Nocturia

1. Gaurav Nahar
DNB Urology Resident,
MMHRC, Madurai
NOCTURIA

2. DEFINITION

3. DEFINITION
•
Waking because of the desire to void during
intended sleep.
•
Cause: Abnormality in genitourinary tract or
a symptom of an underlying medical
condition.
•
ICS Definition: voiding that occurs during
hours of sleep i.e. voiding preceded and
followed by sleep.
•
Two or more voids per night - clinically
significant.

4. IMPACT OF NOCTURIA

5. IMPACT OF NOCTURIA
•
Definition does not take into account
patient's degree of bother.
•
Increased prevalence of depressive
symptoms.
•
Greater morning fatigue & Decreased work
efficiency.
•
Affects both quality & quantity of life.

6. •
Affects sleep efficiency & sleep latency.
•
Sleep efficiency: actual time asleep
(minutes) divided by total time of intended
sleep (minutes); normal > 85%.
•
Sleep latency: time it takes to go from being
completely awake to being completely
asleep.
•
Sleep latency times > 30min & sleep
efficiency < 80%- nearly twice the risk for
death.

7. EPIDEMIOLOGY

8. EPIDEMIOLOGY
•
Overall prevalence (>1 void per night)-
28.4%; Men- 25.2% and Women- 31.3%.
•
One in every 5-6 people 20-40 years and 3
in every 5 people older than 70 years wake
to void two or more times nightly.
•
Prevalence increases with age.

9. •
An increased risk for mortality, because
nocturia can be a symptom of serious
systemic illnesses including hypertension,
diabetes, heart disease, kidney disease, &
metabolic syndrome.
•
Increased falls and fractures.
•
It decreases immune function, increasing risk
for cardiovascular disease, obesity and type
2 diabetes.

11. EVALUATION

12. EVALUATION
•
Complex & multifactorial etiology.
•
Complete history (medication use ex. Li)
•
Physical examination (Peripheral edema,
obesity & short-neck etc.)
•
24-hour voiding diary or frequency-
volume chart: most valuable objective
instrument in evaluating nocturia.

13. CLASSIFICATION & ETIOLOGY

14. CLASSIFICATION & ETIOLOGY

15. I. NOCTURNAL POLYURIA

16. I. NOCTURNAL POLYURIA
Physiology of renal water handling:
•
Normal circadian urine production is age
dependent.
•
NP in <25 years = 14%, Middle-aged adults
14-34%, Elderly>65 =34%.
•
Major determinant of body water is arginine
vasopressin (AVP)-regulated water excretion
by the kidneys.

17. •
AVP stimultors- high serum
hyperosmolality, hypovolemia, and
angiotensin II
•
Inhibitors- natriuretic peptides(ANP), PGE2
hypercalcemia, hypokalemia, lithium,
tetracyclines and negative feedback via
baroreceptors.

18. Schematic diagram depicting arginine vasopressin regulation of
water reabsorption from renal tubular cells.
Schematic representation of aquaporin 2 trafficking within a cell.

19. OBSTRUCTIVE SLEEP APNEA (OSA):
•
Sudden cessation of respiration during sleep
because of airway obstruction.
•
Mechanism- Increased airway pressures →hypoxia
→ pulmonary vasoconstriction → increased right
atrial transmural pressure → increase in ANP
production →ultimately increased renal sodium and
water excretion.
•
OSA is more likely as nocturia worsens in severity.

20. Management of Nocturnal poyuria:
•
Begin with conservative approach:
cessation of fluid intake 4 hours before bedtime,
use of compressive lower extremity stockings,
administration of diuretics in mid-afternoon for
edema states, and
antidiuretic therapy at bedtime.

21. 1. Diuretics: Furosemide (40mg OD)
•
MoA: preventing water accumulation and forcing
water out of the system.
•
Indicated in lower limb venous insufficiency and
congestive cardiac failure.
•
Timing during midafternoon (6 hours before sleep)
allow for elimination of lower extremity excess
body fluid during normal waking hours.

22. 2. Imipramine TCA (20mg HS): complex
pharmacological profile, non-subtype selective
antimuscarinic effect, varied effects in modulating
AVP release and potentiating renal proximal
tubular sodium and water reabsorption in children.
•
S/E: Prolong PR interval, Prolong QRS interval,
Prolong QTc interval, Increase the heart rate,
Lower T-wave amplitude, Torsades de pointes,
Sudden death.

23. 3. Desmopressin (Intranasal spray 10mcg, oral
25-50mcg "melt" tablets):
•
selective V2-receptor agonist that retains the
antidiuretic properties of vasopressin but
lacks its unwanted pressor activity.
•
Increases water permeability, enhances water
reabsorption, dilutes extracellular fluid, and
concentrates urine.
•
ICI & EAU: GR A & LE 1.

24. •
Women twice more sensitive to desmopressin than
men in terms of effects on nocturnal urine
production and duration of action. This may be
because the gene for the V2 receptor is located on
the X chromosome.
•
OSA treatment with continuous positive airway
pressure (CPAP).

25. II. DIMINISHED GLOBAL &
NOCTURNAL BLADDER
CAPACITY•
Causes: infravesical obstruction, idiopathic
nocturnal detrusor overactivity (NDO),
neurogenic bladder, cystitis (bacterial,
interstitial, tuberculous, radiation), cancer of
bladder, prostate, or urethra, learned voiding
dysfunction, anxiety disorders, bladder
calculi, ureteral calculi, and drugs such as
xanthines (caffeine, theophylline) and β-
blockers.

26. Management:
•
Treating bladder outlet obstruction (BOO)
improves nocturia by lowering postvoid
residual (PVR) volume, increasing
functional bladder capacity, reducing urinary
frequency, also diminished input from
afferents in the bladder neck and the
prostatic urethra.
•
α-blockers, TURP, TUMT etc. for BOO.
•
Antimuscarinics for OAB (Tolterodine,
Solifenacin, Trospium, Mirabegron)

27. MIXED NOCTURNAL POLYURIA & ↓
NOCTURNAL BLADDER CAPACITY
Behavioral modifications:
•
Reduced caffeine and alcohol intake,
•
Limited nighttime fluid intake,
•
improved sleep hygiene through moderate exercise,
•
attention to room temperature, noise, and lighting,
•
early evening leg elevation and
•
compression stockings if patients has bilateral lower
extremity edema.

28. III. GLOBAL POLYURIA
•
24-hour urine output greater than 40 mL/kg.
•
Urinary frequency both day and night.
•
Common causes of polyuria include diabetes
mellitus, diabetes insipidus, and primary
polydipsia (dipsogenic and psychogenic).

29. •
Diabetes insipidus can be central or nephrogenic.
•
Central DI: a deficiency in the synthesis or
secretion of endogenous ADH, can be due to loss
of neurosecretory neurons in the hypothalamus or
the posterior pituitary gland as a result of trauma,
primary pituitary tumors (e.g., craniopharyngioma),
metastatic disease (e.g., breast, lung), infiltrative
diseases (e.g., sarcoid), infarction (e.g., Sheehan
syndrome postpartum), or infection (e.g.,
tuberculosis, meningitis) or can be idiopathic.

30. •
Nephrogenic DI is diuresis in the setting of
normal ADH secretion, but the kidneys do
not respond appropriately to the hormone, as
in some patients with chronic kidney disease.
•
To distinguish central from nephrogenic
diabetes insipidus, a renal concentrating
capacity test (RCCT) performed.

31. Management of Global polyuria:
•
Water restriction during day & night.
•
Lifestyle modification.
•
Diabetes mellitus: controlling glycosuria
may improve the polyuria.
•
Central DI: synthetic vasopressin analogues.
•
Compulsive water drinkers may benefit from
psychotherapy.

32. ALGORITHM FOR EVALUATION & TREATMENT OF NOCTURIA

33. Thank You !!!