Diagnosis of Autoimmune Diabetes Insipidus
Autoimmune Diabetes Insipidus Diagnosis: Book Excerpts
Diagnostic Tests for Autoimmune Diabetes Insipidus: Online Medical Books
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POLYDIPSIA:
Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)
- Is there a history of drug ingestion? Diuretics and arsenic poisoning are among the many causes of excessive thirst.
- Is there associated polyphagia and weight loss? The presence of these symptoms would suggest diabetes mellitus and hyperthyroidism.
- Is there massive polyuria? The presence of massive polyuria suggests diabetes insipidus or psychogenic polydipsia.
- Is there mild polyuria? The presence of mild polyuria should suggest chronic renal failure, renal tubular acidosis, hyperparathyroidism, and febrile illnesses.
DIAGNOSTIC WORKUP
The basic workup includes a CBC, sedimentation rate, urinalysis, 24-hr urine volume, a serum and urine osmolality, a thyroid profile, and x-rays of the skull and long bones.
The diagnosis of hyperparathyroidism may be assisted by ordering a serum parathyroid hormone level. Also, a 24-hr urine collection for calcium may be done to help diagnose this condition. Microscopic examination of the urinary sediment will help diagnose renal disease, as will renal biopsies. If pituitary diabetes insipidus is suspected, a CT scan of the brain and blood tests for serum growth hormone, FSH, LH, ACTH, and TSH may be done. The Hickey-Hare test and monitoring intake and output before and after vasopressin (Pitressin®) will be useful in differentiating pituitary diabetes insipidus from nephrogenic diabetes insipidus. The concentrations of circulating vasopressin may be measured by immunoassay.
An endocrinologist should be consulted before ordering these expensive diagnostic tests.
» READ BOOK EXCERPT ONLINE »
Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
Polydipsia:
Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)
-
Diabetes mellitus (type I and type II)
–Hyperglycemia drives an osmotic diuresis that causes polyuria, which then leads to dehydration, increased thirst, and polydipsia
-
Diabetes insipidus
–Abnormal water balance due to vasopressin (ADH) deficiency or resistance, causing excretion of large amounts of dilute urine
-
Central or neurogenic diabetes insipidus
(vasopressin deficiency)
–Congenital
–Familial (autosomal dominant)
–Acquired: Neurosurgery, tumor (e.g.,
craniopharyngioma), head trauma, infiltrative/inflammatory, infectious
-
Nephrogenic diabetes insipidus (decreased responsiveness of the kidneys to vasopressin)
–Familial (X-linked dominant and recessive forms)
–Acquired: Renal disease, obstructive uropathy, hypercalcemia/hypercalciuria
–Hypokalemia, drug-induced (e.g., lithium, diuretics, ethanol, cisplatin)
–Gestational DI: Increased clearance of ADH by placental vasopressinase, lower osmolar threshold for thirst and ADH release
-
Primary polydipsia
–Compulsive water drinking
–Dipsogenic DI
-
Primary hyperaldosteronism
-
Diabetes insipidus, diabetes mellitus, optic atrophy, and deafness (DIDMOAD) syndrome
-
Bartter syndrome
-
Hypertension (e.g., pheochomocytoma)
-
Neuroblastoma
-
Cystinosis
-
Congestive heart failure
Workup and Diagnosis
-
History: Quantification of fluid intake and urine output, drinking overnight, polyphagia, polyuria, nocturia, enuresis, psychosocial factors, interference with normal activities, growth progression, weight loss, weakness, fatigue, leg cramps/muscle aches, neurologic symptoms (headaches, visual changes)
-
Physical exam: Vital signs (HR, BP), weight, height, hydration assessment (mucous membranes, capillary refill, extremities’ temperature, skin turgor), neurologic exam (optic discs, EOM), energy level, muscle pain
-
Initial labs
–Serum electrolytes, BUN, creatinine, glucose, calcium
–Urinalysis with specific gravity, glucose and ketones
–Simultaneous serum and urine osmolality (mOsm/kg)
–Serum osm >300 and urine osm <300 =DI
–If serum osm <270 and urine osm >600 DI unlikely
- Further diagnostic workup
–Water deprivation test in case of ambiguous history and labs (patient deprived of water, then ability to concentrate urine is assessed)
–Differentiates between DI and water intoxication, and between central DI and nephrogenic DI (by response to a dose of vasopressin administered at the end of the study)
-
MRI of brain with special attention to the pituitary
-
Imaging of adrenal glands if hyperaldoterone suspected
>>
» READ BOOK EXCERPT ONLINE »
Source: In A Page: Pediatric Signs and Symptoms, 2007
POLYDIPSIA:
Approach to the Diagnosis
(Differential Diagnosis in Primary Care)
The approach to the diagnosis of polydipsia involves establishing the presence or absence of other symptoms such a polyuria, polyphagia, weakness, and weight loss. Polydipsia with polyuria and excessive appetite (polyphagia) should suggest diabetes mellitus or hyperthyroidism, whereas polydipsia with polyuria alone should suggest a form of diabetes insipidus (pituitary, renal, or psychogenic). The laboratory workup involves checking intake and output, blood sugars, electrolytes, and a thyroid profile.
» READ BOOK EXCERPT ONLINE »
Source: Differential Diagnosis in Primary Care, 2007
Polydipsia:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
Obtain a history. Find out how much fluid the patient drinks each day. How often and how much does he typically urinate? Does the need to urinate awaken him at night? Determine if he or anyone in his family has diabetes or kidney disease. What medications does he use? Has his lifestyle changed recently? If so, have these changes upset him?
If the patient has polydipsia, take his blood pressure and pulse when he’s in supine and standing positions. A decrease of 10 mm Hg in systolic pressure and a pulse rate increase of 10 beats/
minute from the supine to the sitting or standing position may indicate hypovolemia. If you detect these changes, ask the patient about recent weight loss. Check for signs of dehydration, such as dry mucous membranes and decreased skin turgor. Infuse I.V. replacement fluids, as needed.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Diabetes insipidus:
Diagnosis
(Professional Guide to Diseases (Eighth Edition))
Urinalysis reveals almost colorless urine of low osmolality (50 to 200 mOsm/kg, less than that of plasma) and low specific gravity (less than 1.005).
CONFIRMING DIAGNOSIS Diagnosis requires evidence of vasopressin deficiency, resulting in the kidneys’ inability to concentrate urine during a water deprivation test.
In this test, after baseline vital signs, weight, and urine and plasma osmolalities are obtained, the patient is deprived of fluids and observed to make sure he doesn’t drink anything surreptitiously. Hourly measurements then record the total volume of urine output, body weight, urine osmolality or specific gravity, and plasma osmolality. Throughout the test, blood pressure and pulse rate must be monitored for signs of orthostatic hypotension. Fluid deprivation continues until the patient loses 3% of his body weight (indicating severe dehydration). When urine osmolality stops increasing in three consecutive hourly specimens, patients receive 5 units of aqueous vasopressin subcutaneously (S.C.).
Hourly measurements of urine volume and specific gravity continue after S.C. injection of aqueous vasopressin. Patients with pituitary diabetes insipidus respond to exogenous vasopressin with decreased urine output and increased specific gravity. Patients with nephrogenic diabetes insipidus show no response to vasopressin.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Polydipsia:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
Obtain a history. Find out how much fluid the patient drinks each day. How often and how much does he typically urinate? Does the need to urinate awaken him at night? Determine if he or anyone in his family has diabetes or kidney disease. What medications does he use? Has his lifestyle changed recently? If so, have these changes upset him?
If the patient has polydipsia, take his blood pressure and pulse when he’s in supine and standing positions. A decrease of 10 mm Hg in systolic pressure and a pulse rate increase of 10 beats/minute from the supine position to the sitting or standing position may indicate hypovolemia. If you detect these changes, ask the patient about recent weight loss. Check for signs of dehydration, such as dry mucous membranes and decreased skin turgor. Infuse I.V. replacement fluids as needed.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Polydipsia:
History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
Thirst, which is the chief complaint of patients with DM, DI, and psychogenic polydipsia, is associated with polyuria. Nocturia occurs more frequently with DM and DI than with psychogenic polydipsia. Polydipsia usually starts abruptly in central DI and patients often have a preference for ice cold water (3). In eliciting the history, take note of neurologic symptoms (problems with visual fields, headaches, numbness), a prior history of cancer (particularly metastatic brain cancer), a history of trauma, neurosurgery, and infections (e.g., encephalitis). The patient’s psychiatric history may also be relevant.
Physical examination
A thorough general physical examination, including vital signs, is helpful in making the diagnosis, but the emphasis is on the neurologic examination (i.e., visual fields, cranial nerve deficits, oculomotor palsies, and reflexes). Signs of recent weight loss or presence of peripheral neuropathy is helpful in making the diagnosis of DM (Chapters 2.13 and 4.6).
» READ BOOK EXCERPT ONLINE »
Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Diabetes insipidus:
Diagnosis
(Handbook of Diseases)
Urinalysis reveals almost colorless urine of low osmolality (50 to 200 mOsm/kg, less than that of plasma) and low specific gravity (less than 1.005). However, a diagnosis requires the water deprivation test to provide evidence of vasopressin deficiency, resulting in the kidneys’inability to concentrate urine.
Water deprivation test
In this test, after baseline vital signs, weight, and urine and plasma osmolalities are obtained, the patient is deprived of fluids and observed to make sure he doesn’t drink anything surreptitiously. Hourly measurements then record the total volume of urine output, body weight, urine osmolality or specific gravity, and plasma osmolality. Throughout the test, blood pressure and pulse rate must be monitored for signs of orthostatic hypotension.
Fluid deprivation continues until the patient loses 3% of his body weight (indicating severe dehydration). When urine osmolality stops increasing in three consecutive hourly specimens, the patient receives 5 units of aqueous vasopressin subcutaneously (S.C.).
Hourly measurements of urine volume and specific gravity continue after S.C. injection of aqueous vasopressin. Patients with pituitary diabetes insipidus respond to exogenous vasopressin with decreased urine output and increased specific gravity. Patients with nephrogenic diabetes insipidus show no response to vasopressin.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Chronic fatigue and immune dysfunction syndrome:
Diagnosis
(Handbook of Diseases)
The cause and nature of CFIDS are still unknown, and no single test unequivocally confirms its presence. Therefore, the diagnosis is based on the patient’s history and the CDC criteria. Because the CDC criteria are admittedly a working concept that may not include all forms of this disease and are based on symptoms that can result from other diseases, diagnosis is difficult and uncertain. Considerable overlap exists between CFIDS and fibromyalgia syndrome, with many patients having features of both.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Polydipsia:
History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Obtain a history. Find out how much fluid the patient drinks each day. How often and how much does he typically urinate? Does the need to urinate awaken him at night? Determine if he or anyone in his family has diabetes or kidney disease. What medications does he use? Has his lifestyle changed recently? If so, have these changes upset him?
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Polyuria and Polydipsia:
Clinical Features and Diagnosis
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
Diabetes Mellitus
By far,most common cause of polyuria and polydipsia in pediatric populationis diabetes mellitus.Most common form is insulin-dependentdiabetes mellitus (type 1), in which autoimmune destruction of betacells of pancreas causes diminished insulin secretion and hyperglycemia.Subsequent glucosuria produces osmotic diuresis with polyuria, polydipsia,and polyphagia.Second form is non–insulin-dependentdiabetes mellitus (type 2), which is characterized by insulin resistanceand usually relative insulin deficiency.Criteria for diagnosis of diabetesmellitus have been established by American Diabetes Association(1999) and include symptoms of diabetes mellitus plus plasma glucoseconcentration ≥200 mg/dL at any time of day regardlessof time of last meal or fasting plasma glucose concentration ≥126 mg/dL(fasting is defined as no caloric intake for ≥8 hrs). Diabetes Insipidus
2 formsof diabetes insipidus are antidiuretic hormone (ADH) deficiencyand ADH resistance.Primary clinical manifestations arepolyuria and polydipsia. Episodes of hypernatremic dehydration withhypotonic urine also may occur. Antidiuretic Hormone Deficiency (Central Diabetes Insipidus)
Kidney isunable to conserve water with ADH deficiency because of absenceor lack of release of ADH (arginine vasopressin).Genetic transmission of primary formis autosomal-dominant, and gene locus has been mapped to chromosome20p13.Secondary form includes lesions thatdamage neurohypophyseal system: head trauma, infection (meningitis,encephalitis), tumors (most commonly craniopharyngioma), Langerhanscell histiocytosis, and metastatic neoplasia (leukemia).Specific gravity of morning urine specimenshould be ≥1.018 in normal children without any overnight fluidintake. Presence of inappropriately dilute urine with hyperosmolarserum suggests ADH deficiency, and water deprivation test shouldbe performed under controlled supervised conditions.Inability to concentrate urine by waterdeprivation and resolution with administration of exogenous argininevasopressin confirm diagnosis. Antidiuretic Hormone Resistance (Nephrogenic Diabetes Insipidus)
The defectin this form of diabetes insipidus is inability of renal tubuleto respond to ADH.Primary form is usually due to X-linkeddisorder with defect in vasopressin receptor; however, autosomal-dominantand -recessive forms also occur.Secondary form is due to several disorders(renal dysplasia, medullary cystic disease, cystinosis, sickle celldisease, chronic renal failure, Fanconi syndrome, Bartter syndrome,hypercalcemia) and drugs (lithium, demeclocycline, methoxyflurane,amphotericin B, phenytoin) that produce renal concentrating defects. Primary Polydipsia
Is the excessiveingestion of water, when it is not needed to maintain fluid balance.Causes include compulsive water drinkingfor psychological reasons and frequent presentation of fluids toinfants. Another cause of primary polydipsia is hypothalamic damagethat affects thirst center but not ADH release.When overnight fluids are withheld,concentrated urine can be produced in the morning. Serum vasopressinlevels are low but increase to normal with fluid deprivation. Diagnostic Approach
Polyuriamust be distinguished from small volume urinary frequency, whichis common in pediatric practice. Children with polyuria often havenocturia and are unable to sleep through the night without wakingup to urinate. Most children with urinary frequency do not havepolyuria or a defect in urinary concentrating ability. Common causesof isolated urinary frequency are habit, attention-seeking behavior,and urinary tract infection.Random sample of urine with specificgravity of >1.028 and absence of polyuria rules out a concentrationdefect. Even urinary specific gravity of >1.020 on randomor early morning sample indicates sufficient urinary concentrationsuch that symptomatic diabetes insipidus is unlikely. Children whohave urine with a somewhat lower than normal specific gravity butwho can sleep through the night without passing urine do not needfurther evaluation.Presence of polyuria, dehydration,and high urinary specific gravity is evidence for osmotic diuresis,which is most commonly caused by diabetes mellitus. Dilute urineassociated with polyuria suggests diabetes insipidus or psychogenicpolydipsia. If blood glucose and urea nitrogen are normal, high serumosmolality with hyposmolar urine suggests ADH deficiency or resistance.Low serum osmolality with hyposmolar urine suggests primary polydipsia.With either ADH deficiency or resistance,urine specific gravity rarely exceeds 1.005 and urinary osmolalityrarely exceeds 200 mOsm/kg. Water deprivation test thatdemonstrates inability to concentrate urine indicates diabetes insipidusand distinguishes it from primary polydipsia. If urine remains hypotonicwith dehydration, next step is to determine response to exogenousvasopressin, which distinguishes ADH deficiency from resistance.With ADH deficiency, administration of vasopressin causes diminishingof symptoms and increase in urine specific gravity, whereas no responseoccurs with ADH resistance.With suspected renal disease, certaintests should be performed: CBC and differential; UA; urine culture;serum electrolytes, calcium, phosphorus, and creatinine; blood ureanitrogen; hemoglobin electrophoresis; and renal U/S. Othertests (e.g., determination of serum and urinary amino acids, voiding cystourethrography,and renal biopsy) may be necessary to define specific renal abnormality.Psychosocial history of emotional disturbance,including episodes of compulsive water drinking and formation ofconcentrated urine with fluid deprivation, are evidence for psychogenicpolydipsia. This disorder may sometimes be difficult to distinguishfrom hypothalamic thirst defect, and consultation with a pediatricendocrinologist is recommended.
» READ BOOK EXCERPT ONLINE »
Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Polydipsia:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
Obtain a medical history. Find out how much fluid the patient drinks each day. How often and how much does he typically urinate? Does the need to urinate awaken him at night? Determine if he or anyone in his family has diabetes or kidney disease. What medications does he use? Has his lifestyle changed recently?
If the patient has polydipsia, take his blood pressure and pulse when he's in supine and standing positions. A decrease of 10 mm Hg in systolic pressure and a pulse rate increase of 10 beats/minute from the supine to the sitting or standing position may indicate hypovolemia. Ask the patient about recent weight loss. Check for signs of dehydration, such as dry mucous membranes and decreased skin turgor.
» READ BOOK EXCERPT ONLINE »
Source: Nursing: Interpreting Signs and Symptoms, 2007
POLYDIPSIA:
Approach to the Diagnosis
(Differential Diagnosis in Primary Care)
The approach to the diagnosis of polydipsia involves establishing the
presence or absence of other symptoms such a polyuria, polyphagia, weakness,
and weight loss. Polydipsia with polyuria and excessive appetite
(polyphagia) should suggest diabetes mellitus or hyperthyroidism, whereas
polydipsia with polyuria alone should suggest a form of diabetes insipidus
(pituitary, renal, or psychogenic). The laboratory workup involves checking
intake and output, blood sugars, electrolytes, and a thyroid profile.
» READ BOOK EXCERPT ONLINE »
Source: Differential Diagnosis in Primary Care, 2007
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