Polyuria and Polydipsia (Case 38)

Chapter 46
Polyuria and Polydipsia (Case 38)


Kavita Iyengar MD


Case: The patient is a 68-year-old woman with a medical history of hypertension, hyperlipidemia, and obesity. She presents to the outpatient office because for the last few weeks she has been more tired than usual and feels that she has been drinking more water. She has also been going to the bathroom more frequently, particularly at night. In addition, she has blurry vision and headaches. Her husband is also your patient. He has trouble maintaining control over his blood sugar and is also obese. Both the patient and her husband often miss scheduled follow-up appointments.


The patient’s medications are hydrochlorothiazide, atorvastatin, and an aspirin. Her father had hypertension and coronary artery disease, and her mother was recently diagnosed with type 2 diabetes mellitus. The patient works as an administrative assistant. She smokes half a pack of cigarettes a day and drinks a glass of wine occasionally.


On examination she is pleasant and conversant and appears comfortable. She states that she thinks she may have “a little sugar” like her husband. Her vital signs are within normal limits, but her body mass index (BMI) is 37. Her lungs are clear to auscultation, and heart sounds are normal. Her abdomen is obese. Her neurologic exam is normal except for a decreased monofilament sensation in her feet.


Differential Diagnosis











Diabetes mellitus, type 1


Diabetes mellitus, type 2


Diabetes insipidus (DI)


Hypercalcemia


Gestational diabetes


 


Speaking Intelligently



Polyuria is most often caused when the kidneys are subjected to an increased osmotic load, such as that from glucose or calcium. Alternatively, it may be due to endocrine disorders of fluid regulation such as vasopressin (antidiuretic hormone, ADH) deficiency. Conditions that cause bladder irritability or obstruction such as cystitis or prostatic enlargement can cause increased urinary frequency, but usually not polyuria. When most clinicians are assessing an obese patient with polyuria and polydipsia, type 2 diabetes mellitus, which affects over 20 million persons in the United States, is the first diagnosis that comes to mind. A point-of-care capillary glucose by finger-stick or a urinalysis can quickly make the diagnosis of uncontrolled diabetes, so that this patient can quickly get the appropriate care.


PATIENT CARE


Clinical Thinking


• Diabetes mellitus is diagnosed with two fasting blood glucose measurements greater than 125 mg/dL or a random value greater than 200 mg/dL in a patient with symptoms. At this point, you have to determine how sick the patient is and whether the patient needs inpatient management to treat symptomatic hyperglycemia or has life-threatening complications such as diabetic ketoacidosis (DKA) or a nonketotic hyperosmolar state.


• Patients with type 1 diabetes may present to the emergency department in DKA, with an elevated blood glucose, or an anion gap metabolic acidosis with positive serum ketones and electrolyte imbalances.


• Patients with type 2 diabetes may present in a hyperosmolar state with severe volume depletion, hypernatremia, and very high blood glucose levels.


• If the glucose and calcium are normal, other conditions such as DI or primary polydipsia should be considered.


History


• Hyperglycemia can present as a spectrum from one in which the patient is completely asymptomatic to one in which the patient has DKA or a hyperosmolar state.


• In an asymptomatic patient, hyperglycemia may be an incidental finding on laboratory work done for other reasons, or it could be seen in a patient admitted to the hospital in acute stress (e.g., from a myocardial infarction or severe infection). At times, medications such as corticosteroids can be the cause.


• If a patient’s blood glucose has been consistently high for some time, symptoms such as polydipsia, polyuria, and nocturia can be seen, since excess glucose delivered to the kidneys causes an osmotic diuresis. Hyperglycemia can also manifest as blurry vision from the effects of glucose on the lens, or tingling and numbness in the toes from peripheral neuropathy. Other symptoms that should be sought are weight loss and fatigue.


• A patient who presents in DKA or a hyperosmolar state may be too sick to give a history but may have an obvious inciting insult such as infection or a myocardial infarction. Nausea, vomiting, and abdominal pain are common symptoms in patients with DKA.


• A family history of diabetes can be found, which is more common in patients with type 2 diabetes.


• Patients with DI may have pituitary tumors; they should be questioned about headaches and visual changes, and other endocrinopathies. Patients with primary polydipsia may be drinking excessive amounts of water because of a psychiatric or central nervous system (CNS) disorder.


Physical Examination


• Look for signs of complications of long-standing hyperglycemia.


• Patients with type 2 diabetes are typically overweight, while those with type 1 diabetes are often not.


• An exam of the skin may reveal signs of insulin resistance such as acanthosis nigricans and skin tags.


• Patients with type 1 diabetes may have other signs of autoimmune disorders such as vitiligo and goiter.


• Screening for chronic complications of diabetes should include a monofilament exam looking for sensory neuropathy, a foot exam assessing for peripheral vascular disease, and a dilated funduscopic exam screening for retinopathy.


• In a patient admitted to the hospital with DKA, Kussmaul respirations and ketotic breath may be noted; very sick patients may present with mental status changes and signs of volume depletion such as hypotension and tachycardia.


Tests for Consideration






































































Fasting plasma glucose: Obtained to diagnose diabetes.
A value of 100 to 125 mg/dL indicates pre-diabetes, while a value above 125 mg/dL obtained twice indicates diabetes.


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Random plasma glucose: Can also be used to diagnose diabetes. A value of 140 to 200 mg/dL indicates pre-diabetes or glucose intolerance, while a value above 200 mg/dL, in the presence of symptoms, is diagnostic of diabetes.


$7


Fingerstick blood glucose: Checked by the patient at home, using a glucometer. This should typically be checked once daily in patients on oral hypoglycemic agents and three to four times a day in patients on insulin. This could also be checked in an emergency, while awaiting serum blood glucose values from the lab.


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Hemoglobin A1c (HbA1c or glycosylated hemoglobin): Gives an idea of the average blood glucose over the 3- to 4-month period before the blood sample is drawn. The average blood sugar of a normal person should be less than 120 mg/dL, which corresponds to an HbA1c of 6%. For every point increase in HbA1c, a 30-point increase in the average blood glucose can be expected. For example, an HbA1c of 8% would suggest the patient’s blood glucose averaged 180 mg/dL over the previous 3 months. An HbA1c of less than 7% suggests good blood sugar control.


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Urine microalbumin-to-creatinine ratio: Elevated in early diabetic nephropathy.


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Serum creatinine: Elevated in later stages of diabetic nephropathy.


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Arterial blood gas and serum ketones: Used to assess patients with DKA in which an anion gap metabolic acidosis (pH < 7.30) and positive serum ketones are seen.


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Sodium: The osmotic effect of hyperglycemia can shift water from the extravascular to the intravascular space, which is measured as hyponatremia. This is particularly evident in the hyperosmolar state. As a general rule, for each 100 mg/dL of glucose over 100 mg/dL, the serum sodium concentration is lowered by approximately 1.6 mEq/L. Conversely, when glucose levels fall, the serum sodium level rises by a corresponding amount.


$6


Urine and serum osmolality: Patients who have lost excessive free water because of hyperglycemia or hypercalcemia will have high serum osmolality. Patients with DI usually have high serum osmolality and low urine osmolality. Patients with primary polydipsia will have normal or even low serum osmolality and appropriately dilute urine.


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Potassium: Hyperkalemia may be seen in patients with DKA.
Hypokalemia can be expected on treating an acutely ill patient with insulin. An electrocardiogram (ECG) may be used to evaluate the cardiac effects of extremes in serum potassium.


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Bicarbonate: Used in conjunction with the anion gap to assess the degree of acidosis.


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Phosphorus: Should be checked and repleted while treating DKA.


 


Blood urea nitrogen (BUN): Elevated in patients with volume depletion.


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Serum osmolality: Measured as 2(Na+) (mEq/L) + glucose (mg/dL)/18 + BUN (mg/dL)/2.8. Values above 330 mOsm/kg H2O are typically seen in hyperosmolar patients.


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Complete blood count (CBC): An elevated white blood cell (WBC) count may indicate infection as a precipitating cause of hyperglycemia.


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Urinalysis: To look for glycosuria and ketonuria.


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Amylase and lipase: Elevated in pancreatitis.


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Calcium and albumin, ionized calcium: Total calcium is elevated in patients with hypercalcemia. If the albumin is low, total calcium can be mathematically corrected for albumin, or ionized calcium may be measured.


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Parathyroid hormone (PTH): Elevated in patients with hyperparathyroidism; low in patients with hypercalcemia of malignancy or vitamin D intoxication.


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C-peptide level and glutamic acid decarboxylase (GAD) antibodies: Used to diagnose type 1 diabetes. In these patients C-peptide may be low, since no insulin is being secreted in vivo, and GAD antibodies are positive, suggesting autoimmune destruction of the insulin-producing cells of the pancreas.


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Lipids: Should be in the normal range; low-density lipoprotein (LDL) cholesterol, in particular, should be as close to 70 mg/dL as possible to lower the risk of cardiovascular disease.


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Ankle-brachial index: Should be assessed in patients with poor lower extremity pulses to evaluate for peripheral arterial disease.


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Clinical Entities Medical Knowledge

















Diabetes Mellitus Type 1



Destruction of the β-cells of the pancreas from autoimmune, environmental (virus, toxin, stress), or other causes. This results in insulin deficiency; patients are symptomatic when the majority of the β-cells are destroyed.


Previously called IDDM (insulin-dependent diabetes mellitus) or juvenile-onset diabetes mellitus.


TP


Patients are younger at diagnosis, sometimes just 10–14 years of age. Signs and symptoms of hyperglycemia include the following: increased thirst and hunger, frequent urination especially at night, weight loss, and fatigue. Often, a DKA picture at diagnosis.


Dx


High blood and urine glucose, elevated HbA1c, positive GAD antibodies, and nondetectable C-peptide level. In patients with DKA, anion gap metabolic acidosis, low serum bicarbonate, high serum and urine ketones.


Tx


Insulin, subcutaneously with frequent fingersticks to monitor blood glucose. This can be given as multiple daily injections or via an insulin pump. Patients should receive basal insulin (e.g., glargine or detemir) once or twice daily, and prandial (mealtime) insulin (e.g., lispro, aspart, or glulisine) with each meal. Insulin pumps contain short-acting insulin, set for basal doses to be running continuously and bolus doses to cover meals. In addition, diet, exercise, and diabetes and nutrition education are critical.


Patients presenting with DKA require IV fluid hydration and IV insulin infusion, with close monitoring of blood glucose and serum electrolytes; particular attention must be given to potassium and phosphorus repletion. See Cecil Essentials 69.


















Diabetes Mellitus Type 2



Usually a combination of insulin resistance at the periphery, decreased insulin production from the pancreas, and excess glucose production by the liver. Previously called NIDDM (non–insulin-dependent diabetes mellitus) or adult-onset diabetes mellitus.


TP


Patients are typically obese, with a sedentary lifestyle and a strong positive family history in first-degree relatives. They are usually over 30 years of age at diagnosis, but this is now frequently seen at younger ages as well. There is a higher incidence in African Americans, Hispanics, and Native Americans. Patients usually have hyperglycemia for several months before diagnosis. They may have symptoms of hyperglycemia as in type 1 patients and frequently also have blurred vision, tingling/numbness in the feet, and poor wound healing. Other features associated with insulin resistance/metabolic syndrome, such as acanthosis nigricans, hyperlipidemia, and hypertension, may be seen. Sometimes, with uncontrolled hyperglycemia, patients may present in a hyperosmolar state, with severe dehydration and high serum osmolality; serum ketones are usually absent.


Dx


High blood and urine glucose, elevated HbA1c. Diagnosis is made with at least two fasting blood glucose measurements > 125 mg/dL or random blood glucose > 200 mg/dL with symptoms of hyperglycemia.


Tx


Diet and exercise play an important role in management, and all patients should receive diabetes and nutrition education. Oral hypoglycemic agents should be started, with a goal HbA1c of <6.5% or 7.0%. Typically, metformin is the first agent of choice. Patients could also use one of the secretagogues, sulfonylureas, and meglitinides, which stimulate the pancreatic β-cells to secrete insulin. Other agents used are thiazolidinediones and α-glucosidase inhibitors. More recently, the dipeptidyl peptidase IV inhibitor sitagliptin and the incretin mimetic exenatide, which have been proven to have other beneficial effects in addition to blood glucose control, are gaining popularity.


For a patient presenting in a hyperosmolar state, IV hydration and IV insulin should be started, although it is important to volume-resuscitate the patient adequately before insulin is administered, because intracellular fluid shifts following reduction in serum glucose may worsen systemic tissue perfusion. Electrolyte imbalances are common, so close monitoring and repletion with correct use of IV fluids are crucial.


During outpatient follow-up, patients should have annual eye and foot exams to detect retinopathy and neuropathy/vascular disease, respectively. In addition, patients should be advised to take a low-dose aspirin daily to prevent cardiovascular complications. Urine microalbumin-to-creatinine ratio should be checked routinely and the patient started on an angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) if early nephropathy is found. Blood pressure control and cholesterol lowering are crucial for the reduction of cardiovascular risk. See Cecil Essentials 69.


 


















Gestational Diabetes Mellitus



Insulin resistance during pregnancy.


TP


Abnormal fasting or oral glucose tolerance on routine blood tests performed at prenatal visits. Patients are usually asymptomatic or may have symptoms of hyperglycemia.


Dx


Fasting blood glucose > 95 mg/dL, or 100 mg oral glucose tolerance test with the following results: >180 mg/dL at 1 hour, >155 mg/dL at 2 hours, and >140 mg/dL at 3 hours.


Tx


Diet and exercise through diabetes and nutrition education. Insulin is the mainstay of therapy during pregnancy; metformin could be used in the first trimester. Postnatal follow-up, with at least an annual fasting blood glucose measurement, should be performed, keeping in mind that these patients are at a high risk of developing type 2 diabetes in the future. See Cecil Essentials 69, 71.


 


















Diabetes Insipidus



Deficiency of ADH (also known as vasopressin) from either a hypothalamic-pituitary disorder (central DI) or renal resistance to the action of ADH (nephrogenic DI). ADH is synthesized in the hypothalamus and secreted by the posterior pituitary, so damage to these areas (from trauma, tumor, infection, infiltration, or vascular lesion) results in ADH deficiency and central DI. On the other hand, impaired renal tubule response to ADH can result in nephrogenic DI, which may be inherited or acquired. A common acquired cause is from a side effect of the drug lithium.


TP


Insidious onset of polydipsia and polyuria at any age. Alternatively, with an insult to the hypothalamus or pituitary, the onset of symptoms may be acute, resulting in volume depletion and hypernatremia.


Dx


ADH levels (not routinely measured) are low in central DI and high in nephrogenic DI. Diagnostic tests should include measurement of serum electrolytes and osmolality as well as urine specific gravity and osmolality. The water deprivation test reveals the inability to concentrate urine; injecting vasopressin improves symptoms and increases urine osmolality in central DI but not in nephrogenic DI.


Tx


Desmopressin (a synthetic analogue of ADH) treats central DI effectively. Diuretics (i.e., thiazides), which may reduce distal sodium delivery in the renal tubules, may improve nephrogenic DI. Intake of free water, a low-salt, low-protein diet, and correcting the underlying cause, if possible, may be helpful in management. See Cecil Essentials 27, 28, 65.


 


















Hypercalcemia



Hypercalcemia may be PTH-mediated (hyperparathyroidism with increased intestinal calcium absorption) or non–PTH-mediated (localized bone destruction or via PTH-related peptide activity from malignancies, granulomatous disorders, and medications such as thiazides or lithium). Other causes are prolonged immobilization, milk-alkali syndrome, ingestion of calcium supplements, vitamin A or D excess, multiple myeloma, Paget disease, familial hypocalciuric hypercalcemia, and hyperthyroidism.


TP


Patients with mild hypercalcemia may have no symptoms. In more severe cases the patient may have nausea, vomiting, abdominal pain, constipation, altered mental status, headache, muscle/joint aches, and polyuria. These symptoms are more common in the elderly. On exam, hyperreflexia, tongue fasciculations, altered mental status, abdominal tenderness, proximal muscle weakness, and volume depletion may be seen.


Dx


High serum calcium, after correcting for albumin. Ionized calcium levels may also be measured. Other helpful lab tests, including PTH, phosphorus, vitamin D levels, creatinine, and 24-hour urine calcium, should be done to evaluate for the potential cause. If suspected, malignancy should be ruled out.


Tx


Adequate hydration followed by loop diuretics (furosemide), bisphosphonates, steroids, calcitonin, and calcimimetics may be used. Treatment of the underlying cause is also important for management. See Cecil Essentials 74.


 


Oct 3, 2016 | Posted by in MANUAL THERAPIST | Comments Off on Polyuria and Polydipsia (Case 38)

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