal stated urine production
exceeding 200 mL/hour in 2 consecutive hours or greater than 3 L/day (1)
while other journal stated 4L/day.(2)
 Dramatic increase in urine output after the release of Urinary tract
Obstruction which influenced by: (3)
 Accumulation of total body water, sodium, and urea
 Impairment ofTubular re-absorptive capabilities
 Clinically more significant in bilateral ureteral obstruction or unilateral
obstruction of solitary kidney.
1. Halbgewachs C, Domes T. Postobstructive diuresis. Can Fam Physician. 2015 Feb; 61(2): 137-42
2. Hamdi A, Hajage D, Glabeke EV. Severe post-renal acute kidney injury, post-obstructive diuresis and renal recovery. BJUI International. 2012 Dec;110(11 Pt C):E1027-34.
3. Campbell-Walsh: 10th Edition.
 The incidence of POD is unclear but estimates suggest 0.5% to 52% of
patients will experience POD after relief of obstruction.(1)
 Further studies is needed to acquire more accurate number of
incidence.
1. Halbgewachs C, Domes T. Postobstructive diuresis. Can Fam Physician. 2015 Feb; 61(2): 137-42
 There are certain risk factors which must be monitored in
patient post obstruction which can lead to post obstructive
diuresis:
 Edema
 Congestive Heart Failure
 Hypertension
 Azotemia (high levels of nitrogen-containing compounds such as
urea and creatinine)
Physiological Pathological
Urea
Diuresis
Sodium
Diuresis
Water
Diuresis
• Self-limiting
• Normal response to volume expansion
and solute accumulation during
obstruction
• Excess Na and water retention
• Urea retention + non-
reabsorbable solutes
• Accumulation of ANP
• Once solute and fluid homeostasis is
achieved, diuresis ends – euvolumia
• Most common
• Self-limiting
• Lasts 24-28 hours
• Uosm > 250
• Fluid balance and
electrolytes should
be monitores
• Unless
contraindicated,
fluid intake should
be increased and
suffices
• Second most
common
• Usually self-limiting
• Uosm > 250
• Longer duration (>
72 hours)
• Requires more
aggressive
monitoring for
larger diuresis
potential
• Rare
• Self limiting
• Uosm < 150
• Secondary to
impaired renal
tubular response to
• ADH
 Numerous mechanisms have been proposed to describe the
pathophysiology of Post Obstructive Diuresis:(1)
 Progressive reduction in the medullary concentration gradient
secondary to vascular washout and down-regulation of sodium
transporters in the thick ascending loop of Henle.
 Reduction in glomerular filtration rate, which leads to ischemia and
loss of juxtamedullary nephrons.
 Reduced response of the collecting duct to circulating antidiuretic
hormone, leading to nephrogenic diabetes insipidus.
1. Singh I, Strandhoy JW, Assimos DG. Pathophysiology of urinary tract obstruction. In: Wein AJ, Kavoussi LR, Novick AC, Partin AW, Peter CA, editors. Campbell-Walsh urology. 10th ed. Philadelphia, PA:
Elsevier Saunders; 2012. pp. 1107–8.
Obstruction
Retention of Solute (Sodium and Urea)
Volume Expansion
Physiologic Diuresis
Relief of Obstruction
Release of Solute Retention andVolume Expansion
Pathologic Diuresis
Continue > 48hrs
Urine production >200ml/hr in 2 consecutive hrs
Urine production > 3-4L/day
Release of Natriuretic Peptide
peptide induces natriuresis
(the discharge of sodium through urine)
Decrease reabsorption of Sodium (NaCl) in tubule (a)
Loss of medullary gradient (a)
Reduced response of cortical duct to Anti Diuretic Hormone (b)
Impairment ofTubuloGlomerularFeedback (c
)
Water cannot be taken out from the tubule
 Massive sustained polyruria post-relief of obstruction
 Signs of dehydration
 Altered mental status
 Decompensated heart failure and arrhythmias
1. Singh I, Strandhoy JW, Assimos DG. Pathophysiology of urinary tract obstruction. In: Wein AJ, Kavoussi LR, Novick AC, Partin AW, Peter CA, editors. Campbell-Walsh urology. 10th ed. Philadelphia, PA:
Elsevier Saunders; 2012. pp. 1107–8.
 Treatment of POD should be directed toward complete relief
of urinary tract obstruction, replacement of electrolytes,
correction of intravascular volume, and appropriate patient
monitoring.(1)
 In signs of urosepsis, draw appropriate blood and urine
cultures before administering broad-spectrum intravenous
antibiotics.(1)
 Post-Obstructive Diuresis patients have azotemia  dose
adjustment of antibiotics should be made, and some agents (i.e.,
gentamicin) should be avoided.
1. Gonzales CM. Pathophysiology, Diagnosis, and Treatment of the Postobstructive Diuresis. In: McVary KT,editors. Management of Benign Prostatic Hypertrophy. New Jersey: Humana Press; 2004.p:35-45.
Obstruction Relieved
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
Post Obstructive Diuresis
POD Management Discharge
Yes No
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 48 hrs
Fluid Management,Tight Monitoring,
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:(1)
 Volume depletion
 Hyponatremia or hypernatremia
 Hypokalemia
 Hypomagenesemia
 Metabolic acidosis
 Shock
 Death
1. Halbgewachs C, Domes T. Postobstructive diuresis. Can Fam Physician. 2015 Feb; 61(2): 137-42
Post obstructive diuresis

Post obstructive diuresis

  • 1.
  • 2.
     Post-obstructive diuresisis a polyuric state in which copious amounts of salt and water are eliminated after the relief of a urinary tract obstruction.(1)  The Basic Parameter is variable between one journal stated urine production exceeding 200 mL/hour in 2 consecutive hours or greater than 3 L/day (1) while other journal stated 4L/day.(2)  Dramatic increase in urine output after the release of Urinary tract Obstruction which influenced by: (3)  Accumulation of total body water, sodium, and urea  Impairment ofTubular re-absorptive capabilities  Clinically more significant in bilateral ureteral obstruction or unilateral obstruction of solitary kidney. 1. Halbgewachs C, Domes T. Postobstructive diuresis. Can Fam Physician. 2015 Feb; 61(2): 137-42 2. Hamdi A, Hajage D, Glabeke EV. Severe post-renal acute kidney injury, post-obstructive diuresis and renal recovery. BJUI International. 2012 Dec;110(11 Pt C):E1027-34. 3. Campbell-Walsh: 10th Edition.
  • 3.
     The incidenceof POD is unclear but estimates suggest 0.5% to 52% of patients will experience POD after relief of obstruction.(1)  Further studies is needed to acquire more accurate number of incidence. 1. Halbgewachs C, Domes T. Postobstructive diuresis. Can Fam Physician. 2015 Feb; 61(2): 137-42
  • 4.
     There arecertain risk factors which must be monitored in patient post obstruction which can lead to post obstructive diuresis:  Edema  Congestive Heart Failure  Hypertension  Azotemia (high levels of nitrogen-containing compounds such as urea and creatinine)
  • 5.
    Physiological Pathological Urea Diuresis Sodium Diuresis Water Diuresis • Self-limiting •Normal response to volume expansion and solute accumulation during obstruction • Excess Na and water retention • Urea retention + non- reabsorbable solutes • Accumulation of ANP • Once solute and fluid homeostasis is achieved, diuresis ends – euvolumia • Most common • Self-limiting • Lasts 24-28 hours • Uosm > 250 • Fluid balance and electrolytes should be monitores • Unless contraindicated, fluid intake should be increased and suffices • Second most common • Usually self-limiting • Uosm > 250 • Longer duration (> 72 hours) • Requires more aggressive monitoring for larger diuresis potential • Rare • Self limiting • Uosm < 150 • Secondary to impaired renal tubular response to • ADH
  • 6.
     Numerous mechanismshave been proposed to describe the pathophysiology of Post Obstructive Diuresis:(1)  Progressive reduction in the medullary concentration gradient secondary to vascular washout and down-regulation of sodium transporters in the thick ascending loop of Henle.  Reduction in glomerular filtration rate, which leads to ischemia and loss of juxtamedullary nephrons.  Reduced response of the collecting duct to circulating antidiuretic hormone, leading to nephrogenic diabetes insipidus. 1. Singh I, Strandhoy JW, Assimos DG. Pathophysiology of urinary tract obstruction. In: Wein AJ, Kavoussi LR, Novick AC, Partin AW, Peter CA, editors. Campbell-Walsh urology. 10th ed. Philadelphia, PA: Elsevier Saunders; 2012. pp. 1107–8.
  • 7.
    Obstruction Retention of Solute(Sodium and Urea) Volume Expansion Physiologic Diuresis Relief of Obstruction Release of Solute Retention andVolume Expansion Pathologic Diuresis Continue > 48hrs Urine production >200ml/hr in 2 consecutive hrs Urine production > 3-4L/day
  • 8.
    Release of NatriureticPeptide peptide induces natriuresis (the discharge of sodium through urine) Decrease reabsorption of Sodium (NaCl) in tubule (a) Loss of medullary gradient (a) Reduced response of cortical duct to Anti Diuretic Hormone (b) Impairment ofTubuloGlomerularFeedback (c ) Water cannot be taken out from the tubule
  • 9.
     Massive sustainedpolyruria post-relief of obstruction  Signs of dehydration  Altered mental status  Decompensated heart failure and arrhythmias 1. Singh I, Strandhoy JW, Assimos DG. Pathophysiology of urinary tract obstruction. In: Wein AJ, Kavoussi LR, Novick AC, Partin AW, Peter CA, editors. Campbell-Walsh urology. 10th ed. Philadelphia, PA: Elsevier Saunders; 2012. pp. 1107–8.
  • 10.
     Treatment ofPOD should be directed toward complete relief of urinary tract obstruction, replacement of electrolytes, correction of intravascular volume, and appropriate patient monitoring.(1)  In signs of urosepsis, draw appropriate blood and urine cultures before administering broad-spectrum intravenous antibiotics.(1)  Post-Obstructive Diuresis patients have azotemia  dose adjustment of antibiotics should be made, and some agents (i.e., gentamicin) should be avoided. 1. Gonzales CM. Pathophysiology, Diagnosis, and Treatment of the Postobstructive Diuresis. In: McVary KT,editors. Management of Benign Prostatic Hypertrophy. New Jersey: Humana Press; 2004.p:35-45.
  • 11.
    Obstruction Relieved Instatement ofUrine Collection Instruments Mental Status Impairment Edema Congestive Heart Failure Hypertension Azotemia Folley Catheter Condom Catheter Assess Hydration status and Post-Obstructive Diuresis Risk Post Obstructive Diuresis POD Management Discharge Yes No
  • 12.
    POD Management Monitoring Urine volumeevery 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 48 hrs Fluid Management,Tight Monitoring, 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
  • 13.
    There are fewcomplications noted in literatures of untreated post obstructive diuresis:(1)  Volume depletion  Hyponatremia or hypernatremia  Hypokalemia  Hypomagenesemia  Metabolic acidosis  Shock  Death 1. Halbgewachs C, Domes T. Postobstructive diuresis. Can Fam Physician. 2015 Feb; 61(2): 137-42