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ENDO HOUR. Dr. 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

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  1. ENDO HOUR Dr. Marianne Joy B. Advincula

  2. K.J.M • 5/M • Pampanga • Chief complaint: Headache

  3. 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

  4. 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

  5. Review of systems • (+) vomiting (-)cough • (- ) colds (-) fever • ( -) headache (-) LBM • (-) seizure (-) changes in sensorium • (+) good appetite (+) good activity

  6. Past Medical History • (-) BA • (-) PTB • (-) allergies • (+) previous hospitalization • April 2008- underwent Ommaya insertion in PGH

  7. 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

  8. Nutritional History • Breastfed at birth up to 1 year • Started on complementary feeding at 6 months • Presently eats regular table food

  9. 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

  10. Immunization History • Completed Epi

  11. Personal social history • Third of 4 children, mother is 35 yrs old while father is a 38 yr old jeepney driver

  12. 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 • Anictericsclerae, 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

  13. Neurologic exam • GCS-15 • Pupils 2 mm ERTL • Intact EOMs • (-) facial asymmetry • (+) intact gross hearing • (+) gag • (+) tongue midline

  14. MMT- gr 5/5 all extremities • Sensory- intact • (+) Babinski

  15. Admitting Impression • Suprasellar mass secondary to craniopharyngioma with obstructive hydrocephalus • S/P endoscopic guided ommaya shunt insertion- 4/2008 • Hypothyroidism, Hypocortisolism • Central DI, resolved

  16. 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

  17. 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

  18. 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

  19. Case Discussion

  20. Diabetes Insipidus • Presents with polyuria and polydipsia • central DI- result from vasopressin deficiency • nephrogenic DI- vasopressin insensitivity at the level of the kidney

  21. 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

  22. 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

  23. 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.

  24. 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.

  25. 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.

  26. 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.

  27. 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.

  28. 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.

  29. 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.

  30. 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%.

  31. 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.

  32. 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.

  33. 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.

  34. 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%.

  35. INPUT/OUTPUT

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