Download polydepsia

polydepsia
• excessive thirst accompanied by temporary or
prolonged dryness of the mouth
• Causes of polydipsia
• Increased thirst is often the reaction to fluid
loss during exercise, or to eating salty or spicy
foods
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It may be due to an organic lesion or have a psychological cause.
Diabetes mellitus
Diabetes insipidus
Dehydration(Diarrhoe –Vomiting -Profuse sweating -Significant
blood loss – decreased thirst sensation – cognitive impairment)
• drug-induced polydipsia
• diuretics, anticholinergic, salt, ,
megestrol acetate , mannitol, sorbitol
may cause a polyuria and, secondarily, a polydipsia
Loss of body fluids from the bloodstream into the tissues due to:
burns – sepsis, or heart, liver, or kidney failure
• Psychogenic polydipsia - compulsive water drinking associated with
mental/psychiatric disorders
The physiology of thirst
• An important factor in the maintenance of fluid balance is the
secretion of antidiuretic hormone (ADH). ADH, also known as
vasopressin:
– Is secreted by the hypothalamus when plasma osmolality increases.
– Acts mainly on the distal renal tubule, where ADH binds to receptor
sites and stimulates the reabsorption of water.
• The physiological driving force is thus the maintenance of blood
osmolality.
• Sensory osmoreceptors in the brain stimulate cortical effector
regions, principally in the anterior cingulate cortex , to trigger the
sensation of thirst in response to a rise in blood osmolality.[This
sensation usually starts at 280 mOsmol/kg. The intensity of thirst
and the amount of water required are directly proportional to
blood osmolality
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Circulating angiotensin II is known to play a role. It is known that the area of the
hypothalamus which releases angiotensin II is anatomically close to, and linked
neuronally with, the area that releases ADH, so there is clearly a close connection
between the two systems.[ angiotensin II binds to the angiotensin type 1 receptor,
stimulating thirst
oropharyngeal sensors quell the thirst desire before any changes in osmolality
drinking water quenched thirst more rapidly than when the same amount of
water was mixed with food (eg, in soup).
Acute falls in blood pressure and/or blood volume will also stimulate thirst.
15% or more reduction in circulating blood volume is required for this effect.
However, the effect of osmolality changes on thirst is more significant.
the habit of drinking with meals (secondary drinking ) compensated by renal
excretion
With increasing age the thirst stimulus becomes blunted (hypodipsia) with a
reduction in primary drinking. This is usually compensated for by secondary
drinking.However, it may be a contributory factor in causing dehydration
• Diabetes mellitus in which an excessive concentration
of glucose in the blood osmotically pulls intracellular fl
uid into the bloodstream and increases the
excretion of fluid via increased urination, which leads
to hypovolemia and thirst.
• In diabetes insipidus the deficiency of the pituitary ant
idiuretic hormone results in excretion of copious amou
nts of dilute urine, reduced fluid volume in
the body, and polydipsia. In nephrogenic diabetes insipi
dus there is also copious excretion of urine with conse
quent polydipsia
Diabetes insipidus
• hyposecretion of, or insensitivity to the effects of
(ADH), also known as arginine vasopressin (AVP). ADH
is synthesised in the hypothalamus and transported as
neurosecretory vesicles to the posterior pituitary.
• There it is released into the circulation, governed by
plasma osmolality. Its deficiency or failure to act causes
an inability to concentrate urine in the distal renal
tubules, leading to the passage of copious volumes of
dilute urine. Usually the sufferer passes >3 litres/24
hours of low osmolality (<300 mOsmol/kg) urine.
There are two major forms of DI:
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Cranial DI: decreased secretion of ADH. This is usually due to disease of the
hypothalamus Posterior pituitary disease tends not to cause DI, as secretion
continues in the hypothalamus.
– Causes:
– idiopathic
– Brain Tumours , craniopharyngioma, hypothalamic metastases (especially
breast carcinoma), hypothalamic glioma, large pituitary tumours with
suprasellar extension, lymphoma
– Intracranial surgery
– Head injury.
– Granulomata - sarcoidosis, tuberculosis (TB),
– Infections - encephalitis, meningitis, cerebral abscess
– Vascular disorders - haemorrhage/thrombosis, aneurysms, , Sheehan's
syndrome (postpartum pituitary necrosis).
– Post-radiotherapy.
Inherited:
Autosomal recessive combination of DI, diabetes mellitus, optic atrophy, deafness
(DIDMOAD)
– Autosomal dominant mutations of vasopressin gene
Nephrogenic DI
• decreased ability to concentrate urine because of
resistance to ADH in the kidney.
• Acquired nephrogenic DI:
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Idiopathic.
Hypokalaemia.
Hypercalcaemia.
Chronic kidney disease.
Renal tubular acidosis.
• obstructive uropathy
• Congenital/genetic nephrogenic DI:
• X-linked mutation ADH-receptor gene.
Presentation
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Symptoms
vague and insidious,
marked polyuria. variable between patients (3-20 litres).
Polydipsia.
Nocturia occurring several times per night is common, particularly
in older adults.
urinary incontinence
Signs
signs of dehydration (confusion –dizziness – sunken eyes rapid
heart rate –low blood pressure )and the bladder can be grossly
enlarged and palpable
24-hour urinary collection will show urine volume >3 litres/24 hours
Investigations
• plasma glucose, and plasma and urine osmolality .
• Fluid deprivation test with response to desmopressin. The patient
is deprived of fluids for up to eight hours following which
desmopressin (DDAVP®) 2 micrograms (IM) is given. See table
below for interpretation of the results.
• A therapeutic trial of low-dose desmopressin is another option,
with careful monitoring of plasma osmolality or serum sodium.
Cranial DI patients improve, and those with nephrogenic DI are
unaffected. Those with PP develop hyponatraemia and may stop
drinking.
• MRI of the pituitary, hypothalamus and surrounding tissues
• Renal tract ultrasound or intravenous pyelogram (IVP) may be used
to assess for obstructive complications caused by the high urinary
back-pressure.
Classification of causes of diabetes
insipidus on basis of water
deprivation and DDAVP® response
Urine osmolality after
fluid
deprivation (mOsm/kg)
Urine osmolality after
DDAVP® (mOsm/kg)
Likely diagnosis
<300
>800
CDI
<300
<300
NDI
>800
>800
Primary/psychogenic
polydipsia
Interpretation of results
• Renal function tests and glucose levels should
be assessed to rule out chronic kidney disease
and diabetes mellitus.
A urine specific gravity of 1.005 or less and a
urine osmolality less than 200 mOsmol/kg are
highly suggestive of diabetes insipidus.
Random plasma osmolality is usually greater
than 287 mOsmol/kg.
• In normal individuals, the urine osmolality is 2-4 times greater than
the plasma osmolality. Administration of vasopressin results only in
a small increase in urine osmolality (less than 9%). It takes between
4-18 hours to achieve maximal concentration of urine.
• In central diabetes insipidus (due to decreased production of ADH),
there is an excessive increase in plasma osmolality but not in urine
osmolality. Administration of vasopressin results in an increase in
urine osmolality of 50% or more. ADH levels are minimal.
• In nephrogenic diabetes insipidus (due to resistance of renal tissue
to the action of ADH), ADH levels are normal to elevated and the
kidney fails to respond to exogenous ADH during the water
deprivation test.
• In psychogenic polydipsia, water deprivation will show the same
changes as normal individuals, There is no response to exogenous
ADH.
Management
• Cranial DI
• As the primary problem is a hormone deficiency, physiological
replacement with desmopressin is usually effective. This can be
given orally, intranasally or parenterally.
• Mild cases of DI (urine output 3-4 litres/24 hrs) can be managed by
ingestion of water to quench thirst.
• It is essential to avoid chronic overdosage with desmopressin,
which will cause hyponatraemia.
• Long-term management:
– Because of the risk of hyponatraemia, (1- to 3-monthly)
measurements of serum sodium are advised.
– Some endocrinologists recommend missing desmopressin treatment
one day each week to avoid the development of hyponatraemia.
Nephrogenic DI
• If daily urine volume is <4 litres/24 hrs and the
patient is not suffering from severe dehydration
then definitive therapy is not always necessary.
• Correct any metabolic abnormality.
• Stop any drugs that may be causing the problem.
• High-dose DDAVP® may be used with success in
mild to moderate cases of nephrogenic DI..
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Complications
• DDAVP® can worsen myocardial ischaemia in
susceptible patients
• Patients with genetic causes of nephrogenic DI
are prone to bladder dysfunction and hydroureter/hydronephrosis if the condition is
undiagnosed or untreated for an appreciable
period of time
• Patients with genetic causes or severe
nephrogenic DI may need, intermittent
catheterisation to reduce urinary tract backpressure complications
Prognosis
• Death is rare, the elderly with acute illness or
surgery are more at risk of severe
dehydration, hypernatraemia, fever,
cardiovascular collapse and death
• Patients with inborn errors are more likely to
suffer complications as the underlying cause
cannot be removed.
Psychogenic Polydipsia
(Exessive Fluid Seeking Behaviour)
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type of polydipsia exhibited by patients with mental illness
Psychogenic polydipsia, is a condition of psychological rather than physiologic origin. When
the intake of water exceeds the body’s ability to manage it, imbalance ensues
Psychogenic polydipsia is a serious disorder that often leads to institutionalization.
It should be taken very seriously and can be life-threatening, as serum sodium is diluted to
an extent that seizures and cardiac arrest can occur.
The urine produced by these clients will have a low electrolyte concentration, and it will be
produced in large quantities (i.e., polyuria).
close monitoring by staff is necessary to control fluid intake.
the kidneys will be unable to deal with fluid overload and
a more serious symptom of selfinduced water intoxication (i.e.,SIWI). Individuals diagnosed
with ”psychogenic polydipsia” — of which 80% are diagnosed with schizophrenia have a fluid
intake that is usually 4 – 10L/day, some drink up to 22L/day!
Hyponatremia 25% of polydipsia patients have acute development of hyponatremia
Behavioral management programs should be mandatory.Psychosocial rehabilitation (PSR)
programs for individuals diagnosed with psychogenic polydipsia,
Clozapine is an atypical antipsychotic medication,
antipsychotics such as risperidone and angiotensin-II receptor antagonists, such as
irbesartan.
Complications of polydepsia
• A distinction between organic and psychogenic
polydipsia.
• In the former, once the underlying condition is
treated, complications from the polydipsia are
few. This is because homeostasis tends to be
preserved.
• In psychogenic polydipsia, water continues to be
drunk in excess irrespective of the osmotic status
of plasma and urine. This can result in water
intoxication with subsequent cardiac failure, and
urinary tract abnormalities
Management
• The management of polydipsia depends on
the underlying cause
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