eMedicine Specialties > Endocrinology > Diabetes Mellitus

Diabetes Mellitus, Type 1: Follow-up

Author: Aneela Naureen Hussain, MD, FAAFM, Assistant Professor, Department of Family Medicine, State University of New York Downstate Medical Center; Consulting Staff, Department of Family Medicine, University Hospital of Brooklyn
Coauthor(s): Miriam T Vincent, MD, PhD, Professor and Chair, Department of Family Practice, State University of New York Downstate Medical Center
Contributor Information and Disclosures

Updated: Jul 2, 2009

Follow-up

Further Inpatient Care

• Hypoglycemia/hyperglycemia (DKA)
  • Patients with type 1 diabetes mellitus (DM) can have coexisting illnesses that aggravate hyperglycemia, such as infection, coronary artery disease, or fever; additionally, certain medications can aggravate the condition.
  • Regular insulin doses may cause hypoglycemia if the patient becomes anorectic or has another cause for reduced food intake, has gastroparesis, or is vomiting.
  • The insulin coverage, with a sliding scale for insulin administration, should not be the only intervention because it is reactive, rather than proactive, in correcting hyperglycemia. Also, insulin may be used inappropriately when hyperglycemia reflects hepatic gluconeogenesis in response to previously uncorrected hypoglycemia.
  • Continue intermediate (ie, NPH, lente) insulin at 50-70% of the daily dose divided bid or, occasionally, tid. Administer supplemental regular insulin on a sliding scale. Blood glucose should be monitored before meals and at bedtime.
• Care during surgical procedures
  • Surgical procedures, inclusive of presurgery emotional stress, the effects of general anesthesia, and the trauma of the procedure, can markedly increase plasma glucose levels and induce DKA in patients with type 1 DM. In patients who normally take 1-2 daily injections of insulin, a third to a half of the usual morning dose can be administered in the morning before the operation and an IV infusion of 5% glucose in either 0.9% sodium chloride solution or water administered at a rate of 1 L (50 g glucose) over 6-8 hours. For additional information, see Perioperative Medication Management and Perioperative Management of the Diabetic Patient.
  • After the operation, check plasma glucose levels and assess for a reaction to ketones. Unless a change in dosage is indicated, repeat the preoperative dose of insulin when the patient recovers from the anesthesia and continue the glucose infusion.
  • Monitor plasma glucose and ketones at 2- to 4-hour intervals and administer regular insulin every 4-6 hours as needed to maintain the plasma glucose level at 100-250 mg/dL (ie, 5.55-13.88 mmol/L). Continue until the patient can be switched to oral feedings and a 2- or 3-dose insulin schedule.
  • Some physicians prefer to withhold subcutaneous insulin on the day of the operation and to add 6-10 units of regular insulin to 1 L of 5% glucose in 0.9% sodium chloride solution or water infused initially at 150 mL/h on the morning of the operation, depending on the plasma glucose level. The infusion is continued through recovery, with insulin adjustments depending on the plasma glucose levels obtained in the recovery room and at 2- to 4-hour intervals thereafter. The use of an intravenous insulin infusion in the postoperative period after major surgical procedures now is considered the standard of care in most hospitals.

Further Outpatient Care

• The primary care physician should help patients both to acknowledge and to understand the course of diabetes, and the physician should reassure patients about the prognosis. Patients with diabetes should be taught that they have a chronic condition that requires lifestyle modification. Patients should be made aware that they are likely to have chronic complications if they do not take control of their disease.
• Plasma glucose monitoring is very important for better control of the disease.
  • All patients with type 1 DM should learn how to self-monitor and record their blood glucose levels with home analyzers and adjust their insulin doses accordingly.
  • Insulin-dependent patients ideally should test their plasma glucose daily before meals, in some cases 1-2 hours after meals, and at bedtime. In practice, however, patients often obtain 2-4 measurements each day, including fasting levels and at various other times, including preprandially and at bedtime.
  • In patients with well-controlled diabetes, physicians must monitor blood sugar level and Hb A1c every 3 months.
  • Instruct patients with type 1 DM in the method of testing for urine ketones using commercially available reagent strips. Also, advise patients to test for urine ketones whenever they develop symptoms of a cold, flu, or other intercurrent illness; nausea, vomiting, or abdominal pain; polyuria; or if they find an unexpectedly high plasma glucose level on self-monitoring. Recommend testing for ketones in all urine samples from patients with type 1 DM who exhibit persistent, rapid, and marked fluctuation in their degree of hyperglycemia.
  • Because people with diabetes have an increased risk of acute renal failure, perform radiographic studies that require IV injection of contrast dyes only when absolutely necessary and only when the patient is well hydrated.
  • Hypercholesterolemia and hypertension increase the risk for specific late complications and require special attention and appropriate treatment. Although physicians can safely use beta-blockers (eg, propranolol) in most patients, these agents can mask the adrenergic symptoms of insulin-induced hypoglycemia and can impair the normal counter-regulatory response. ACE inhibitors are the drugs of choice for hypertension because of their renal protective action, especially early in the course of the disease.
• Increased bedtime doses of hypoglycemic agents with nighttime peaks in action may correct early morning hyperglycemia but may be associated with undesirable nocturnal hypoglycemia. Targeted continuous subcutaneous insulin infusion programming can facilitate the prevention of early morning hyperglycemia in selected patients.

Deterrence/Prevention

• Due to significant improvement in prediction of type 1 DM, several prevention trials are ongoing (eg, Diabetes Prevention Trial – Type 1 [DPT-1], European Nicotinamide Diabetes Intervention Trial [ENDIT]).
  • Diabetes Prevention Trial - Type 1: The objective of this multicenter US trial was to determine whether antigen-based (insulin) treatment of nondiabetic relatives prevents or delays the onset of clinical disease. As compared to the general population, in which the risk of developing type 1 diabetes is 1 per 300, the risk increases 15- to 20-fold in relatives of people with type 1 diabetes, especially first-degree relatives. Accurate assignment of risk in these relatives is determined by assessing immune, genetic, and metabolic markers. The strategy for DPT-1 was to screen for islet cell antibodies (ICA), which further enhances risk, in approximately 80,000 first- and second-degree relatives who are younger than 45 years. Researchers randomized subjects who fall into the high-risk group (ie, 5-y risk >50%) to receive either an annual 4-day intravenous insulin infusion followed by twice-daily low doses of subcutaneous injections of ultralente insulin or to be in a closely observed group.
  • The European Nicotinamide Diabetes Intervention Trial: The ENDIT study will prospectively address whether nicotinamide will reduce the rate of progression to DM in relatives. Forty thousand first-degree relatives (aged 5-40 y) have been screened, with 552 subjects (ICA titers ³ 20 Juvenile Diabetes Foundation [JDF] U) randomized to nicotinamide or placebo. This study is designed with 90% power to detect a 35% reduction in disease (placebo group estimated at 40% risk over 5 y). Analysis of data is expected in 2003.
• Pilot studies, nondiabetic relatives: Pilot studies conducted in high-risk nondiabetic relatives in the United States and in Germany (Fuchtenbusch) further suggest that parenteral insulin therapy may delay the onset of the disease.

Complications

Complications can be acute or chronic.

• Acute complications include the following:
• Hypoglycemia
• Local allergic reactions
• DKA
• Chronic complications are further subdivided into macrovascular, microvascular, and miscellaneous.
• Macrovascular complications
• Atherosclerosis
• Cerebrovascular disease
• Ischemic heart disease
• Ischemia of lower limb (ie, gangrene)
• Microvascular complications
• Peripheral neuropathy
• Peripheral neuropathy with trophic ulceration
• Diabetic retinopathy, cataract, glaucoma
• Diabetic nephropathy
• Miscellaneous complications
• Skin infections
• Necrobiosis lipoidica

A more detailed discussion of some of the possible complications is as follows:

• Hypoglycemia
• This may be due to change in insulin dose, a small or missed meal, or strenuous exercise. Common symptoms are light-headedness, dizziness, confusion, shakiness, sweating, and headache.
• Patients should be educated about symptoms of hypoglycemia and to respond rapidly with sugar intake. These patients should be advised to carry candy or sugar cubes. Family members can be taught to administer a subcutaneous injection of glucagon. In emergency, initial treatment is a bolus injection of 25 mL of 50% glucose solution followed by a continuous glucose infusion.
• The dawn phenomenon is the normal tendency of the blood glucose to rise in the early morning before breakfast. This rise in glucose, which may be due to the nocturnal spikes in growth hormone causing insulin resistance, is probably enhanced by increased hepatic gluconeogenesis secondary to the diurnal rise in serum cortisol. However, in some patients, nocturnal hypoglycemia may be followed by a marked increase in fasting plasma glucose with an increase in plasma ketones (Somogyi phenomenon). Thus, both the dawn and Somogyi phenomena are characterized by morning hyperglycemia, but the latter is due to rebound (counter-regulation) hyperglycemia. In cases of dawn phenomenon, the patient should check blood glucose levels at 2-4 am. The dawn and Somogyi phenomena can be ameliorated by administering intermediate insulin at bedtime.
• Local allergic reactions
• Local allergic reactions can occur at the site of insulin injections and can cause pain, burning, local erythema, pruritus, and induration. These complications are less common with human insulin than observed previously with animal insulins.
• These reactions usually resolve spontaneously without any intervention.
• Generalized insulin allergy is rare. Symptoms occur immediately after the injection and include urticaria, angioedema, pruritus, bronchospasm, and, rarely, circulatory shock. It may be treated with antihistamines. Some cases may require epinephrine and IV steroids.
• Diabetic ketoacidosis
• DKA is acute metabolic changes in the body due to lack of insulin or poor response to insulin due to stress or illness. It is characterized by hyperglycemia, ketosis, and acidosis, leading to osmotic diuresis and dehydration.
• The key to treatment of DKA is volume repletion, insulin therapy, and specific metabolic corrections.
• Macrovascular complications (ie, atherosclerosis): People with diabetes experience accelerated atherosclerosis. It affects small arterioles with the following predominant effects:
• Heart: Coronary atherosclerosis often occurs earlier and is more severe and extensive than in those without diabetes, increasing the risk of ischemic heart disease.
• Brain: Atherosclerosis of the internal carotid and vertebrobasilar arteries and their branches predisposes to cerebral ischemia.
• Lower extremity: Severe atherosclerosis of the iliofemoral and smaller arteries of the lower legs predisposes to gangrene. Ischemia of a single toe or ischemic areas on the heel are characteristic of diabetic peripheral vascular disease. This is due to the involvement of much smaller and more peripheral arteries.
• Kidneys: Atherosclerosis of the main renal arteries and their intrarenal branches causes chronic nephron ischemia. It is a significant component of multiple renal lesions in diabetes. Nephropathy is a significant life-threatening complication and is due to the adverse effects of glucose-induced preglomerular vasodilation on glomerular hemodynamics. Glomerulosclerosis is initiated early in the course of diabetic nephropathy by exacerbated expression of cytokines like tumor growth factor beta 1. However, not all people with type 1 DM are at risk of nephropathy because of some polymorphisms in the various factors involved in its pathogenesis, which can modulate the course of this disease from one person to the other. Although end-stage renal disease (ESRD) is one of the most severe complications of type 1 DM, the incidence of ESRD has been very low, 2.2% at 20 years after diagnosis and 7.8% at 30 years after diagnosis.³
• Microvascular disease
• This is a significant feature of diabetes and causes multiple pathological complications. Hyaline arteriosclerosis, a characteristic pattern of wall thickening of small arterioles and capillaries is wide- spread and is responsible for ischemic changes in the kidney, retina, brain, and peripheral nerves.
• In the kidneys, this wall thickening leads to diabetic nephropathy, which is characterized by proteinuria, glomerular hyalinization (Kimmelstiel-Wilson), and chronic renal failure.
• In the retina, this condition causes diabetic retinopathy. It is the leading cause of blindness in the United States in people younger than 60 years and affects the eyes in the following different ways:
• Background retinopathy: This complication is due to retinal small vessel abnormality leading to hard exudates, hemorrhages, and microaneurysms. It does not affect acuity.
• Proliferative retinopathy: This is due to extensive proliferation of new retinal small blood vessels. A sudden loss of vision can occur due to vitreous hemorrhage from proliferating new vessels or retinal detachment.
• Maculopathy: This complication is due to edema and hard exudate or retinal ischemia. It causes a marked reduction of acuity.
• Cataract: This is frequent in people with diabetes.
• Glaucoma: This condition relates to the neovascularization of the iris, rubeosis iridis.
• In the brain, the condition causes lacunar infarction and ischemic white matter degeneration.
• In the peripheral nerves, diabetes causes peripheral neuropathy. Four types of diabetic neuropathies develop, including (1) peripheral distal symmetrical polyneuropathy, predominantly sensory; (2) autonomic neuropathy; (3) proximal painful motor neuropathy; and (4) cranial mononeuropathy (ie, III, IV, VI). Sensory and autonomic neuropathy are due to axonal degeneration and segmental demyelination. Motor neuropathy and cranial mononeuropathy are due to vascular disease in blood vessels supplying nerves.
• Infections: People with diabetes are susceptible to various types of infections. The most common sites affected are the skin and urinary tract system. Increased risk of staphylococcal follicular skin infections, superficial fungal infections, cellulitis, erysipelas, and oral or genital candidal infections exists. These patients develop frequent lower urinary tract infections and are at increased risk of acute pyelonephritis.
• Necrobiosis lipoidica: Local fat atrophy or hypertrophy at injection sites is not unusual and usually improves by switching to human insulin and injecting it directly into the affected area. Patients do not require any specific treatment of local fat hypertrophy, but injection sites should be rotated.
• Charcot joint is a type of arthropathy observed in people with diabetes. It is a progressive deterioration of foot joints caused by underlying neuropathy. Tarsometatarsal and midtarsal joints are affected most commonly. Other neuromuscular foot deformities also may be present. Early diagnosis and treatment is important to prevent further joint degeneration.

Prognosis

Controlling blood glucose, Hb A1c, lipids, blood pressure, and weight are important prognostic factors and predict the development of long-term macrovascular and microvascular complications. More than 60% of patients with type 1 DM fare reasonably well over the long term. Many of the rest develop blindness, end-stage renal disease, and, in some cases, early death. If a patient with type 1 DM survives the period 10-20 years after onset of disease without fulminant complications, he or she has a high probability of reasonably good health. Other factors affecting long-term outcomes are the patient's education, awareness, motivation, and intelligence level.

Patient Education

• Education is the most important aspect of diabetes management. The physician or the health care provider should educate the patient and, in the case of children, the parents about the disease process, management, goals, and long-term complications. They should be made aware of the signs and symptoms of hypoglycemia and ways to manage it.
• A dietitian should provide specific diet control education to the patient and family.
• A nurse should educate the patient about self–insulin injection and performing finger sticks for blood glucose level monitoring.
• For excellent patient education resources, visit eMedicine's Diabetes Center. Also, see eMedicine's patient education article Diabetes.

Miscellaneous

Medicolegal Pitfalls

The physician is often required to evaluate diabetes control in regards to personal and commercial drivers' licenses, pilots' licenses, and employment. Legal issues are often different in different locations. Loss of consciousness due to hypoglycemia is an event that a physician is often legally required to report.

Special Concerns

• People with diabetes are at high risk of acute renal failure under certain circumstances. Therefore, administer the intravenous contrast media required for some radiological studies cautiously and only when it is necessary in a well-hydrated patient.
• Because pregnancy in patients with type 1 diabetes is at risk for multiple poor maternal and fetal outcomes, prepregnancy counseling, good glycemic control prior to and during pregnancy, and complete medical evaluation are essential. High-risk areas include exacerbation of existing hypertension, renal insufficiency, retinopathy, and more frequent congenital anomalies. These patients should be referred to obstetricians specializing in high-risk pregnancies.
• Adequate education for managing hypoglycemia is essential. Self-treatment techniques and glucagon use by family in emergencies are important skills.

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