 k.j.m  5/m  pampanga  chief complaint: headache

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Slide 2 K.J.M 5/M Pampanga Chief complaint: Headache Slide 3 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 Slide 4 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 Slide 5 (+) vomiting (-)cough (- ) colds (-) fever ( -) headache (-) LBM (-) seizure (-) changes in sensorium (+) good appetite (+) good activity Slide 6 (-) BA (-) PTB (-) allergies (+) previous hospitalization April 2008- underwent Ommaya insertion in PGH Slide 7 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 Slide 8 Breastfed at birth up to 1 year Started on complementary feeding at 6 months Presently eats regular table food Slide 9 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 Slide 10 Completed Epi Slide 11 Third of 4 children, mother is 35 yrs old while father is a 38 yr old jeepney driver Slide 12 Conscious, coherent, not in distress BP- 100/60 CR- 84/min RR- 20 T- 37.1C 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 Slide 13 GCS-15 Pupils 2 mm ERTL Intact EOMs (-) facial asymmetry (+) intact gross hearing (+) gag (+) tongue midline Slide 14 MMT- gr 5/5 all extremities Sensory- intact (+) Babinski Slide 15 Suprasellar mass secondary to craniopharyngioma with obstructive hydrocephalus S/P endoscopic guided ommaya shunt insertion- 4/2008 Hypothyroidism, Hypocortisolism Central DI, resolved Slide 16 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 1 st 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 Slide 17 3 rd HD- Na was noted to be 146, minirin 0.1 mg/tab, tab was given as stat dose UO- 770 ml after minirin Slide 18 8 th HD- minirin started 0.1 mg/tab, tab at bedtime 9 th 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 Slide 19 Slide 20 Presents with polyuria and polydipsia central DI- result from vasopressin deficiency nephrogenic DI- vasopressin insensitivity at the level of the kidney Slide 21 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 1248 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 Slide 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 Slide 23 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. Slide 24 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. Slide 25 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. Slide 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. Slide 27 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 individuals endogenous release of ADH. Slide 28 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. Slide 29 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. Slide 30 Interpretation: Normal subjects and primary polydipsia: Urine osms are greater than plasma Osms after water restriction. Urine osms increase minimally (