Special Considerations for Intensive Care Management of Pediatric Patients With Cancer

Central Diabetes Insipidus

CDI can occur in more than 50% of patients after transsphenoidal surgery (TSS) to resect intrasellar or suprasellar tumors. The diagnosis of CDI is made on the basis of both clinical and biochemical findings. Polyuria (>4 mL/kg/h of urine output) and polydipsia, in combination with increased serum osmolality (>300 mOsm/L) and decreased urine osmolality with a urine/plasma osmolality ratio <1, is the hallmark of CDI in the postoperative period. Patients with an intact thirst mechanism and free access to oral fluids may not develop symptoms or hypernatremia. However, patients who are unable to maintain normal plasma osmolality and serum sodium levels need immediate intervention or they will develop symptoms of CDI, such as acute dehydration, nausea and vomiting, and alterations in mental status.

Monitoring of CDI includes following hourly urine output, hourly fluid intake, as well as measurements of serum and urine osmolality, serum electrolytes, and blood glucose levels every 6–8 h in the immediate postoperative period.

For patients who show laboratory and/or clinical evidence of CDI, management will depend on the patients’ thirst mechanism and access to oral fluids. For patients without an intact thirst mechanism or without free access to oral fluids, supplemental intravenous (IV) fluids are necessary. Institutional guidelines are very helpful in these circumstances, as a multidisciplinary approach to monitoring and treatment is warranted for consistency. A reasonable approach to IV fluids with either normal saline or ½ normal saline with dextrose at one-third of maintenance needs or 400 mL/m ² /h, plus urine output replacement mL:mL with ½ normal saline or other balanced solution. If this fluid replacement method of CDI treatment is not successful, an alternative approach is to administer oral 1-desamino-8- d -arginine vasopressin (DDAVP) or vasopressin infusion for the hormonal replacement of endogenous vasopressin, which is often due to transient direct surgical injury or localized edema at the site of surgery. The course of CDI most typically lasts up to 48 h from the immediate postoperative period ^{, ,} but may undergo what is termed a triphasic pattern of immediate postoperative CDI, followed by a period of SIADH for 5–7 days, followed once again by CDI, which may persist after discharge. ^, This triphasic pattern persists in more than 3% of patients undergoing TSS, and approximately 1% of patients experience the biphasic pattern of immediate postoperative CDI followed by SIADH. ^,

Syndrome of Inappropriate Antidiuretic Hormone

SIADH can occur in the immediate postoperative phase following TSS, either in isolation or as part of the triphasic pattern discussed earlier. SIADH occurs in isolation following TSS in up to 20% of patients. ^, The mechanism is likely the uncontrolled release of ADH from either degenerating posterior pituitary or from magnocellular neurons with damaged axons. With this release of ADH, urine output decreases, and the patient remains in either a euvolemic or hypervolemic state with a subsequent drop in serum osmolality <270 mOsm/L. The most important therapeutic intervention is fluid restriction and cessation of IV fluids, as soon as the patient is able to drink. Sodium replacement is only required for prolonged SIADH or in cases of severe hyponatremia. Symptoms of severe hyponatremia from SIADH include visual changes, focal neurologic changes, respiratory depression, and seizures. These symptoms are consistent with cerebral edema and can be treated carefully with hypertonic saline until symptoms resolve. ^,

Cerebral Salt Wasting

Cerebral salt wasting (CSW), characterized by polyuria and natriuresis, occurs in about 4% of children following neurosurgery. CSW is thought to be due to a tubular defect in sodium transport, leading to extracellular volume depletion. CSW and SIADH can be present in both surgical and nonsurgical settings. Making a distinction between the two is important, as the treatment of CSW is different from that of SIADH. The treatment of CSW involves water and sodium repletion. The fundamental difference between these two syndromes is the presence of polyuria, which leads to dehydration in CSW. Replacement of both free water and sodium is therefore necessary because of the significant urine sodium losses and high urine output. ^, Depending on the severity, sodium replacement needs can be met with oral sodium, or CSW may require aggressive fluid and sodium replacement in the PICU with central venous pressure monitoring of intravascular volume status. In severe CSW, the mineralocorticoid fludrocortisone may be used, although CSW typically resolves within a month of onset.