3. Assess: Serum electrolytes (K , Na , Mg , Cl , bicarbonate, phosphate), acid_base status—pH, HCO3_, PCO2, ^-hydroxybutyrate, renal function (creatin-ine, urine output)

4. Replace fluids: 2_3 L of 0.9% saline over first 1_3 hours (5_10 mL/kg/h); subsequently, 0.45% saline at 150_300 mL/h; change to 5% glucose and 0.45% saline at 100_200 mL/h when plasma glucose reaches 250 mg/dL (14 mmol/L)

5. Administer regular insulin: IV (0.1 unit/kg) or IM (0.4 unit/kg), then 0.1 unit/kg/h by continuous IV infusion; increase 2- to 10-fold if no response by 2_4 hours. If initial serum potassium is less than 3.3 mmol/L (3.3 mEq/L), do not administer insulin until the potassium is corrected to greater than 3.3 mmol/L (3.3 mEq/L)

6. Assess patient: What precipitated the episode (e.g., nonadherence, infection, trauma, infarction, cocaine)? Initiate appropriate workup for precipitating event (cultures, chest x-ray, ECG)

7. Measure capillar y glucose ever y 1_2 hours; measure elec trol y tes (espe cially K+, bicarbonate, phosphate) and anion gap every 4 hours for first 24 hours

8. Monitor blood pressure, pulse, respirations, mental status, and fluid intake and output every 1-4 hours

9. Replace K+: 10 mEq/h when plasma K+ less than 5.5 mEq/L (5.5 mmol/L), ECG normal, urine flow and normal creatinine documented; administer 40-80 mEq/h when plasma K+ less than 3.5 mEq/L (3.5 mmol/L) or if bicarbonate is given

10. Continue above until patient is stable, glucose goal is 150-250 mg/dL (8.3-14 mmol/L), and acidosis is resolved. Insulin infusion may be decreased to 0.05-0.1 unit/kg/h

11. Administer intermediate or long-acting insulin as soon as patient is eating. Allow for overlap in insulin infusion and subcutaneous insulin injection

Cl, chloride; HCO3, serum bicarbonate; IM, intramuscular; K, potassium; Mg, magnesium; Na, sodium; PCO2, partial pressure of carbon dioxide in the arterial blood.

Hyperosmolar Hyperglycemic State

Hyperosmolar hyperglycemic state (HHS) is a life-threatening condition similar to DKA that also arises from inadequate insulin, but HHS occurs primarily in older patients with T2DM. DKA and HHS also differ in that HHS lacks the lipolysis, ketonemia, and acidosis associated with DKA. Patients with hyperglycemia and dehydration lasting several days to weeks are at the greatest risk of developing HHS. Illness and infection are common precipitating causes of HHS. Two main diagnostic criteria for HHS are a plasma glucose value of greater than 600 mg/dL (33.3 mmol/ L) and a serum osmolality of greater than 320 mOsm/kg. The extreme hyperglycemia and large fluid deficits resulting from osmotic diuresis are major challenges to overcome with this condition. Similar to DKA, the treatment of HHS consists of aggressive rehydration, correction of electrolyte imbalances, and continuous insulin infusion to normalize serum glucose. However, in patients with HHS, blood glucose levels should be reduced gradually to minimize the risk of cerebral edema.

Treatment of Long-Term Complications


Diabetic retinopathy occurs when the microvasculature that supplies blood to the retina becomes damaged. This damage permits leakage of blood components through the vessel walls. Diabetic retinopathy is the leading cause of blindness in adults 20 to 74

years of age in the United States. Retino-pathy is staged as either nonproliferative or proliferative.

Nonproliferative retinopathy often causes no visual disturbances and may remain asymptomatic for years. Proliferative retinopathy occurs when new retinal vessels form as a result of retinal ischemia in a process called neovascularization. Vision loss from proliferative retinopathy may range from mild blurring to obstruction of vision to complete blindness. Blurred vision is the presenting symptom for many patients who are diagnosed with diabetes. The ADA recommends that patients with DM receive a dilated eye examination annually by an ophthalmologist or optometrist. Gly-cemic control is the best prevention for slowing the progression of retinopathy. Early retinopathy may be reversed with improved glucose control.


O Peripheral neuropathy is the most common complication reported in T2DM. This complication generally presents as pain, tingling, or numbness in the extremities. The feet are affected more often than the hands and fingers. A number of treatment options have been tried with mixed success. Current options include pregabalin, gabapentin, low-dose tricyclic antidepressants, duloxetine, venlafaxine, topiramate, nonsteroidal anti-inflammatory drugs, and topical capsaicin.

Autonomic neuropathy is also a common complication as DM progresses. Clinical presentation of autonomic neuropathy may include gastroparesis, resting tachycardia, orthostatic hypotension, impotence, constipation, and hypoglycemic autonomic failure. Therapy for each individual autonomic complication is addressed separately.

Microalbuminuria and Nephropathy

DM is the leading contributor to end-stage renal disease. Early evidence of nephropathy is the presence of albumin in the urine. Therefore, as the disease progresses, larger amounts of protein spill into the urine. The ADA recommends urine protein tests annually in T2DM patients. For children with T1DM, annual urine protein testing should begin with the onset of puberty or 5 years after the diagnosis of diabetes. The most common form of screening for protein in the urine is a random collection for measurement of the urine albumin/creatinine ratio. The desirable value is less than 30 mcg of albumin per mg of creatinine.

Microalbuminuria is defined as between 30 and 300 mcg of albumin per mg of creatinine. The presence of micro-albuminuria is a strong risk factor for future kidney disease in T1DM patients. In T2DM patients, micro albuminuria has been found to be a strong risk factor for macrovascular disease.

Glycemic control and blood pressure control are primary measures for the prevention of progression of nephropathy. ACE inhibitors and angiotensin II receptor blockers prevent the progression of renal disease in T2DM patients. Treatment of advanced nephropathy includes dialysis and kidney transplantation.

Foot Ulcers

© Lower extremity amputations are one of the most feared and disabling sequelae of long-term uncontrolled DM. A foot ulcer is an open sore that develops and penetrates to the subcutaneous tissues. Complications of the feet develop primarily as a result of peripheral vascular disease, neuropathies, and foot deformations.

Peripheral vascular disease causes ischemia to the lower limbs. This decreased blood flow deprives the tissues of oxygen and nutrients, and impairs the ability of the immune system to function adequately. Symptoms of peripheral vascular disease include intermittent claudication, cold feet, pain at rest, and loss of hair on the feet and toes. Smoking cessation is the single most important treatment for peripheral vascular disease. In addition, exercising by walking to the point of pain, and then resting and resuming can be a vital therapy to maintain or improve the symptoms of peripheral vascular disease. Pharmacologic intervention with pentoxifylline or cilostazol also may be useful to improve blood flow and reduce the symptoms of peripheral vascular disease.

Neuropathies play a large part in the development of foot ulcers. Loss of sensation in the feet allows trauma to go unnoticed. Autonomic neuropathy can cause changes in the blood flow, perspiration, skin hydration, and possibly bone composition of the foot. Motor neuropathy can lead to muscle atrophy, resulting in weakness and changes in the shape of the foot. To prevent foot complications, the ADA recommends daily visual examination of the feet and a foot check performed at every physician visit. Sensory testing with a 10-gauge monofilament can detect areas of neuropathy. Treatment consists of glycemic control, preventing infection, debriding dead tissues, applying dressings, treating edema, and limiting ambulation. Untreated foot problems may develop gangrene, necessitating surgical intervention.

Patient Encounter, Part 2: Follow-Up Visit

EP comes in 1 week later for more education and brings in his blood glucose readings for you to download and review with him. See below. Readings are in units of mg/dL (mmol/L)

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