AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Diabetes mellitus is a chronic disease that requires long-term medical attention both to limit the development of its devastating complications and to manage them when they do occur. It is a disproportionately expensive disease; in 2002, the per-capita cost of health care was $13,243 for people with diabetes, while it was $2560 for those without diabetes.

This article focuses on the ED evaluation and treatment of the acute and chronic complications of diabetes other than those directly associated with hypoglycemia and severe metabolic disturbances, such as diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS). (Please see Hypoglycemia, Diabetic Ketoacidosis, and Hyperosmolar Hyperglycemic Nonketotic Coma for more information on these disorders.)

Pathophysiology

Type 1 diabetes mellitus can occur at any age and is characterized by the marked and progressive inability of the pancreas to secrete insulin because of autoimmune destruction of the beta cells. It commonly occurs in children, with a fairly abrupt onset; however, newer antibody tests have allowed for the identification of more people with the new-onset adult form of type 1 diabetes mellitus called latent autoimmune diabetes of the adult (LADA). The distinguishing characteristic of a patient with type 1 diabetes is that, if his or her insulin is withdrawn, ketosis and eventually ketoacidosis develop. Therefore, these patients are dependent on exogenous insulin.

Type 2 diabetes mellitus is discussed in Diabetes Mellitus, Type 2 - A Review. A variety of other types of diabetes, previously called secondary diabetes, are caused by other illnesses or medications. Depending on the primary process involved (eg, destruction of pancreatic beta cells or development of peripheral insulin resistance), these types of diabetes behave similarly to type 1 or type 2 diabetes. The most common are diseases of the pancreas that destroy the pancreatic beta cells (eg, hemochromatosis, pancreatitis, cystic fibrosis, pancreatic cancer), hormonal syndromes that interfere with insulin secretion (eg, pheochromocytoma) or cause peripheral insulin resistance (eg, acromegaly, Cushing syndrome, pheochromocytoma), and diabetes induced by drugs (eg, phenytoin,glucocorticoids, estrogens).

Gestational diabetes mellitus (GDM) is defined as any degree of glucose intolerance with onset or first recognition during pregnancy. GDM is a complication of approximately 4% of all pregnancies in the United States. Untreated GDM can lead to fetal macrosomia, hypoglycemia, hypocalcemia, and hyperbilirubinemia. In addition, mothers with GDM have increased rates of cesarean delivery and chronic hypertension. To screen for GDM, a 50-g glucose screening test should be done at 24-28 weeks of gestation. This is followed by a 100-g, 3-hour oral glucose tolerance test if the patient's plasma glucose concentration at 1 hour after screening is greater than 140 mg/dL.

Frequency

United States

In 2005, people with diabetes were estimated to account for 7% of the US population, or approximately 20.8 million people. Of these 20.8 million people, 14.6 million have a diagnosis of diabetes, and diabetes is undiagnosed in another 6.2 million. Approximately 10% have type 1 diabetes, and the rest have type 2. Additionally, an estimated 54 million people have pre-diabetes. Pre-diabetes, as defined by the American Diabetes Association, is that state in which blood glucose levels are higher than normal but not high enough to be diagnosed as diabetes. It is presumed that most persons with elevated glucose levels approaching the level needed for the diagnosis of diabetes will subsequently progress to diabetes.

Mortality/Morbidity

The morbidity and mortality associated with diabetes are related to the short- and long-term complications.

• Complications include hypoglycemia and hyperglycemia, increased risk of infections, microvascular complications (eg, retinopathy, nephropathy), neuropathic complications, and macrovascular disease.
• Diabetes is the major cause of blindness in adults aged 20-74 years, as well as the leading cause of nontraumatic lower-extremity amputation and end-stage renal disease (ESRD).

Race

Whites seem to be affected more often than blacks, who have the lowest overall incidence of type 1 diabetes.

Sex

The male-to-female ratio is approximately 1:1.

Age

Long called juvenile-onset diabetes, type 1 diabetes is typically diagnosed in childhood, adolescence, or early adulthood. Type 1 diabetes may also develop in older adults and is increasingly being recognized through the measurement of islet–glutamate decarboxylase (GAD) antibodies.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

Correctly determining whether a patient has type 1 or type 2 diabetes is important because patients with type 1 diabetes are dependent on a continuous source of exogenous insulin and carbohydrate for survival. Patients with type 2 diabetes may not need any treatment for hyperglycemia during periods of fasting or decreased oral intake. A patient whose diabetes is controlled with diet or an oral antidiabetic agent clearly has type 2 diabetes. A lean patient who has had diabetes since childhood, who has always been dependent on insulin, or who has a history of DKA almost certainly has type 1 diabetes.

Distinguishing the type of diabetes can be difficult in (1) patients who are treated with insulin and who are younger but clinically appear to have type 2 diabetes and (2) older patients with late onset of diabetes who nonetheless take insulin and seem to share characteristics of patients with type 1 diabetes. (This latter group is now said to have LADA). When in doubt, treat the patient with insulin and closely monitor his or her glucose levels. Some adolescents or young adults, mostly Hispanic or African American patients, present as with classic DKA are subsequently found to have type 2 diabetes.

See Workup for more information on diagnosis of diabetes. See Diabetes Mellitus, Type 2 - A Review for more information on the asymptomatic patient with diabetes.

During history taking, inquire about the type and duration of the patient's diabetes and about the care the patient is receiving for diabetes.

• Type of diabetes: The diagnosis is based on history, therapy, and clinical judgment, as described above.
• Duration of diabetes: The chronic complications of diabetes are related to the length of time the patient has had the disease.
• Diabetes care: Inquire about the type of insulin being used, delivery system (pump vs injections), dose, and frequency. Also ask about oral antidiabetic agents, if any. Patients using a pump or a multiple-injection regimen have a basal insulin (taken through the pump or with the injection of a long-acting insulin analogue) and a premeal rapid-acting insulin, the dose of which is determined as a function of the carbohydrate count plus the correction (to adjust for how high the premeal glucose level is). In these patients, ask about the following:
• • Basal rate (eg, units per hour by pump, generally 0.4-2 unit/h)
  • Carbohydrate ratio (ie, units of insulin per grams of carbohydrate, generally 1 unit of rapid-acting insulin per 10-15 g carbohydrate)
  • Correction dose (ie, how far the blood glucose level is expected to decrease per unit of rapid-acting insulin, often 1 unit of insulin per 50-mg/dL decrease, but individuals with insulin resistance may need 1 per 25-mg/dL decrease)
  • Some patients may be taking premeal pramlintide.

A focused diabetes history should also include the following questions:

• Is the patient's diabetes generally well controlled (with near-normal blood glucose levels)? Patients with poorly controlled blood glucose levels heal more slowly and are at increased risk for infection and other complications.
• Does the patient have severe hypoglycemic reactions? If the patient has episodes of severe hypoglycemia and therefore is at risk for losing consciousness, this possibility must be addressed, especially if the patient drives.
• Does the patient have peripheral neuropathy?
• Does the patient have any unrecognized foot ulcers or lesions that need treatment?
• Does the patient have diabetic nephropathy that might alter the use of medications or intravenous radiographic contrast material?
• Does the patient have macrovascular disease, such as coronary artery disease (CAD) that should be considered in the ED?

As circumstances dictate, additional questions may be warranted.

• Treatment monitoring
• • Does the patient self-monitor his or her blood glucose levels? Note the frequency and range of values at each time of day. An increasing number of patients monitor with continuous sensors.
  • When was the patient's hemoglobin A_1c (HbA_1c) value (an indicator of long-term glucose control) last measured? What was it?
• Hyperglycemia: Does the patient give a history of recent polyuria, polydipsia, nocturia, or weight loss?
• Hypoglycemia
• • Has the patient had episodes of unexplained hypoglycemia? If so, when, how often, and how does the patient treat these episodes?
  • Does the patient have hypoglycemia unawareness (ie, does the patient lack the adrenergic warning signs of hypoglycemia)? Hypoglycemia unawareness indicates an increased risk of subsequent episodes of hypoglycemia. 
• Microvascular complications
• • Retinopathy: When was the patient's last dilated eye examination? What were the results?
  • Nephropathy: Does the patient have known kidney disease? What were the dates and results of the last measurements of urine protein and serum creatinine levels?
• Macrovascular complications
• • Hypertension: Does the patient have hypertension? What medications are taken?
  • CAD: Does the patient have CAD?
  • Peripheral vascular disease: Does the patient have symptoms of claudication or a history of vascular bypass?
  • Cerebrovascular disease: Has the patient had a stroke or transient ischemic attack?
  • Hyperlipidemia: What are the patient's most recent lipid levels? Is the patient taking lipid-lowering medication?
• Neuropathy: Does the patient have a history of neuropathy or symptoms of peripheral neuropathy or autonomic neuropathy present (including impotence if the patient is male)?
• Diabetic foot disease: Does the patient have a history of foot ulcers or amputations? Are any foot ulcers present?
• Infections: Are frequent infections a problem? At what site?

Physical

A diabetes-focused physical examination includes an assessment of vital signs, funduscopic examination, limited vascular and neurologic examinations, and a foot assessment. Other organ systems should be examined, as indicated by the patient's clinical situation.

• Assessment of vital signs
• • Is the patient hypertensive or hypotensive? Orthostatic vital signs may be useful in assessing the patient's volume status as well as suggesting the presence of an autonomic neuropathy.
  • If the respiratory rate and pattern suggest Kussmaul breathing, DKA must be considered immediately, and appropriate tests obtained.
• Funduscopic examination
• • Funduscopic examination should include a careful view of the retina, including both the optic disc and the macula.
  • If hemorrhages or exudates are seen, the patient should be referred to an ophthalmologist as soon as possible. Examiners who are not ophthalmologists tend to underestimate the severity of retinopathy, especially if the patients' pupils are not dilated.
• Foot examination
• • The dorsalis pedis and posterior tibialis pulses should be palpated and their presence or absence noted. This is particularly important in patients who have foot infections because poor lower-extremity blood flow can delay healing and increase the risk of amputation.
  • Documenting lower-extremity sensory neuropathy is useful in patients who present with foot ulcers because decreased sensation limits the patient's ability to protect the feet and ankles.
  • If peripheral neuropathy is found, the patient should be made aware that foot care (including daily foot examination) is very important for the prevention of foot ulcers and lower-extremity amputation.

Causes

• Patients with type 1 diabetes are believed to have a genetic susceptibility to developing the disease.
• • Exposure to a trigger (viral, environmental, toxin) stimulates immunologically mediated destruction of the beta cells.
  • As beta-cell mass declines with ongoing immunologic destruction, insulin secretion decreases until the available insulin no longer is adequate to maintain normal blood glucose levels.
  • After 80-90% of the beta cells are destroyed, hyperglycemia develops and diabetes may be diagnosed.
• In studies of identical twin pairs in which 1 twin has type 1 diabetes, antibodies to the islet cell (IA2) and to insulin (IAA) are positive for several years in the nondiabetic twin before overt diabetes develops.
• Autoantibodies to GAD (anti-GAD65) may also be present in type 1 diabetes, especially in adults.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• A fingerstick glucose test is appropriate in the ED for virtually all patients with diabetes. All other laboratory studies should be individualized to the clinical situation.
• Most patients who present to the ED with undiagnosed type 1 diabetes have the classic symptoms of uncontrolled hyperglycemia, including polyuria, polydipsia, nocturia, fatigue, and weight loss.
• • In these patients, a confirmatory random plasma glucose level of >200 mg/dL is adequate to establish the diagnosis of diabetes.
  • On occasion, a patient who is ultimately found to have type 1 diabetes presents with subtle symptoms because of residual insulin secretion.
• A fasting C-peptide level >1 ng/dL in a patient who has had diabetes for more than 1-2 years is suggestive of type 2 diabetes (ie, residual beta-cell function).
• Islet-cell autoantibodies are present in early type 1 but not type 2 diabetes.
• • Measurements of these autoantibodies (IA2) within 6 months of diagnosis can help differentiate type 1 and type 2 diabetes.
  • Titers of islet-cell autoantibodies decrease after 6 months.
  • Anti-GAD65 antibodies can be present at diagnosis and are persistently positive over time.
• See Diabetes Mellitus, Type 2 - A Review for a discussion of the diagnosis of diabetes in the asymptomatic patient.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Prehospital Care

In the absence of an acute hypoglycemic reaction or a severe metabolic disturbance such as DKA, most patients with diabetes do not require prehospital treatment of their diabetes. Typically, it is the complications of diabetes, such as accelerated macrovascular disease leading to acute myocardial ischemia, rather than the diabetes itself that results in the need for prehospital care and emergency transport.

Emergency Department Care

The ED care of patients with type 1 diabetes requires attention to both the patient's glycemic control and any of the numerous complications of diabetes the patient may have. See Diabetic Ketoacidosis and Hypoglycemia for specific details about their care.

• New-onset diabetes
• • In patients with new-onset type 1 diabetes, lifelong insulin therapy must be started. Many patients present with DKA.
  • On occasion, the patient with new-onset type 1 diabetes who presents with mild manifestations and who is judged to be compliant can begin insulin therapy as an outpatient. However, this approach requires close follow-up and the ability to provide immediate and thorough education about the use of insulin; the signs, symptoms, and treatment of hypoglycemia; and the need to self-monitor blood glucose levels.
• Abnormalities caused by hyperglycemia
• • Acute hyperglycemia, even when not associated with DKA or hyperglycemic hyperosmolar nonketotic syndrome (HNKS), is harmful for a number of reasons. If the blood glucose level exceeds the renal threshold for glucose, an osmotic diuresis ensues, with loss of glucose, electrolytes, and water. Hyperglycemia impairs leukocyte function through a variety of mechanisms. Patients with diabetes have an increased rate of wound infection, and hyperglycemia also may impair wound healing.
  • In patients with known, poorly controlled type 1 diabetes, no absolute level of blood glucose elevation requires admission to the hospital or the administration of insulin in the ED. In general, lowering the patient's glucose level in the ED does not correct the underlying cause and has no long-term effect on the patient's glucose levels. Therefore, a plan for lowering and monitoring the patients' glucose levels is needed. Adequacy of follow-up is extremely important. Whether insulin is given in the ED is of less consequence and can be decided on an individual basis.
• Hyperglycemia during medical illness and surgery
• • Serious medical illness and surgery produce a state of increased insulin resistance and relative insulin deficiency. Hyperglycemia can occur, even in patients without diabetes, because of stress-induced insulin resistance plus the use of dextrose-containing intravenous fluids. Increases in glucagon, catecholamines, cortisol, and growth hormone levels antagonize the effects of insulin, and the alpha-adrenergic effect of increased catecholamine levels inhibit insulin secretion. Counterregulatory hormones also directly increase hepatic gluconeogenesis.
  • To maintain normal blood glucose levels, treatment regimens must be modified to compensate for both decreased caloric intake and increased physiologic stress. Near-normal blood glucose levels should be maintained in medical and surgical patients with diabetes for the following reasons:
  • • To prevent the development of ketosis
    • To prevent electrolyte abnormalities and volume depletion secondary to osmotic diuresis
    • To prevent impairment of leukocyte function that occurs when blood glucose levels are elevated
    • To prevent impairment of wound healing that occurs when glucose levels are elevated
  • Patients with type 1 diabetes must take in insulin and carbohydrate at all times to prevent ketosis. For seriously ill patients and those undergoing general anesthesia, the optimal regimen includes continuous intravenous infusions of dextrose and insulin. This technique requires that the blood glucose level be measured hourly and that the insulin and dextrose infusion rates be adjusted accordingly to prevent hypoglycemia or persistent hyperglycemia. Many different insulin infusion protocols are available, and it is recommended that protocols be adopted and followed at each institution to avoid medication errors.
  • Frequent blood glucose monitoring is not always possible, and patients with less serious illness or those undergoing minor surgery may do as well with subcutaneously injected insulin. In patients who are on a basal bolus insulin regimen (generally with a basal long-acting insulin and premeal rapid-acting insulin), the basal insulin dose can simply be continued before surgery. Rapid-acting insulin should be given as a correction dose to keep blood glucose levels in the normal range during and after surgery. If a patient is on an NPH-based regimen, their total daily NPH dose should be calculated and half of the total given the morning before surgery. In all patients given insulin prior to surgery, an intravenous infusion of 5% dextrose should be started at a rate of 125 mL/h. Blood glucose levels should be checked every 2 hours, and small doses of rapid-acting or regular insulin should be given if values are greater than 120 mg/dL.
  • The same principles of providing a constant source of insulin and carbohydrate apply to patients with type 1 diabetes who must also take nothing by mouth (NPO) for medical reasons. Patients should receive a basal insulin, such as glargine or detemir insulin, with additional correction doses using regular insulin or a rapid-acting insulin (eg, lispro). To avoid hypoglycemia, regular insulin should not be given more often than every 3-4 hours because a dose is effective for up to 6 hours. Rapid-acting insulins may be given every 3 hours.
  • Cardiovascular disease or renal dysfunction increases surgical morbidity and mortality, and diabetic autonomic neuropathy increases the risk of cardiovascular instability. The emergency physician caring for patients with diabetes who require emergency surgery must notify the surgeon and the anesthesiologist of the patient's condition, consult medical specialists when appropriate, and promptly initiate a thorough medical evaluation.
• Infections in general
• • Infections cause considerable morbidity and mortality in patients with diabetes. Infections may precipitate metabolic derangements and, conversely, the metabolic derangements of diabetes may facilitate infection. Infections have been identified as the precipitant of 26-77% cases of DKA.
  • A few infections, such as malignant otitis externa, rhinocerebral mucormycosis, and emphysematous pyelonephritis, occur almost exclusively in patients with diabetes. Infections such as staphylococcal sepsis occur more frequently and result in greater mortality rates in patients with diabetes than in others. Infections such as pneumococcal pneumonia affect patients with diabetes and others the same.
  • Hyperglycemia and acidemia exacerbate impairments in humoral immunity and polymorphonuclear leukocyte and lymphocyte functions but are substantially reversed when pH and blood glucose levels return to normal. Although the exact level above which leukocyte function is impaired is not defined, in vitro evidence suggests that glucose levels greater than 200 mg/dL impair leukocytic function.
  • Patients with long-standing diabetes tend to have microvascular and macrovascular disease with resultant poor tissue perfusion and increased risk of infection. The ability of the skin to act as a barrier to infection may be compromised when the diminished sensation of diabetic neuropathy results in unnoticed injury.
• Ear, nose, and throat infections
• • Two head and neck infections that are associated with high rates of morbidity and mortality are malignant otitis externa and rhinocerebral mucormycosis; these are seen almost exclusively in patients with diabetes.
  • Malignant or necrotizing otitis externa principally occurs in patients with diabetes who are older than 35 years and is almost always due to Pseudomonas aeruginosa.
  • • Infection starts in the external auditory canal and spreads to adjacent soft tissue, cartilage, and bone. Patients typically present with severe ear pain and otorrhea. Although they often have preexisting otitis externa, progression to invasive disease is usually rapid.
    • Examination of the auditory canal may reveal granulation tissue, but spread of infection to the pinna, preauricular tissue, and mastoid often makes the diagnosis apparent. Involvement of the cranial nerves, particularly the facial nerve, is common; when infection extends to the meninges, it is often lethal.
    • CT helps define the extent of disease.
    • Prompt surgical consultation is mandatory for malignant otitis externa because surgical debridement is often an essential part of therapy. Intravenous antipseudomonal antibiotics should be started immediately in patients with invasive disease. Patients with diabetes with severe otitis externa but no evidence of invasive disease can be treated with an otic antibiotic drop and oral ciprofloxacin; they require close follow-up.
  • Mucormycosis collectively refers to infections caused by various ubiquitous molds. Invasive disease occurs in patients with poorly controlled diabetes, especially with DKA. Organisms colonize the nose and paranasal sinuses, spreading to adjacent tissues by invading blood vessels and causing soft tissue necrosis and bony erosion.
  • • Patients usually present with periorbital or perinasal pain, swelling, and induration. Bloody nasal discharge may be present. Involvement of the orbits, with lid swelling, proptosis, and diplopia, is common.
    • The nasal turbinates may appear dusky red or frankly necrotic. Black necrotic tissue is an important visual clue. The infection may invade the cranial vault through the cribriform plate, resulting in cerebral abscess, cavernous sinus thrombosis, or thrombosis of the internal carotid artery.
    • Wet smears of necrotic tissue often reveal broad hyphae and distinguish mucormycosis from severe facial cellulitis. CT helps delineate the extent of disease.
    • Treatment consists of controlling the predisposing hyperglycemia and acidemia, giving intravenous amphotericin B, and immediate surgical debridement. Until the diagnosis is confirmed, antistaphylococcal antibiotic therapy is appropriate.
• Urinary tract infections
• • Patients with diabetes have an increased risk of cystitis and, more important, serious upper urinary tract infection. Intrarenal bacterial infection should be considered in the differential diagnosis of any patient with diabetes who presents with flank or abdominal pain.
  • The treatment of cystitis is essentially the same as that in patients without diabetes, except that longer courses of therapy are generally recommended (eg, 7 d for uncomplicated cystitis). Individuals with a neurogenic bladder due to diabetic neuropathy may not empty their bladder well and may require urologic referral.
  • Treatment of pyelonephritis does not differ for patients with diabetes, but a lower threshold for hospital admission is appropriate. First, pyelonephritis makes control of diabetes more difficult by causing insulin resistance; in addition, nausea may limit the patient's ability to maintain normal hydration. The ensuing hyperglycemia further compromises their immune response. Second, patients with diabetes are more susceptible than others to complications of pyelonephritis (eg, renal abscess, emphysematous pyelonephritis, renal papillary necrosis, gram-negative sepsis).
  • More than 70% of cases of emphysematous pyelonephritis occurred in patients with diabetes. Emphysematous pyelonephritis is an uncommon necrotizing renal infection caused by Escherichia coli, Klebsiella pneumoniae, or other organisms capable of fermenting glucose to carbon dioxide. The presentation is usually similar to that of uncomplicated pyelonephritis, and the diagnosis is established by identifying renal gas on plain radiography, CT, or sonography. Surgery is indicated after diagnosis.
• Skin and soft tissue infections
• • Sensory neuropathy, atherosclerotic vascular disease, and hyperglycemia all predispose patients with diabetes to skin and soft tissue infections. These can affect any skin surface but most commonly involve the feet.
  • Cellulitis; lymphangitis; and, most ominously, staphylococcal sepsis can complicate even the smallest wound. Minor wound infections and cellulitis are typically caused by Staphylococcus aureus or hemolytic streptococci. Treatment with a penicillinase-resistant synthetic penicillin or a first-generation cephalosporin has been effective for the outpatient treatment of minor infections, but the increasing prevalence of community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) must now be considered when selecting an antibiotic. Patients with diabetes do not appear to have a higher prevalence of CA-MRSA than comparable patients without diabetes.
  • Outpatient treatment of minor infections is appropriate for patients who are reliable, who monitor their blood glucose and urine ketone levels, and who have access to close follow-up.
  • Necrotizing infections of the skin, subcutaneous tissues, fascia, or muscle can also complicate wounds and particularly cutaneous ulcers. These infections are typically polymicrobial, involving group A streptococci, enterococci, S aureus, Enterobacteriaceae, and various anaerobes. Radiographs of any spreading soft tissue infection in a patient with diabetes should be obtained to look for the soft tissue gas that characterizes necrosis. Surgical debridement is necessary for necrotizing infections. Gram stains and surface cultures are not helpful; antibiotic coverage should reflect the range of potential pathogens.
• Osteomyelitis
• • Contiguous spread of a polymicrobial infection from a skin ulcer to adjacent bone is common in patients with diabetes.
  • In one study, osteomyelitis was found in the bone under 68% of diabetic foot ulcers, and findings on physical examination and plain radiographs did not help in diagnosing one half of the cases. Unfortunately, these diagnostic modalities are often the only ones available in the ED, and the diagnosis might be suspected but not established. MRI, if available on an emergent basis, has better sensitivity and specificity in diagnosing osteomyelitis. 
  • If osteomyelitis is apparent on physical examination (eg, if the wounds are deep enough to expose tendons or bone), radiography, or MRI, the patient should be admitted for intravenous antibiotics. If osteomyelitis is suspected but the soft tissue infection or metabolic disturbances do not warrant admission, the patient can be discharged for outpatient workup.
• Other infections
• • Although cholecystitis is probably no more common in patients with diabetes than in the general population, severe fulminating infection, especially with gas-forming organisms, is more common. The early clinical manifestations of emphysematous cholecystitis are indistinguishable from those of usual cholecystitis. The diagnosis can be made by finding gas in the gallbladder lumen, wall, or surrounding tissues. Even with immediate surgery, the rate of mortality is high. Clostridial species are found in more than 50% of cases.
  • The incidence of staphylococcal and K pneumoniae infections are greater in people with diabetes than in people without diabetes.
  • Diabetes is a risk factor for reactivation of tuberculosis.
  • Cryptococcal infections and coccidioidomycoses are more virulent in patients with diabetes.
• Ophthalmologic complications
• • Diabetes can affect the lens, vitreous, and retina, causing visual symptoms that may prompt the patient to come to the ED. Visual blurring may develop acutely as the lens changes shape with marked changes in blood glucose concentrations. This effect, which is caused by osmotic fluxes of water into and out of the lens, usually occurs as hyperglycemia increases, but it also may be seen when high glucose levels are lowered rapidly. In either case, recovery to baseline visual acuity can take up to a month, and some patients are almost completely unable to read small print or do close work during this period.
  • Patients with diabetes tend to develop senile cataracts sooner than persons without diabetes, though this is not related to the degree of glycemic control.
  • Whether patients develop diabetic retinopathy depends on the duration of their diabetes and on the level of glycemic control. The following are the 5 stages in the progression of diabetic retinopathy:
  • 1. Dilation of the retinal venules and formation of retinal capillary microaneurysms
    2. Increased vascular permeability 
    3. Vascular occlusion and retinal ischemia 
    4. Proliferation of new blood vessels on the surface of the retina
    5. Hemorrhage and contraction of the fibrovascular proliferation and the vitreous
  • The first 2 stages of diabetic retinopathy are known as background or nonproliferative retinopathy. Initially, the retinal venules dilate, then microaneurysms (tiny red dots on the retina that cause no visual impairment) appear.
  • • The microaneurysms or retinal capillaries become more permeable, and hard exudates appear, reflecting the leakage of plasma. Rupture of intraretinal capillaries results in hemorrhage. If a superficial capillary ruptures, a flame-shaped hemorrhage appears.
    • Hard exudates are often found in partial or complete rings (circinate pattern), which usually include multiple microaneurysms. These rings usually mark an area of edematous retina.
    • The patient may not notice a change in visual acuity unless the center of the macula is involved. Macular edema can cause visual loss; therefore, all patients with suspected macular edema must be referred to an ophthalmologist for evaluation and possible laser therapy. Laser therapy is effective in decreasing macular edema and preserving vision but less effective in restoring lost vision.
  • Preproliferative and proliferative diabetic retinopathy are the next stages in the progression of the disease. Cotton-wool spots can be seen in preproliferative retinopathy. These represent retinal microinfarcts due to capillary occlusion and appear as off-white to gray patches with poorly defined margins.
  • Proliferative retinopathy is characterized by neovascularization, or the development of networks of fragile new vessels that often are seen on the optic disc or along the main vascular arcades. The vessels undergo cycles of proliferation and regression. During proliferation, fibrous adhesions develop between the vessels and the vitreous. Subsequent contraction of the adhesions can result in traction on the retina and retinal detachment. Contraction also tears the new vessels, which hemorrhage into the vitreous.
  • Patients may notice a small hemorrhage, which appears as a floater; larger hemorrhage may result in marked visual loss. Patients with preproliferative or proliferative retinopathy must immediately be referred for ophthalmologic evaluation because laser therapy is effective in this condition, especially before actual hemorrhage occurs. Patients with retinal hemorrhage should be advised to limit their activity and to keep their head upright (even while sleeping) so that the blood settles to the inferior portion of the retina, minimizing obscuration of their central vision.
  • Patients with active proliferative diabetic retinopathy are at increased risk of retinal hemorrhage if they receive thrombolytic therapy; therefore, this condition is a relative contraindication to the use of thrombolytic agents.
• Nephropathy
• • ESRD affects 30-35% of patients with type 1 diabetes whose disease was diagnosed before 1965 and in 10-15% of those whose diabetes was diagnosed after 1965. All patients with diabetes should be considered to have the potential for renal impairment unless proven otherwise. Therefore, extreme care should be exercised when using any nephrotoxic agent in a patient with diabetes.
  • The use of contrast media can precipitate acute renal failure in patients with underlying diabetic nephropathy. Caution should be used when contrast-enhanced studies are being considered in patients with diabetes having a creatinine level greater than 2 mg/dL; such studies should absolutely be avoided in patients with a creatinine level greater than 3 mg/dL. Although most recover from contrast medium–induced renal failure within 10 days, some have irreversible renal failure. Patients with diabetes who must undergo such studies should be well hydrated before, during, and after the study, and their renal function should be carefully monitored. A better solution is to seek equivalent clinical information by using an alternative study that does not require the use of contrast material (eg, sonography, noncontrast CT, MRI).
  • Potentially nephrotoxic drugs should be avoided whenever possible. Renally excreted or potentially nephrotoxic drugs should be given at reduced doses appropriate to the patient's serum creatinine level. Because chronically elevated blood pressure contributes to the decline in renal function, hypertensive patients with diabetes must be referred for long-term management of their blood pressure. If antihypertensive therapy is started in the ED, an angiotensin-converting enzyme (ACE) inhibitor should be used because this class of agents decreases proteinuria and slows the decline in renal function independent of its effect on blood pressure. ACE inhibitors tend to increase the serum potassium levels and therefore should be used with caution in patients with renal insufficiency or elevated serum potassium levels.
• Neuropathy
• • Of the many types of peripheral and autonomic diabetic neuropathy, distal symmetric sensorimotor polyneuropathy (in a glove-and-stocking distribution) is the most frequent. Besides causing pain in its early stages, this type of neuropathy eventually results in the loss of peripheral sensation. The combination of decreased sensation and peripheral arterial insufficiency often leads to foot ulceration and eventual amputation.
  • Acute-onset mononeuropathies in diabetes include acute cranial mononeuropathies, mononeuropathy multiplex, focal lesions of the brachial or lumbosacral plexus, and radiculopathies. Of the cranial neuropathies, the third cranial nerve (oculomotor) is most commonly affected, followed by the sixth nerve (abducens) and the fourth nerve (trochlear). Patients can present with diplopia and eye pain. In diabetic third-nerve palsy, the pupil is usually spared, whereas in third-nerve palsy due to intracranial aneurysm or tumor, the pupil is affected in 80-90% of cases.
  • Consideration of nondiabetic causes of cranial nerve palsies is important because 42% are due to causes other than diabetes. Therefore, evaluation should include nonenhanced and contrast-enhanced CT or, preferably, MRI. Neurologic consultation is recommended. Acute cranial-nerve mononeuropathies usually resolve in 2-9 months. Acute thrombosis or ischemia of the blood vessels supplying the structure involved is thought to cause these neuropathies.
  • Autonomic dysfunction can involve any part of the sympathetic or parasympathetic chains and produce myriad manifestations. Patients likely to seek care in the ED are those with diabetic gastroparesis and vomiting, severe diarrhea, bladder dysfunction and urinary retention, or symptomatic orthostatic hypotension.
  • • Treatment of gastroparesis is symptomatic, and symptoms tend to wax and wane. Patients with gastroparesis may benefit from metoclopramide or erythromycin. Before these therapies are started, the degree of dehydration and metabolic imbalance must be assessed, and other serious causes of vomiting must be excluded. In severe cases, gastric pacing has been used.
    • Patients with disabling orthostatic hypotension may be treated with salt tablets, support stockings, or fludrocortisone.
    • Alleviating the functional abnormalities associated with the autonomic neuropathy is often difficult and frustrating for both doctor and patient. The patient's physician should be involved in devising a long-term treatment plan.
• Diabetic foot disease
• • About 50-70% of all nontraumatic lower-extremity amputations occur in patients with diabetes. The insensate, poorly perfused foot is at risk for ulcers from pressure necrosis or inflammation from repeated skin stress and unnoticed minor trauma. These can evolve into cellulitis, osteomyelitis, or nonclostridial gangrene and end in amputation.
  • Patients with diabetes presenting with wounds, infections, or ulcers of the foot should be treated intensively. In addition to appropriate use of antibiotics, avoidance of further trauma to the healing foot by using crutches, wheelchairs, or bed rest is mandatory. Patients should be treated by a podiatrist or an orthopedist with experience in the care of diabetic foot disease. If bone or tendon is visible, osteomyelitis is present, and hospitalization for intravenous antibiotics is often necessary. Many patients need a vascular evaluation in conjunction with local treatment of the foot ulcer because a revascularization procedure may be required to provide adequate blood flow for wound healing.
  • Because curing ulcers and foot infections is difficult, their prevention is extremely important. At one clinic, the rate of amputation was halved after patients were required to remove their shoes and socks at every visit. The emergency physician can facilitate this practice by briefly inspecting the feet of patients with diabetes and by educating them about the need for proper foot care. Patients with distal sensory neuropathy to pinprick or light touch, decreased peripheral pulses, moderate-to-severe onychomycosis, or impending skin breakdown should be referred to a podiatrist.
• Macrovascular disease
• • This is the leading cause of death in patients with diabetes, causing 75% of deaths in this group but approximately 35% of deaths in people without diabetes. Diabetes increases the risk of myocardial infarction (MI) 2-fold in men and 4-fold in women, and many patients have other risk factors for MI as well. The risk of stroke in patients with diabetes is double that of nondiabetic people, and the risk of peripheral vascular disease is 4 times that of people without diabetes. Subtle differences in the pathophysiology of atherosclerosis in patients with diabetes result in both earlier development and a more malignant course. Therefore, lipid abnormalities must be treated aggressively to lower the risk of serious atherosclerosis.
  • Patients with diabetes may have increased incidence of silent ischemia. However, silent ischemia is common in many patients with CAD, and the apparently increased incidence may be because patients with diabetes are more likely than others to have CAD to begin with. Nevertheless, an ECG is prudent in patients with diabetes and a serious illness or who present with generalized weakness, malaise, or other nonspecific symptoms that are not expected to be due to myocardial ischemia.
  • Diastolic dysfunction is common in patients with diabetes and should be considered in the patient with symptoms of congestive heart failure and a normal ejection fraction.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Target glucose levels

The fact that chronic hyperglycemia is associated with an increased risk of microvascular complications of type 1 diabetes was demonstrated in the Diabetes Control and Complications Trial (DCCT). In that trial, intensive therapy designed to maintain normal blood glucose levels greatly reduced the development and progression of retinopathy, microalbuminuria, proteinuria, and neuropathy, as assessed over 7 years.

The ongoing Epidemiology of Diabetes Interventions and Complications Study (EDIC), an observational study that continues to follow the patients previously enrolled in the DCCT, demonstrates that benefit has continued since the DCCT trial ended in 1993. Intensive therapy was not associated with increased mortality or major macrovascular events and did not decrease the quality of life, although it did increase the likelihood of severe hypoglycemic episodes. Therefore, the goal of treatment is to lower blood glucose levels to the near-normal range (eg, preprandial blood glucose levels of 90-130 mg/dL,HbA_1c levels of <7%) and to maintain them in this range throughout the patient's life.

Some patients should not aim for near-normal blood glucose levels. In elderly patients who have a life expectancy of less than 5 years or in any patient with a terminal disease, tight control may be unnecessary. Patients with known CAD or cerebrovascular disease also should have higher preprandial blood glucose targets (eg, 100-160 mg/dL) to prevent extreme hypoglycemia. Patients with advanced microvascular and neuropathic diabetic complications may not particularly benefit from maintenance of near-euglycemia.

Additionally, patients with alcoholism or other serious substance abuse and patients with severe uncontrolled mental illness may be unable to effectively participate in the care of their diabetes, placing them at high risk for severe hypoglycemic reactions if near-normal glucose levels are targeted. Finally, patients with hypoglycemia unawareness (ie, lack adrenergic warning signs of hypoglycemia) or those with recurrent episodes of severe hypoglycemia (ie, hypoglycemia requiring treatment by another person) should also have high target levels at least temporarily.

Self-monitoring of glucose levels

Optimal diabetic control requires frequent self-monitoring of blood glucose levels. Frequent monitoring allows for rational adjustments in insulin doses. Most patients with type 1 diabetes require 2 or more injections of insulin daily with doses adjusted based on self-monitoring of blood glucose levels.

Subcutaneous continuous glucose sensors are now available, making the continuous glucose monitor (CGM) possible. These devices measure interstitial glucose levels every 1-5 minutes, providing alarms when glucose levels are too high or too low or are rapidly rising or falling. CGM transmits to a receiver, which is either a pagerlike device or is integral to an insulin pump. Looking at the continuous glucose graph and responding to the alarms can help patients avoid serious hyperglycemia or hypoglycemia.

Several drawbacks exist; first, there is a lag between glucose levels in the interstitial space and capillary blood, so the levels recorded by the CGM may differ from a finger stick (capillary) glucose. For that reason, the trends (whether the glucose levels are rising or falling) tend to be more helpful. Second, patients may overtreat hyperglycemia (repeatedly giving insulin because the glucose levels do not fall rapidly enough—a phenomenon known as stacking) as well as overtreat lows (the glucose levels rise slowly with ingestion of carbohydrate).

Patients using CGM and/or insulin pumps can often provide very detailed information as to their insulin regimens as well as recent alterations in blood glucose levels.

Types of insulin

By definition, patients with type 1 diabetes require lifelong treatment with insulin to promote glucose utilization. Rapid-, short-, intermediate-, and long-acting insulin preparations are available. Although pork, beef, and beef-pork insulins were previously used, recombinant human insulin is now available and used almost exclusively. Commercially prepared mixtures of insulin are also available.

Insulin is sensitive to heat and exposure to oxygen. Once a bottle of insulin is open, it should be used for no more than 28 days and then discarded, even if insulin remains in the bottle. Use of old insulin can result in a lack of clinical effectiveness. Insulin in a pump reservoir for longer than 3 days also loses its clinical effectiveness. Sometimes, insulin distributed from the pharmacy has been exposed to heat or other environmental factors and may be less active. If a patient is experiencing unexplained high blood sugar levels, new insulin vials should be opened and used.

Common insulin regimens

Although emergency physicians rarely start new therapy for patients with diabetes, being acquainted with the various forms of insulin and the common regimens is useful.

When treating patients with type 1 diabetes, the goal is to provide insulin in a manner that is as physiologic as possible. Insulin replacement is given as a basal insulin (either long-acting [glargine or detemir] or intermediate-acting [NPH]) and preprandial (premeal) insulin (either rapid-acting [lispro, aspart, or glulisine] or short-acting [regular]). For patients on intensive insulin regimens (multiple daily injections or insulin pumps), the preprandial dose is based on the carbohydrate content of the meal (the carbohydrate ratio) plus a correction dose if their blood glucose level is elevated (eg, 2 additional units of rapid-acting insulin to correct the blood glucose from a level of 200 mg/dL to a target of 100 mg/dL). This method allows patients more flexibility in caloric intake and activity, but it requires more blood glucose monitoring and attention to the control of their diabetes.

Common insulin regimens include the following: (1) split or mixed, such as NPH with rapid-acting (eg, lispro or aspart) or regular insulin before breakfast and supper; (2) split or mixed variant: NPH with rapid-acting or regular insulin before breakfast, rapid-acting or regular insulin before supper, NPH before bedtime (designed to reduce fasting hypoglycemia by giving the NPH latter in the evening); (3) multiple daily injections (MDI), a long-acting insulin (eg, glargine) once a day in the morning or evening (or twice a day in about 20% of patients), and a rapid-acting insulin before meals or snacks (dose adjusted based on the carbohydrate intake and the blood glucose level); and (4) continuous subcutaneous insulin infusion (CSII), rapid-acting insulin infused continuously 24 hours a day through an insulin pump at one or more basal rates, with additional boluses given before each meal, and correction doses administered if blood glucose levels exceed target levels.

Drug Category: Rapid-acting injectable insulins

With the most rapid onset of action, these insulins are used whenever a rapid onset and short duration is appropriate (eg, before meals or when the blood glucose level exceeds target and a correction dose is needed). Rapid-acting insulins are associated with less hypoglycemia than regular insulin.

Drug Name	Insulin glulisine (Apidra)
Description	Onset of action is 5-15 min, peak effect is in 30-90 min, and usual duration of action is 4 h. Has FDA approval for use in insulin pumps.
Adult Dose	Individualize dose; intended for intermittent SC injection with meals or use by external infusion pump
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; hypoglycemia
Interactions	Corticosteroids, danazol, diazoxide, diuretics, sympathomimetic agents (eg, epinephrine, albuterol, terbutaline), glucagon, isoniazid, phenothiazines, growth hormone, thyroid hormone, estrogen, progestogens, protease inhibitors, and atypical antipsychotics (eg, olanzapine, clozapine) may increase blood glucose level and reduce glucose-lowering effect of insulin; oral antidiabetic agents, ACE inhibitors, disopyramide, fibrates, fluoxetine, MAOIs, pentoxifylline, propoxyphene, salicylates, and sulfonamides may decrease blood glucose level and cause additive effects to insulin
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	Careful blood glucose monitoring required to prevent hypoglycemia and maintain glucose control; dose reduction may be required with renal or hepatic impairment; must be administered within 15 min before meals or immediately after a meal; may cause lipodystrophy, pruritus, rash, or injection site reaction

Drug Name	Insulin lispro (Humalog)
Description	Onset of action is 5-15 minutes, and usual duration of action is 4h.
Adult Dose	Doses vary; adjust dose according to patient's metabolic needs; titrate to maintain a premeal and bedtime glucose of 80-140 mg/dL
Pediatric Dose	<3 years: Not established >3 years: Administer as in adults
Contraindications	Documented hypersensitivity; hypoglycemia
Interactions	Medications that may decrease hypoglycemic effects of insulin include acetazolamide, AIDS antivirals, asparaginase, phenytoin, nicotine, isoniazid, diltiazem, diuretics, corticosteroids, thiazide diuretics, thyroid hormone, estrogens, ethacrynic acid, calcitonin, oral contraceptives, diazoxide, dobutamine, phenothiazines, cyclophosphamide, dextrothyroxine, lithium carbonate, epinephrine, morphine sulfate, and niacin Medications that may increase hypoglycemic effects of insulin include calcium, ACE inhibitors, alcohol, tetracyclines, beta-blockers, lithium carbonate, anabolic steroids, pyridoxine, salicylates, MAO inhibitors, mebendazole, sulfonamides, phenylbutazone, chloroquine, clofibrate, fenfluramine, guanethidine, octreotide, pentamidine, and sulfinpyrazone
Pregnancy	B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions	Because of insulin lispro's prompt onset of action, administer within 15 min before or immediately after meal; monitor glucose carefully; dose adjustments may be necessary in patients with renal or hepatic dysfunction

Drug Category: Short-acting injectable insulins

Currently, short-acting insulins are less commonly used than the rapid-acting insulins in patients with type 1 diabetes. They are used when a slightly slower onset of action or greater duration of action is desired. 

Drug Category: Intermediate-acting injectable insulins

With their relatively slow onset of action and relatively long duration of action, these insulins usually are combined with faster-acting insulins to maximize benefits of a single injection.

Drug Category: Long-acting injectable insulins

These insulins offer a long duration of action and are effective basal insulins. In patients with type 1 diabetes, they must be used in conjunction with a rapid-acting or short-acting insulin given before meals.

Drug Name	Insulin glargine (Lantus)
Description	Onset of action 4-6 h, generally no discernible peak effect, but an increased effect may occur at 10-20 h; usual duration of action 24-28 h.
Adult Dose	Doses vary; adjust dose according to patient's metabolic needs; titrate doses to maintain a premeal and bedtime glucose of 80-140 mg/dL
Pediatric Dose	Doses vary and must be adjusted for patient's metabolic needs; titrate doses to maintain target glucose levels
Contraindications	Documented hypersensitivity; hypoglycemia
Interactions	Acetazolamide, AIDS antivirals, asparaginase, phenytoin, nicotine, isoniazid, diltiazem, diuretics, corticosteroids, thiazide diuretics, thyroid replacement, estrogens, ethacrynic acid, calcitonin, oral contraceptives, diazoxide, dobutamine, phenothiazines, cyclophosphamide, dextrothyroxine, lithium carbonate, epinephrine, morphine sulfate, and niacin may decrease hypoglycemic effects Calcium, ACE inhibitors, alcohol, tetracyclines, beta-blockers, lithium carbonate, anabolic steroids, pyridoxine, salicylates, MAOIs, mebendazole, sulfonamides, phenylbutazone, chloroquine, clofibrate, fenfluramine, guanethidine, octreotide, pentamidine, and sulfinpyrazone may increase hypoglycemic effects
Pregnancy	A - Fetal risk not revealed in controlled studies in humans
Precautions	Monitor glucose levels carefully; dose adjustments may be necessary in renal or hepatic dysfunction

Drug Category: Inhaled insulins

The first inhaled insulin was approved by the US FDA in January 2006 for use as an alternative to injectable insulin. On October 18, 2007, Pfizer Inc announced that it is no longer making inhaled insulin (Exubera). The decision is not based on any safety concerns but is due to economic feasibility resulting from too few patients taking the inhaled insulin. Pfizer will work with physicians to transition patients from inhaled insulin to other treatment options over the next several months.

Drug Category: Amylin analogs

Elicit endogenous amylin effects by delaying gastric emptying, decreasing postprandial glucagon release, and modulating appetite.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Most patients with new-onset type 1 diabetes require hospitalization. For patients with known diabetes, inpatient care is generally warranted only for the management of major acute complications such as severe recurrent hypoglycemia, major infections, or DKA.
• Patients who cannot tolerate oral fluids require hospitalization. Likewise, if the precipitating cause of hyperglycemia cannot be treated adequately in the ED, the patient should be admitted.

Further Outpatient Care

• Although a few complications require hospitalization, type 1 diabetes can be managed almost entirely on an outpatient basis.

Complications

• The complications of diabetes include hypoglycemia and hyperglycemia, increased risk of infections, microvascular complications (ie, retinopathy, nephropathy), neuropathic complications, and macrovascular disease. (See Emergency Department Care for more information.)
• Diabetes is the major cause of blindness in adults aged 20-74 years.
• Diabetes is the leading cause of nontraumatic lower-extremity amputation and ESRD.

Prognosis

• Patients with diabetes have a lifelong challenge to achieve and maintain blood glucose levels as close to the normal range as possible. With appropriate glycemic control, the risk of both microvascular and neuropathic complications is decreased markedly. In addition, if hypertension and hyperlipidemia are treated aggressively, the risk of macrovascular complications decreases as well.
• These benefits are weighed against the risk of hypoglycemia and the short-term costs of providing high-quality preventive care. Studies have shown cost savings due to a reduction in acute diabetes-related complications within 1-3 years of starting effective preventive care.
• With each physician encounter, patients with diabetes should be educated about and encouraged to follow an appropriate treatment plan. The physician must ensure that the care for each patient with diabetes includes all necessary laboratory tests, examinations (eg, foot and neurologic examinations), and referrals to specialists (eg, ophthalmologist, podiatrist).

Patient Education

• Patients with new-onset type 1 diabetes require extensive education if they are to manage their disease safely and effectively and to minimize long-term complications. Such education is beyond the scope of ED practice and is best coordinated by the patient's long-term care providers.
• For excellent patient education resources, see eMedicine's Diabetes Center. Also, visit eMedicine's patient education article, Diabetes.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Overtreatment or undertreatment of hypoglycemia such as premature discharge of a patient who develops hypoglycemia due to long-acting insulin
• • After an episode of severe hypoglycemia, patients should be discharged home with a prescription for glucagon.
  • If the hypoglycemia resulted in a loss of consciousness while driving, patients with diabetes should be educated about how to drive safely with their condition. In many states, a loss of consciousness while driving must be reported to the state department of motor vehicles, though if a patient has a monitored treatment plan for their diabetes, this notification may not be required.
• Failure to treat the blood glucose levels of patients with wounds or active infections when they are greater than 200 mg/dL.
• Underestimation of the severity of diabetic retinopathy on funduscopic examination because of a failure to dilate the pupils or the failure to urgently refer any patient with lesions near the macula to an ophthalmologist.
• Failure to provide adequate hydration to patients with mild di