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ENDO HOURDr. Marianne Joy B. Advincula
K.J.M 5/M Pampanga Chief complaint: Headache
History of present illness
2 yrs PTA- diagnosed to have craniopharyngioma with obstructive hydrocephalus
-presented with headache and nystagmus.
- S/p endoscopic guided ommaya insertion (April 2008)
- diagnosed to have central DI last June 2009, during OR, px was noted to have Na 151 and urine sg 1.000, urine volume ~1,000 cc in 3 hrs
History of present illness
6 days PTA- (+) headache, right parietal area 5 days PTA- (+) headache and vomiting -sought consult with MD, advised NSS
ff up 3 days PTA- consult done c/o NSS OPD. Vent tap
was done, no relief of symptoms Day of admission- due to persistence of
symptoms, px was brought to PGH Admission
Review of systems
(+) vomiting (-)cough (- ) colds (-) fever ( -) headache (-) LBM (-) seizure (-) changes in sensorium (+) good appetite (+) good activity
Past Medical History
(-) BA (-) PTB (-) allergies (+) previous hospitalization
› April 2008- underwent Ommaya insertion in PGH
Birth and maternal History
Born full term to a 30 yr old G3P2 (2002) mother via SVD at a local hospital assisted by an OB-Gyn
Mother had regular PNCU No feto-maternal complications No exposure to teratogenic substances No intake of abortifacient substances
Nutritional History
Breastfed at birth up to 1 year Started on complementary feeding at 6 months Presently eats regular table food
Developmental history
Creeps at 9 months Able to walk independently at 1 yr and 3 months Able to say “mama” and “papa” at 1 year old Speaks in sentences at 2 yrs old
Immunization History
Completed Epi
Personal social history
Third of 4 children, mother is 35 yrs old while father is a 38 yr old jeepney driver
Physical examination on admission
Conscious, coherent, not in distress BP- 100/60 CR- 84/min RR- 20 T- 37.1°C Wt: 19 kg Ht- 110 cm HC- 52 cm Anicteric sclerae, pink conjunctivae, (+) good shunt
rebound SCE, no retractions, CBS AP, normal rate and regular rhythm, no murmurs Abdomen flat, soft, normoactive bowel sound, no
masses Full and equal pulses, no edema, no cyanosis
Neurologic exam
GCS-15 Pupils 2 mm ERTL Intact EOMs (-) facial asymmetry (+) intact gross hearing (+) gag (+) tongue midline
MMT- gr 5/5 all extremities Sensory- intact (+) Babinski
Admitting Impression
Suprasellar mass secondary to craniopharyngioma with obstructive hydrocephalus
S/P endoscopic guided ommaya shunt insertion- 4/2008
Hypothyroidism, Hypocortisolism Central DI, resolved
COURSE AT THE WARD
Upon admission, baseline serum electrolytes showed Na 134, K 3.6, Cl 96, Ca 2.51. Baseline urinalysis showed light yellow/ clear/ 1.010/ 7.0/ neg sugar and alb/ RBC 4/ WBC 1.
On the 1st HD- 24 hr urine output was 4,150 ml. Serum and urine electrolytes were done, showing Na 146/ K 4/ Cl 112. Urine electrolytes showed Na 36/ K 4.9/ Cl 37. Plan was to do water deprivation test. Urine losses were replaced in excess of 3 cc/kg/hr with OFI
3rd HD- Na was noted to be 146, minirin 0.1 mg/tab, ½ tab was given as stat dose
UO- 770 ml after minirin
8th HD- minirin started 0.1 mg/tab, ½ tab at bedtime
9th HD- Na 128, K 3.5, Cl 94, NaCl tabs started, 1 tab q 3 hrs
Urine Na 33/ K 8.3/ Cl 26 Serum Na 135/ K 4.0/ Cl 102 Minirin put on hold
Case Discussion
Diabetes Insipidus
Presents with polyuria and polydipsia
central DI- result from vasopressin deficiency nephrogenic DI- vasopressin insensitivity at the
level of the kidney
Central diabetes insipidus
Etiologies: 1. genetic mutations in the vasopressin gene 2. trauma (accidental or surgical) to vasopressin
neurons› triphasic response – after surgery, refers to an initial
phase of transient DI, lasting 12–48 hr, followed by a 2nd phase of syndrome of inappropriate antidiuretic hormone secretion, lasting up to 10 days, which may be followed by permanent DI
3. congenital malformations of the hypothalamus or pituitary
4. neoplasms- tumors that cause DI must either be very large and infiltrative or be strategically located near the base of the hypothalamus, where vasopressin axons converge before their entry into the posterior pituitary
5. infiltrative 6. autoimmune 7. infectious diseases affecting vasopressin neurons
or fiber tracts 8. increased metabolism of vasopressin
Symptoms
The major symptoms of central DI are polyuria and polydipsia.
Polyuria is defined as a urine output of over 3 L/day in adults. The onset of polyuria is usually abrupt in CDI. This is in contrast to nephrogenic DI and primary polydipsia,
in which onset of polyuria is almost always gradual.
Symptoms
Nocturia is often the first sign of CDI. This is because urine is usually most concentrated in
the morning due to lack of fluid ingestion overnight. As a result, nocturia is usually the first manifestation
of a loss of concentrating ability. Thus, a relatively dilute urine is excreted, with a
urine osmolality of less than 200 mOsmol/kg. Dry skin and constipation are other symptoms that
may occur in CDI.
Diagnostics
serum for osmolality, sodium, potassium, blood urea nitrogen, creatinine, glucose, and calcium; urine for osmolality, specific gravity, and glucose determination.
The diagnosis of DI is established if the serum osmolality is greater than 300 mOsm/kg and the urine osmolality is less than 300 mOsm/kg.
DI is unlikely if the serum osmolality is less than 270 mOsm/kg or the urine osmolality is greater than 600 mOsm/kg
If serum osmolality is less than 300 mOsm/kg (but greater than 270 mOsm/kg) and pathologic polyuria and polydipsia are present, a water deprivation test is indicated to establish the diagnosis of DI and to differentiate central from nephrogenic causes.
Water Restriction Test
In healthy individuals, water deprivation increases plasma osmolality, which stimulates secretion of ADH by the posterior pituitary.
This then acts on the kidney to increase urine osmolality to 1000 to 1200 mOmol/kg and to restore plasma osmolality to normal levels.
Giving exogenous ADH does not increase urine osmolality further because it is already maximal in response to an individual’s endogenous release of ADH.
Water Restriction Test
Method:› Water restriction lasts 4 to 18 hours.› Overnight fluid restriction should be avoided, as
severe volume depletion and hypernatremia can be induced in patients with severe polyuria.
› Measure the urine volume and osmolality every hour and serum sodium concentration and osmolality every two hours.
Water Restriction Test
The test should be continued until one of the following occurs:› The urine osmolality reaches a normal value, which is above 600
mOsm/kg, indicating that both ADH release and effect are intact. › The urine osmolality is stable on 2 or 3 successive measurements
despite a rising plasma osmolality.› The plasma osmolality exceeds 295 to 300 mOsm/kg.› In the last two settings, the serum ADH level is measured, which is
also performed at the start of the test, and then exogenous ADH is administered (10 microgm of dDAVP nasally or 4 microgm sq).
› Urine osmolality is then measured every 30 minutes for the next 3 hours.
Water Restriction Tests
Interpretation:› Normal subjects and primary polydipsia:
Urine osms are greater than plasma Osms after water restriction. Urine osms increase minimally (<10%) after exogenous ADH.
› Central Diabetes Insipidus: Urine osms remain less than plasma osms after water restriction. After ADH is given, urine osms increase 100% in complete CDI and
over 50% in partial CDI.› Nephrogenic Diabetes Insipidus:
Urine osms remain less than plasma osms. After ADH, urine osms increase by less than 50%.
Treatment
Treatment is primarily aimed at decreasing the urine output, usually by increasing the activity of ADH.
Replacement of previous and ongoing fluid losses is also important, either with oral water intake or IVF such as D5W if the patient is unable to take fluids by mouth.
There are several medications available for the treatment of CDI, of which desmopressin is the most common.
Desmopressin
Desmopressin is a two-amino acid substitute of ADH that has potent antidiuretic activity but no vasopressor activity.
It is also known as dDAVP, which stands for 1-deamino-8-D-arginine vasopressin.
It is currently the drug of choice for long-term therapy of CDI to control polyuria.
It is safe during pregnancy for both the mother and the fetus.
Risks of Desmopressin
Potential risks of desmopressin include water retention and the development of hyponatremia.
This may occur because once dDAVP is given, the patient has nonsuppressible ADH activity and may be unable to excrete ingested water normally.
This can be avoided by giving the minimum daily dose required to control the polyuria.
Other Drugs
For the vast majority of patients with CDI, dDAVP is readily available, safe, and effective.
Therefore, it is rarely necessary to add other drugs to the regimen.
The other agents available are less effective and associated with more adverse effects than desmopressin.
Chlorpropamide, carbamazepine, and clofibrate can be used in cases of partial CDI and can lower the urine output by as much as 50%.
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Serum elestrolytes
Na 134 146 136 134 128 125 134 135 137 148 136
K 3.6 4.0 4.3 3.7 3.5 3.8 3.9 4.0 4.3 3.4 3.8
Cl 96 112 99 100 94 90 103 102 103 115 99
Urine electrolytes
Na 20 36 33 19 26 75 36
K 6.4 4.9 8.3 4.3 17.5 4.7 11
Cl 22 37 26 24 41 75 24
USG 1.015
1.004
1.027
1.002
1.005
1.006
1.003
INPUT/OUTPUT
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Input 4076 4250 1235 2550 4685 3630 3965 2465 3463 5175
Output
2880 3060 1210 3110 4030 3420 3980 2380 4280 5900
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