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
History
• 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.
Physical Examination
• Look for signs of complications of long-standing hyperglycemia.
Tests for Consideration
| Clinical Entities | Medical Knowledge |
Diabetes Mellitus Type 1 | |
Pφ | 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. |
Pφ | 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. |
Gestational Diabetes Mellitus | |
Pφ | 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 | |
Pφ | 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. |
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 | |
Pφ | 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. |
