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You may need to add more. - replace hypophosphatemia by using Kphos for 1/2of potassium replacement - example fluids: NS + 20 mEq KCl/L + 20 mEq Kphos/L 4. Correct metabolic acidosis by interrupting ketone production - begin with continuous insulin drip 0.05- 0.1 units/kg/hr IV - start with lower dose and titrate to achieve glucose drop no more than 50-100 mg/dL/hour - monitor blood glucose q1-2 hours Æ when glucose reaches 250-300 mg/dL add D5 to fluids, change to D10 (try to increase dextrose in IVF’s to keep blood sugar 200-300 rather than decreasing rate of insulin drip until acidosis is corrected) - monitor venous blood gas and electrolytes q2-4 hours until out of DKA - monitor urine for ketones and glucose with each void - when acidosis resolved (HCO3 >18), pt tolerating PO and mental status normal consider switching to SQ insulin = 0.5-1.0 unit/kg/day 2/3 total dose in am (1/3 Regular, 2/3 NPH) 1/3 total dose in pm (1/2 Regular at dinner, 1/2 NPH at bedtime) 5. Assess for and treat any underlying causes for DKA (e.g. infection) 6. Closely monitor for and treat any complications of DKA Complications: 1. Cerebral edema- the leading cause of mortality; occurs in 1-2% of children with DKA; risk factors include rapid shifts in osmolality, excessive fluid administration, use of hypotonic fluid; symptoms include declining/fluctuating mental status, symptoms of increased intracranial pressure such as dilated or unequal pupils, Cushing’s triad. Treatment: Mannitol, consider intubation, mechanical ventilation 2. Cardiac arrhythmia- due to electrolyte disturbance (hypo/hyperkalemia) - 12 - 3. Fluid overload 4. Hypoglycemia Reference: White, Heil. Diabetic Ketoacidosis in Children. Endocrinology and Metab Clinics 29(4): December 2000. Diabetes Insipidus: Definition: 1. Absence of or inability to respond to argentine vasopressin (AVP) 2. Polydipsia, polyuria with dilute urine, hypernatremia and dehydration 3. Polyuria exceeding 5cc/kg/hr, specific gravity < 1.010 4. Serum sodium > 145mmol/L 5. Central DI Æ vasopressin deficiency 6. Nephrogenic DI Æ renotubular resistance to vasopressin Pathophysiology:
1. The secretion of antidiuretic hormone, argentine vasopressin, occurs from the posterior pituitary gland in response to changes in serum osmolality and is regulated by the paraventricular & supraoptic nuclei AVP acts at the cortical collecting ducts in the kidney and binds to the vasopressin2 receptor 2. Binding initiates a G protein/cAMP signaling cascade leading to the insertion of aquaporin protein in the cortical tubular cells allowing water to enter the cell 3. A deficiency of vasopressin is caused by destruction of the posterior pituitary gland by tumors or trauma 4. Nephrogenic diabetes arises from end-organ resistance to vasopressin, either from a receptor defect or medications that interfere with aquaporin transport of water Epidemiology: 1. Incidence of diabetes insipidus in the general population is 3 in 100,000 slightly higher incidence in males (60%) 2. Central diabetes insipidus: - approximately 29% cases are idiopathic (isolated or familial) 50% of childhood cases are due to primary brain tumors of the hypophyseal fossa - up to 16% of childhood cases result from Histiocytosis X - 2% of childhood cases are due to postinfectious complications and another 2% result from head trauma - inherited forms of central DI may be autosomal dominant (usu. present >1year of life) or autosomal recessive (present <1 year) 3. Nephrogenic DI: - may be x-linked recessive, autosomal dominant or recessive and usually presents <1 week of life - acquired forms of nephrogenic DI may be secondary to medications (lithium, amphotericin, cisplatin, lasix, gentamicin, rifampin, vinblastine), electrolyte disorders (hypokalemia, hypercalcemia or hypercalciuria) or due to systemic disorders (Fanconi Syndrome, diffuse renal injury, obstructive uropathy, RTA, sarcoidosis, Sjogren syndrome, Sickle cell disease and trait) Evaluation: 1. Clinical history: poor feeding, failure to thrive, irritability, soaking of diapers in infants; polyuria, polydipsia, nocturia, large volume of water; growth retardation, seizures 2. Physical examination: irritability, signs of dehydration (decreased tearing, depressed fontanelle, sunken eyes, mottled or poor skin turgor), signs of shock (hypotension, weak pulses) 3. Laboratory tests: - hypernatremia >145 mmol/L, (>180 in nephrogenic DI) - hyperchloremia, azotemia, acidosis, high osmolarity - low urinary sodium and chloride, osmols - urine specific gravity < 1.010 (first morning void) - 24 hour hure collection- usu. > 5cc/kg/hour 4. Diagnostic tests: - water deprivation test (perform only w/close monitoring and involvement of endocrine team) - a rise in plasma osmolality >10mOsm/kg over baseline with specific gravity remaining <1.0101 establishes diagnosis of DI to differentiate types, administer DDAVP; if urine osmolality rises by more than 450 mOsm/kg, central DI is established; if urine osmols remain <200 mOsm/kg, nephrogenic DI is the likely diagnosis 5. Imaging: consider MRI scan to delineate cause of central diabetes insipidus (suprasellar mass/ pituitary cyst/ hypoplasia/ ectopic gland, etc) Differential Diagnosis:
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