Acute Complications

Introduction

Patients with type 2 diabetes (T2D) are prone to developing acute complications such as:

• Metabolic:
  • Diabetic ketoacidosis (DKA)
  • Hyperosmolar hyperglycemic syndrome (HHS)
  • Hypoglycemia
  • Infection (poor wound healing)
• Quality of life:
  • Nocturia
  • Poor sleep
  • Daytime tiredness
  • Tooth and gum disease
  • Cognitive impairment
  • Gastrointestinal issues

The most common acute complications of T2D are metabolic problems (DKA, HHS, hypoglycemia) and infection. In addition, the quality of life of patients with acute complications is adversely affected. Characteristic symptoms of tiredness and lethargy can become severe and lead to increased falls and bedsores in the elderly, decreased school performance in children with T2D and decreased work performance in adults.

Metabolic

Diabetic Ketoacidosis

This acute metabolic complication of diabetes typically results from a profound insulin deficiency (absolute or relative) associated with uncontrolled type 1 Diabetes (T1D) mellitus and less commonly in severely decompensated T2D. Simply stated, the insulin deficiency causes the body to breakdown fatty acids for fuel, leading to a buildup of toxic blood acids called ketones. The accumulation of ketones eventually leads to hyperglycemia, metabolic acidosis, electrolyte abnormalities and volume depletion requiring hospitalization.

Individuals with T2D may develop DKA under certain conditions:

• Poor nutrition that contributes to dehydration and catabolism of fat to provide necessary calories.
• Severe physiologic stress (e.g., infection, myocardial infarction) that leads to increased levels of counter-regulatory hormones (e.g., epinephrine, cortisol, and glucagon), which stimulate lipolysis, elevate free fatty acids and stimulate hepatic ketogenesis.
• Chronic poor metabolic control that leads to decreased insulin secretion and decreased glucose uptake (glucose toxicity).
• Dehydration that leads to decreased excretion of ketones in urine and a buildup of ketone bodies in the blood.
• Treated with an SGLT2 inhibitor; in this case, DKA may present with euglycemia (glucose less than 250 mg/dl).

The biochemical criteria for DKA include:

• Hyperglycemia (blood glucose >250 mg/dL)
• Venous pH <7.3 or bicarbonate <15 mmol/L
• Ketonemia and ketonuria.

Precipitating Factors

Precipitating factors vary from individual to individual, occurring typically in people with T2D of long duration and insulin deficient, and may include the following (approximately 50% of which are preventable):

• Illness and infection; increased production of glucagon and glucocorticoids by the adrenal gland promotes gluconeogenesis; increased production of epinephrine and norepinephrine increases glycogenolysis. Both processes promote hyperglycemia and the subsequent development of DKA.
• Inadequate insulin dosage due to omission or reduction of doses by patient, physician, or clinic; patients with gastrointestinal (GI) distress often decrease or eliminate their insulin doses thinking that less insulin is needed when food intake is decreased; this practice can be dangerous because GI symptoms are key features of DKA. Once again people with T2D who are insulin deficient are at risk for DKA. More recently, sodium glucose cotransporter type 2 (SGLT2) inhibitors have been shown to cause DKA and more specifically euglycemic DKA (glucose level below 250mg/dl) and this warning is in all of the package inserts from medication (Invokana, Farxiga, Jardiance and Steglatro).
• Initial manifestation of T1D in the elderly misdiagnosed as T2D (LADA or latent autoimmune diabetes in adults).
• Chronic untreated hyperglycemia (glucose toxicity).

Of note, the precipitating factor in up to 25% of all cases admitted to the hospital is the reduction or omission of insulin by the patient after refraining from eating because of nausea or vomiting. It is imperative that patients be advised to not stop insulin therapy and be instructed when and how to adjust the dosage when necessary. Frequent glucose testing with blood glucose monitoring (BGM) or continuous glucose monitoring (CGM) is essential for treatment.

Additional precipitation factors for DKA are presented in Table 22-1.

Closer Look at the Pathophysiology of Diabetic Ketoacidosis

Insulin deficiency results in hyperglycemia and the production of excess levels of counterregulatory hormones (e.g., glucagon, catecholamines, cortisol, growth hormone) that allow the body to access alternative sources of fuel. Increased lipolysis breaks down adipose tissue into free fatty acids, some of which are used to produce energy. The remainder is catabolized into ketones (acetone, acetoacetate and β-hydroxybutyrate), which can be used for fuel but rapidly accumulate, resulting in metabolic acidosis. Increased proteolysis and glycogenolysis respectively catabolize proteins and glycogen to produce glucose. Collectively, these mechanisms further promote hyperglycemia, resulting in osmotic diuresis followed by progressive dehydration, electrolyte disturbances and a hyperosmolar state that act to further increase hormone release. This negative cycle rapidly leads to a widespread catabolic state and life-threatening metabolic decompensation.

Symptoms and Signs of DKA

The symptoms and signs of DKA are polyuria, polydipsia and signs of dehydration (tachycardia, poor skin turgor, dry mucous membranes) that result from osmotic diuresis secondary to hyperglycemia. Kussmaul’s respiration, characterized by rapid deep respirations, is a ventilatory response to metabolic acidosis and a fruity scent on a patient’s breath is a sign of increased levels of acetone.

Other common signs include:

• Weight loss
• Fatigue
• Dyspnea
• Nausea
• Vomiting
• Abdominal pain
• Polyphagia
• Altered mental status
• Somnolence
• Lethargy
• Fever when infection is present
• Progressive obtundation and loss of consciousness
• Increased leukocyte count with left shirt
• Nonspecific elevation of serum amylase.

These are classic for DKA in type 1 diabetes (T1D), although they are not as severe in patients with T2D because some endogenous insulin secretion is maintained. Polyuria and polydipsia are symptoms of osmotic diuresis secondary to hyperglycemia. Nonspecific symptoms include weakness, lethargy, headache and myalgia; specific symptoms of DKA are GI and respiratory. The GI symptoms probably are related to the ketosis and/or acidosis.

Because the signs are not specific to DKA, physicians should be alert to a constellation of evidence that points to the possibility of DKA.

Laboratory Evaluation

The diagnosis of DKA must be made quickly. The presence of typical clinical signs of DKA should prompt the clinician to confirm diagnosis by testing for:

• Hyperglycemia: >250 mg/dL
• Increased anion gap on basic chemistry
• Serum ketone level: 7-10 mmol/L
• Arterial pH: <7.3
• Serum bicarbonate level: <15 mmol.

Table 22-2 presents a comparison of the key features of DKA and HHS.

Differential Diagnosis

Patients may have ketosis without DKA. Starvation ketosis and alcoholic ketoacidosis (AKA) are differentiated by clinical history and by plasma glucose concentrations that range from mildly elevated (rare >250 mg/dL) to hypoglycemia. While DKA can lead to serious acidosis, the serum bicarbonate concentration in starvation ketosis usually does not fall below 18 mEq/L. DKA must also be distinguished from other causes of high anion-gap metabolic acidosis (eg, ingestion of substances such as salicylate, methanol, ethylene glycol and paraldehyde), chronic renal failure and lactic acidosis. Clinical history of previous drug intoxications or metformin use should be obtained. Measurement of blood lactate, serum salicylate and blood methanol level can be useful. Table 22-3 presents the differential diagnosis of DKA.

Treatment of DKA

Although aggressive therapy is not usually necessary in T2D, the following treatment strategies are for severe cases and for true T1D misdiagnosed as T2D because of the patient’s age at presentation. The goals of treatment are to:

• Correct fluid and electrolyte disturbances
• Correct acidosis and ketogenesis
• Restore and maintain normal glucose metabolism.

The cornerstones of DKA therapy are administering fluids and insulin immediately. Potassium and phosphate replacement and bicarbonate therapy also may be necessary for certain patients, depending on the severity of the DKA. This is rarely the case in patients with T2D. The following treatment guidelines provide an overview for managing DKA. It is not unusual that patients with T2D can be treated adequately in a general hospital ward and not in an intensive care unit.

Fluid Therapy

• This is based on the degree of dehydration and the patient’s CV status.
• It also plays a critical role in lowering glucose concentrations; hyperglycemia will continue despite appropriate insulin therapy if hydration is not adequate.
• Oral hydration with a sodium-containing fluid is appropriate for a patient with mild DKA who is not vomiting.
• For most patients, begin fluid replacement with 0.9% saline, 1 L of normal saline within first hour followed by a continuous infusion with either 0.45% NaCl or 0.9% NaCl. The rate of infusion is typically 250 to 500 mL/hour, depending on each patient’s clinical situation.
• IV fluids are continued until intravascular volume has been fully restored, as indicated by normal filling of neck veins or when the patient can tolerate fluids.

Insulin Infusion

• Despite the significant reductions in hyperglycemia following fluid replacement therapy, insulin is still required to normalize blood glucose, attenuate lipolysis and ketogenesis and reverse acidosis.
• Initial volume expansion typically occurs within 1 to 2 hours following the start of fluid therapy and IV insulin infusion should be initiated at that time. However, before starting insulin therapy, it is important to confirm the level of electrolytes. In the relatively unusual circumstance of hypokalemia, insulin therapy must be postponed until potassium levels are corrected.
• Insulin infusion with human regular insulin should begin without an IV priming bolus, which may increase the risk of cerebral edema.
• The standard infusion rate is 0.1 U/kg/hour and maintained until DKA has resolved, as indicted by a pH >7.30, normal anion gap, bicarbonate >15 mmol/L and β-OHB <0.6 mmol/L.
• If a 10% decrease in glucose concentration from the initial level is not observed after 2 hours, the infusion rate should be doubled to 10 units per hour.
• The insulin infusion rate can be decreased when blood glucose measures 250 to 300 mg/dL, at which time dextrose (5%) may be added to prevent hypoglycemia.
• The major mistake with severe DKA is premature discontinuation of aggressive fluid and insulin therapy. Ketogenesis must be curtailed and this requires insulin therapy. Serum glucose levels are not reflective of ketone body generation.
• In patients with uncomplicated DKA or in whom IV administration is not possible, subcutaneous or intramuscular administration of a rapid-acting insulin analog may be substituted for IV regular insulin infusion.

Potassium Replacement

• Not usually necessary in patients with T2D.
• Patients presenting with DKA often have a potassium deficit of 500 to 700 mEq/L, which must be replaced to a minimum level of 3.3 mEq/L before initiation of insulin therapy. This is because IV insulin moves potassium from extracellular to intracellular domains, while IV fluids increase renal plasma flow.
• Replacement should not begin until serum potassium concentration is <5.5 mEq/L. If the patient presents with low serum potassium, the clinician should assume that the deficit in total body potassium is severe and initiate potassium therapy at 20-40 mmol/L at the same time as fluid therapy and before implementing insulin therapy.
• In patients with hyperkalemia, potassium replacement should be deferred until after documentation of urine output. For all other patients, potassium therapy should be instituted after fluid therapy and at the same time as the start of insulin therapy.
• Electrocardiogram monitoring is recommended during potassium therapy in patients with hypokalemia or in patients with abnormal cardiac rhythms.
• Carbohydrate intake is also very important to turn off the brain’s drive to break down fatty acids for energy leading to acidosis. Many patients and providers are surprised by this recommendation, however it is an important way for patients who are still at home to reverse DKA before nausea and vomiting appears necessitating a visit to the emergency room. Of course, the carbohydrates are given with insulin to prevent hyperglycemia. This latter recommendation was developed for patients with T1D but it also pertains to those with T2D on multiple daily injection (MDI) or pump therapy.

Phosphate Replacement

• Phosphate levels should be measured initially.
• Current guidelines call for replacing phosphate if levels decrease below 1.0 mg/dL by adding 20 to 30 mEq/L of potassium phosphate to the IV solution over 2 to 3 hours. Serum calcium levels should be checked to avoid hypocalcemia, which is a potential complication.

Bicarbonate Therapy

• Bicarbonate administration in patients with DKA has shown no clinical benefit in controlled clinical studies and routine treatment is not recommended.
• In selected patients, including those with live-threatening hyperkalemia or who present with a pH <6.9 with decreased peripheral vasodilatation and cardiac contractility may further reduce tissue perfusion, bicarbonate may be administered cautiously at 1-2 mmol/kg over 60 minutes.

Glucose concentrations should be decreased by about 75 to 100 mg/dL/h with low-dose insulin infusion, reaching levels of 200 to 300 mg/dL within 4 to 5 hours. Dextrose (5%) is generally added to the infusion at this point in therapy to avoid hypoglycemia from continued insulin administration, which still is necessary to treat ketosis and acidosis. Approximately 12 to 24 hours of treatment is necessary to reverse ketosis for most patients; some patients may have ketone bodies for several days. The addition of dextrose also minimizing the potential for hypoglycemia. Too rapid a decrease in blood glucose can also cause cerebral edema, which is an especially important consideration in young children and the elderly, both of whom are at greater risk for overhydration and attendant cerebral edema.

Complications of Treatment

Common complications of therapy for DKA include hypoglycemia, hypokalemia, hypophosphatemia, hyperchloremic metabolic acidosis and pulmonary edema. Cerebral edema, which occurs in in 0.7% to 1.0% of children with DKA, is associated with hypotonic fluid replacement of overaggressive treatment of hyperglycemia. Neurologic deterioration can be rapid, with headache, lethargy and progressive decrease in arousal, leading to seizures, bradycardia and respiratory arrest. Once symptoms progress beyond lethargy, a mortality risk of >70% has been shown and permanent morbidity is estimated at 86% to 93%. Reduction in colloid osmotic pressure leading to increased pulmonary water content and decreased lung compliance is associated with hypoxemia. Patients with rales on exam are at higher risk for developing pulmonary edema.

Prevention of DKA

In the majority of cases, DKA results from an intentional or inadvertent interruption of insulin therapy, especially in patients with T2D who have pancreatic exhaustion do to a long duration of diabetes and on an MDI regimen or insulin pump. SGLT2 inhibitors are an additional cause of DKA in both T1D and T2D. Education should include instructions on back-up insulin administration in the event of pump failure and the protocol to follow when the patient is sick and an interruption in therapy is most likely to occur. A visit to the emergency room can be averted if the patient is educated to take in lots of non-caloric fluids, administer insulin and ingest 30 grams of carbohydrates, which turns off the brain’s drive to produce ketones.

Hyperosmolar Hyperglycemic Syndrome

The terms hyperosmolar hyperglycemic nonketotic state or coma have been replaced with HHS since ketosis may be present to various degrees and alterations of sensoria may occur in the absence of coma. This acute metabolic complication is a life-threatening crisis with a high mortality rate that is more common in patients with T2D and is usually seen in:

• Elderly patients with T2D (particularly those in nursing homes without access to free water)
• People with undiagnosed diabetes
• Those with diabetes that is diagnosed after a long period of uncontrolled hyperglycemia.

Pathophysiology of HHS

HHS is usually brought on by another condition, such as an illness or infection. The hallmarks of this metabolic complication are:

• Severe hyperglycemia: >600 mg/dL (>33.3 mM)
• Severe hyperosmolarity: >320 mOsm/L.

In clinical practice, patients often are seen who have these characteristics but also have mild ketosis and acidosis. Although HHS and DKA represent opposite ends of a continuum, many patients have some aspects of each syndrome. The two conditions have some similarity in pathophysiology, clinical signs and symptoms and treatments, with certain important exceptions.

Symptoms and Signs of HHS

Patients typically develop excessive thirst, confusion,and physical signs of severe dehydration. A comparison of the key features of HHS and DKA is shown in Table 22-2; several important differences exist in the symptoms and signs:

• GI symptoms usually are milder in HHS than in DKA in the absence of ketosis and acidosis. Because of a lack of severe GI problems (which prompt patients with DKA to seek medical attention within 1 to 2 days), patients with HHS may tolerate polyuria and polydipsia for weeks and consequently lose significant quantities of fluids and electrolytes before seeking help. Average fluid loss in HHS is 9 L vs 6.5 L in DKA.
• Residual insulin secretion in patients with T2D is usually sufficient to prevent significant keto acid production, explaining why ketosis is generally absent in HHS. Since keto acid production in the liver is relatively mild compared with patients with DKA, severe acidosis and Kussmaul’s respiration are rarely observed.
• Decreased mentation (mild confusion, lethargy) and lack of normal responsiveness are common and correlate best with serum osmolality. These are the usual reasons that patients with HHS seek medical attention.
• Focal neurologic signs may be present and may mimic a cerebrovascular event (hemisensory deficits, hemiparesis, aphasia, seizures); these signs decline as biochemical status returns to normal.

A diagnosis of HHS usually is easily made if one has a high index of suspicion. Patients may be admitted to the neurology or neurosurgical service because only neurologic conditions are considered initially. Routine urine and blood tests can help clarify the diagnosis of HHS. Health care professionals need to be alert for signs of HHS in patients at chronic-care facilities because this diagnosis tends to be overlooked in such settings.

Laboratory Evaluation

Laboratory values reflect the effects of uncontrolled diabetes and dehydration. Typical laboratory values in HHS are shown in Table 22-2.

Treatment

Lifesaving measures may be needed immediately. The primary treatment goal is rehydration to restore circulating plasma volume and correct electrolyte deficits. In addition, the precipitating event should be identified and corrected and other goals similar to those described for treatment of DKA should be instituted, including providing adequate insulin to restore and maintain normal glucose metabolism. Glucose concentration is the major biochemical end point because patients with HHS do not have ketosis or acidosis.

• CV status should be monitored closely and frequently during fluid replacement to avoid precipitating CHF, given the fact that most patients with HHS are older and have preexisting heart disease.
• Insulin is administered in the same manner as in patients with DKA. At glucose concentrations of 250 mg/dL, the rate of insulin infusion should be decreased to 2 to 3 U/h and 5% dextrose should be added to the replacement fluids when blood glucose concentrations are <300 mg/dL.
• Insulin dose should be adjusted (decreased 1 to 3 U/h) based on plasma glucose measurements every 4 hours.
• Since HHS signals insulin deficiency, insulin replacement therapy should be discussed with the patient prior to discharge.
• Potassium replacement follows the same guidelines as for DKA, with consideration of the special conditions of patients with HHS (underlying renal disease is associated with lower urinary potassium losses; preexisting heart disease is associated with greater susceptibility to the effects of potassium).
• Bicarbonate therapy is contraindicated in absence of acidosis.
• Phosphate replacement follows the same guidelines as for DKA, with consideration of the effect of phosphate on underlying renal disease.

Hypoglycemia

This metabolic problem occurs in both T1D and less commonly in T2D. The American Diabetes Association classifies hypoglycemia into three distinct levels: Level 1 hypoglycemia is defined as blood glucose <70 mg/dL and ≥54 mg/dL; Level 2 hypoglycemia as <54 mg/dL; and Level 3 hypoglycemia as a severe event characterized by an altered mental and/or physical status which requires assistance for treatment of hypoglycemia.

Hypoglycemia occurs when there is an imbalance between food intake, insulin therapy and physical activity. This can result from factors such as inadequate nutrition or delayed meals; inappropriate form, dose, or timing of insulin; and intensive or prolonged exercise without adjusting food intake or insulin dosage. Biologic and behavioral factors also contribute to the development of hypoglycemia. Biologic factors include low blood glucose, insulin sensitivity, comorbid conditions and medications and GI illness. Behavioral factors include impaired awareness of low blood glucose and symptoms (hypoglycemic unawareness) and failure to treat promptly or effectively.

Signs of Hypoglycemia

The incidence of hypoglycemia in patients with T2D is several orders of magnitude lower than in T1D. Nonetheless, patients taking insulin, SFUs and/or glinides are prone to hypoglycemia.

The symptoms of hypoglycemia are classified as adrenergic or neuroglycopenic. Additional symptoms, such as hunger, weakness, headache, nausea, mood changes and a sense of unease have no known etiology:

• Adrenergic symptoms
  • Trembling/shaking
  • Diaphoresis
  • Tachycardia
  • Palpitations
  • Paresthesias
  • Heavy breathing
• Neuroglycopenic
  • Inability to concentrate
  • Slow thinking
  • Slurred speech
  • Numbness
  • Slowed reaction time
  • Aggressive behavior
  • Blurred vision
  • Incoordination
  • Completely automatic/disoriented behavior
  • Fatigue or sleepiness
  • Loss of consciousness
  • Seizures
  • Death.

Adrenergic symptoms are typically the earliest subjective signs of falling blood glucose levels. However, it is important to understand that hypoglycemia does not necessarily progress in a linear fashion from mild to severe. For example, some patients might develop neuroglycopenic symptoms before adrenergic or cholinergic symptoms and other patients may overlook or ignore adrenergic or cholinergic symptoms and progress to neuroglycopenia.

Treatment

The goal of treatment is to normalize the plasma glucose level as quickly as possible. Recommendations for treatment are listed below:

• Mild to moderate hypoglycemia (<70 mg/dL) is treated most effectively by having the patient ingest approximately 15-20 g of readily available glucose or carbohydrate that contains glucose. Sources of rapidly-acting carbohydrate (15-20 g) include:
  • 3-4 glucose tablets (5 g each)
  • 4-6 oz of fruit juice
  • 2 tablespoons of raisins
  • 8-10 Lifesavers candies
  • 10 Airheads
  • 8-10 Brach’s Hard Candies
  • 4-6 oz of regular soda (not diet)
  • 8 oz no- or low-fat milk
  • If SMBG/CGM is performed 15 minutes after ingestion of glucose or carbohydrates and continues to indicate hypoglycemia, the treatment should be repeated. If SMBG/CGM shows normal or returning-to-normal glucose levels, the patient should consume a meal or substantial snack to prevent another episode of hypoglycemia, but this depends on the circumstances of why the patient became hypoglycemic in the first place.
• Severe hypoglycemia requires rapid treatment. IV glucose (50 cc 50% dextrose or glucose followed by 10% dextrose drip) is the most effective route; however, glucagon (1 mg for adults) can be administered intramuscularly at home with positive results. Several older emergency kits for intramuscular administration of glucagon by a family member or friend are available from Lilly (glucagon for injection vials and emergency kit) and Novo Nordisk (BlucaGen HypoKit). Three new formulations
  • Gvoke (Xeris), Zegalogue (Zealand) and Baqsimi (Lilly) - are now available; they are much easier to administer (no mixing needed) and have a longer shelf life. Gvoke comes in two dosage forms (0.5 mg and 1 mg) as well as a vial and syringe application, while Zegalogue is supplied is a single 0.6 mg dosage form. Gvoke and Zegalogue are available as pre-filled syringes, but also (much more conveniently) in the form of pre-filled auto-injectors. Both the Gvoke HypoPen and Zegalogue pen auto-injectors contain glucagon that is stable in solution and can be injected in a few seconds after taking off the cap, in a fashion similar to an epi-pen. By contrast, Baqsimi is glucagon in the form of powder in an intranasal device. Baqsimi is simply sprayed in one of the nostrils of the affected patient using the device plunger. If a rescue glucagon kit is not available, then individuals who are unable to swallow should be given glucose gel, honey, syrup, or jelly on the inside of the cheek. Emergency services may have to be called depending on the situation. After the initial response, a rapid-acting, carbohydrate-containing liquid should be given until nausea subsides; then a small snack or meal can be consumed. Blood glucose levels should be monitored frequently for several hours to assure that the levels remain normal and to avoid over­treatment. The individual’s health care team should be informed of any severe hypoglycemic episodes.
• It is important to educate patients on the proper treatment of hypoglycemia. For example, many eat candy bars that contain excessive amounts of fat, protein and calories, thus leading to delayed recovery from hypoglycemia and unnecessary weight gain.

Prevention of Hypoglycemia

Patients should be advised that the prevention of hypoglycemia is an essential step in the successful management of diabetes. Clinicians should question the patient about the events surrounding the episode to determine triggers and efficacy of treatments and provide instruction on how to both prevent and treat hypoglycemia in the future. Patient education should stress:

• Recognizing the signs and symptoms of hypoglycemia
• The importance of eating meals on a regular schedule
• Carrying a source of fast-acting carbohydrate at all times (at least 15-20 g; small containers of juice work well)
• Performing SMBG regularly for early detection of low blood glucose levels; initiate treatment at the first signs of hypoglycemia and assess efficacy of treatment. CGM alerts and alarms can also be invaluable, especially in a patient with little or no hypoglycemic symptoms. The lower alert is typically set at 80mg/dl or higher.
• Take mealtime insulin at least 15 to 30 minutes before eating (patients who take their fast-acting insulin immediately before or after a meal will be prone to delayed hypoglycemia). Afrezza can be given at the time of ingestion because of its rapid on and off Pk/Pd characteristics
• Understanding when hypoglycemic reactions are most likely to occur (eg, when the insulin(s) is peaking, during or following intense exercise, after skipping meals, during sleep)
• Recognizing situations that can be potentially dangerous in the event of a hypoglycemic episode
• Checking blood glucose level before going to sleep to avoid nocturnal hypoglycemia; perform nocturnal (3 am) monitoring:
  • If hypoglycemia has occurred during the night
  • When evening insulin has been adjusted
  • When strenuous activity has occurred the previous day
  • During times of irregular eating schedules or erratic glucose control
• Scheduling exercise appropriately; adjust meal times, caloric intake, or insulin dosing to accommodate physical activity; use SMBG (before, during, after strenuous activity) to determine the effect of exercise on blood glucose levels and to detect low blood glucose levels.

Infection

Infection is the primary cause of metabolic abnormalities leading to diabetic coma in patients with diabetes. Because of the potentially severe consequences of untreated infections, prompt diagnosis and treatment are essential. Infections are often occult in diabetic patients and require a high index of suspicion. Common infections in patients with diabetes are shown in Table 22-4.

Quality of Life

Patients with blood glucose values consistently >200 mg/dL will have a reduced quality of life. Poorly controlled blood glucose values will lead to excessive thirst and urination, causing nocturia and poor sleep. Poor sleep will lead to daytime tiredness and poor work performance in adults. Patients will have frequent urinary tract infections, tooth and gum disease and blurry vision. It has also been shown that the elderly experience cognitive impairment and a higher incidence of falls.

This article was last updated: October 26, 2022