Endocrine Clinical Assessment and Diagnostic Procedures

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Endocrine Clinical Assessment and Diagnostic Procedures

Mary E. Lough

Assessment of the patient with endocrine dysfunction is a systematic process that incorporates history taking and physical examination. Most of the endocrine glands are deeply encased in the human body. Although the placement of the glands provides security for the glandular functions, their resulting inaccessibility limits clinical examination. Nevertheless, the endocrine glands may be assessed indirectly. The critical care nurse who understands the metabolic actions of the hormones produced by endocrine glands assesses the physiology of the gland by monitoring that gland’s target tissue as listed in Figure 31-1 in Chapter 31. This chapter describes clinical and diagnostic evaluation of the pancreas, the posterior pituitary, and the thyroid gland.


The initial presentation of the patient determines the rapidity and direction of the interview. For a patient in acute distress, the history is curtailed to only a few questions about the patient’s chief complaint and precipitating events. For the patient without obvious distress, the endocrine history focuses on four areas: 1) current health status, 2) description of the current illness, 3) medical history and general endocrine status, and 4) family history. Data collection in the endocrine history for diabetes complications is outlined in Box 32-1.

Box 32-1   Data Collection

Complications of Diabetes


Physical Assessment

Insulin, which is produced by the pancreas, is responsible for glucose metabolism. The clinical assessment provides information about pancreatic functioning. Clinical manifestations of abnormal glucose metabolism often include hyperglycemia, which is the initial assessment priority for the patient with pancreatic dysfunction.1,2 Patients with hyperglycemia may ultimately be diagnosed with type 1 or type 2 diabetes or be hyperglycemic in association with a severe critical illness.1,2 All of these conditions have specific identifying features. More information on the specific pathophysiology and management of each condition is available in Chapter 33.


Because severe hyperglycemia affects a variety of body systems, all systems are assessed. The patient may complain of blurred vision, headache, weakness, fatigue, drowsiness, anorexia, nausea, and abdominal pain. On inspection, the patient has flushed skin, polyuria, polydipsia, vomiting, and evidence of dehydration. Progressive deterioration in the level of consciousness, from alert to lethargic or comatose, is observed as the hyperglycemia exacerbates. If ketoacidosis occurs, the patient’s breathing becomes deep and rapid (Kussmaul respirations), and the breath may have a fruity odor. Auscultation of the abdomen may reveal hypoactive bowel sounds. Palpation elicits abdominal tenderness. Percussion may reveal diminished deep tendon reflexes. Because hyperglycemia results in osmotic diuresis, the patient’s fluid volume status is assessed. Signs of dehydration include tachycardia, orthostatic hypotension, and poor skin turgor. The key laboratory tests that assist in assessment are discussed in the following section.

Laboratory Studies

Pertinent laboratory tests for pancreatic function measure short-term and long-term blood glucose levels, which can identify and diagnose diabetes.

Blood Glucose

The fasting plasma glucose (FPG) level is assessed by a simple blood test after the person has not eaten for 8 hours. A normal FPG level is between 70 and 100 milligrams per deciliter (mg/dL).1 A fasting glucose level between 100 and 125 mg/dL identifies a person who is prediabetic.1 Even these individuals are at increased risk for complications of diabetes, such as coronary heart disease and stroke. A FPG level of 126 mg/dL (7 millimoles per liter [mmol/L]) or higher is diagnostic of diabetes (Table 32-1). In nonurgent settings, the test is repeated on another day to ensure that the result is accurate. After a meal, the concentration of glucose increases in the bloodstream. Recommended postprandial blood glucose levels should not exceed 180 mg/dL (10 mmol/L).1

TABLE 32-1


Hypoglycemia <70 < 3.9
Normal 70-100 >3.9-5.6
Prediabetes 100-125 5.6-6.9
Diabetes ≥126 ≥7.0

BG, Blood glucose; mg/dL, milligram per deciliter; mmol/L, millimole per liter.

Data from American Diabetes Association. Standards of medical care in diabetes—2012, Diabetes Care. 2012;35(suppl 1):S11.

All critically ill patients must have their blood glucose levels monitored frequently while in the hospital. Clinical practice guidelines from the American Association of Clinical Endocrinologists (AACE) and the American Diabetes Association (ADA) recommend instituting insulin therapy when the blood glucose is greater than 180 mg/dL in critical illness.3 A target blood glucose range of 140 to 180 mg/dL is recommended.3

When a continuous insulin infusion is administered, point-of-care blood glucose testing is performed hourly or according to hospital protocol by the critical care nurse to achieve and maintain the blood glucose within the target range.3

Hypoglycemia is defined as a blood glucose level below 70 mg/dL (3.9 mmol/L).1,3 A complication of intensive glucose control is that hypoglycemic episodes may occur more frequently both in the hospital and with self-management of glucose levels in diabetes.3

Before discharge to home, patients with diabetes should be taught to monitor their blood glucose levels.4 Maintaining blood glucose within the normal range is associated with fewer long-term diabetes related complications.4 Laboratory blood tests and point-of-care or self-monitoring of blood glucose represent the standard of care for management of diabetes. Unfortunately, home monitoring of blood glucose is not the norm despite research evidence that maintaining blood glucose levels as close to normal as possible prolongs life and reduces complications.

Glycated Hemoglobin

Blood testing of glucose is useful for daily management of diabetes. However, a different blood test is used to achieve an objective measure of blood glucose over an extended period. The glycated hemoglobin test, also known as glycosylated hemoglobin (HbA1C or A1C) provides information about the average amount of glucose that has been present in the patient’s bloodstream over the previous 3 to 4 months. During the 120-day life span of red blood cells (RBCs; erythrocytes), the hemoglobin within each cell binds to the available blood glucose through a process known as glycosylation. Typically, 4% to 6% of hemoglobin contains the glucose group A1C. A normal A1C value is less than 5.4%, with an acceptable target level for diabetic patients below 6.5%.1,2,5 The A1C value correlates with specific blood glucose levels as shown in Table 32-2.1,2 The American Diabetes Association recommends use of the A1C value both during initial assessment of diabetes mellitus, and for follow-up to monitor treatment effectiveness.1

TABLE 32-2


6 126 7.0
7 154 8.6
8 183 10.2
9 212 11.8
10 240 13.4
11 269 14.9
12 298 16.5

HbA1c, Glycosylated hemoglobin; mg/dL, milligram per deciliter; mmol/L, millimole per liter.

Data from American Diabetes Association. Standards of medical care in diabetes—2012. Diabetes Care. 2012;35(suppl 1):S11.

Blood Ketones

Ketone bodies are a byproduct of rapid fat breakdown. Ketone blood levels rise in acute illness, fasting, and with sustained elevation of blood glucose in type 1 diabetes in the absence of insulin. In diabetic ketoacidosis (DKA), fat breakdown (lipolysis) occurs so rapidly that fat metabolism is incomplete, and the ketone bodies (acetone, beta-hydroxybutyric acid, and acetoacetic acid) accumulate in the blood (ketonemia) and are excreted in the urine (ketonuria). It is recommended that all patients with diabetes perform self-test, or have their blood or urine tested, for the presence of ketones during any alteration in level of consciousness or acute illness with an elevated blood glucose.6 A blood test that measures beta-hydroxybutyrate, the primary metabolite of ketoacidosis, provides the most accurate measurement.6,7 Self-test meters to measure blood ketones from a fingerstick are now available.6

Elevated levels of ketones (ketonemia) may be detected by a fruity, sweet-smelling odor on the exhaled breath. This distinctive breath odor derives from the elimination of acetone as part of the compensatory response to maintain a normal pH.

Pituitary Gland

The pituitary gland, recessed in the base of the cranium, is not accessible to physical assessment. The critical care nurse must, therefore, be aware of the systemic effects of a normally functioning pituitary to be able to identify dysfunction. One essential hormone formed in the hypothalamus but secreted through the posterior pituitary gland is antidiuretic hormone (ADH), also known as vasopressin.

Physical Assessment

ADH controls the amount of fluid lost and retained within the body. Acute dysfunction of the posterior pituitary or the hypothalamus may result in insufficient or excessive ADH production. The clinical signs of posterior pituitary dysfunction often manifest as fluid volume deficit (insufficient ADH production) or fluid volume excess (excessive ADH production).

Hydration Status

The nurse determines the effectiveness of ADH production by conducting a hydration assessment. A hydration assessment includes observations of skin integrity, skin turgor, and buccal membrane moisture. Moist, shiny buccal membranes indicate satisfactory fluid balance. Skin turgor that is resilient and returns to its original position in less than 3 seconds after being pinched or lifted indicates adequate skin elasticity. The skin over the forehead, clavicle, and sternum is the most reliable for testing tissue turgor because it is less affected by aging and more easily assessed for changes related to fluid balance. The skin in the groin and axilla is slightly moist to touch in a well-hydrated patient. In older patients, these typical assessment findings may be absent.

Other indicators that the patient’s hydration status is adequate for metabolic demands include a balanced intake and output and absence of thirst. Absence of thirst, however, is not a reliable indicator of dehydration in those with decreased thirst mechanisms such as the older or critically ill patients. Absence of abrupt changes in mental status may also indicate normal hydration. Other indicators of normal hydration include absence of edema, stable weight, and urine specific gravity that falls within the normal range (1.005 to 1.030).

Laboratory Assessment

No single diagnostic test identifies dysfunction of the posterior pituitary gland. Diagnosis usually is made through the patient’s clinical presentation and history. Although serum measurement of ADH is available, it is rarely obtained in critical illness.

Serum Antidiuretic Hormone

The normal serum ADH range is 1 to 5 picogram per milliliter (pg/mL). Prior to ADH measurement, all medications that may alter the release of ADH are withheld for a minimum of 8 hours. Common medications that affect ADH levels include morphine sulfate, lithium carbonate, chlorothiazide, carbamazepine, oxytocin, and selective serotonin reuptake inhibitors (SSRIs). Nicotine, alcohol, positive-pressure and negative-pressure ventilation, and emotional stress also influence ADH.

Serum ADH levels are then compared with the blood and urine osmolality to differentiate syndrome of inappropriate antidiuretic hormone (SIADH) from central diabetes insipidus (DI). Increased ADH levels in the bloodstream compared with a low serum osmolality and elevated urine osmolality confirms the diagnosis of SIADH. Reduced levels of serum ADH in a patient with high serum osmolality, hypernatremia, and reduced urine concentration signal central DI. Chapter 33 provides more information about SIADH and DI.

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