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Accurate patient history contributes to differentiating diabetes insipidus: a case study.

Abstract: This case study highlights the important contribution of nursing in obtaining an accurate health history. The case discussed herein initially appeared to be neurogenic diabetes insipidus (DI) secondary to a traumatic brain injury. The nursing staff, by reviewing the patient's health history with his family, discovered a history of polydipsia and long-standing lithium use. Lithium is implicated in drug-induced nephrogenic DI, and because the patient had not received lithium since being admitted to the hospital, his treatment changed to focus on nephrogenic DL By combining information from the patient history, the physical examination, and radiologic and laboratory studies, the critical care team demonstrated that the patient had been self-treating his lithium-induced nephrogenic DI and developed neurogenic DI secondary to brain trauma. Thus successful treatment required that nephrogenic and neurogenic DI be treated concomitantly.



Obtaining an accurate health history can often provide the clinician with crucial clues to improving patient care management. This was the case when RJ was transferred to the neuro critical care unit (NCCU) with a diagnosis of diabetes insipidus (DI) after falling from a moving vehicle. RJ, a 73-year-old white male trauma patient, was admitted to the emergency department (ED). Records indicated that he had fallen from a moving pickup truck and had a witnessed seizure in the ambulance. He arrived at the ED intubated and sedated with bilateral wrist restraints and a cervical collar in place. His Glasgow Coma Scale (GCS) score was 7, indicating a moderate head injury. A brain computed tomography (CT) scan in the ED confirmed the diagnosis of a closed head injury.

RJ was admitted to the surgical intensive care unit (SICU) at 2:30 am and was successfully extubated to supplemental oxygen (4 I/min via nasal cannula) at 1 pm. His GCS score after extubation was 15 per chart documentation. However, the chart indicated that he was confused, difficult to arouse and oriented to name only, which would imply a GCS of 12 at best (eye = 4, verbal = 3, motor = 5). As his sedation wore off, his agitation and combativeness increased, requiring four-point restraints. Serial chemistries showed a serum sodium level that had risen to 163 mmol/L, serum osmolality of 353 mOs/kg, and urine output ranging from 150 to 890 ml/hr. The decision was made to begin a continuous infusion of intravenous (IV) vasopressin to combat neurogenic diabetes insipidus (DI), presumably resulting from his closed head injury. He received a 7-ml/hr infusion of 5 units of vasopressin added to 1000 ml 0.9% sodium chloride (NaCl). Additional measures included hourly fluid replacement with 0.9% NaCl at a rate of 1 ml/hr for each 1 ml of urine output. By 8 am the next day his sodium levels had risen to 166 mmol/L, and the decision was made to transfer him to the NCCU. A stat CT scan, obtained just prior to transfer, showed no further increase in injury or edema.

At 11:15 am on day 2, RJ was transferred to the NCCU unit. Although a brief history had been obtained upon admission, a more complete history was obtained from the patient's family upon arrival in the NCCU as well as a comprehensive neurological assessment. His neurological assessment showed his GCS to be 14 (oriented to name only, following commands and opening eyes spontaneously). Cranial nerves II-XII were intact except for unequal pupils; his right pupil was 4 mm and the left pupil was 3 mm; both were round and reactive to light. He had periods during which he was calm and relaxed interspersed with periods of acute confusion, agitation, and combativeness. His sodium level upon admission to the NCCU was 170 mmol/L.

The health history obtained by the NCCU admitting nurse was different than that documented by the SICU staff nurse. This more complete health history became an essential factor in determining complete diagnoses and a plan of care for RJ. He had not fallen out of a moving vehicle; he had stumbled backwards while attempting to remove an object from the bed of a pickup truck. Catching his heel, he had stumbled backwards and struck his head against a brick wall. He then slid to the ground, landing on his buttocks, and became unconscious. His son, who witnessed the event, was immediately at his side and activated the 911 emergency system. RJ had a 30-year history of manic depression for which he was taking lithium; this was not given during his hospital stay. Additional history revealed that RJ drank copious amounts of water and had occasional episodes of incontinence at night. His fluid intake pattern included taking a thermos of water to bed each night. His family also reported several previous episodes of falling and near-falling.

With this additional historical perspective, we began to question the diagnosis of DI secondary to closed head injury. Diabetes insipidus is most commonly a diagnosis of inclusion. Typically practitioners look at three elements to make a diagnosis of DI: urine outputs of greater than 300 ml/hr, urine specific gravity of less than 1.003, and a serum sodium concentration of greater than 155 mmol/L (Williams & Wilson, 1998).

This more complete health history and understanding of neurogenic DI led the NCCU nurse practitioner to increase the vasopressin infusion to a rate of 40 ml/hr. Serum sodium levels were ordered q2h. Over the next 16 hours RJ's sodium continued to rise, eventually reaching 172 mmol/L. An endocrinology consult was obtained, and after learning of the history of lithium use, the consult recommended the administration of large amounts of free water fluid replacement (D5W) and concurred with stopping lithium therapy.


Diabetes insipidus is characterized by the excretion of a large volume (usually greater than 4 L/day) of hypotonic, insipid (tasteless) urine, usually accompanied by polyuria and polydipsia (Williams & Wilson, 1998). Serum sodium levels are elevated, and urine sodium as well as urine osmolarity levels are below normal. Urine specific gravity approaches 1.000 as the kidneys lose the ability to concentrate urine. There are five types of DI:

* Neurogenic (also called central), which occurs most commonly with changes to the brain structure through injury, tumor, or invasion involving the pituitary gland resulting in decreased levels of antidiuretic hormone (ADH). It is characterized by polyuria, polydipsia and increased serum sodium and potassium levels.

* Nephrogenic, which is caused by a decreased ability of the kidneys to respond to antidiuretic hormone (ADH). Typically, diagnosis of nephrogenic DI is made after the administration of a test dose of vasopressin administered intravenously fails to result in an increase in urine sodium, urine osmolarity, and urine specific gravity.

* Dipsogenic, which is caused by an injury to the hypothalamus directly. Dipsogenic DI occurs when changes in the hypothalamus cause ADH to be suppressed and urine output to increase in the setting of an abnormal increase in thirst and water intake.

* Gestational, which occurs only during pregnancy and is caused by an enzyme secreted from the placenta that interferes with the mother's ADH.

* Idiopathic, a condition in which the cause of DI is unknown. Idiopathic DI is made as a diagnosis of exclusion when it is not possible to infer that the cause is neurogenic, nephrogenic, dipsogenic, or gestational.

Lithium is the most common cause of drug-induced nephrogenic diabetes insipidus. As many as 10%-20% of patients receiving chronic lithium therapy may develop nephrogenic DI. Lithium is known to interfere with the production of cAMP (Bendz, Sjodin, & Aurell, 1996; Christensen, Kusano, Yusufi, Murayama, & Dousa, 1985). The defect is both of aquaporin-2 on the luminal surface of the collecting duct and of aquaporin-3 on the basal lateral membrane, producing a severe defect in aquaporin production that parallels the lithium-induced polyuria (Marples, Christensen, Christensen, Ottosen, & Nielsen, 1995). There is as much as a 95% decrease in aquaporin-2 content, and even the 5% of aquaporin-2 that persists is not normally transported to the collecting duct membrane (Marples et al.).


Intravenous D5W was started and the vasopressin drip was stopped per renal consult recommendation to treat the lithium-induced nephrogenic DI. The primary treatment for nephrogenic DI is cessation of any causative agent and free water replacement, the administration of thiazide diuretics, and the administration of chlorpropamide, which may increase ADH release (Litwack, 1998). RJ's lithium had already been discontinued. A psychiatric consult was obtained, and the decision was made to postpone the addition of any antidepressants to his current drug regime pending further evaluation. Unfortunately, the DI symptoms worsened and vasopressin was resumed as 5-mg subcutaneous injections every 6 hours. A vasopressin level obtained 2 hours after the first subcutaneous vasopressin dose confirmed that RJ was also experiencing neurogenic DI. The primary treatment for neurogenic DI is the administration of hormonal replacements either intravenous or subcutaneous aqueous pitressin, nasal vasopressin, or desmopressin acetate (DDAVP) (Litwack, 1998). RJ was started on subcutaneous aqueous pitressin. Over the next 48 hours, his sodium levels normalized, and the patient's cognitive ability continued to improve.

Determining an accurate history of events helped us to develop an appropriate plan of care. The initial diagnosis of a closed head injury sustained as the result of falling from moving vehicle was found to be only partially accurate, and ultimately misleading. The subsequent development of DI was initially presumed to be neurogenic in origin. Throughout the past 30 years, RJ had steadily increased his water intake, effectively self-treating his lithium-induced nephrogenic DI. Discovering the history of lithium use and polydipsia changed the primary diagnosis from neurogenic DI to nephrogenic DI. Ultimately it was not until we realized that RJ's DI was both nephrogenic and neurogenic in origin that we were able to develop an effective treatment strategy. After 6 days in the NCCU, RJ was transferred to the step-down unit for further care, where the aqueous pitressin was discontinued.


Obtaining a full and accurate medical history upon admission is essential. RJ's history of lithium use was noted, but there was no recording of his polydipsia or polyuria, which would have linked his lithium use to nephrogenic DI. Also missing from his admission history was an accurate account of his trauma. A more thorough history, in this case, could have led the medical team to seek earlier alternative explanations for RJ's symptoms and avoid the pitfall of assuming that his DI symptoms could be explained entirely from his closed head injury. Without the combined teamwork and communication of the neuroscience staff nurses, nurse practitioner, and medical attending, an accurate diagnosis would likely have been delayed. This case study is a clear example of the valuable contribution that nursing and the nursing history play in the care of neurologically compromised patients.


This study was supported by T32 NR07091, "Interventions to Prevent and Manage Chronic Illness."


Bendz, H., Sjodin, I., & Aurell, M. (1996). Renal function on and off lithium in patients treated with lithium for 15 years or more. A controlled, prospective lithium-withdrawal study. Nephrology Dialysis Transplantation, 11(3), 457-460.

Christensen, S., Kusano, E., Yusufi, A. N., Murayama, N., & Dousa, T. P. (1985). Pathogenesis of nephrogenic diabetes insipidus due to chronic administration of lithium in rats. Journal of Clinical Investigation, 75(6), 1869-1879.

Litwack, K. (1998). The endocrine system. In J. Alspach (Ed.), American Association of Critical Care Nurses core curriculum for critical care nursing (5th ed., pp. 565-600). Philadelphia: Saunders.

Marples, D., Christensen, S., Christensen, E.I., Ottosen, P.D., & Nielsen, S. (1995). Lithium-induced downregulation of aquaporin-2 water channel expression in rat kidney medulla. Journal of Clinical Investigation, 95(4), 1838-1845.

Williams, R.H., & Wilson, J.D. (1998). Williams textbook of endocrinology (9th ed.). Philadelphia: Saunders.

Questions or comments about this article may be directed to DaiWai M. Olson, BSN RN CCRN, by phone at 919/681-4241 or by e-mail at He is a clinical nurse TV at Duke University Hospital North, Durham, NC.

LorieAnn G. Meek, RN CCRN, is a clinical nurse IV at Duke University Hospital North.

John R. Lynch, MD, is an associate professor of neurology at Duke University School of Medicine, Durham, NC.
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Author:Olson, DaiWai M.; Meek, LorieAnn G.; Lynch, John R.
Publication:Journal of Neuroscience Nursing
Date:Aug 1, 2004
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