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An Approach to Polydipsia

Diabetes Insipidus

Tiffany Chan

on 17 January 2013

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Transcript of An Approach to Polydipsia

History Tiffany Chan
January 16th 2013 Investigations Neurologic HEENT Cardiovascular Respiratory Abdominal Alert and oriented x3, GCS 15
Cranial nerves II-XII normal
Normal muscle and sensory testing
Normal reflexes in upper and lower extremities
Normal fine motor coordination
Normal gait and Romber's test
No photophobia or phonophobia on exam Past Medical History Healthy adolescent female with no medical history
No previous hospitalizations or surgeries
Met all normal developmental milestones
Immunizations up to date
No medications, NKDA
Takes OTC multivitamins and herbal supplements Adopted at 8 months of age
Unknown pre-natal, birth, or new-born history
Unknown maternal or paternal medical history Back to the Case Social History Differential Diagnosis Primary Polydipsia Increase in water intake = increase in urine output
Often seen in anxious, middle-aged woman with psychiatric illness 1. Consult
2. History
3. Physical
4. Differential Diagnosis
5. Investigations
6. Back to the Case 1 month history of polydipsia, with no specific triggering factors
Previously drank 4-5 cups of fluids per day and currently doubled in amount
Constant feeling of unsatisfied thirst Increasing urinary frequency and polyuria, up to 10-12 times during the day
Noticeably more immediately after drinking
No urinary retention, dribbling, interrupted flow, or incomplete voiding
No nocturia, bed-wetting, or urinary incontinence
No dysuria or hematuria An Approach to Polydipsia Progressively worsening pain in left lower leg, worse at night and early morning
Non-radiating, cramping sensation about 5/10 in severity
Previously noted but only intermittently 16y/o female with urinary concerns Family History Currently living with adopted mother and father
Grade 10 high-school student, enjoys science
Physical active, no recent change in diet
No alcohol, smoking, or other elicit drug use
Reached menarche at 12 years of age and has irregular menses, every 1-2 months
Not sexually active Normal ears, nose, mouth, and throat
No palpable cervical lymphadenopathy
Moist mucous membranes, no tongue furrows
No palpable massess or nodes in thyroid Neurogenic Diabetes Insipidus Nephrogenic Diabetes Insipidus Polyuria = urine output greater than 3L/day in adults Deficient secretion of ADH hormone, due to idiopathic (25%), traumatic (17%), iatrogenic (9%), tumours (20%), or infectious causes (20%) Normal ADH secretion but varying degrees of renal resistance to ADH's effect, causing impaired urine concentrating abilities Mostly acquired nephrogenic DI, due to infection, renal failure, and electrolyte imbalance
Underlying minimal CRF is not enough to cause symptomatic polyuria
Nephrogenic DI in adults is often due to chronic lithium use, hypercalcemia, or hypokalemia
Nephrogenic DI in children is often inherited "Water Overload" Serum [Na] < 137mEq/L
Urine osmolality
N. Water restriction test Serum [Na] > 142mEq/L
Urine osmolality
AbN. Water restriction test Serum [Na] > 142mEq/L
Urine osmolality
AbN. Water restriction test Intermittent non-radiating frontal headaches, 5/10 in severity, no triggering factors
No associated symptoms or red flags Increased
osmolality Elevated ADH release "Water Wasting" "Water Wasting" Increased
osmolality Maximum ADH effect once plasma osmolality reaches 295-300 mOsmol/kg or plasma sodium reaches 145mEq/L or urine osmolality reaches at least 600mOsmol/kg or urine specific gravity reaches at least 1.020

No response to desmopressin administration Administer
1ug IV Measure urine osmolality and volume q30 minutes Urine osmolality would be far less than 300mOsmol/kg and typically does not increase by more than 100mOsmol/kg over baseline in response to water deprivation test.
Urine osmolality may increase up to 45% in partial cases (between 300-750mOmol/kg) and by 0% in complete cases with Desmopressin. Measure baseline urine osmolality 2 hours Administer
1ug IV Measure urine osmolality and volume q30 minutes Urine osmolality would be around 300mOsmol/kg in response to water deprivation test.
Urine osmolality will increase further by 15-50% in partial cases (between 300-750mOmol/kg) and by 100% in complete cases (usually >750mOsmol/kg) with Desmopressin Measure baseline urine osmolality 2 hours Start after breakfast, once child spontaneously voids Measure body weight and continue to monitor vitals Baseline plasma sodium and plasma osmolality Repeat plasma sodium and plasma osmolality 4 hours Record each urine void's volume, specific gravity, osmolality Repeat q2 hours Urine specific gravity > 1.020
Urine osmolality > 600mOsmol/kg
Plasma osmolality > 295-300mOsmol/kg
Plasma Na > 145mEq/L
Decrease body weight by more than 5% or signs of volume depletion
T = 6hrs (< 6m) OR 8hrs (6-18m) OR 12hrs (> 2yrs) Final plasma sodium and plasma osmolality
Plasma ADH level
Final urine osmolality and specific gravity Water restriction test if plasma osmolality stabilized and reached at least 295mOsmol/kg or plasma sodium concentration 150mEq/L No signs of respiratory disress
Equal air entry bilateral, with no crackles or wheezes Soft, non-tender, non-distended abdomen
No CVA tenderness
No evidence of scars, discolouration, masses, or asymmetry
No palpable organomegaly STOP 15 year-old previously healthy female with an acute onset of polyuria, likely secondary to polydipsia. No underlying medical history and normal developmental history. No recent steroid therapy. Unknown family history.
No specific triggering factors, with no recent head trauma/injury, meningitis/encephalitis, or surgeries
Not associated with dysuria or hematuria.
No recent change in appetite or weight, no fatigue or weakness, or headaches or vision changes.
Never been sexual active and no previous drug use

Associated with intermittent frontal headaches, but no red flags
Associated with mild localized left leg cramp Physical On exam, she is alert and oriented, with no obvious alterations in her mental state. She is VSS and appears well hydrated.

Physical exam is grossly benign. There is no evidence of Cushingnoid features. VSS. At this point in our exam, the history and physical are suggestive of diabetes insipidus. We continue with our investigations to determine the underlying cause: Serum
Labwork CBC
Extended electrolytes - Ca
Creatinine and urea
Albumin:Creatinine ratio
Serum osmolality
Serum lithium
Serum ADH levels Urine
Studies 24-hour urine collection
Urine cultures
Urine electrolytes
Urine osmolality Laboratory Investigations Questions? Serum Labwork:
Osmolality 304mOsmol/kg
Lithium Normal
ADH Levels Pending Urinalysis:
Colour Yellow
SG 1.001
pH 5.5
Protein Negative
Glucose Negative
Ketones Negative
Blood Negative
Nitrite Negative

Urine Culture:
No growth Treatment Water Restriction (after 4 hours):
Urine SG 1.018
Urine osmolality 294mOsmol/kg
Serum Na 140mEq/L
Serum osmolality 290mOsmol/kg
Serum ADH Pending

Desmopressin Challenge:
Urine osmolality 600mOsmol/kg
Serum ADH Pending Urine Studies:
Electrolytes Pending
Osmolality 158 mOsmol/kg 2 138 r. glucose 5.2
CK Normal
TSH Normal 125 334 4.6 Cr 54 3.7 105 22 Urea 2.1 At this point, the patient's history, physical, and laboratory investigations point towards neurogenic diabetes insipidus. Consider the following:
MRI/CT head
Anterior pituitary studies General Considerations Specific Considerations Neurogenic DI: Desmopressin therapy
Nephrogenic DI: Diuretics (Thiazide/Potassium-sparing) and NSAID (Indomethacin) Adequate fluid replacement
Dietary suggestions
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