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Diabetes Insipidus Nursing Diagnosis and Nursing Care Plan

Last updated on December 31st, 2022 at 11:49 am

Diabetes Insipidus Nursing Care Plans Diagnosis and Interventions

Diabetes insipidus is a disorder that causes fluid imbalances in the body, which can lead the patient to have polyuria, large amounts of urine, and polydipsia, which makes them feel very thirsty despite drinking fluids.

A healthy adult usually produces about 1 to 2 liters of urine a day. However, an adult who has severe diabetes insipidus may produce up to 20 liters of urine in 24 hours or may pass urine more than 7 times in a day.

Because of its distinctive signs and symptoms, strict input and output monitoring and accurate fluid management are both required for patients with this uncommon disorder. Diabetes insipidus is believed to be caused by a hormone imbalance of the antidiuretic hormone (ADH), also known as vasopressin or AVP.

Diabetes insipidus is not related to diabetes mellitus, as it does not involve a disturbance in the blood glucose levels compared to the latter.

Signs and Symptoms of Diabetes Insipidus

The following are the signs and symptoms of diabetes insipidus:

  • Polydipsia – feeling of extreme thirst despite drinking the usual amounts of fluids
  • Polyuria  – passing urine in large amounts and usually pale in color
  • Nocturia  – increased urinary frequency at night
  • Preference for cold drinks

In infants or young children, the following signs and symptoms of diabetes insipidus may be observed:

  • Bed-wetting
  • Heavy, wet diapers
  • Trouble  sleeping
  • Weight loss
  • Delayed growth
  • Constipation

Causes of Diabetes Insipidus

The fluid part of the blood called plasma is filtered by the kidneys to take away the waste products. After the filtering process, the hormone vasopressin or anti-diuretic hormone (ADH) helps the filtered plasma to return to the bloodstream.

ADH is produced in the hypothalamus and is stored in a small gland called the pituitary gland of the brain. Any deficiency of ADH or blockage of its effect causes an increase in the production of excess urine. Problems with ADH levels can cause imbalances in the fluid levels of the body.

Types of Diabetes Insipidus

There are two main types of diabetes insipidus: central and nephrogenic. The other two rare types include gestational diabetes insipidus and dipsogenic or primary polydipsia. In some cases, the cause could be an autoimmune response that results in unwanted damage to the vasopressin-making cells.

  • Central diabetes insipidus . The normal process of producing, storing, and releasing ADH can be affected by any damage to the hypothalamus or the pituitary gland. Conditions such as brain tumors or malignancy, brain infections, head injuries, or even surgery can cause this type of diabetes insipidus. Rarely, the disease can also result from a genetic disorder inherited from the person’s parents.
  • Nephrogenic diabetes insipidus . This type of diabetes insipidus is caused by any defect in the parts of the kidneys. When the kidney structures are damaged, the organ will not be able to respond appropriately to ADH. This will result in polyuria and nocturia. The damage can be caused by a chronic or long-term kidney disorder, a genetic disease, and/or the use of certain medications such as some antivirals and the drug lithium.
  • Gestational diabetes insipidus. A rare disorder during pregnancy, gestational diabetes insipidus happens when ADH is destroyed by a placenta-produced enzyme.
  • Dipsogenic diabetes insipidus . Also called primary polydipsia, this type of diabetes insipidus involves damage to the mechanism that regulates thirst in the hypothalamus. Recent studies relate it to some mental health disorders, such as schizophrenia. It causes the patient to drink very large amounts of fluids and pass huge amounts of diluted, pale urine.

Risk Factors for Diabetes Insipidus

The following are risk factors for the development of diabetes insipidus:

  • Genetics . The disease can be hereditary and can develop at birth or shortly after being born. There could be permanent changes in the structures of the kidneys, disabling the baby to concentrate urine.
  • Sex. Males are usually affected by nephrogenic diabetes insipidus. However, women may pass the gene to their kids.

Complications of Diabetes Insipidus

  • Dehydration. Diabetes insipidus may result in dehydration if left untreated. A dehydrated patient may have increased fatigue, thirst, dryness of the mouth, and poor skin elasticity or skin turgor.
  • Electrolyte imbalance. Diabetes insipidus can affect the balance of the electrolytes, particularly serum sodium and potassium, which are the two main electrolytes involved in fluid balance. An imbalance of these electrolytes can result in muscular weakness and cramps, acute confusion, loss of appetite, nausea, and/or vomiting.

Diagnosis of Diabetes Insipidus

  • Water deprivation test. In this exam, the patient will be subjected to oral fluid cessation for a few hours. The nurse should measure the changes in the urine output, body weight, and concentration of blood and urine while the body is deprived of water and other fluids. The test aims to check if the body’s production of ADH is adequate and to assess the response of the kidneys to ADH. The physician may order the administration of synthetic ADH during the water deprivation test.
  • Magnetic resonance imaging (MRI). To check for any abnormalities in the pituitary gland, an MRI of the head may be ordered. An MRI can help see detailed images of the brain tissues in and around the pituitary gland through the non-invasive method of using radio waves in a magnetic field.
  • Genetic testing. The doctor may order a genetic screening procedure if the patient’s family members also suffer from excessive urine production or polyuria.

Treatment for Diabetes Insipidus

The type of diabetes insipidus determines the treatment required, which may include the following:

  • Central diabetes insipidus. The physician may prescribe a synthetic replacement for ADH called desmopressin, which can help reduce urination. It is usually available in tablet form, but can also be given by injection or as a nasal spray. The drug may result in unwanted water retention and hyponatremia or low sodium levels if taken too much, so the amount of desmopressin may vary depending on the ADH level in the body. Another type of medication is one that can help increase the availability of ADH in the body.
  • Nephrogenic diabetes insipidus. This type of D.I. is usually treated with a low-sodium diet to facilitate the reduction of urine that is produced by the kidneys. The doctor may prescribe a diuretic called hydrochlorothiazide to improve polyuria. The patient will also be encouraged to drink adequate amounts of water daily. Desmopressin will not be helpful in this type of D.I.
  • Gestational diabetes insipidus. Synthetic hormone desmopressin is usually the treatment of choice in pregnant women with D.I.
  • Dipsogenic diabetes insipidus. The physician will instruct the patient to decrease oral fluid intake. As this type of D.I. can be strongly related to an underlying mental health condition, treating the specific mental health disorder may have a positive effect on primary polydipsia.
  • Lifestyle changes. The patient will be instructed to take measures to prevent dehydration and electrolyte imbalance, which are the two most common complications of diabetes insipidus. The patient should carry water wherever they go and must never stop the prescribed medication abruptly or on their own. It is also recommended to carry a medical alert card in their wallet or wear a medical alert bracelet which can help if the patient has a medical emergency.

Nursing Diagnosis for Diabetes Insipidus

Diabetes insipidus nursing care plan 1.

Deficient Knowledge

Nursing Diagnosis: Deficient Knowledge related to lack of understanding of the condition and its treatment regimen and unfamiliarity with the complications secondary to diabetes insipidus as evidenced by asking numerous questions and verbal expression of misconceptions about the illness

Desired Outcome: The patient will verbally express their complete comprehension of diabetes insipidus and the medications used in the treatment.

Diabetes Insipidus Nursing Care Plan 2

Deficient Fluid Volume

Nursing Diagnosis: Deficient Fluid Volume related to endocrine regulatory mechanism dysfunction, hypophysectomy, impairment of the neuro-hypophyseal, and hypopituitarism secondary to diabetes insipidus as evidenced by polyuria, polydipsia, and rapid weight loss

Desired Outcome: The patient will have average fluid volume, as evidenced by the noticeable lack of thirst, a standard blood sodium level, and an unchanging weight.

Diabetes Insipidus Nursing Care Plan 3

Risk for Impaired Skin Integrity

Nursing Diagnosis: Risk for Impaired Skin Integrity related to urinary recurrence, large volume output, and the possibility of incontinence secondary to diabetes insipidus

Desired Outcome: The patient’s skin will be intact and remain undamaged.

Diabetes Insipidus Nursing Care Plan 4

Disturbed Sleep Pattern

Nursing Diagnosis: Disturbed Sleep Pattern related to an increase in urinary frequency and anxiety about the condition secondary to diabetes insipidus, as evidenced by discontentment with sleeping habits, waking up earlier or later than desired, general fatigue, and sleep disruption.

Desired Outcome: The patient will get an adequate amount of sleep, as demonstrated by a refreshed appearance, verbalization of feeling relaxed, and an improvement in sleeping habits.

Diabetes Insipidus Nursing Care Plan 5

Nursing Diagnosis: Nausea related to disparities in minerals in the blood, such as potassium and sodium (electrolytes), which preserve the body’s fluid equilibrium secondary to diabetes insipidus as evidenced by dizziness and lethargy.

Desired Outcome: The patient will report less severe or complete elimination of nausea.

Nursing References

Ackley, B. J., Ladwig, G. B., Makic, M. B., Martinez-Kratz, M. R., & Zanotti, M. (2020).  Nursing diagnoses handbook: An evidence-based guide to planning care . St. Louis, MO: Elsevier.  Buy on Amazon

Gulanick, M., & Myers, J. L. (2022).  Nursing care plans: Diagnoses, interventions, & outcomes . St. Louis, MO: Elsevier. Buy on Amazon

Ignatavicius, D. D., Workman, M. L., Rebar, C. R., & Heimgartner, N. M. (2020).  Medical-surgical nursing: Concepts for interprofessional collaborative care . St. Louis, MO: Elsevier.  Buy on Amazon

Silvestri, L. A. (2020).  Saunders comprehensive review for the NCLEX-RN examination . St. Louis, MO: Elsevier.  Buy on Amazon

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3 Diabetes Insipidus Nursing Care Plans

Diabetes Insipidus Nursing Care Plans and Nursing Diagnosis

Diabetes insipidus (DI) is a disorder in which there is an abnormal increase in urine output, fluid intake and often thirst. It causes symptoms such as urinary frequency, nocturia (frequent awakening at night to urinate) or enuresis (involuntary urination during sleep or “bedwetting”). Urine output is increased because it is not concentrated normally.

Table of Contents

1. deficient fluid volume, 2. risk for impaired skin integrity, 3. deficient knowledge.

Consequently, instead of being a yellow color, the urine is pale, colorless or watery in appearance and the measured concentration (osmolality or specific gravity) is low.

Nursing Care Plans

Here are three (3) nursing care plans for diabetes insipidus.

May be related to

  • Compromised endocrine regulatory mechanism
  • Neurophypophyseal dysfunction
  • Hypopituitarism
  • Hypophysectomy
  • Nephrogenic DI

Defining Characteristics

  • Output exceeds intake
  • Polydipsia (increased thirst)
  • Sudden weight loss
  • Urine specific gravity less than 1.005
  • Urine osmolality less than 300 mOsm/L
  • Hypernatremia
  • Altered mental status
  • Requests for cold or ice water

Desired outcomes

  • Patient experiences normal fluid volume as evidenced by absence of thirst, normal serum sodium level, and stable weight.

Risk factors

  • Urinary frequency with high volume output and the potential for incontinence

Desired outcome

  • Patient’s skin remains intact.
  • New condition
  • Unfamiliarity with the disease and treatment

Defining characteristics

  • Questioning
  • Requests for more information
  • Verbalization of misconceptions or misinterpretations
  • Patient verbalizes correct understanding of DI and the medications used in treatment

3 thoughts on “3 Diabetes Insipidus Nursing Care Plans”

I am a school nurse this was helpful. Thank you

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very informative. Thank you for the big help. May I please know what are your references? Thank you.

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A Case of Diabetes Insipidus

By David F. Dean (rr)

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A Case of Diabetes Insipidus

“Amanda Richards,” a 20-year-old junior in college, is majoring in biology and hopes to be a pediatrician one day. For about a month, she has been waking up frequently at night to go to the bathroom. Most recently, she has noticed that she needs to go to the bathroom during the day more often, almost hourly. Students read about these symptoms and then answer a set of directed questions designed to teach facts and principles of physiology using reference books, textbooks, the Internet, and each other as sources of information. The case has been used in a sophomore-level course in human anatomy and physiology as well as in senior-level course in general physiology.

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  • Learn about the similarities and dissimilarities between diabetes insipidus and diabetes mellitus.
  • Understand the basic differences between the four types of diabetes insipidus.
  • Be able to define and describe excessive thirst and urination in adults.
  • Understand the methods by which diabetes insipidus is diagnosed and treated.
  • Learn about other conditions which produce symptoms similar to those produced by diabetes insipidus.
  • Be able to describe the physiological effects of antidiuretic hormone other than the maintenance of body water balance.

Pituitary diabetes insipidus; diabetic; antidiuretic hormone; ADH; vasopressin; osmoreceptors; osmolarity; polyuria; polydipsia; supraoptic nuclei; kidney function

  

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Undergraduate lower division, Undergraduate upper division

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Endocrine Abstracts

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ICEECE2012 Poster Presentations Clinical case reports - Pituitary/Adrenal (58 abstracts)

Central diabetes insipidus: about two clinical cases

C. nogueira 1, , m. matos 1, , c. esteves 1, , g. jorge 1 , j. couto 2 , c. neves 1, , j. queirós 1 , e. vinha 1 , i. bernardes 1 & d. carvalho 1,.

1 Centro Hospitalar São João, Porto, Portugal; 2 Instituto Português de Oncologia, Porto, Portugal; 3 University of Porto, Porto, Portugal.

Introduction: Central diabetes insipidus (CDI) is produced by the destruction of the magnocellular neurons of the hypothalamic supraoptic and paraventricular nuclei which results in decreased arginine vasopressin (AVP) synthesis and secretion.

Case report 1: Forty-five year old female, previously healthy, was observed in April 2011 complaining of polydipsia, polyuria, nocturia and weight loss since January. Diabetes mellitus (DM) was excluded and she was admitted for study of possible diabetes insipidus. Water deprivation test was suggestive of CDI. Magnetic resonance imaging (MRI) showed infundibular hypophysitis and no hyperintense signal in the neurohypophysis. Autoimmune diseases, infections and infiltrative diseases were excluded. Imaging (chest x-ray, abdominal ultrasound, mammography, breast ultrasound and thoracoabdominal CT) was normal. No other pituitary deficits were shown. She started therapy with oral desmopressin with clinical improvement.

Case report 2: Fourty-three year old man, previously healthy, was seen in August 2011 complaining of polydipsia, polyuria and nocturia during the previous 3 months. DM was excluded. Water deprivation test was positive for CDI. Pituitary MRI was normal, with normal signal of high intensity in the neutohypophysis. He had no other hormonal deficits. Autoimmune and infectous diseases were excluded. After initiation of oral desmopressin the symptoms disappeared.

Discussion: In both cases it was not determined the etiology of CDI, as it may occur in 20–50% of CDI cases. In our institution is not possible to determine antibodies towards vasopressin secretory cells, which does not allow the diagnosis of this autoimmune form of CDI. The infundibular hypophysitis, observed in the first case, can occur in about 50% of idiopathic cases and more frequently in women. The lymphocytic hypophysitis can be diagnosed by pituitary biopsy, but it’s a very aggressive procedure and almost never performed. These cases highlight the difficulty of the etiologic diagnosis of CDI. However, proper treatment allows the symptoms control.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.

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Clinical Case Seminar

Central diabetes insipidus: a previously unreported side effect of temozolomide.

Temozolomide (TMZ) is an alkylating agent primarily used to treat tumors of the central nervous system. We describe 2 patients with apparent TMZ-induced central diabetes insipidus. Using our institution's Research Patient Database Registry, we identified 3 additional potential cases of TMZ-induced diabetes insipidus among a group of 1545 patients treated with TMZ.

Case Presentations:

A 53-year-old male with an oligoastrocytoma and a 38-year-old male with an oligodendroglioma each developed symptoms of polydipsia and polyuria approximately 2 months after the initiation of TMZ. Laboratory analyses demonstrated hypernatremia and urinary concentrating defects, consistent with the presence of diabetes insipidus, and the patients were successfully treated with desmopressin acetate. Desmopressin acetate was withdrawn after the discontinuation of TMZ, and diabetes insipidus did not recur. Magnetic resonance imaging of the pituitary and hypothalamus was unremarkable apart from the absence of a posterior pituitary bright spot in both of the cases. Anterior pituitary function tests were normal in both cases. Using the Research Patient Database Registry database, we identified the 2 index cases and 3 additional potential cases of diabetes insipidus for an estimated prevalence of 0.3% (5 cases of diabetes insipidus per 1545 patients prescribed TMZ).

Conclusions:

Central diabetes insipidus is a rare but reversible side effect of treatment with TMZ.

Temozolomide (TMZ) is an oral alkylating agent and an imidazotetrazine derivative of dacarbazine ( 1 ). TMZ is currently approved in the United States for treatment of glioblastoma multiforme and recurrent anaplastic astrocytoma. Off-label uses include the treatment of other tumors such as oligodendrogliomas, metastatic melanoma, nonpituitary neuroendocrine tumors, and aggressive pituitary neoplasms that are resistant to standard therapies ( 2 ). Treatment with TMZ is generally well tolerated. Common side effects include nausea/vomiting, headache, fatigue, and myelosuppression ( 3 , 4 ). In this paper we describe 2 cases of central diabetes insipidus that developed after TMZ initiation and resolved after discontinuation of TMZ. To search for other cases, we used our institution's Research Patient Database Registry (RPDR) to examine the records of patients treated with TMZ in several affiliated medical centers. In addition to the 2 index cases, 3 additional potential cases of TMZ-induced diabetes insipidus were identified. No prior report describes an association between diabetes insipidus with TMZ therapy.

A 53-year-old male initially presented with left-hand weakness and was found to have a 4.5-cm right posterior parietal lobe mass. He underwent a right parietal craniotomy and was diagnosed with a World Health Organization (WHO) grade II oligoastrocytoma. Surgery was followed by treatment with TMZ (150 mg daily). The patient developed new symptoms of polydipsia (approximately 5.5 L daily fluid intake) and polyuria/nocturia (urination of large volumes on an hourly basis during the day and nighttime) approximately 2 months after the initiation of TMZ. Laboratory tests obtained concurrently demonstrated hypernatremia and the presence of a urinary concentrating defect: serum sodium 151 mmol/L (normal 135–145 mmol/L), serum osmolality 319 mOsm/kg (normal: 280–296 mOsm/kg), and urine specific gravity 1.005. A modified overnight water deprivation test was also attempted, but it could not be completed. (The patient was instructed to avoid fluid intake overnight and have serum and urine laboratory tests performed in the morning. However, the patient consumed 1 L of fluid prior to the morning sample collection due to intense thirst.) Nonetheless, morning laboratory tests showed a serum sodium concentration of 149 mmol/L and a urine osmolality of 222 mOsm/kg.

Anterior pituitary function was assessed at the time of diagnosis and was normal ( Table 1 ). Treatment with twice-daily oral 1-desamino-8- D -arginine vasopressin acetate (DDAVP) (300 μg every morning and 400 μg every night) alleviated the patient's symptoms. Subsequent laboratory measures showed a serum sodium concentration of 145 mmol/L, serum osmolality 295 mOsm/kg, and urine osmolality of 508 mOsm/kg. TMZ was discontinued after 20 months of treatment due to durable tumor response/resolution, and additional antineoplastic treatment was not required. DDAVP was tapered off several months later, and polydipsia and polyuria did not recur. A modified overnight water deprivation test was repeated 4 weeks after DDAVP had been withdrawn. Laboratory tests on the following morning showed a serum sodium concentration of 140 mmol/L and a urine osmolality of 667 mOsm/kg. Whole-brain magnetic resonance imaging (MRI) scans performed before, during, and after TMZ treatment did not show any evidence of a mass lesion or infiltrative process in the pituitary or hypothalamus. The posterior pituitary bright spot was not visible before, during, or after development of diabetes insipidus. The patient did not receive any radiation therapy or additional chemotherapy for his malignancy before, during, or immediately after treatment with TMZ. Figure 1 illustrates a time line of the patient's biochemical test results. He has not experienced a recurrence of diabetes insipidus since discontinuation of TMZ. He has been followed by serial radiological imaging for approximately 6 years since completion of TMZ.

Anterior Pituitary Function Tests, Cases 1 and 2

Assay normal ranges are as follows: free T 4 (0.9–1.8 ng/mL); IGF-I (114–492 ng/mL); total T (270–1070 ng/dL); and prolactin (0–15 ng/mL).

An external file that holds a picture, illustration, etc.
Object name is zeg9991301590001.jpg

The development and resolution of diabetes insipidus in case 1. ♦ and □ denote serum sodium concentration and urine osmolality, respectively.

A 38-year-old male was treated with TMZ for a WHO grade II oligodendroglioma located in the left frontal lobe. The patient underwent 2 craniotomies 4 years and 2 months prior to treatment with TMZ, respectively. Two months after starting TMZ (140 mg daily), the patient began to note an increased sense of thirst and frequency of urination. He voided large volumes of urine on an hourly basis during the daytime and woke approximately 10 times per night to urinate and to drink liquids. He developed mild hypernatremia (serum sodium concentration 146 mmol/L).

Concurrent serum and urine laboratory measurements showed a serum sodium concentration of 143 mmol/L, serum osmolality of 302 mOsm/kg, and urine specific gravity of 1.006. An additional set of laboratory tests demonstrated a serum osmolality of 296 mOsm/kg with a concurrent urine osmolality of 196 mOsm/kg. Anterior pituitary function tests assessed at the time of diagnosis were normal ( Table 1 ). Intranasal DDAVP (10 μg once to twice daily) relieved the patient's symptoms. TMZ was stopped 6 months after DDAVP was started due to tumor regression/resolution. The total duration of treatment with TMZ was 9 months. DDAVP was withdrawn 2 months after TMZ was discontinued, and the patient did not experience recurrent polydipsia or polyuria. Laboratory studies obtained 2 weeks after cessation of DDAVP showed a serum sodium concentration of 139 mmol/L, and concurrent urine-specific gravity of 1.019. Whole-brain MRIs performed before and after TMZ treatment and a dedicated pituitary MRI during active diabetes insipidus did not show any evidence of a mass lesion or infiltrative process in the pituitary or hypothalamus ( Figure 2 ). The posterior pituitary bright spot was not visible before, during, or after development of diabetes insipidus. The patient has not had any tumor recurrence since the completion of TMZ treatment and has not required any additional antineoplastic therapy. He has been followed by serial radiologic imaging for approximately eight years since completion of TMZ. He has not experienced a recurrence of diabetes insipidus since discontinuation of TMZ.

An external file that holds a picture, illustration, etc.
Object name is zeg9991301590002.jpg

Postcontrast T1-weighted MRI sagittal images obtained from case 2 (A) prior to TMZ treatment and the development of diabetes insipidus, during TMZ treatment and active diabetes insipidus (B), and after TMZ was discontinued and diabetes insipidus had resolved (C).

Additional cases

The RPDR is an electronic data repository that compiles clinical and demographic data from patients in the Partners Healthcare system dating back to the early 1990s. The database contains records from more than 4.6 million patients and includes more than 1.2 billion clinical and demographic data entries. The registry may be searched using coded fields for medication prescriptions, medical diagnoses, laboratory parameters, radiological studies, interventional procedures, demographic details, vital signs, and certain examination findings. We queried patient records from the Massachusetts General Hospital, Brigham and Women's Hospital, and the Dana Farber Cancer Institute and identified 1545 patients (878 males and 667 females) treated with temozolomide.

We then performed a secondary query of these patients to identify individuals whose clinical records included a coded diagnosis of hypernatremia or diabetes insipidus or had received a prescription for desmopressin acetate or DDAVP. Forty-four of 1545 patients met these search criteria. The medical records of these 44 patients were thoroughly examined. Clinical histories and/or laboratory records were suggestive of possible TMZ-induced diabetes insipidus in 5 of these patients. Two of the 5 patients were the index cases 1 and 2 described above, and 3 additional potential cases were also identified. In most of the 39 excluded patients, individuals were diagnosed with hypernatremia in the days or weeks preceding their deaths, often in the context of alterations in mental status. Laboratory records indicate that these patients did not have urinary concentrating defects. A minority of the 39 patients were diagnosed with diabetes insipidus prior to treatment with TMZ (in the context of metastatic disease involving the pituitary and/or hypothalamus) or experienced transient diabetes insipidus after transsphenoidal surgery or a craniotomy.

A 45-year-old male received TMZ (140 mg daily) for treatment of a right frontal oligodendroglioma. Three months after the initiation of TMZ, he abruptly developed polydipsia and polyuria that was independent of fluid intake. Approximately 4 weeks later, TMZ was discontinued, and the patient began treatment with DDAVP by rhinal tube. DDAVP (10 μg once daily) successfully relieved his symptoms of polyuria and polydipsia. Shortly thereafter, the patient departed on a trip, but he did not remember to bring any DDAVP. He did not develop polydipsia and polyuria during his trip, and he had no further recurrence of these symptoms after his travels despite remaining off DDAVP. Serum and urine laboratory tests were not obtained prior to the initiation of DDAVP. Laboratory tests measured 3 months after discontinuation of DDAVP showed a serum sodium concentration of 144 mmol/L, serum osmolality 294 mOsm/kg, and a concurrent urine osmolality of 496 mOsm/kg. Whole-brain MRIs performed prior to TMZ therapy and 3 months after its conclusion did not show any evidence of a mass lesion or infiltrative process in the pituitary or hypothalamus. The patient did not receive any radiation therapy or additional chemotherapy before, during, or immediately after TMZ.

A 49-year-old male was treated with TMZ (280 mg daily for 7 days on alternate weeks separated by 7 days off treatment) for a clinically nonfunctioning pancreatic neuroendocrine tumor that had metastasized to the liver. Approximately 2 months after starting TMZ, the patient developed polydipsia and polyuria. He experienced persistent hypernatremia for approximately 1 month (serum sodium concentrations of 143–146 mmol/L, normal range of 136–142 mmol/L). Concurrent measurements of urine-specific gravity ranged from 1.003 to 1.006. (Serum osmolality and urine osmolality were not assessed.) The patient's serum creatinine rose from 1.2 to 1.6 mg/dL, and a fractional excretion of sodium was calculated to be 0.7%. The patient's polydipsia and polyuria spontaneously resolved after 2 months. TMZ was continued throughout this period of time and was terminated 13 months later. Prophylactic antibiotic therapy with trimethoprim/sulfamethoxazole was started approximately 2 weeks before the patient developed polyuria and polydipsia and acute renal insufficiency. The patient was given a presumptive diagnosis of acute interstitial nephritis. Laboratory evaluation did not show the presence of peripheral eosinophilia or urine eosinophils. The patient did not have any intracranial metastases or receive additional chemotherapy before or during treatment with TMZ. Whole-brain MRIs performed 1 year prior to TMZ treatment and 10 months after the resolution of polyuria and polydipsia did not reveal any mass lesion of infiltrative process involving the pituitary or hypothalamus.

A 44-year-old male received TMZ (150 mg daily) plus bevacizumab (10 mg/kg every 2 weeks) for treatment of an astrocytoma with gliomatosis cerebri. Serum sodium values and urinalyses were obtained on a biweekly basis during TMZ therapy. Three months after initiation of TMZ, laboratory measures demonstrated an increase in baseline serum sodium values from a range of 138–140 mmol/L to 142–145 mmol/L, and concurrent values of urine-specific gravity had decreased from 1.010–1.020 to less than 1.006–1.010. This probable urinary-concentrating defect reversed after approximately 6 weeks. Available records did not indicate whether the patient experienced symptoms of polydipsia or polyuria, but clinical notes did describe that he experienced new sleep difficulties during this period of time. Whole-brain MRI studies obtained before the initiation of TMZ, while the urinary concentrating defect was present, and 2 months after its resolution did not indicate the presence of a mass lesion or infiltrative process in the pituitary or hypothalamus. The patient did receive fractionated whole-brain irradiation (50.4 Gy, divided over 28 fractions) 6 months before starting TMZ.

We demonstrate for the first time that treatment with TMZ may be associated with the development of new central diabetes insipidus. In these cases, diabetes insipidus developed within 2–3 months after starting TMZ. Patients' symptoms and laboratory abnormalities corrected after treatment with DDAVP. Urinary concentrating defects eventually resolved in each of the cases. Reversal was documented within several months of TMZ cessation in 3 cases. In 2 potential cases of diabetes insipidus, spontaneous resolution occurred despite continuation of treatment with TMZ.

The precise mechanism for TMZ-induced diabetes insipidus is unclear. Posterior pituitary bright spots on MRI indicate the presence of antidiuretic hormone (ADH)-containing granules ( 5 , 6 ). This area of hyperintensity on T1-weighted images is absent in some normal individuals ( 7 ) and most patients with central diabetes insipidus ( 8 – 10 ). Posterior pituitary bright spots were not visible on precontrast T1-weighted images in cases 1 or 2 prior to treatment with TMZ, during active diabetes insipidus, or after TMZ had been discontinued (posterior pituitary bright spots also were not visible in the MRIs of cases 3, 4, and 5). TMZ may affect ADH production. Alternatively, TMZ might interfere with ADH storage and/or secretion from the neurohypophysis. An in vitro study demonstrated that treatment with TMZ causes actin depolymerization in human glioma cells ( 11 ). Filamentous actin regulates exocytosis in the neurons of the posterior pituitary, and disruption of the cytoskeleton may potentially impair intracellular transport of ADH to the axon terminal and hormone release ( 12 ). TMZ forms methyl adducts with purine bases ( 1 ). Potential modification of purinergic receptor signaling by TMZ and inhibition of protein kinase C activity may also affect ADH release ( 13 , 14 ).

Although standard TMZ dosing regimens typically consist of 5 days of treatment in every 28-day cycle, more intensive dosing strategies have also been studied ( 15 ). Four of the 5 patients described in this series received daily TMZ. One patient (case 4) was treated with daily TMZ on alternate weeks. It is unclear whether TMZ-induced diabetes insipidus occurs in patients receiving standard dosing regimens. Although approximately 43% of the 1545 patients treated with TMZ were female, all 5 cases of apparent TMZ-induced diabetes insipidus occurred in males. Due to the limited number of cases, however, we are unable to determine whether diabetes insipidus represents a gender-specific effect of TMZ.

Clinically significant diabetes insipidus appears to be a rare side effect of treatment with TMZ. If all 5 of the reported cases are included, the prevalence of diabetes insipidus was 0.3% in our survey of 1545 patients treated with TMZ. We postulate, however, that this figure likely underestimates the true prevalence of TMZ-induced diabetes insipidus in this population. Urinary incontinence and increased urinary frequency were reported in 8% and 6%, respectively, of patients with anaplastic astrocytoma treated with TMZ ( 16 ). It is possible that a portion of these adverse events represented undiagnosed cases of diabetes insipidus. We performed an additional query of the 1545 patients treated with TMZ using the following coded diagnoses: incontinence of urine, urinary frequency, polyuria, or polydipsia. Two hundred eight patients met these search criteria. One hundred sixty-four of these patients (approximately 11% of the original cohort of 1545 patients) did not receive a prescription for desmopressin acetate or DDAVP or have clinical records that included a coded diagnosis of hypernatremia or diabetes insipidus. Although we can not confirm the presence of a urinary concentrating defect in these individuals, it is possible that a portion of these cases represent undiagnosed or mild diabetes insipidus.

We were able to successfully identify several possible cases of diabetes insipidus by searching an electronic database registry. Nonetheless, patient record analyses in the RPDR are retrospective and are limited by factors that affect data entry, such as variability in diagnostic coding or the choice of clinical descriptors by medical providers. The RPDR is also unable to conduct medication dose search queries, and therefore, the proportion of patients receiving dose-dense TMZ regimens is unclear. As such, it is difficult to quantify the true prevalence of this side effect and its relationship to the dose schedule of TMZ. MRI protocol selection represents an additional limitation in our case series. With the exception of the MRI performed during the period of active diabetes insipidus in case 2, previously described brain MRIs were not dedicated pituitary studies. It is possible that posterior pituitary bright spots would have been visible in some patients if a greater number of image slices were obtained from the sella.

To our knowledge, this case series represents the first report of central diabetes insipidus occurring in association with TMZ or any other alkylating chemotherapeutic agent. Diabetes insipidus in these patients is reversible and responds readily to vasopressin analog replacement therapy. The prevalence of TMZ-induced diabetes insipidus appears to be rare, but it may be underdiagnosed in this patient population. The recognition and treatment of diabetes insipidus in these patients can potentially improve quality of life and functional capacity.

Acknowledgments

We thank the Partners Health Care Research Patient Data Registry group for facilitating the use of their database.

This work was supported by the National Institutes of Health Grant K23DK087857 (to H.M.).

Disclosure Summary: H.M. has received investigator-initiated research support from Pfizer, Inc unrelated to the manuscript. The other authors have nothing to declare.

Abbreviations:

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Case study: a patient with uncontrolled type 2 diabetes and complex comorbidities whose diabetes care is managed by an advanced practice nurse.

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Geralyn Spollett; Case Study: A Patient With Uncontrolled Type 2 Diabetes and Complex Comorbidities Whose Diabetes Care Is Managed by an Advanced Practice Nurse. Diabetes Spectr 1 January 2003; 16 (1): 32–36. https://doi.org/10.2337/diaspect.16.1.32

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The specialized role of nursing in the care and education of people with diabetes has been in existence for more than 30 years. Diabetes education carried out by nurses has moved beyond the hospital bedside into a variety of health care settings. Among the disciplines involved in diabetes education, nursing has played a pivotal role in the diabetes team management concept. This was well illustrated in the Diabetes Control and Complications Trial (DCCT) by the effectiveness of nurse managers in coordinating and delivering diabetes self-management education. These nurse managers not only performed administrative tasks crucial to the outcomes of the DCCT, but also participated directly in patient care. 1  

The emergence and subsequent growth of advanced practice in nursing during the past 20 years has expanded the direct care component, incorporating aspects of both nursing and medical care while maintaining the teaching and counseling roles. Both the clinical nurse specialist (CNS) and nurse practitioner (NP) models, when applied to chronic disease management, create enhanced patient-provider relationships in which self-care education and counseling is provided within the context of disease state management. Clement 2 commented in a review of diabetes self-management education issues that unless ongoing management is part of an education program, knowledge may increase but most clinical outcomes only minimally improve. Advanced practice nurses by the very nature of their scope of practice effectively combine both education and management into their delivery of care.

Operating beyond the role of educator, advanced practice nurses holistically assess patients’ needs with the understanding of patients’ primary role in the improvement and maintenance of their own health and wellness. In conducting assessments, advanced practice nurses carefully explore patients’ medical history and perform focused physical exams. At the completion of assessments, advanced practice nurses, in conjunction with patients, identify management goals and determine appropriate plans of care. A review of patients’ self-care management skills and application/adaptation to lifestyle is incorporated in initial histories, physical exams, and plans of care.

Many advanced practice nurses (NPs, CNSs, nurse midwives, and nurse anesthetists) may prescribe and adjust medication through prescriptive authority granted to them by their state nursing regulatory body. Currently, all 50 states have some form of prescriptive authority for advanced practice nurses. 3 The ability to prescribe and adjust medication is a valuable asset in caring for individuals with diabetes. It is a crucial component in the care of people with type 1 diabetes, and it becomes increasingly important in the care of patients with type 2 diabetes who have a constellation of comorbidities, all of which must be managed for successful disease outcomes.

Many studies have documented the effectiveness of advanced practice nurses in managing common primary care issues. 4 NP care has been associated with a high level of satisfaction among health services consumers. In diabetes, the role of advanced practice nurses has significantly contributed to improved outcomes in the management of type 2 diabetes, 5 in specialized diabetes foot care programs, 6 in the management of diabetes in pregnancy, 7 and in the care of pediatric type 1 diabetic patients and their parents. 8 , 9 Furthermore, NPs have also been effective providers of diabetes care among disadvantaged urban African-American patients. 10 Primary management of these patients by NPs led to improved metabolic control regardless of whether weight loss was achieved.

The following case study illustrates the clinical role of advanced practice nurses in the management of a patient with type 2 diabetes.

A.B. is a retired 69-year-old man with a 5-year history of type 2 diabetes. Although he was diagnosed in 1997, he had symptoms indicating hyperglycemia for 2 years before diagnosis. He had fasting blood glucose records indicating values of 118–127 mg/dl, which were described to him as indicative of “borderline diabetes.” He also remembered past episodes of nocturia associated with large pasta meals and Italian pastries. At the time of initial diagnosis, he was advised to lose weight (“at least 10 lb.”), but no further action was taken.

Referred by his family physician to the diabetes specialty clinic, A.B. presents with recent weight gain, suboptimal diabetes control, and foot pain. He has been trying to lose weight and increase his exercise for the past 6 months without success. He had been started on glyburide (Diabeta), 2.5 mg every morning, but had stopped taking it because of dizziness, often accompanied by sweating and a feeling of mild agitation, in the late afternoon.

A.B. also takes atorvastatin (Lipitor), 10 mg daily, for hypercholesterolemia (elevated LDL cholesterol, low HDL cholesterol, and elevated triglycerides). He has tolerated this medication and adheres to the daily schedule. During the past 6 months, he has also taken chromium picolinate, gymnema sylvestre, and a “pancreas elixir” in an attempt to improve his diabetes control. He stopped these supplements when he did not see any positive results.

He does not test his blood glucose levels at home and expresses doubt that this procedure would help him improve his diabetes control. “What would knowing the numbers do for me?,” he asks. “The doctor already knows the sugars are high.”

A.B. states that he has “never been sick a day in my life.” He recently sold his business and has become very active in a variety of volunteer organizations. He lives with his wife of 48 years and has two married children. Although both his mother and father had type 2 diabetes, A.B. has limited knowledge regarding diabetes self-care management and states that he does not understand why he has diabetes since he never eats sugar. In the past, his wife has encouraged him to treat his diabetes with herbal remedies and weight-loss supplements, and she frequently scans the Internet for the latest diabetes remedies.

During the past year, A.B. has gained 22 lb. Since retiring, he has been more physically active, playing golf once a week and gardening, but he has been unable to lose more than 2–3 lb. He has never seen a dietitian and has not been instructed in self-monitoring of blood glucose (SMBG).

A.B.’s diet history reveals excessive carbohydrate intake in the form of bread and pasta. His normal dinners consist of 2 cups of cooked pasta with homemade sauce and three to four slices of Italian bread. During the day, he often has “a slice or two” of bread with butter or olive oil. He also eats eight to ten pieces of fresh fruit per day at meals and as snacks. He prefers chicken and fish, but it is usually served with a tomato or cream sauce accompanied by pasta. His wife has offered to make him plain grilled meats, but he finds them “tasteless.” He drinks 8 oz. of red wine with dinner each evening. He stopped smoking more than 10 years ago, he reports, “when the cost of cigarettes topped a buck-fifty.”

The medical documents that A.B. brings to this appointment indicate that his hemoglobin A 1c (A1C) has never been <8%. His blood pressure has been measured at 150/70, 148/92, and 166/88 mmHg on separate occasions during the past year at the local senior center screening clinic. Although he was told that his blood pressure was “up a little,” he was not aware of the need to keep his blood pressure ≤130/80 mmHg for both cardiovascular and renal health. 11  

A.B. has never had a foot exam as part of his primary care exams, nor has he been instructed in preventive foot care. However, his medical records also indicate that he has had no surgeries or hospitalizations, his immunizations are up to date, and, in general, he has been remarkably healthy for many years.

Physical Exam

A physical examination reveals the following:

Weight: 178 lb; height: 5′2″; body mass index (BMI): 32.6 kg/m 2

Fasting capillary glucose: 166 mg/dl

Blood pressure: lying, right arm 154/96 mmHg; sitting, right arm 140/90 mmHg

Pulse: 88 bpm; respirations 20 per minute

Eyes: corrective lenses, pupils equal and reactive to light and accommodation, Fundi-clear, no arteriolovenous nicking, no retinopathy

Thyroid: nonpalpable

Lungs: clear to auscultation

Heart: Rate and rhythm regular, no murmurs or gallops

Vascular assessment: no carotid bruits; femoral, popliteal, and dorsalis pedis pulses 2+ bilaterally

Neurological assessment: diminished vibratory sense to the forefoot, absent ankle reflexes, monofilament (5.07 Semmes-Weinstein) felt only above the ankle

Lab Results

Results of laboratory tests (drawn 5 days before the office visit) are as follows:

Glucose (fasting): 178 mg/dl (normal range: 65–109 mg/dl)

Creatinine: 1.0 mg/dl (normal range: 0.5–1.4 mg/dl)

Blood urea nitrogen: 18 mg/dl (normal range: 7–30 mg/dl)

Sodium: 141 mg/dl (normal range: 135–146 mg/dl)

Potassium: 4.3 mg/dl (normal range: 3.5–5.3 mg/dl)

Lipid panel

    • Total cholesterol: 162 mg/dl (normal: <200 mg/dl)

    • HDL cholesterol: 43 mg/dl (normal: ≥40 mg/dl)

    • LDL cholesterol (calculated): 84 mg/dl (normal: <100 mg/dl)

    • Triglycerides: 177 mg/dl (normal: <150 mg/dl)

    • Cholesterol-to-HDL ratio: 3.8 (normal: <5.0)

AST: 14 IU/l (normal: 0–40 IU/l)

ALT: 19 IU/l (normal: 5–40 IU/l)

Alkaline phosphotase: 56 IU/l (normal: 35–125 IU/l)

A1C: 8.1% (normal: 4–6%)

Urine microalbumin: 45 mg (normal: <30 mg)

Based on A.B.’s medical history, records, physical exam, and lab results, he is assessed as follows:

Uncontrolled type 2 diabetes (A1C >7%)

Obesity (BMI 32.4 kg/m 2 )

Hyperlipidemia (controlled with atorvastatin)

Peripheral neuropathy (distal and symmetrical by exam)

Hypertension (by previous chart data and exam)

Elevated urine microalbumin level

Self-care management/lifestyle deficits

    • Limited exercise

    • High carbohydrate intake

    • No SMBG program

Poor understanding of diabetes

A.B. presented with uncontrolled type 2 diabetes and a complex set of comorbidities, all of which needed treatment. The first task of the NP who provided his care was to select the most pressing health care issues and prioritize his medical care to address them. Although A.B. stated that his need to lose weight was his chief reason for seeking diabetes specialty care, his elevated glucose levels and his hypertension also needed to be addressed at the initial visit.

The patient and his wife agreed that a referral to a dietitian was their first priority. A.B. acknowledged that he had little dietary information to help him achieve weight loss and that his current weight was unhealthy and “embarrassing.” He recognized that his glucose control was affected by large portions of bread and pasta and agreed to start improving dietary control by reducing his portion size by one-third during the week before his dietary consultation. Weight loss would also be an important first step in reducing his blood pressure.

The NP contacted the registered dietitian (RD) by telephone and referred the patient for a medical nutrition therapy assessment with a focus on weight loss and improved diabetes control. A.B.’s appointment was scheduled for the following week. The RD requested that during the intervening week, the patient keep a food journal recording his food intake at meals and snacks. She asked that the patient also try to estimate portion sizes.

Although his physical activity had increased since his retirement, it was fairly sporadic and weather-dependent. After further discussion, he realized that a week or more would often pass without any significant form of exercise and that most of his exercise was seasonal. Whatever weight he had lost during the summer was regained in the winter, when he was again quite sedentary.

A.B.’s wife suggested that the two of them could walk each morning after breakfast. She also felt that a treadmill at home would be the best solution for getting sufficient exercise in inclement weather. After a short discussion about the positive effect exercise can have on glucose control, the patient and his wife agreed to walk 15–20 minutes each day between 9:00 and 10:00 a.m.

A first-line medication for this patient had to be targeted to improving glucose control without contributing to weight gain. Thiazolidinediones (i.e., rosiglitizone [Avandia] or pioglitizone [Actos]) effectively address insulin resistance but have been associated with weight gain. 12 A sulfonylurea or meglitinide (i.e., repaglinide [Prandin]) can reduce postprandial elevations caused by increased carbohydrate intake, but they are also associated with some weight gain. 12 When glyburide was previously prescribed, the patient exhibited signs and symptoms of hypoglycemia (unconfirmed by SMBG). α-Glucosidase inhibitors (i.e., acarbose [Precose]) can help with postprandial hyperglycemia rise by blunting the effect of the entry of carbohydrate-related glucose into the system. However, acarbose requires slow titration, has multiple gastrointestinal (GI) side effects, and reduces A1C by only 0.5–0.9%. 13 Acarbose may be considered as a second-line therapy for A.B. but would not fully address his elevated A1C results. Metformin (Glucophage), which reduces hepatic glucose production and improves insulin resistance, is not associated with hypoglycemia and can lower A1C results by 1%. Although GI side effects can occur, they are usually self-limiting and can be further reduced by slow titration to dose efficacy. 14  

After reviewing these options and discussing the need for improved glycemic control, the NP prescribed metformin, 500 mg twice a day. Possible GI side effects and the need to avoid alcohol were of concern to A.B., but he agreed that medication was necessary and that metformin was his best option. The NP advised him to take the medication with food to reduce GI side effects.

The NP also discussed with the patient a titration schedule that increased the dosage to 1,000 mg twice a day over a 4-week period. She wrote out this plan, including a date and time for telephone contact and medication evaluation, and gave it to the patient.

During the visit, A.B. and his wife learned to use a glucose meter that features a simple two-step procedure. The patient agreed to use the meter twice a day, at breakfast and dinner, while the metformin dose was being titrated. He understood the need for glucose readings to guide the choice of medication and to evaluate the effects of his dietary changes, but he felt that it would not be “a forever thing.”

The NP reviewed glycemic goals with the patient and his wife and assisted them in deciding on initial short-term goals for weight loss, exercise, and medication. Glucose monitoring would serve as a guide and assist the patient in modifying his lifestyle.

A.B. drew the line at starting an antihypertensive medication—the angiotensin-converting enzyme (ACE) inhibitor enalapril (Vasotec), 5 mg daily. He stated that one new medication at a time was enough and that “too many medications would make a sick man out of me.” His perception of the state of his health as being represented by the number of medications prescribed for him gave the advanced practice nurse an important insight into the patient’s health belief system. The patient’s wife also believed that a “natural solution” was better than medication for treating blood pressure.

Although the use of an ACE inhibitor was indicated both by the level of hypertension and by the presence of microalbuminuria, the decision to wait until the next office visit to further evaluate the need for antihypertensive medication afforded the patient and his wife time to consider the importance of adding this pharmacotherapy. They were quite willing to read any materials that addressed the prevention of diabetes complications. However, both the patient and his wife voiced a strong desire to focus their energies on changes in food and physical activity. The NP expressed support for their decision. Because A.B. was obese, weight loss would be beneficial for many of his health issues.

Because he has a sedentary lifestyle, is >35 years old, has hypertension and peripheral neuropathy, and is being treated for hypercholestrolemia, the NP performed an electrocardiogram in the office and referred the patient for an exercise tolerance test. 11 In doing this, the NP acknowledged and respected the mutually set goals, but also provided appropriate pre-exercise screening for the patient’s protection and safety.

In her role as diabetes educator, the NP taught A.B. and his wife the importance of foot care, demonstrating to the patient his inability to feel the light touch of the monofilament. She explained that the loss of protective sensation from peripheral neuropathy means that he will need to be more vigilant in checking his feet for any skin lesions caused by poorly fitting footwear worn during exercise.

At the conclusion of the visit, the NP assured A.B. that she would share the plan of care they had developed with his primary care physician, collaborating with him and discussing the findings of any diagnostic tests and procedures. She would also work in partnership with the RD to reinforce medical nutrition therapies and improve his glucose control. In this way, the NP would facilitate the continuity of care and keep vital pathways of communication open.

Advanced practice nurses are ideally suited to play an integral role in the education and medical management of people with diabetes. 15 The combination of clinical skills and expertise in teaching and counseling enhances the delivery of care in a manner that is both cost-reducing and effective. Inherent in the role of advanced practice nurses is the understanding of shared responsibility for health care outcomes. This partnering of nurse with patient not only improves care but strengthens the patient’s role as self-manager.

Geralyn Spollett, MSN, C-ANP, CDE, is associate director and an adult nurse practitioner at the Yale Diabetes Center, Department of Endocrinology and Metabolism, at Yale University in New Haven, Conn. She is an associate editor of Diabetes Spectrum.

Note of disclosure: Ms. Spollett has received honoraria for speaking engagements from Novo Nordisk Pharmaceuticals, Inc., and Aventis and has been a paid consultant for Aventis. Both companies produce products and devices for the treatment of diabetes.

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Diabetes Insipidus (DI) NCLEX Review for Nursing Students + Free Download

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Understanding Diabetes Insipidus (DI) is Important for Nursing Students 

Endocrine Disorder: Diabetes insipidus is a rare but important endocrine disorder characterized by excessive thirst and urination due to the inability to regulate water balance. Nurses should be knowledgeable about its pathophysiology, clinical presentation, and management. Potentially Life-Threatening: Severe cases of diabetes insipidus can lead to dehydration, electrolyte imbalances, and complications such as hypovolemic shock. Nurses need to understand the potential severity of this condition and how to provide appropriate care. Assessment Skills: Nurses should be skilled in assessing patients for signs of diabetes insipidus, including excessive thirst, polyuria, and signs of dehydration.

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Fluid and Electrolyte Imbalance: Diabetes insipidus can lead to significant fluid and electrolyte imbalances. Nurses need to understand the implications of these imbalances and how to address them. Diagnostic Tests: Nurses should be familiar with the diagnostic tests used to confirm diabetes insipidus, such as water deprivation tests and urine osmolality measurements. Medication Management: Understanding the medications used to manage diabetes insipidus, such as desmopressin, and their administration is important for nurses. Fluid Replacement: In cases of severe dehydration, nurses need to understand fluid replacement protocols to address the increased water loss associated with diabetes insipidus. Documentation: Accurate documentation of signs, symptoms, interventions, and patient education is crucial for tracking the patient's condition and providing continuity of care. NCLEX Preparation: The NCLEX exam may include questions related to diabetes insipidus, its pathophysiology, assessment, interventions, and patient education. A solid understanding of this topic is essential for answering these questions accurately. Overall, understanding diabetes insipidus equips nursing students to provide safe, patient-centered care to individuals affected by this condition. It ensures that nursing students are prepared to address the unique challenges and needs of patients with diabetes insipidus and contribute to positive patient outcomes.

Diabetes Insipidus nclex prep

Overview of Diabetes Insipidus

Hyposecretion or failure to respond to antidiuretic hormone (ADH) from the posterior pituitary, which leads to excess water loss

General Information forDiabetes Insipidus

1. Urine output → 4L to 30L in a 24 hour period 2. Excessive dehydration 3. Causes        a. Neurogenic→ stroke, tumor       b. Infection       c. Pituitary surgery (pituitary gland secretes ADH)

Assessment for Diabetes Insipidus

1. Polyuria → Excessive urine output→ dilute urine, Urine Specific Gravity <1.006 2. Polydipsia (extreme thirst) 3. Hypotension leading to cardiovascular collapse 4. Tachycardia 5. Hypernatremia, neurological changes

Therapeutic Management for Diabetes Insipidus

1. Water replacement         a. PO Free Water (plain water)         b. D5W if IV replacement required 2. Hormone replacement→ DDAVP (Desmopressin/ Vasopressin) → Synthetic ADH 3. Monitor urine output hourly (Report UO >200mL/ hour), monitor urine specific gravity 4. Daily weight monitoring

Nursing Case Study for Diabetes Insipidus

Patient Profile: Lucas Carter, a 10-year-old boy, is admitted to the pediatric unit with complaints of excessive thirst and urination. His parents report that he has been drinking large amounts of water and needing to use the bathroom frequently, even during the night. Assessment: Upon assessment, Lucas appears alert and oriented but slightly dehydrated. He reports feeling thirsty and requests water frequently. His urine output is significantly increased, and his urine appears dilute. His serum electrolyte levels are within normal range, but his serum osmolality is low.

  • Collaborate with the healthcare provider to initiate fluid replacement to address Lucas's dehydration and maintain adequate fluid balance.
  • Collaborate with the healthcare provider to order diagnostic tests, such as water deprivation tests and urine osmolality measurements, to confirm the diagnosis of diabetes insipidus.
  • Collaborate with the healthcare provider to initiate desmopressin therapy, a synthetic form of antidiuretic hormone, to manage Lucas's symptoms and help regulate his fluid balance.
  • Monitor Lucas's vital signs regularly, especially his blood pressure and heart rate, to ensure he remains hemodynamically stable.
  • Perform neurological assessments to monitor Lucas's level of consciousness and cognitive function, as electrolyte imbalances or dehydration can affect neurological status.
  • Educate Lucas and his family about the condition, the importance of adhering to medication therapy, and the signs of dehydration to watch for.
  • Collaborate with the healthcare team to monitor Lucas's fluid intake and output, as well as his serum electrolyte levels, to prevent imbalances.
  • Provide emotional support to Lucas and his family, addressing their concerns and helping them cope with the challenges of managing a chronic condition.
  • Schedule regular follow-up appointments to monitor Lucas's response to treatment, adjust medication doses as needed, and provide ongoing support.

Outcome:  With comprehensive care and proper management, Lucas's condition improves. His excessive thirst and urination subside as he receives desmopressin therapy. His fluid balance is maintained, and he is educated about his condition to actively participate in self-management.

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Affiliation.

  • 1 St. Michael's Hospital, Toronto, Ontario, Canada. [email protected]
  • PMID: 12042694
  • DOI: 10.1097/00003465-200205000-00005

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STUDY OF A CASE OF DIABETES INSIPIDUS WITH SPECIAL REFERENCE TO THE MECHANISM OF THE DIURESIS AND OF THE ACTION OF PITUITARY EXTRACT ON IT

From the Department of Medicine of Lakeside Hospital and the H. K. Cushing Laboratory of Experimental Medicine, Western Reserve University.

The case of diabetes insipidus reported in this paper presented, on account of the high degree of the diuresis, an unusually good opportunity for the study of certain points in connection with the mechanism of the diuresis and the influence on it of extracts of the posterior lobe of the pituitary body. Although it was not possible to induce the patient to remain long enough in the hospital to enable us to complete our program, the results obtained seem worthy of being recorded.

The manner in which the excretion of water by the kidney is regulated has formed the subject of recent papers by Priestley 1 and by Haldane and Priestley. 2 They find, as T. M. Wilson, 3 working under the direction of one of us, previously showed, that the drinking of water is followed by a small diminution of the specific conductivity of the blood serum. According to Wilson, the meaning

CHRISTIE CD , STEWART GN. STUDY OF A CASE OF DIABETES INSIPIDUS WITH SPECIAL REFERENCE TO THE MECHANISM OF THE DIURESIS AND OF THE ACTION OF PITUITARY EXTRACT ON IT. Arch Intern Med (Chic). 1917;XX(1):10–23. doi:10.1001/archinte.1917.00090010017002

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Med-Surg Endocrine System, part 10: Diabetes Insipidus and SIADH

by Cathy Parkes August 11, 2020 Updated: August 09, 2023 8 min read 3 Comments

In this article, we cover two disorders, diabetes insipidus and syndrome of inappropriate ADH (SIADH). These are disorders that result from improper amounts of ADH in the body, so we begin with a quick review of ADH. Knowing the pathophysiology, symptoms, diagnosis and treatment for these two disorders will be key in your Med-Surg exams as well as your nursing practice.

These disorders are covered in our Medical-Surgical Flashcards (Endocrine system).

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What is the difference between SIADH and DI?

With diabetes insipidus, the body has too little antidiuretic hormone (ADH), and with SIADH, the body has too much ADH.

If you would like more in-depth information about ADH, we gave an overview of ADH in the pathophysiology section of this playlist.

Antidiuretic hormone review

As a quick overview, ADH is released by the posterior pituitary gland in response to:

  • Low blood volume
  • Low blood pressure
  • Hypernatremia (increased blood osmolarity)

If the body senses any of these three things, it will release ADH from the posterior pituitary gland, which will cause the kidneys to reabsorb more water, which helps to:

  • Increase blood volume
  • Increase blood pressure
  • Dilute the blood so the blood osmolarity drops to a normal level

Diabetes insipidus

Diabetes insipidus is sometimes jokingly called “the other diabetes,” meaning it’s not related to the much more common diabetes mellitus. The word diabetes comes from Latin and Greek meaning “siphon” or “to pass through,” referring to excessive urination common with the disease. The word insipidus comes from Latin meaning “tasteless,” referring to the diluteness of the urine.

Pathophysiology

Neurogenic diabetes insipidus.

Neurogenic diabetes insipidus happens when there is some kind of trauma or tumor in the hypothalamus or pituitary gland which is causing insufficient ADH to be released. Without enough ADH being released from the posterior pituitary gland, the kidneys are not getting the signal to reabsorb water.

The prefix neuro- in neurogenic means nervous system, or more specifically, brain. The hypothalamus and pituitary gland are in the brain, so that’s how you can remember neurogenic diabetes insipidus.

Nephrogenic diabetes insipidus

With nephrogenic diabetes insipidus, the posterior pituitary gland is actually releasing the correct amount of ADH. But there’s a problem with the kidneys. They are not responding appropriately to the ADH signal. They are getting the ADH, but they don’t respond and don’t reabsorb more water.

Why don’t the kidneys respond to the ADH? It may be due to some kind of kidney infection or damage. Sometimes kidney damage occurs from use of nephrotoxic medications.

The prefix nephro- in nephrogenic means kidneys, so that’s how you can remember nephrogenic diabetes insipidus is a problem with the kidneys. Pretty easy!

If you’d like to learn more about prefixes and suffixes that can help you easily decode disease names, check out our Medical Terminology Flashcards .

Signs and symptoms of diabetes insipidus

One of the telltale symptoms of diabetes insipidus is large amounts of dilute urine. Dilute urine is urine that has a higher concentration of water than is expected -- in this case, because the kidneys are not reabsorbing the water. Dilution or concentration of urine is measured by the urine specific gravity test, which we will cover shortly.

Another key symptom of diabetes insipidus is polydipsia, which is excessive thirst. If you think about it, these two symptoms will exacerbate one another. If you are very thirsty, you will increase your water intake, but drinking tons of water will cause you to excrete large quantities of diluted urine, which can cause even more thirst in response to fluid loss!

Easy way to remember polydipsia

Cool Chicken

Other signs and symptoms of diabetes insipidus include dehydration, hypotension, and loss of appetite.

Lab values associated with diabetes insipidus

Urine specific gravity.

A urine specific gravity test measures the relative densities of a patient’s urine to the density of water. More specifically, it’s a ratio of the mass of urine to the mass of an equal volume of water, so it measures how dense or heavy the urine is compared to water. The closer the urine specific gravity ratio is to 1, the closer the urine’s density is to water.

The expected range for urine specific gravity is 1.010 - 1.025. Lower than that is dilute urine, and higher than that is concentrated urine. Very low urine specific gravity, under 1.005, can indicate diabetes insipidus.

Urine osmolality

A urine osmolality test measures urine concentration, or the amount of dissolved substances in the urine.

The expected range for urine osmolality is 300 - 900 mOsm/kg. Lower than that is dilute urine, and higher than that is concentrated urine. Very low urine osmolality, under 200, can indicate diabetes insipidus.

Serum osmolality (blood osmolality)

Blood (serum) osmolality is the amount of dissolved substances in the liquid part ( plasma ) of the blood. A large portion of these substances is sodium. Remember that one of the tasks that ADH gives the kidneys is to dilute the blood so its osmolality drops to a normal level. Without the kidneys doing that job, the blood becomes more concentrated and its osmolality rises.

The expected range for serum osmolality is 275-295 mOsm/L. Lower than that is dilute blood, and higher than that is concentrated blood. Very high serum osmolality, over 300, can indicate diabetes insipidus. This is opposite of the urine osmolality, because the fluid shifting into the urine results in excessively dilute urine, but significant fluid loss from the blood.

Sodium is an electrolyte that’s important for nerve and muscle function and maintaining fluid balance. Remember that a large portion of the substances in the blood is sodium — so as blood fluid levels drop and serum osmolality increases, sodium (Na) levels will also be high in a patient with diabetes insipidus.

The expected range for sodium (na) is 136 - 145 mEq/L. Lower than that can indicate hyponatremia, and higher than that can indicate hypernatremia. In diabetes insipidus, the expected sodium level would be above 145 mEq/L.

Having trouble remembering all these lab values? Urine specific gravity, urine osmolality, serum osmolality, and sodium are all covered in our Lab Values Flashcards . You can use these to practice for your nursing exams and as a reference guide if you’re a practicing nurse.

Diagnosis of diabetes insipidus

Water deprivation test.

Remember that one of the symptoms of diabetes insipidus is producing large volumes of dilute urine. Well, large volumes of dilute urine can also be a result of drinking large volumes of water.

A water deprivation test basically checks to see what happens when you take the water away. Does the body behave normally when the water is taken away, or abnormally? Is the dilute urine due to too much water, or is the body actually unable to concentrate urine?

Normally, water deprivation would cause increased production of ADH, which would trigger the kidneys to preserve fluid, resulting in smaller volumes of more concentrated urine. But if the patient is deprived of water in this test, and still produces dilute urine, this is abnormal and can indicate diabetes insipidus

Vasopressin test

The vasopressin test helps differentiate between neurogenic and nephrogenic diabetes insipidus. Remember that neuro means brain (pituitary gland) and nephro means kidneys.

Vasopressin is a drug used as a hormone replacement for ADH. We expect it to do the same thing as ADH: trigger the kidneys to reabsorb water. If we give a patient vasopressin and their kidneys do not reabsorb water, we know it’s a kidney problem and we have nephrogenic diabetes insipidus. If we give the patient vasopressin and their kidneys successfully reabsorb water, then we know it was a problem with the pituitary gland not producing enough ADH, and we have neurogenic diabetes insipidus.

Treatment (medications) for diabetes insipidus

In the case of neurogenic diabetes insipidus, we can provide the patient medications like vasopressin or desmopressin (DDAVP) as an ADH replacement. Check out Cathy’s easy way to remember the side effects of antidiuretic hormones .

Nursing care for diabetes insipidus

When a patient has diabetes insipidus, you will want to montior their intake and output (I&Os), urine specific gravity, and daily weight. Weight is important because weight loss can occur with excessive fluid loss.

Also, monitor for signs of fluid volume deficit: tachycardia, hypotension, poor skin turgor, dry/sticky mucus membranes.

Syndrome of inappropriate ADH (SIADH)

Pathophysiology of siadh.

You can think of SIADH as basically the opposite of diabetes insipidus. With SIADH, there is excess secretion of ADH from the posterior pituitary gland.

Why does excess ADH get released? It can be due to a brain tumor, head injury, meningitis, or because of a medication. This excess ADH will be released even when serum osmolality is low (when the blood is diluted). This results in the kidneys reabsorbing more water — meaning the body retains too much water.

Signs and symptoms of SIADH

The key symptom of SIADH is a very small amount of concentrated urine. The body is holding onto the water so it’s not being released in the urine.

There will also be signs and symptoms of fluid volume excess. This includes tachycardia (fast heart rate), hypertension (high blood pressure), crackles, jugular vein distention, and weight gain. Some other symptoms the patient may have are headache, weakness, and muscle cramping.

With the blood diluted, this can lead to hyponatremia (abnormally low sodium), and one symptom of hyponatremia is confusion, especially in elderly patients.

Check out Cathy’s nursing tip for the easy way to remember SIADH symptoms !

Labs values associated with SIADH

Remember that SIADH is the opposite of diabetes insipidus. With DI, the patient has dilute urine and concentrated blood — with SIADH, the patient has concentrated urine and dilute blood

With SIADH a patient has concentrated urine, so that means a high urine specific gravity — the urine is a lot denser than water. Urine specific gravity will be over 1.03.

This concentrated urine will also result in a high urine osmolality, over 900 mOsm/kg.

The blood will be very dilute, which means a decreased serum osmolality, under 270 mOsm/L.

Remember that a large portion of the substances in the blood is sodium — so when serum osmolality is low, sodium (Na) levels will also be low in a patient with SIADH. Sodium levels will be under 136 mEq/L, indicating hyponatremia.

Treatment (medications) for SIADH

One of the important medications for SIADH is a diuretic to try to eliminate the excess fluid. Within diuretics, you have loop diuretics (furosemide), thiazide diuretics (hydrochlorothiazide), osmotic diuretics (mannitol), and potassium sparing diuretics (spironolactone).

Want to learn about diuretics in more detail? These medications are covered in our Pharmacology Flashcards .

We can also give the patient a vasopressin antagonist. Remember that vasopressin is ADH and an antagonist blocks — blocking production of ADH makes sense for a patient with excess or uncontrolled ADH production.

A patient with SIADH and hyponatremia can also be given hypertonic saline, an IV sodium solution, to slowly raise the sodium levels in their body and allow their electrolytes to balance.

Nursing care for SIADH

For a patient with SIADH, you will monitor their intake & output and weigh daily, just like the patient with diabetes insipidus.

You will restrict fluids and replace sodium as ordered by the provider.

Monitor for fluid volume excess . If the patient has too much fluid volume overload, that can lead to pulmonary edema which is life threatening, so it’s important to monitor for that.

In the case of pulmonary edema, along with calling the healthcare provider, the nurse's priority action is to sit the patient up in tripod position over the bedside table.

Remember that hyponatremia can lead to confusion. So you will want to monitor the patient’s neurological status for that. Also, you may need to implement seizure precautions, because hyponatremia can lead to seizures if it becomes severe.

Diabetes insipidus vs. SIADH labs

Cathy’s teaching on these disorders is intended to help prepare you for Medical-Surgical nursing exams. The Medical-Surgical Nursing video series is intended to help RN and PN nursing students study for nursing school exams, including the ATI, HESI and NCLEX.

Full Transcript

In this video we are going to talk about diabetes insipidus, as well as SIADH. These are two very important topics. If you happen to be following along with cards, I'm on card 23 [in the endocrine system section of the Medical-Surgical flashcards ], and you'll notice the next four cards, there's a lot of bold and red text on them, because there are several very important nursing concepts for you to know related to these disorders.

So both of these disorders have to do with ADH, either too much ADH, not enough ADH, or the organs in your body aren't responding appropriately to ADH. So let's do a quick review of ADH, and if you want more details about ADH, I did make a whole other video about it. But if you recall, ADH is released by the posterior pituitary gland in response to low blood volume in the body, low blood pressure, or to hypernatremia, or increased blood osmolarity. So if the body senses any of these three things, it will release ADH from the posterior pituitary gland, which will cause the kidneys to reabsorb more water, which helps to bring up that blood pressure, bring up that blood volume, and dilute the blood so that the blood osmolarity is back to a normal level.

So with diabetes insipidus, we have one of two things going on.

We may have neurogenic diabetes insipidus, which means that there is some kind of injury or tumor in the hypothalamus or the pituitary gland such that insufficient ADH is being released from the posterior pituitary gland. So if the posterior pituitary gland is not releasing enough ADH, the kidneys aren't getting the signal to reabsorb that water. So that is neurogenic diabetes insipidus.

The other thing we may have going on is something called nephrogenic diabetes insipidus. So in this situation, the posterior pituitary gland is doing its job fine. It's releasing ADH. But there's some problem in the kidneys and they are not responding appropriately to that signal. Right? They're getting the ADH but they're kind of like, "Ehh." They're not reabsorbing more water. This may be due to some kind of kidney infection, or maybe the kidneys have been damaged due to nephrotoxic medications. But this is called nephrogenic diabetes insipidus.

So in terms of signs and symptoms of diabetes insipidus, the key symptom is that the patient will have large amounts of dilute urine. So we're just dumping water. We're just peeing out tons of dilute urine. We're not reabsorbing that water as we should be. The patient will exhibit polydipsia, so this is where they have excessive thirst. And one way that I remember this symptom, if you look at the word diabetes insipidus, diabetes inSIPidus will make you want to SIP more water, because you're super thirsty.

Other signs and symptoms include dehydration, hypotension, and anorexia.

So in terms of labs, labs are definitely going to be important to know.

The urine, like we talked about, is going to be very dilute. So the specific gravity of the urine will be very low, or under 1.005. Also the osmolarity of the urine will also be very low, because it's very dilute. So it will be under 200, and then we would expect kind of decreased sodium levels in the urine as well.

In the blood though, that's a totally different story. Because we're getting rid of all those fluids, the blood's going to be really concentrated, so the serum, or blood osmolarity is going to be over 300, and the sodium levels are also going to be really high, so we're going to see hypernatremia.

In terms of diagnosis of diabetes insipidus, we can do a water deprivation test to test the ability of the kidneys to concentrate urine. We can also do a vasopressin test. So vasopressin is essentially the same as ADH. And if we give the patient vasopressin, we would expect their kidneys to reabsorb water. If their kidneys don't do that, then we know it's a problem with the kidneys and we have nephrogenic diabetes insipidus. If we give the patient vasopressin and their kidneys do do their job and reabsorb water, then we know it was an issue with the pituitary gland not producing enough ADH.

And if that is the case, then we can provide medications such as vasopressin or desmopressin, which you can find on Pharm card 110 [in our Pharmacology Flashcards ] in terms of getting more information about those medications.

So in terms of nursing care, when a patient has diabetes insipidus, we're definitely going to want to monitor the patient's I&Os, as well as their urine specific gravity and their daily weight.

Let's move on to syndrome of inappropriate ADH, or SIADH. With SIADH, we have excess release of ADH from the posterior pituitary gland due to a brain tumor, head injury, meningitis, or because of a medication. So even though the blood is very dilute, the posterior pituitary gland still releases ADH, even though it should not. So because it's releasing all this extra ADH inappropriately, it's causing the kidneys to reabsorb more water.

So signs and symptoms of SIADH will include a very small amount of very concentrated urine. And then we'll have signs and symptoms of fluid volume excess because we have all this extra fluid being reabsorbed. So the patient may exhibit signs and symptoms such as tachycardia, hypertension, crackles, jugular vein distention, as well as weight gain. They may also complain of a headache, weakness, and muscle cramping. And then they may also exhibit confusion because we have hyponatremia due to all this dilution, and that can cause the patient to be confused.

So one way to remember what SIADH does, if you look at the first two letters of that, S-I, you can think of super inflated, and that's basically what happens. When you have SIADH, you reabsorb all this extra fluid, and you are super inflated.

In terms of labs, we're going to have, basically, the exact opposite as we saw with diabetes insipidus.

So the urine with SIADH will be super concentrated. So the urine specific gravity will be elevated. It will be over 1.03, and the urine osmolality or osmolarity will also be increased because it's so concentrated.

The blood or the serum will be a completely different story. It will be very dilute, so the serum osmolality will be decreased. It will be under 270 and we'll see hyponatremia because the sodium is diluted with all this extra fluid volume.

In terms of treatment, we're definitely going to give the patient diuretics to try to get rid of some of this excess fluid. We can also give them a vasopressin antagonist, and then we can also give them hypertonic saline to help bring up the sodium levels and allow for those electrolyte levels to be more in balance.

In terms of nursing care, again, we're going to want to monitor the patient's I&Os, we're going to weigh our patients daily, and we're going to restrict fluids and replace sodium as ordered by the provider. We're going to monitor for fluid volume excess. So if we have too much fluid volume overload, we can end up with pulmonary edema, which is life threatening. So we're definitely going to want to monitor for that. And then we're going to want to continually monitor the patient's neurologic status because of the confusion that can result from hypernatremia, and we're also going to need to implement seizure precautions, because hypernatremia can result in seizures if it gets too bad.

So hopefully that was useful in terms of a review of diabetes insipidus, and SIADH. If you appreciated this review, be sure to like our video and subscribe to us here. Take care.

Cathy Parkes

Cathy Parkes

3 responses.

Steven

September 23, 2021

Very good review of DI vs SIADH

April

April 26, 2021

Thank you much – had worse 1st time doc appointment w Diabetes ,Osteoporosis,Endocrinologist -In & out in less than 1/2 hr-didnt fill out all paperwork before saw / moved to 2 dif. Rms blood pressure cuff not working-heard nurse comment on meds taking through closed door,and when did see doc she seemed rude ,didn’t explain why thought had SIADH

Berthe

October 29, 2020

Very helpful information.

Leave a comment

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IMAGES

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  1. Diabetes Insipidus Case Study (60 min)

    View Answer Mrs. Ford's vital signs are as follows: BP 124/68 MAP 86 HR 84 Temp 98.9 RR 16 (ventilated) ICP 12 She is not on any sedation. You determine her GCS is 6, she withdraws to pain, but does not open her eyes.

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    Diabetes insipidus (DI) is a rare condition affecting approximately 1 out of 25,000 people. Characterized by the passage of large amounts of dilute urine, increased thirst, and an increased likelihood of dehydration, this disorder is seen across the lifespan, equally among men and women.

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    Trouble sleeping Weight loss Delayed growth Constipation Vomiting Causes of Diabetes Insipidus The fluid part of the blood called plasma is filtered by the kidneys to take away the waste products. After the filtering process, the hormone vasopressin or anti-diuretic hormone (ADH) helps the filtered plasma to return to the bloodstream.

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    1. Deficient Fluid Volume 2. Risk for Impaired Skin Integrity 3. Deficient Knowledge Consequently, instead of being a yellow color, the urine is pale, colorless or watery in appearance and the measured concentration (osmolality or specific gravity) is low. Nursing Care Plans Here are three (3) nursing care plans for diabetes insipidus. 1.

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    The principal hormone of diabetes insipidus is the posterior pituitary hormone ADH, which is one of the main determinants regarding water homeostasis within the body. antidiuretic hormone (ADH) acts on its target organ, the kidney, to increase urine osmolality [ 3 ].

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    Case report 1: Forty-five year old female, previously healthy, was observed in April 2011 complaining of polydipsia, polyuria, nocturia and weight loss since January. Diabetes mellitus (DM) was excluded and she was admitted for study of possible diabetes insipidus. Water deprivation test was suggestive of CDI. Magnetic resonance imaging (MRI ...

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  10. Clinical Case Seminar: Central Diabetes Insipidus: A Previously

    Laboratory studies obtained 2 weeks after cessation of DDAVP showed a serum sodium concentration of 139 mmol/L, and concurrent urine-specific gravity of 1.019. ... With the exception of the MRI performed during the period of active diabetes insipidus in case 2, previously described brain MRIs were not dedicated pituitary studies. It is possible ...

  11. Case Study: A Patient With Uncontrolled Type 2 Diabetes and Complex

    The following case study illustrates the clinical role of advanced practice nurses in the management of a patient with type 2 diabetes. Case Presentation A.B. is a retired 69-year-old man with a 5-year history of type 2 diabetes. Although he was diagnosed in 1997, he had symptoms indicating hyperglycemia for 2 years before diagnosis.

  12. Diabetes Insipidus (DI) NCLEX Review for Nursing Students + Free Download

    1. Urine output → 4L to 30L in a 24 hour period 2. Excessive dehydration 3. Causes a. Neurogenic→ stroke, tumor b. Infection c. Pituitary surgery (pituitary gland secretes ADH) Assessment for Diabetes Insipidus 1.

  13. Accurate patient history contributes to differentiating diabetes

    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 …

  14. Central diabetes insipidus from a patient's perspective: management

    Summary Background Central diabetes insipidus is a rare neuroendocrine condition. Data on treatment-associated side-effects, psychological comorbidities, and incorrect management are scarce. The aim of this study was to investigate patients' perspectives on their disease. Methods

  15. Nursing Care Plan (NCP) for Diabetes Insipidus

    Outline Lesson Objective for Diabetes Insipidus (DI) Understanding of Diabetes Insipidus: Define Diabetes Insipidus, distinguishing it from other forms of diabetes. Explain the pathophysiology of DI, emphasizing the role of antidiuretic hormone (ADH) and its impact on fluid balance. Identification of Signs and Symptoms:

  16. Treating nephrogenic diabetes insipidus: a case study

    Treating nephrogenic diabetes insipidus: a case study Dimens Crit Care Nurs. May-Jun 2002;21(3):98-9. doi: 10.1097/00003465-200205000-00005. ... Diabetes Insipidus, Nephrogenic / nursing Diabetes Insipidus, Nephrogenic / therapy* Humans ...

  17. Study of A Case of Diabetes Insipidus With Special Reference to The

    The case of diabetes insipidus reported in this paper presented, on account of the high degree of the diuresis, an unusually good opportunity for the study of certain points in connection with the mechanism of the diuresis and the influence on it of extracts of the posterior lobe of the pituitary body.

  18. Diabetes Insipidus Case Study (60 min)

    Critical thinking nursing case study on diabetes insipidus for nursing students. Diabetes Insipidus Case Study (60 min) Start a free trial to unlock videos, outlines, cheatsheets, and quizzes. ...

  19. Case Discussion on Central Diabetes Insipidus

    CNS examination: Conscious, oriented and cooperative. Intelligence and memory intact. Speech normal. Vision normal, no nystagmus. Bilateral pupil round regular and reactive. Eye movement and field of vision normal. Fundus examination: bilateral disc edema. Other cranial nerves were intact. Bulk, tone, power were normal of all major muscle groups.

  20. Med-Surg Nursing: Diabetes Insipidus and SIADH

    Cathy's teaching on these disorders is intended to help prepare you for Medical-Surgical nursing exams. The Medical-Surgical Nursing video series is intended to help RN and PN nursing students study for nursing school exams, including the ATI, HESI and NCLEX.. Full Transcript. In this video we are going to talk about diabetes insipidus, as well as SIADH.

  21. Diabetes insipidus: Nursing process (ADPIE)

    Finally, the fourth type is dipsogenic diabetes insipidus, also called psychogenic or primary polydipsia, which is caused by drinking far too much water and it is often associated with a psychiatric disorder, such as schizophrenia, but can also be caused by damage to the hypothalamic osmoreceptors that regulate the feeling of thirst.

  22. Case Study

    Case Study - Diabetes Insipidus. A 19 yr old undergraduate nursing student who is working part-time as a CNA. Lately she realizes that she has to go to the bathroom very frequently - almost every hour- and that she is drinking more than 5 L of water a day. She goes to see her NP, who finds her physical exam to be normal, with a BP of 105/70 and ...

  23. Diabetes Insipidus

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