Disorders of Glucose Homeostasis
Most disorders of carbohydrate metabolism are related to diabetes mellitus (DM) and represent a broad category of emergency conditions. Toxin ingestion, medications, multisystem trauma, head injury, cardiovascular disease, cerebrovascular disease, and infection can mimic or exacerbate these conditions. Clinical appearance may vary dramatically. Patients may present with significant mental status changes or appear well while on the brink of metabolic decompensation.
- Symptoms and signs include fatigue, tachypnea (Kussmaul’s respirations), tachycardia, altered mental status, abdominal pain, vomiting, polyuria, and polydipsia
- Arterial pH < 7.3, serum glucose ≥ 250 mg/dL, and serum bicarbonate ≤ 15 mEq/L
Diabetic ketoacidosis (DKA) is the most common acute life-threatening complication of diabetes. It is more commonly seen in type 1 diabetes but may occur in type 2. Patients with type 1 DM have an absolute insulin deficiency. When the production of insulin in the pancreas fails, the decreased glucose utilization creates a relative state of starvation. Counter-regulatory hormones (cortisol, glucagon, catecholamine, and growth hormone) that help maintain blood glucose levels adequate for cellular function during fasting are stimulated. These hormones promote gluconeogenesis and glycogenolysis, increasing glucose levels, and lipolysis, which converts adipose to free fatty acids. Without insulin to allow cellular absorption of glucose, these mechanisms continue to produce glucose. Severe dehydration and electrolyte losses develop as the kidneys filter the highly osmotic glucose. Furthermore, free fatty acids that cannot enter the citric acid cycle without insulin are oxidized into ketones. These accumulate to cause metabolic acidosis, further electrolyte derangement, and exocrine pancreatic dysfunction.
If a diabetes history is elicited or known, ascertain potential precipitating causes of DKA:
- Recent or current infection of any type (most common)
- Injury or trauma
- Acute coronary syndrome or myocardial infarction
- Transient ischemic attack or stroke
- Medications (corticosteroids, thiazides, or sympathomimetics)
- Acute or acute-on-chronic pancreatitis
- Ethanol or drug abuse
- Gastroenteritis or GI bleeding
- Psychosocial factors, such as depression or inability to afford medications, limiting compliance
- Noncompliance with insulin regimen due to psychological or physiological reasons
Although noncompliance or misuse of insulin is a frequent cause of DKA, consideration of other causes of decompensation is imperative. Infection or illness may prompt patients to underdose. Up to 25% of DKA admissions results from new-onset diabetes. Alcoholic ketoacidosis (AKA), starvation, lactic acidosis, renal failure, or ingestions such as salicylates, methanol, ethylene glycol, or paraldehyde should be considered in the differential diagnosis of DKA.
Typical findings include general fatigue and weakness, orthostasis, abdominal pain, and Kussmaul’s respirations (rapid deep respirations attempting to compensate for acidosis). A fruity or acetone-like odor is classically described along with historical findings of polyuria, polydipsia, and polyphagia; nausea and vomiting are found in up to 25% of patients. Emesis may have a coffee ground appearance due to hemorrhagic gastritis. Mental status changes ranging from mild confusion to coma may be seen. DKA alone does not cause fever.
Laboratory features include serum glucose ≥ 250 mg/dL, serum ketones or ketonuria, serum bicarbonate ≤ 15 mEq/L, and arterial pH < 7.3. Arterial blood gas (ABG) determination can be limited to patients with an uncertain diagnosis or respiratory concerns. Venous blood is an acceptable alternative. The pH value is usually 0.03 lower than that of arterial blood. This is especially useful for repeated pH determinations. The degree of leukocytosis often correlates with the degree of ketosis.
Because the initial serum potassium is unpredictable, the determination of serum potassium should precede insulin therapy. Acidosis drives potassium out of the cells causing a relatively higher serum potassium level despite total body deficits that may be as much as 3–5 mEq/kg. If serum potassium is initially low, insulin administration will exacerbate the situation by facilitating the cellular entry of potassium. The rapid development of severe hypokalemia may cause symptoms such as fatigue and muscle cramps or lead to a lethal arrhythmia.
Significant diuresis and emesis frequently lower serum sodium. Osmotic shifts from hyperglycemia also dilute the serum and fictitiously lower the reported sodium value. This effect can be corrected by adding 1.8 mEq/L to the serum sodium concentration for each 100 mg/dL above normal.
Sodium deficits may approach 7–10 mEq/kg; however, rapid correction with increasing osmolality may precipitate cerebral edema, especially in children.
Serum phosphate values may be normal or elevated despite deficits approaching 1 mmol/kg body weight. Routine phosphate repletion does not improve outcome in DKA and is generally not indicated in the emergency department (ED). Severe hypophosphatemia (<1 mg/dL), however, may cause skeletal, cardiac, and respiratory muscle depression. Phosphate should be replaced in this circumstance. This can be done by using potassium phosphate as 1/3 of potassium replacement.
The anion gap is useful to assess severity of acidosis and to follow progress of therapy. The anion gap is obtained from the formula:
Anion Gap = [Na] – ([Cl] + [HCO3])
Normal values are 8–16.
Serum osmolality values above 340 mOsm/kg usually result in mental status changes. Below this value, other causes for lethargy or coma should be investigated. This value may also be used to diagnose hyperosmolar hyperglycemic state (HHS) and ingestions of ethanol, ethylene glycol, or other alcohols. Effective serum osmolality can be estimated by the formula:
Serum osmolality = 2[Na] + (glucose/18) + (blood urea nitrogen/2.8).
The laboratory determination of serum ketones is not always reliable as a diagnostic test. The primary ketone body formed in DKA initially is β-hydroxybutyrate. However, standard ketone assays measure only acetoacetate. Since insulin is required for the conversion of β-hydroxybutyrate to acetoacetate, these assays may be reassuringly negative even in a severely ill patient. Due to insulin’s effect, in most cases serum ketone values will initially increase as the patient improves before resolving.
These levels may be elevated because of severe dehydration, acute tubular necrosis, or renal failure. In these circumstances, establish urine output prior to initiating potassium repletion.
Levels of both enzymes can be elevated in DKA in the absence of pancreatic pathology.
See below.
- Most symptoms relate to severe dehydration
- Absence of acidosis, small or absent serum ketones, and hyperglycemia usually ≥ 600 mg/dL
- Kussmaul’s respirations and abdominal pain are unusual findings
In contrast to DKA, patients with HHS have sufficient insulin activity to prevent lipolysis and ketogenesis. HHS results from gradual diuresis, resulting in severe dehydration and electrolyte depletion without significant early symptoms. This leads to profound electrolyte deficiencies and eventually mental status changes. In contrast, DKA often manifests symptoms more suddenly over hours to a few days due to acidosis.
HHS is often caused by physiologic stressors such as infection, myocardial infarction, cerebrovascular accident, trauma, decreased access to water, and medication effects or interactions.
Risk factors for HHS include age greater than 65, residence in a chronic care facility or nursing home, change in diabetes regimen, addition of medications that may elevate glucose levels (e.g., corticosteroids, thiazides, anticonvulsants, immunosuppressants, sympathomimetics), recent or current infection, and dementia. Other factors include myocardial infarction, Cushing’s syndrome, intracranial hemorrhage, cerebrovascular accident, Down’s syndrome, trauma/burns, hemodialysis, and hyperalimentation.
These include polydipsia, polyuria, or polyphagia; generalized weakness; altered mental status (clouded thinking to confusion to lethargy or coma); dry mucous membranes; poor skin turgor; and delayed capillary refill. Since the average fluid deficit is 9 L, tachycardia and orthostatic hypotension are common.
Abdominal pain is not a typical finding in HHS (in contrast to DKA); its presence merits aggressive investigation for a precipitating cause. Acute cholecystitis and appendicitis may be insidious and have an atypical presentation in elderly patients.
Key findings to diagnose HHS and differentiate it from DKA are as follows:
- HHS typically is associated with a greater fluid deficit (9 L vs. 3–5 L).
- Serum glucose ≥ 600 mg/dL.
- Urine or serum ketones are small or absent (a small amount of ketone may be detected secondary to starvation).
- Glucosuria is prominent.
- Serum bicarbonate is usually >15 mEq/L.
- pH is usually >7.30, but the patient can have acidemia from lactate, starvation ketosis, or renal insufficiency.
- The anion gap may be variable depending on precipitating cause but is usually ≤10.
- Serum osmolality is 320–380 mOsm/kg.
In the early stages of HHS, serum sodium findings are similar to those in patients with DKA. Urinary losses and fluid shifts out of the cell and into the extracellular compartment create hyponatremia usually 125–130 mg/dL. Correct for hyperglycemia with the addition of 1.8–2.4 mg/dL sodium per 100 mg/dL of glucose.
Serum potassium levels will most commonly be normal or low, unless renal failure is present. Total body deficits are often 4–6 mEq/L, which is as much as 500 mEq total.
Blood urea nitrogen (BUN) is often markedly elevated. Gastrointestinal bleeding may also elevate BUN and is a possible precipitating cause of HHS in elderly patients.
Ancillary diagnostic testing should also be considered including serial ECGs and cardiac enzymes, cranial and abdominal tomography, and evaluation for gastrointestinal hemorrhage. Bedside ultrasonography may also be useful.
Treatment of DKA and HHS is very similar. Continuous monitoring of vital signs, mental status, and laboratory parameters is essential. A flow sheet may be helpful during resuscitation due to the complexity of treatment and need for frequent therapeutic changes.
Standard airway management is indicated. If tracheal intubation is required, avoid succinylcholine unless hyperkalemia is excluded. Hypoxia should trigger an investigation for aspiration, pneumonia, or pulmonary edema. Maintain oxygen saturation above 96% or Po2 ≥70 mm Hg for all DKA or HHS patients.
Fluid therapy is dictated by three parameters: vital signs, corrected serum sodium, and serum glucose. Overall fluid deficits approach 6–10 L in most patients. Large-bore (≥18-gauge) intravenous lines are essential. Central venous access may be indicated. Hypotension should prompt a bolus of 1–2 L of 0.9% NaCl solution to restore blood pressure to at least 90 mm Hg.
Caution: Decreased cardiac systolic function and renal failure complicate crystalloid resuscitation. Reassess patients frequently for adequate urine output and signs of pulmonary edema or congestive heart failure. Invasive hemodynamic monitoring may be indicated in very select cases to facilitate fluid management if cardiogenic shock is present.
Serum electrolytes including potassium, bicarbonate, and sodium should be monitored every hour along with hourly glucose determination. The calculated serum osmolality should not decrease more than ∼3 mOsm/kg/h due to increased risk of cerebral edema.
- Usually 1–1.5 L of 0.9% saline is infused over the first hour while initial laboratory values are determined. Subsequent infusion can be decreased to 500 mL/h, then 250–500 mL/h, and then 150–300 mL/h as the hydration status improves. Correct one-half of the fluid deficit over the initial 8 hours, and the other half over the following 24 hours.
If the serum sodium is high normal or high, 0.45% saline is recommended after initial fluid boluses to avoid severe hypernatremia. If serum sodium is low or low normal, 0.9% saline should be continued.
- Once serum glucose reaches approximately 250 mg/dL, 5% dextrose in 0.45% NaCl is the fluid of choice at a rate of 250 mL/h; alternatively, use 5% dextrose in normal saline if the corrected serum sodium remains low.
The clinical relevance of the urine output is unreliable while glucose levels remain high due to osmotic diuresis. Once glucose levels approach normal, urine output may be used to guide therapy; 30–50 cc/h is considered adequate.
Cerebral edema may occur in the following cases: correcting acidosis too rapidly, correcting glucose too rapidly, overaggressive IV fluid resuscitation.
Potassium repletion may begin once continuous urine output is confirmed and an initial potassium level is determined. With target levels of 4.0–5.0 mEq/L, the following algorithm is useful:
- If the serum potassium is 3.3 mEq/L or less, withhold insulin therapy and give potassium replacement. Give 40 mEq potassium chloride intravenously or a mixture of two-thirds potassium chloride and one-third potassium phosphate (∼5 mmol) if serum phosphate is less than 1 mmol/L. Potassium chloride, 40 mEq, may also be given orally or by nasogastric tube. This method allows for safer administration of larger doses of potassium and is the preferred replacement method if oral dosage is tolerated. Assume a deficit of about 100 mEq potassium for each 1 mEq/L below normal.
- If the serum potassium is 3.3–5.0 mEq/L, give 20–30 mEq potassium chloride in each liter of intravenous fluid.
- If the serum potassium is 5.0 mEq/L or more, hold potassium repletion and recheck the serum potassium in 1 hour. If levels remain significantly elevated (above 6 mEq/L) or ECG changes are noted, a regular insulin bolus of 8–12 units can be given along with other standard treatments for hyperkalemia.
- Magnesium is often deficient due to diuresis, and may worsen vomiting.
Intravenous regular insulin is used for initial therapy. Subcutaneous insulin may be absorbed erratically in volume-depleted patients. A continuous infusion of regular insulin at 0.1 units/kg body weight per hour is the treatment of choice. Historically, after the serum potassium determination, a bolus of 0.1–0.15 units/kg body weight of regular insulin was considered (not recommended in pediatric patients). Due to the risk of cerebral edema, one should avoid insulin boluses even in adult patients; continuous infusion of insulin is optimal. If glucose is not decreasing by at least 50–70 mg/dL/h, the insulin dosage should be doubled until this rate of decline is achieved. Decrease insulin infusion by 25–75% if the decline in serum glucose is more than 100 mg/dL/h since this results in rapid shifts in serum osmolality.
Insulin therapy should be delayed if the potassium level is less than 3.3 mEq/L until the potassium level is rising.
Sodium bicarbonate therapy is generally not indicated except for unstable patients with severe acidosis such as an arterial pH < 6.9. Bicarbonate therapy is rarely indicated for HHS patients. The incidence of cerebral edema increases with aggressive bicarbonate use (particularly in children). There is no proven impact on outcome in controlled trials when bicarbonate therapy was used for severe acidosis. However, due to the catastrophic potential of severe acidosis, bicarbonate therapy may be considered in these patients. NaHCO3 (50 mmol) is diluted in 200 mL sterile water and infused at 200 mL/h. This may be repeated every 2 hours until the venous pH is greater than 7.
Infection is the most common pathological precipitant of DKA and HHS. The patient’s entire skin surface should be examined for wounds and cellulitis. A pelvic examination may be indicated to rule out infection. Analysis and cultures of all appropriate body fluids (blood, sputum, urine, cerebrospinal fluid) should be obtained. The empiric administration of broad-spectrum antibiotics should be considered until culture results are available.
Patients with all but very mild cases of DKA and all patients with HHS should have cardiac monitoring and a higher level of nursing care for at least 24 hours. Whether the patient goes to an intermediate care, telemetry unit, or the intensive care unit is based on severity of the case and response to initial therapy as judged by the treating physician.
Hyperglycemia in the absence of metabolic decompensation (DKA or HHS) is a common finding in the ED. Patients with either known or undiagnosed diabetes may present with symptoms due to hyperglycemia, complications of untreated diabetes, or numerous unrelated conditions that incidentally have high blood glucose levels.
Age greater than 45, obesity, physical inactivity, and family history are risk factors for insulin resistance. Personal history of gestational diabetes, impaired glucose tolerance, hypertension, dyslipidemia, vascular disease, or polycystic ovary disease also increases risk.
Symptoms of hyperglycemia may include polydipsia, polyuria, polyphagia, weakness, fatigue, headache, blurred vision, dehydration, lightheadedness, or dizziness.
Infections are much more common in poorly controlled diabetics. Superficial skin infections such as cellulitis, furuncles, abscesses, nonhealing wounds, and ulcers are very common complaints. Urinary tract infections and candidal infections, malignant otitis externa, and rhinocerebral mucormycosis all have epidemiologic associations with hyperglycemia.
A random serum glucose greater than 200 mg/dL with symptoms of hyperglycemia or metabolic decompensation (DKA or HHS) or a fasting serum glucose greater than 126 mg/dL on repeat occasions is diagnostic of diabetes. Impaired fasting glucose is defined as a fasting plasma glucose of 110–126 mg/dL. Glycosylated hemoglobin, or HbA1C, can facilitate the diagnosis of diabetes, and is becoming more valued as a screening test. Levels of 7% or more are nearly always consistent with diabetes.
Severe hyperglycemia (≥400 mg/dL) may foreshadow impending decompensation. An underlying cause should be sought aggressively such as infection, cardiac ischemia, or myocardial infarction. White blood cell count, blood cultures, and ECG with cardiac enzymes may be helpful. Lack of compliance with antidiabetic regimen or diet should always be exclusionary. In this setting evaluate electrolytes, BUN, creatinine, and serum bicarbonate to screen for metabolic decompensation.
If diabetes was previously undiagnosed and insulin deficiency (type 1) cannot be excluded, then the patient should be admitted. Insulin resistance (type 2) is much more common. If hyperglycemia is mild (<250–350 mg/dL) with no signs of decompensation, no specific treatment is required if primary care follow-up is readily available. Newly diagnosed patients should also be counseled on diet and the importance of follow-up. If the serum glucose is greater than 300 mg/dL, treatment is as follows:
Normal saline 1 L given over 1 hour may be adequate monotherapy for hyperglycemia.
Usually 0.1–0.15 units/kg regular insulin, insulin lispro (Humalog), or insulin aspart (NovoLog) can be given subcutaneously or intravenously. Insulin may be rebolused intravenously if glucose does not decline by 50–75 mg/dL in the first hour.
Oral hypoglycemic agents are generally not indicated for acute therapy of severe hyperglycemia. Oral agents may, however, be initiated or continued by emergency physicians when follow-up is available.
Metformin inhibits fasting hepatic glucose production and promotes weight loss. It is an attractive option that should only be prescribed if follow-up is possible, since it is the least likely to cause hypoglycemia. Metformin can be safely started at 500 mg orally once per day; the dosage can be increased by 500 mg/d each week until 1000 mg twice a day is reached. It should not be given if serum creatinine levels are above 1.4 mg/dL, due to the risk of developing lactic acidosis. Metformin should also be avoided in the following circumstances: risk of hypoxemia, CHF, hepatic impairment, renal insufficiency, acute infection, age >80 or <17, alcoholic, exposure to contrast in the past 48 hours, or planned exposure to contrast.
Initial treatment with sulfonylurea, thiazolidinediones, and α-glucosidase inhibitors is best withheld until the patient has received diabetes education. If education can be provided along with supplies such as glucometer and test strips, these agents can be started in conjunction with consultation and close follow-up. When adjusting an existing oral agent or insulin dosage, do not increase insulin dosages by more than 10% or sulfonylurea dosage by more than about 20%.
Most patients with blood glucose less than 250–350 mg/dL in the absence of metabolic decompensation can be safely discharged with follow-up after a thorough evaluation for underlying illness. Patients with serious underlying precipitants or in whom hyperglycemia is resistant to treatment should be hospitalized.
- Common symptoms and signs include irritability, diaphoresis, and tachycardia related to increased circulating catecholamines
- As hypoglycemia progresses, neuroglycopenic effects range from focal neurologic deficits such as diplopia and paresthesias to coma
- Always check the fingerstick blood glucose on every patient presenting with altered mental status or who appears to be acutely ill
Symptoms can include altered mental status, focal neurologic deficits, and coma. Even mild, treated episodes can exacerbate preexisting microvascular disease and lead to cumulative brain damage.
Hypoglycemia is commonly defined as serum glucose of <50 mg/dL. Less than 30 mg/dL is considered severe hypoglycemia. This most commonly occurs in diabetics on exogenous insulin therapy. Changes in daily activities such as diet, exercise, or dosage changes may result in hypoglycemia. Many other factors, however, may result in hypoglycemia such as infection, endocrine disorders, drugs or alcohol, liver failure, intentional overdose of insulin, tumors or malnutrition in both diabetics and nondiabetics.
Other causes of hypoglycemia include glycogen storage disease (esp von Gierke’s), carnitine deficiency, sepsis, Addisonion crisis, beta blocker overdose, pregnancy, salicylate toxicity.
In patients with known diabetes, hypoglycemia may occur as a result of the following:
- Delay in eating after taking insulin, general malnutrition, or inadequate caloric intake due to nausea and vomiting or gastroparesis.
- Increased physical activity.
- Increased physiologic stress resulting from infection or injury.
- Excessive dose of exogenous insulin (Note: Remember to check the patient’s vision and confirm that he or she can read the syringe appropriately.).
- Variable absorption from injection sites.
- Impaired counter-regulatory hormone axis.
- Excessive insulin release produced by sulfonylurea drugs, especially in the presence of renal insufficiency.
- Alterations in therapeutic regimen, particularly increases in insulin or oral agent dosages or the addition of new oral agents such as thiazolidinediones (also known as glitazones), which may reduce insulin resistance and improve therapeutic action of endogenous or exogenous insulin.
- Intentional hypoglycemia may result from insulin or antihyperglycemic agents such as sulfonylurea that may be taken by, or given to, the patients. C-peptide is naturally secreted along with insulin by the pancreas and is not present in manufactured insulin. A high insulin level without a correspondingly high C-peptide level is diagnostic of exogenous insulin.
Tumor of the insulin-secreting β-cells in the islets of Langerhans may cause refractory hypoglycemia and even coma. C-peptide levels will elevate concurrently with insulin levels.
Acute or chronic excessive ethanol intake, especially without adequate caloric intake, may cause severe hypoglycemia (especially in children). Chronic abuse reduces NADH-mediated gluconeogenesis and depletes hepatic glycogen production and storage.
Caution: Administer thiamine, 100 mg, to alcoholic patients with hypoglycemia to avoid Wernicke’s encephalopathy.
The intake of large amounts of concentrated calories in nondiabetics may produce enough excess insulin to induce mildly symptomatic hypoglycemia. Rarely, hypoglycemia may be severe enough to cause briefly decreased level of consciousness.
Try to obtain a history of diabetes from emergency medical services, family, Medic Alert bracelet, necklace, or wallet card. Emergency medical services or family may also be helpful in disclosing alcohol use, recent caloric intake, alterations of medication regimen, and recent illness or injury.
Most early symptoms and signs are the result of increased catecholamine release: tachycardia, irritability, diaphoresis, paresthesias, hunger, and decreased concentration are common. With more severe or prolonged hypoglycemia, symptoms and signs of neuroglycopenia result in mental status changes including confusion or bizarre behavior, lethargy, or coma; visual disturbances such as blurred vision, diplopia, hallucinations; seizures or seizure-like activity or focal neurologic deficits similar to Todd’s paralysis that resolves with glucose administration.
The capillary or fingerstick glucose is a rapid screen to determine blood glucose levels. Glucometers become unreliable at readings less than 40 mg/dL. Obtain a sample for laboratory determination.
Search for ancillary causes of hypoglycemia such as infection or sepsis, myocardial infarction, cerebrovascular accident, renal insufficiency or failure, alcohol use, pregnancy, drug use (particularly stimulants), occult trauma, depression (poor caloric intake or insulin or oral agent overdose), and other endocrinopathies (Addison’s disease, myxedema, thyrotoxicosis, pituitary insufficiency).
If intravenous access is readily obtainable, administer 50 cc of 50% dextrose in water (containing approximately 25 g of glucose, which is enough to resolve most hypoglycemic episodes). Caution: Remember to give thiamine, 100 mg intravenously or intramuscularly, to alcoholic patients to prevent Wernicke’s encephalopathy. Monitor the patient’s mental status and recheck capillary blood glucose 15–30 minutes after glucose administration. Repeat dosages of 50% dextrose or infusion of glucose-containing intravenous fluids (5–10%) may be necessary to maintain adequate blood glucose levels. Neuroglycopenia (altered level of consciousness, seizure-like activity, focal neurologic deficits) may take time to resolve completely. If abnormalities persist longer than 30 minutes after glucose administration and hypoglycemia has not recurred, other causes should be investigated with a cranial CT scan and appropriate laboratory studies.
As soon as the patient regains consciousness (or in an already conscious patient), clear fruit juice (eg, apple, grape; 6 oz ≅ 15 g glucose) is a good choice to maintain glucose levels, a snack or meal is appropriate.
If intravenous access is not readily available, 1 mg of glucagon may be given intramuscularly. The response time is typically 10–15 minutes, and nausea and vomiting along with overcorrection of glucose levels are common. Since glucagon can be given intramuscularly, all patients with insulin-treated diabetes (or their families) should carry and be familiar with the use of glucagon emergency kits.
Consider the duration of action of the insulin or oral agents taken by the patient. Hourly capillary glucose checks should be taken until glucose levels are stable. Generally the patient should be observed through the peak time of the longest-acting insulin, typically 30 minutes to 1–2 hours after the dose with insulin lispro or insulin aspart, 2–4 hours with regular insulin, or 6–8 hours with NPH. Insulin glargine has no peak activity and does not generally cause hypoglycemia by itself. Patients taking long-acting insulins with peak activity, such as lente or ultralente, or patients taking sulfonylurea oral agents should generally be observed in the hospital.
Indications for admission include persistent or recurrent hypoglycemia despite appropriate therapy, hypoglycemia related to an oral agent or long-acting insulin, and unknown cause of hypoglycemia or serious ancillary cause (eg, severe infection, persistent nausea, and vomiting).
Conditions for discharge include well-understood cause of hypoglycemia, easily reversible episode, availability of responsible adult to observe the patient for next 8–12 hours; ability to take oral fluids and food; medical follow-up available within 24–48 hours; and ability to check blood glucose levels.
With advances in the treatment of insulin-dependent diabetes mellitus, more ED physicians will encounter patients who have insulin pumps. These devices come in various brands. The pump consists of a device worn by the patient, which has a reservoir for fast-acting insulin. Tubing connects the reservoir to a subcutaneous site implanted on the trunk or thigh of the patient. Insulin is administered as a continuous basal rate with the addition of bolus therapy with carbohydrate intake. Although associated with iatrogenic hypoglycemia, insulin pumps help the motivated/educated patient achieve tight glycemic control.
