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Complications of Diabetes Insipidus: THE SIGNIFICANCE OF A HEADACHE!

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Complications of Diabetes Insipidus: The Significance of Headache

Mary Jane Hudson, MSN, RN

 

Pediatr Nurs. 2007;33(1):58-59. ?2007 Jannetti Publications, Inc.Posted 05/14/2007spacer.gif

Introduction and Medical History

 

Introduction

Travis was a 10-year-old with panhypopituitarism and recent resection of a craniopharyngioma. One week after discharge, his parents telephoned to report that Travis was complaining of neck and back pain. They were instructed to bring Travis to the hospital immediately. Upon arrival in the Pediatric Clinic, blood was drawn for laboratory tests and intravenous access was obtained. When sodium levels were reported as 181, Travis was admitted to the Pediatric Intensive Care Unit (PICU).

 

 

Medical History

Travis was a healthy young boy until recently when he started complaining of headaches. He was diagnosed with panhypopituitarism and craniopharyngioma. Subsequently, Travis underwent surgical resection of the tumor. Fluctuating sodium levels complicated his immediate postoperative hospital course. Travis had developed diabetes insipidus following the removal of his craniopharyngioma, resulting in extremely high and fluctuating postoperative sodium levels. During his initial postoperative hospital stay, Travis' sodium levels gradually were controlled with intravenous fluids and desmopressin. After his sodium levels were stabilized within normal limits, Travis was discharged on oral desmopressin. Once home, Travis was relatively immobile, gained weight, and spent most of his time in bed and only occasionally left his room or his house.

 

 

Assessment Findings

Travis arrived in the PICU complaining of neck and back pain. The following initial assessment findings were noted:

 

Vital Signs: Temp ? 39.5oC, HR ? 212, RR ? 72, BP ? 119/65 (89), O2 sat ? 96% on room air, Weight ? 27.6 kg.

 

Neurological: Lethargic, oriented, PERRL.

 

Pain: Acute, constant, aching pain in neck, back and extremities; pain rating of 10/10 on numeric scale.

 

Respiratory: Tachypneic, symmetrical, clear, irregular, labored, grunting, 1-liter oxygen via nasal cannula.

 

Cardiovascular: Sinus tachycardia, pulses present, generalized edema, capillary refill sluggish.

 

Musculoskeletal: Spontaneous but limited movement of all extremities due to pain.

 

Gastrointestinal: Abdomen soft & distended; active bowel sounds, adipsia, no hunger.

 

Genitourinary: Clear, pale yellow, polyuria, and specific gravity 1.005.

 

Integumentary: Warm, pale.

 

 

Management Plan

A peripheral intravenous line was initiated and intravenous normal saline was started in the Pediatric Clinic. Pain medication was administered and Travis was placed on 1 liter of oxygen via nasal cannula before transfer to the PICU. Upon arrival in the PICU, his initial chemistry laboratory values were reported as follows: glucose 175, sodium 181, potassium 4.7, chloride 145, carbon dioxide 18, blood urea nitrogen 30, creatinine 1, calcium 9.8, albumin 5.3, Alk 137, Alt 134. The initial complete blood count (CBC) results were: WBC 9.3, RBC 3.09, Hgb 7.5, Hct 25.3 and Plt 315.

 

A second peripheral intravenous line of D51/2 NS was initiated. Initiation of an arterial line was attempted without success. Blood cultures were drawn and cerebrospinal fluid analysis from lumbar puncture (LP) was performed. Travis was sent for a computed tomography (CT) scan and magnetic resonance imaging (MRI). What do you think is causing Travis to decompensate and have neck and back pain?

 

 

Continuing Medical Management

The blood cultures and LP were negative but the MRI showed a sagittal sinus thrombosis. A heparin drip was initiated after a bolus was administered and Travis remained on a heparin drip with several rate adjustments. Several hours after admission to the PICU, the laboratory reported a serum osmolality of 392. At that time, a diagnosis of recurrent or worsened central diabetes insipidus was made. The therapeutic plan was to slowly lower his sodium level while maintaining an appropriate fluid balance. Repeated sodium levels fluctuated between 159 and 178, but by the following day with continuous isotonic intravenous therapy, gradually decreased to the 140 range.

 

Over the next several days, Travis became less lethargic and vocalized hunger. His back and neck pain were greatly decreased and he reported pain scores of 0 to 3/10. Travis' heart rate and respiratory rate also began to slowly decrease. He was eventually transferred to an acute care unit and discharged to home after 2 weeks of close monitoring and treatment.

 

 

Pathophysiology

Sodium is the main extracellular ion that regulates the osmotic pressure in the cells and body fluids. Water and sodium interact to control intravascular volume. Water balance usually determines the concentration of sodium and sodium acts as a buffer to prevent an excessive loss of water from the tissues. Hypernatremia is defined as an elevation in the concentration of serum sodium above 145 mEq/L and is always indicative of dehydration. Signs and symptoms of hypernatremia include irritability, restlessness, weakness, lethargy, fever, hyperglycemia, headache, and seizures. Hypernatremia has also been associated with adipsia in 50% of patients with hypothalamic tumors. Thirst, however, usually prevents severe hypernatremia unless water intake is restricted or water resorption is reduced (Behrman, Kleigman, & Jenson, 2004; Workeneh, Balakumaran, Bichet & Mitch, 2004).

 

Hypernatremic dehydration can develop in patients with central diabetes insipidus when the patient does not drink adequately. An elevated osmolality (> 295) normally causes the secretion of antidiuretic hormone (ADH). Diabetes insipidus (DI) is an ADH deficiency disorder of the hypothalamus. The hypothalamus, which is responsible for regulating water balance, secretes ADH that is subsequently released from the pituitary gland into the bloodstream. ADH tells the body to conserve the right amount of water to prevent dehydration.

 

Causes of deficient amounts of ADH secretion include: (a) a malfunctioning hypothalamus or pituitary gland, ( B) damage to the hypothalamus or pituitary gland during surgery, ? endocrine and metabolic disorders, (d) brain injury, (e) tumor, (f) tuberculosis, and (g) meningitis. Disturbances and disorders of the hypothalamus result in insufficient secretion of ADH. If too little ADH is secreted, fluid and electrolyte imbalance occurs, resulting in water not being reabsorbed, and in excessive, dilute urine production, sodium retention and dehydration (Makaryus & McFarlane, 2006; Robertson, 2003; The Diabetes Insipidus Foundation, 2003).

 

Dehydration is a decrease in the extracellular fluid volume that results in electrolyte imbalance. Signs of dehydration include increased temperature, tachycardia, tachypnea and lethargy. The type of dehydration is determined by the serum sodium concentration. Hypernatremic dehydration is the most devastating type of dehydration because it can result in severe neurological damage from hemorrhage. Normally, an increased osmolality results in water conservation. This does not occur in central DI due to a malfunctioning hypothalamus. In hypernatremic dehydration, extracellular osmolality increases and water moves out of the brain cells. This movement of water causes brain cells to shrink and the blood vessels tear as the brain is pulled away from the skull and the meninges. The tearing of blood vessels results in hemorrhaging and potential for thrombus formation (Behrman et al., 2004).

 

The torn blood vessels are repaired as the platelets migrate and stick to the injured cells to form a thrombin plug. The thrombin plug is converted to a fibrinous deposit on the cell to stop the hemorrhaging. Thrombus formation is greatly affected by the stasis or turbulence of blood flow. With sluggish blood flow, more platelets stick and additional fibrin is deposited to create congestion and edema in the obstructed vessel. The obstructed, fibrin-filled blood vessels constrict blood flow and subsequently cause pain at the site and distal to the site of the thrombus (Kumar, Abbas, & Fausto, 2005).

 

The combination of surgical manipulation of the hypothalamus, physical inactivity, and hypernatremic dehydration with central diabetes insipidus are major factors in thrombus formation. After the hypothalmus is surgically manipulated, management includes closely monitoring body water and electrolyte balance as well as a medication regimen. In diabetes insipidus, hypernatremic dehydration can develop as the result of an inadequately monitored therapeutic regimen. In Travis' case, his postoperative diabetes insipdius was inadequately monitored and his physical inactivity together with restricted fluid intake resulted in inadequate resorption of water, impaired blood circulation and sagittal sinus thrombus formation as a complication of his hypernatremic dehydration.

 

 

Family Matters

Travis was the product of a term delivery without prenatal complications. Travis lived with his mother, father, older brother and younger sister. His parents were very involved in his care and have been physically and emotionally drained since Travis was diagnosed with craniopharyngioma. Travis was a child who required constant emotional support and relied heavily on his mother to provide reassurance and tend to all of his needs. He was a very emotionally fragile child who communicated his needs by mumbling through tears.

 

 

The Rest of the Story

During this PICU admission, Travis' hypernatremia was resolved with intravenous hydration and desmopressin. Travis was discharged on enoxaparin (Lovanox) via insuflon catheter. His parents were instructed on the use and care of the insuflon catheter. Other discharge instructions included weekly checks of his enoxaparin and sodium levels as well as drinking at least four 12-ounce glasses of fluid per day.

 

Home nursing visits were ordered to assess Travis' progress and evaluate his home regimen. Goals of the home nursing care included: 1) changing insuflon catheter once a week, 2) instructing Travis and his family about his medications, diet and fluid intake, and safety factors related to diabetes insipidus and the potential complications of dehydration, and 3) assessing vital signs and evaluating management of Travis' disease process. Since Travis had been immobile since his surgery, physical therapy was ordered to facilitate ambulation and improve his joint and muscle strength. Over the past several months, Travis has been stable. He has been constantly and closely monitored by endocrinology and has maintained his sodium level within normal range.

 

 

The Lesson Learned

Manipulation of the hypothalamus for removal of a tumor results in 90% neuron death that eventually leads to permanent central diabetes insipidus in 70% to 90% of patients during the postoperative period (Behrman et al., 2004;Ghirardello, Hopper, Albanese, & Maghnie, 2006). Early recognition and management of the child with diabetes insipidus demands extremely close monitoring of fluid and electrolyte balance to prevent the complications associated with hypernatremia and dehydration. Nurses need to be attuned to the subtle changes in electrolytes and water balance in patients diagnosed with hypothalamic disorders. An inadequately monitored therapeutic regimen of patients with diabetes insipidus can quickly lead to complications of hypernatremic dehydration and thrombus formation.

 

 

References

  1. Behrman, R., Kliegman, R., & Jenson, H. (2004). Nelson textbook of pediatrics (17th edition) (pp. 193 ? 199, 245 ? 249, 1650, 1656, 1853 ? 1855, 2036 ? 2037). Philadelphia: Saunders, An Imprint of Elsevier.
  2. Ghirardello, S., Hopper, N., Albanese, A., & Maghnie, M. (2006). Diabetes insipidus in craniopharyngioma: Postoperative management of water and electrolyte disorders. Journal of Pediatric Endocrinology, 19(Suppl. 1), 413 ? 421.
  3. Kumar, V., Abbas, A., Fausto, N. (2005). Robbins and Cotran: Pathologic basis of disease (7th edition) (pp. 124-125). Philadelphia: Saunders, An Imprint of Elsevier.
  4. Makaryus, A., & McFarlane, S. (2006). Diabetes insipidus: Diagnosis and treatment of a complex disease. Cleveland Clinic Journal of Medicine, 73 (1), 65 ? 71.
  5. Robertson, G. (2003). What is diabetes insipidus? Retrieved on July 5, 2006 from http://www.diabetesinsipidus.org/whatisdi.htm.
  6. The Diabetes Insipidus Foundation, Inc. (2003). Polyuria and polydipsia: Think of diabetes insipidus (DI) - not just diabetes mellitus. Retrieved on June 30, 2006 from http://www.diabetesinsipidus.org/polydipsia_polyuria.htm.
  7. Workeneh, B., Balakumaran, A., Bichet, D., & Mitch, W. (2004). The dilemma of diagnosing the cause of hypernatraemia: Drinking habits vs diabetes insipidus. Nephrology Dialysis Transplantation, 19 (12), 3165 ? 3167.

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Mary Jane Hudson, MSN, RN, Clinician IV University of Virginia Health Science Center Charlottesville, VA

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Great article!! Good Job!

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Thanks Robin,

 

I had severe DI for 5 days after my first surgery, but not so bad after the second. I did however tell my husband that this is the worst I have felt since being in the hospital. I told him if I do not feel better by tomorrow that I want to go to the ER to get this checked. I have been feeling a lot like I did with the DI. The headache, body aches, cotton mouth, uncontrollable thirst, fatigue, and going to the bathroom a lot.

 

You are always so helpful. We really do appreciate you.

 

Thanks again.

 

PennyL

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