英文ppt精品课件medicalgrandrounds on diabetes

MEDICAL GRANDROUNDS ON DIABETES INSIPIDUS Desiree B. Yano-Simbulan, M.D. Maricel B. Peniero, M.D. November 8, 2007 LEARNING OBJECTIVES l To present a case of a 50 year old female with diabetes insipidus l To provide an overview in the diagnostic approach to polyuria and diabetes insipidus l To discuss nephrogenic versus central diabetes insipidus: etiology, clinical manifestation, work up and management IDENTIFYING DATA l A.G. l 50y/o female l Filipino l cc: epigastric pain HISTORY OF PRESENT ILLNESS 2 weeks PTA (+)epigastric pain (+)bloatedness (+)loss of appetite (-) nausea, vomiting (-)changes in bowel habit EGD: Gastritis Gastric polyp Few days PTA (+)persistence of symptoms A REVIEW OF SYSTEMS l No fever l No blurring of vision, no visual loss l No throat pain, tinnitus, no hearing loss l No dyspnea, no cough, no hemoptysis l No chest pain, no palpitation, no orthopnea l (+) polydipsia (+) polyphagia (+) nocturia l (+) right hip pain (+) low back pain l No skin rash or skin changes PAST MEDICAL HISTORY l Invasive Ductal Carcinoma, Left Breast s/p Modified Radical Mastectomy,left breast 2003 s/p Chemotherapy 2003, 2004 s/p Radiotherapy, 2006 l Hypertension, 2004 Atenolol (Therabloc) 50mg 1/2tab OD Imidapril (Vascor) 5mg OD l Diabetes Mellitus, 2000 Acarbose (Glucobay) 50mg OD Repaglinide (Novonorm) 0.5mg OD l s/p laparoscopic cholecystectomy, 2004 FAMILY HISTORY l (+) Breast cancer 2 cousins l (+) Diabetes Mellitus mother, brother PERSONAL/SOCIAL HISTORY l non smoker l non alcoholic beverage drinker l no history of substance abuse l worked as a general accountant PHYSICAL EXAMINATION Gen. Survey: Awake, alert not in cardiorespiratory distress Vital Statistics: Ht:157cm Wt:58kgs BMI: 23 Vital Signs: BP:110/70 CR:95 RR:20 To:36.6 Skin: warm, moist, no rash HEENT: pink palpebral conjunctivae, anicteric sclerae, supple neck, no tonsillopharyngeal congestion, no neck vein distention, JVP = 10cm Chest: symmetrical chest expansion, (-) intercostal retraction (-) rales (-) wheezes (+) 10cm well healed incisional scar left chest Cardiac: Adynamic Precordium, regular S1S2, apex beat at 5th LICS MCL, (-) murmur (-) thrill Abdomen: Globular, NABS, (-) bruits, normo-tympanic, (+)epigastric tenderness (-) organomegaly Extremities: (-)edema (-) cyanosis, full and equal pulses PHYSICAL EXAMINATION ADMITTING DIAGNOSIS l Gastritis, Gastric polyp s/p EGD l Hypertensive Cardiovascular Disease II l Diabetes Mellitus Type II l Invasive Ductal Carcinoma, Left Breast, 2003 s/p MRM, left breast s/p chemotherapy s/p radiotherapy COURSE IN THE WARDS 1st HOSPITAL DAY l Diagnostics CBC Spec 16 CT of chest and abdomen l Endocrine Referral for blood sugar control CBG monitoring (initial CBG= 243mgs%) FBS (207mgs%), HbA1c (9.6%) Acarbose (Glucobay) 50mg TID Glimepiride (Solosa) 2mg OD CBC Hg 13.3 Hct 38.8 WBC 8400 Seg 74 Lymp 19 Eo 2 Mono 5 Plt 214 Urinalysis Color yellow Transparency clear pH acidic Specific Gravity 1.020 (1.015- 1.025) Sugar (-) Protein (-) Ketones (-) Nitrites (-) Leucocyte Esterases +1 Blood (-) RBC 0.1 WBC 2.5 Epithelial cells 0.2 Bacteria 82 Mucus Threads (-) Crystals (-) Cast (-) SPEC 16 (done as OPD) Na 131 K 2.9 CL 94 CALC 12.1 ALK.P 300 UA 8.0 ALB 3.3 UREA 8.0 CREA 1.1 RBS 426 Corrected Na 136 Corrected Ca 12.6 (CBG-100) x0.016 +Na (4-albumin) x0.8 +Ca l K = 2.9 KCL incorporation (30meqsKCL +PNSS1L x10h) Repeat K 5.0 (n.v. 3.5-5.1) l Ca = 12.6 ionized Ca (1.66mmol/L) (n.v. 1.12-1.32) phosphorus(3.7mgs%) (n.v. 2.3-4.7) intact PTH (1.637pg/ml) (n.v. 10-65) 3rd Hospital Day NEPHROLOGY referral for electrolyte management l Ca = 12.0 ( 12.1) Hydration with PNSS at 200cc/h x 4hours, then back to 120cc/h Diuresis with Lasix 20mg IV q8 Serial electrolyte monitoring Accurate I/O monitoring 4th Hospital Day lCa = 12.2 12.0 after Lasix and PNSS Impression Hypercalcemia of Malignancy Plan Ibandronic Acid (6mg in PNSS500cc x1hr) Lasix discontinued Continue hydration, PNSS 1Lx120cc/h CT Scan of Chest and Abdomen l Multiple osseous lytic lesions in the thoracolumbar spine, likely metastatic l Minimal bilateral pleural effusion with parenchymal consolidation in the right lower lobe, atelectasis vs pneumonia l No interval change in size of subcm nodule in lingula l Mediastinal, right hilar and right axillary lymphadenopathy showing significant increase in size since september 27, 2006 l Heterogeneous enhancement with slight nodularity of the right breast tissue. l Post mastectomy, left 4th Hospital Day lMedical Oncology Referral Impression Breast Ca IV, bone and lung metastases with inflammatory breast changes, right breast Plan For repeat chemotherapy 4th Hospital Day lPain Management Referral for right hip pain, low back pain Paracetamol/Tramadol (Dolcet) 1 tab TID Gabapentin 100mg BID Fentanyl 25mcg IV Fentanyl PCA 5th Hospital Day luncontrolled Hyperglycemia (CBG =406mgs%) OHA discontinued Insulin drip Hourly CBG monitoring K monitoring ( K = 3.3) KCL incorporation 6th Hospital Day Bone Scan Foci of increased radioactivity situated in several areas of the body, namely: frontal, parietal, and occipital regions of the skull, both shoulder regions, both scapulae, both humerii, sternum, all levels of the thoracic and lumbosacral spine, both sides of the pelvis, both femora, both tibia, and multiple rib segments bilaterally. Above findings are not demonstrated in the previous study done in October 2006 Impression: Findings are compatible with Osseous Metastases lZoledronic acid (Zometa) 4mg in D5W100cc x20min lAllopurinol 300mg OD 8th HOSPITAL DAY MRI of the Cervical and Thoracic Spine Extensive bone metastases involving the cervical and thoracic spine with compression deformities of T2 and T6 vertebral bodies. No evidence of spinal canal metastasis Extensive mediastinal lymphadenopathy lDexamethasone 5mg IV q 6hr RTC lNexium 40mg IV OD 10th Hospital Day lRadiation Oncology Referral for spinal cord compression For radiation therapy 900 cGy to upper thoracic spines, 10 sessions over 2 weeks 12th Hospital Day lPolyuria (Urine output 8.8/L) Na (155) Urine Osmolality (120 mosm/kg) (n.v.301-1093) Plasma Osmolality (326 mosm/kg) (n.v.275-295) Increase oral fluid intake Increased hydration with D5W 1L x100cc/h 150cc/h, later shifted to 0.3% NSS 1L x 150cc/h Urinalysis Color yellow Transparency hazy pH neutral Specific Gravity 1.010 (1.015- 1.025) Sugar +2 Protein trace Ketones (-) Nitrites (-) Leucocyte Esterases +1 Blood (-) RBC 0.2 WBC 6.6 Epithelial cells 1.3 Bacteria 291 Mucus Threads (-) Crystals (-) Cast (-) Osmolar Clearance vs Free Water Clearance Solute H20 urine Osmolar Clearance (Cosm) = Uosm x V - Posm Uosm = 120 Posm = 326 Vol = 8.8L Cosm = 120 x 8.8 326 Cosm = 3.23L Urine vol =8.8L 3.3L (Osm) 5.5L (H20) Conclusion lPolyuria is secondary to water diuresis l Polyuria secondary to water diuresis Nephrogenic DI (? hypercalcemia) vs Central DI (? metastasis) l Trial of DESMOPRESSIN (0.2mcg 1/2tab BID) Effect on urine volume and osmolality After the trial of Desmopressin l Urine Volume 100% 8.8L 4.6L l Urine Osmolality 100% 120 423 Conclusion : CENTRAL Diabetes Insipidus WITHDRAWAL OF DESMOPRESSIN Urine OSMOLALITY: 423 213 Urine VolumeUrine Osmolality Input and Output Monitoring 16th HOSPITAL DAY Brain MRI Nodules in the pineal region and hypothalamus with thickening of the pituitary stalk. Enhancing nodules in the left parieto occipital area, head of the right caudate nucleus, left basal ganglia, left cerebellar hemisphere. Leptomeningeal thickening and enhancement, left temporal area. Enhancing bone foci in both frontoparietal and left temporal bones. Above findings considered metastases Clinical Outcome lDischarged stable on the 24th hospital day POLYURIA AND DIABETES INSIPIDUS POLYURIA lPolyuria can be arbitrarily defined as a urine output exceeding 3 L/day in adults and 2 L/m2 in children lCauses Primary polydipsia Central Diabetes Insipidus Nephrogenic Diabetes Insipidus Diagnostic Approach to Polyuria l Onset of polyuria l Family history l Plasma Na concentration Na 142 meq/L, due to water loss, points toward DI l Water restriction test l Plasma ADH measurement Water Restriction Test Solute Diuresis l Glucosuria l High-protein feedings l Volume expansion due to saline loading l Differentiated from diabetes insipidus Water diuresis Uosm 300 mosmol/kg Total solute excretion markedly increased Central Diabetes Insipidus l Decreased release of ADH l Lack of ADH can be caused by disorders that act at one or more of the sites involved in ADH secretion: hypothalamic osmoreceptors supraoptic or paraventricular nuclei superior portion of the supraopticohypophyseal tract Etiology of central diabetes insipidus l Idiopathic l Neurosurgery a. Craniopharyngioma b. Transphenoidal surgery l Head trauma l Hypoxic or ischemic encephalopathy a. Cardiopulmonary arrest b. Shock c. Sheehan syndrome l Neoplastic a. Primary : craniopharyngioma, cyst, pinealoma b. Metastatic : breast, lung l Miscellaneous Review of Literature SYSTEMIC CANCER PRESENTING AS DIABETES INSIPIDUS - Clinical and radiographic features of 11 patients with a review of metastatic-induced diabetes insipidus “of 100 consecutive cases of DI of any cause, diabetes insipidus was the initial presentation in 11 patients with systemic cancer. In these 11 patients, the most common sources metastatic to the posterior pituitary-hypothalamic region were lung, breast, leukemia and lymphoma. CT scanning demonstrated pituitary stalk enlargement, suprasellar masses, or both” Kimmel D.W., ONeill B.P., Systemic cancer presenting as diabetes insipidus. Clinical and radiographic features of 11 patients with a review of metastatic-induced diabetes insipidus. Cancer 1983 Dec 15;52(12):2355-8. Review of Literature PITUITARY METASTASIS IN BREAST CARCINOMA “ the incidence of metastasis to pituitary in breast cancer is reported as 0.95%. Breast cancer and lung cancer are the most common primary sites, in women and men respectively, which metastasize to the pituitary. The presenting symptoms include diabetes insipidus, anterior pituitary insufficiency and retro-orbital pain. Metastases to the posterior lobe are more common than to the anterior lobe.” Rao SR, Rao RS, Pituitary metastases in carcinoma breast. Shushrusha Hospital, Mumbai, India. JPGM 2001 Volume 47 Issue2 Page 135-6 Drug therapy of central diabetes insipidus l ADH preparations a. Desmopressin nasal spray b. Aqueous vasopressin c. Lysine vasopressin nasal spray d. Vasopressin tannate in oil l Drugs that potentiate ADH effect a. Chlorpropamide b. Carbamazepine c. NSAIDS l Drugs that increase ADH secretion a. Clofibrate l Drugs not requiring ADH b. Thiazide diuretics Nephrogenic Diabetes Insipidus l Decrease in urinary concentrating ability that results from ADH resistance l Resistance at the ADH site of action in the collecting tubules, or interference with the countercurrent mechanism due to medullary injury or to decreased sodium chloride reabsorption in the medullary aspect of the thick ascending limb of the loop of Henle Etiology of nephrogenic diabetes insipidus l Congenital ( mutations in AVPR2 gene and aquaporin-2 gene l Hypercalcemia l Hypokalemia l Drugs a. Lithium b. Demeclocycline c. Streptozotocin l Pregnancy l Acute and chronic renal failure Drug therapy of nephrogenic diabetes insipidus lLow sodium, low protein diet lThiazide diuretic lAmiloride, K sparing diuretic lNSAIDS * Thank you! Xeloda (Capecitabine) 150mg, 500mg lAntimetabolite lPyrimidine analog lInhibits DNA, RNA synthesis lRenal dose adjustment lCrCl 30-50 : decr start dose 25% lCrCl 30 : contraindicated Serial Electrolyte Monitoring d0 d2 d4 d5 d7 d9 d10 d12 am d12 pm d13 am d13p m Na 131 136 142 140 155 153 160 158 K 2.9 5.0 3.3 3.9 3.2 3.2 3.2 3.4 3.2 CL 94 Calc 12.1 12.0 12.2 9.3 8.6 7.1 Alb 3.3 Urea 8.0 15