Diabetes Mellitus, Diabetes Insipidus and Diabetic Ketoacidosis in Children

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Text of Diabetes Mellitus, Diabetes Insipidus and Diabetic Ketoacidosis in Children

Clinical Performance of a Fully Implanted Long Term Glucose Sensor (LTGS)

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Basic Science LectureMa. Giselle G. Genovata, MD3rd Year Pedia ResidentMedical Center ParanaqueDiabetes InsipidusDiabetes MellitusDiabetic Ketoacidosisa. the passage of large volumes (>4ml/kg/hr) of dilute urine (< 300 mOsm/kg).c. A common chronic metabolic syndrome characterized as hyperglycemia as a cardinal biochemical featureb. A combination of hyperglycemia, acidosis and ketonesGist Definitions

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Diabetes InsipidusDiabetes Insipidus (DI) a heterogeneous clinical syndrome of disturbance in water balance, characterized by polyuria (urine output > 4 ml/kg/hr), polydypsia (water intake > 2 L/m2/d) and failure to thrive.

CENTRAL DIABETES INSIPIDUSVassopresin deficiencyNEPHROGENIC DIABETES INSIPIDUSVassopresin insensitivity at the level of the kidney

both central and nephrogenic DI can be hereditary, or secondary to variety of causesSource: Nelsons Textbook of Pediatrics 19th Ed.DI presents clinically with plyuria and polydipsia and may result from either vasopressin deficiency (central DI) or vasopressin insensitivity at the level of the kidney (nephrogenic DI). They can both rise from inherited defects with congenital or neonatal onset or secondary to variety of causesNelson's Textbook of Pediatrics 19th Edition

Regulation of VP secretion and Serum Osmolality

This table represents the regulation of vasopressin secretion and serum osmolality. *Hyperosmolality, hypovolemia and hypotension are sensed by *osmosensors, volume sensors and barosensors. These stimulate vasopressin secretion and thirst. Vasopressin acts on the kidney to increase water reabsorption (antidiuresis). Thirst causes increased water ingestion. The results of this negative feedback loop causes reduction in hyperosmolaloty or hypotension/hypovolemia. Additiional stimuli for vp secretion includes nausea, hypoglycemia and pain. Nelson's Textbook of Pediatrics 19th EditionCauses of Diabetes Insipidus

Central diabetes insipidus can result from multiple etiologies, including genetic mutations in the vasopressin gene; trauma (accidental or surgical) to vasopressin neurons; congenital malformations of the hypothalamus or pituitary; neoplasms; infiltrative, autoimmune, and infectious diseases affecting vasopressin neurons or fiber tracts; and increased metabolism of vasopressin. In approximately 10% of children with central DI, the etiology is idiopathic. Other pituitary hormone deficiencies may be present Nephrogenic (vasopressin-insensitive) DI (NDI) can result from genetic or acquired causes. Genetic causes are less common but more severe than acquired forms of NDI. The polyuria and polydipsia associated with genetic NDI usually presents within the first several weeks of life, but may only become apparent after weaning or with longer periods of nighttime sleep. Many infants initially present with fever, vomiting, and dehydration. Failure to thrive may be secondary to the ingestion of large amounts of water resulting in calorie malnutrition. Long-standing ingestion and excretion of large volumes of water may lead to nonobstructive hydronephrosis, hydroureter, and megabladder.Acquired nephrogenic DI may result from hypercalcemia or hypokalemia and is associated with the following drugs: lithium, demeclocycline, foscarnet, clozapine, amphotericin, methicillin, and rifampin. Impaired renal concentrating ability can also be seen with ureteral obstruction, chronic renal failure, polycystic kidney disease, medullary cystic disease, Sjgren syndrome, and sickle cell disease. Decreased protein or sodium intake or excessive water intake, as in primary polydipsia, can lead to diminished tonicity of the renal medullary interstitium and nephrogenic DINelson's Textbook of Pediatrics 19th Edition Clinical Presentation of DI

Establishment of pathologic polyuria or polydipsia (exceeding 2L/m2/24hr)Careful history must be obtainedNon specific features Poor suck, failure to thrive, irritabilityEarliest signs include vigorous suck w/ vomiting, fever w/o apparent cause, constipation, excessively wet diapersIn older infants and children, they can be irritableNocturiaSigns of dehydration on PE

The cause of pathologic polyuria or polydipsia (exceeding 2 L/ m2/24 hr) may be difficult to establish in children.Carefully quantify the intake and urine output of patient (ask for nocturia, secondary enuresis)Diagnosis of diabetes insipidus (DI) may be difficult in infants and children because of nonspecific presenting features (eg, poor feeding, failure to thrive, irritability). Accordingly, a high index of suspicion is necessary.The earliest signs of DI include a vigorous suck with vomiting, fever without apparent cause, constipation, and excessively wet diapers from urination. In older infants and young children, irritability is generally due to a borderline state of dehydration coupled with hypernatremia and, sometimes, fever. Nocturia is common and expected because of increased urine production. Central DI tends to develop suddenly

The typical examination reveals an irritable infant with a dripping wet diaper, along with detectable signs of dehydration (eg, dry mucous membranes, diminished skin turgor, decreased tearing, tachycardia). Often, skin turgor is not diminished in individuals with hypernatremic dehydration despite significant dehydration. In severely dehydrated patients, the pulse may be thready and rapid. Hypotension may be present because of hypovolemic shock. Mobile fecaliths may be palpable in the abdomenNelson's Textbook of Pediatrics 19th Edition Complications of DIGrowth failureNocturia and enuresisHypernatremic dehydrationSeizuresMental retardation

Dehydrationresults from an inability to reabsorb free water at a site distal to electrolyte reabsorption. Any patient unable to continuously replace water loss is vulnerable to dehydration, especially in warm weather when insensible water loss through perspiration and respiration substantially increases risk.Electrolyte abnormalities are caused by the loss of urinary free water, which produces hyperosmolar dehydration, leading to hypernatremia, hyperchloremia, and prerenal azotemia. Diminished blood volume increases blood viscosity and the risk of sludging and thrombosis.Failure to thriveoccurs because of the patients constant thirst conferring a sense of fullness that offsets the sense of hunger. The affected individual eats less than necessary for normal growth.Seizures are a consequence of the electrolyte abnormalities introduced in the central nervous system (CNS) by severe hypernatremia and hyperosmolar dehydration. Mental retardation results from the damage to the CNS caused by severe hyperosmolarity, seizures, and potential hypoxia, all of which are thought to account for the frequent occurrence of mental retardation. Death can occur from a hypovolemic shock or a hypernatremic seizure.

Nelson's Textbook of Pediatrics 19th Edition Approach to Patient with Suspected DIThe diagnosis of DI is established if:the serum osmolality is greater than 300 mOsm/kg (if 600, it is unlikely)

If pathologic polyuria or polydipsia is present, the following should be obtained: 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 the patient's 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. Nelson's Textbook of Pediatrics 19th Edition Water Deprivation Test: How it is done? (Step 1)Should be done in the morning under observation8 hours fasting enough for childrenWeigh the child hourly and measure plasma and urine osmolality q2 hoursWATER DEPRIVATION TEST IS NEEDED FOR PATIENTS WITH PARTIAL AVP DEFICIENCY & ALSO TO DIFFERENTIATE DI FROM PRIMARY POLYDIPSIA WHICH IS VERY RARE IN CHILDRENSHOULD BE DONE IN THE MORNING UNDER OBSERVATION8 HOURS FAST IS ENOUGH FOR CHILDRENWEIGH THE CHILD HOURLY AND MEASURE PLASMA & URINE OSMOLALITY EVERY 2 HOURSIN NORMAL SUBJECTS PLASMA OSMOLALITY HARDLY RISES (< 300) BUT THE URINE OUTPUT IS REDUCED & ITS OSMOLALITY RISES (800-1200)

Nelson's Textbook of Pediatrics 19th Edition Water Deprivation Test: Initial Interpretation(Step 2)WATER DEPRIVATION TEST IS NEEDED FOR PATIENTS WITH PARTIAL AVP DEFICIENCY & ALSO TO DIFFERENTIATE DI FROM PRIMARY POLYDIPSIA WHICH IS VERY RARE IN CHILDRENSHOULD BE DONE IN THE MORNING UNDER OBSERVATION8 HOURS FAST IS ENOUGH FOR CHILDRENWEIGH THE CHILD HOURLY AND MEASURE PLASMA & URINE OSMOLALITY EVERY 2 HOURSIN NORMAL SUBJECTS PLASMA OSMOLALITY HARDLY RISES (< 300) BUT THE URINE OUTPUT IS REDUCED & ITS OSMOLALITY RISES (800-1200)

Nelson's Textbook of Pediatrics 19th Edition Water Deprivation Test: The VP challenge test (Step 3)At the end of the test, ADH is given (20mg DDAVP intranasally or 2mg IM) then fluid intake was allowedConcentration of dilute urine confirms central DI and failure suggest nephrogenic causesWATER DEPRIVATION TEST IS NEEDED FOR PATIENTS WITH PARTIAL AVP DEFICIENCY & ALSO TO DIFFERENTIATE DI FROM PRIMARY POLYDIPSIA WHICH IS VERY RARE IN CHILDRENSHOULD BE DONE IN THE MORNING UNDER OBSERVATION8 HOURS FAST IS ENOUGH FOR CHILDRENWEIGH THE CHILD HOURLY AND MEASURE PLASMA & URINE OSMOLALITY EVERY 2 HOURSIN NORMAL SUBJECTS PLASMA OSMOLALITY HARDLY RISES (< 300) BUT THE URINE OUTPUT IS REDUCED & ITS OSMOLALI

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