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Diagnosis and Management of Type 2 Diabetes, 10th Edition, Ch 14, Pt1

Acute Complications: Metabolic – DKA

Diagnosis_and_Management_of_Type_2_Diabetes

Steve V. Edelman, MD
Robert R. Henry, MD

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

METABOLIC

Diabetic Ketoacidosis (DKA)

This acute metabolic complication typically results from a profound insulin deficiency (absolute or relative) associated with uncontrolled Type 1 diabetes mellitus and less commonly in severely decompensated Type 2 diabetes.

Individuals with Type 2 diabetes 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 counterregulatory 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.

Key characteristics include:

  • Hyperglycemia (300 to 800 mg/dL although usually
  • Ketosis: serum ketones usually 10 to 20 mM and acidosis (pH 6.8-7.3, HCO3 <15mEq/L)
  • Dehydration caused by:
    • Nausea
    • Vomiting
    • Inadequate oral intake
  • Electrolyte depletion (e.g., potassium, magnesium, etc).

Precipitating factors vary from individual to individual and may include the following (approximately 50% of which are preventable):

  • Illness and infection; increased production of glucagon and glucocorticoids by adrenal gland promotes gluconeogenesis; increased production of epinephrine and norepinephrine increases glycogenolysis
  • Inadequate insulin dosage due to omission or reduction of doses by patient, physician, or clinic; patients with 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
  • Initial manifestation of Type 1 diabetes in the elderly misdiagnosed as Type 2 diabetes
  • Chronic untreated hyperglycemia (glucose toxicity) and hyperinsulinemia. 

Pathophysiology of DKA 

DKA is a metabolic acidosis caused by a significant insulin deficiency. The following physiologic abnormalities are characteristic of DKA and require prompt correction:

  • Chronic hyperglycemia and glucose toxicity
  • Acidosis caused by catabolism of fat and the buildup of ketone bodies
  • Low blood volume because of dehydration (loss of fluid and electrolytes)
  • Hyperosmolality because of renal water loss and water depletion from sweating, nausea and vomiting; and associated potassium loss. 

Symptoms and Signs of DKA 

The symptoms and signs of DKA are shown in Table 14.1. These are classic for DKA in Type 1 diabetes, although they are not as severe in patients with Type 2 diabetes because some 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. The chief respiratory complaint of dyspnea actually is an inability to catch one’s breath. This type of hyperventilation unrelated to exertion is the ventilator response to metabolic acidosis termed Kussmaul’s respiration.

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

Because other diseases and conditions may mimic DKA and precipitate and/or coexist with DKA, the following differential diagnoses (and representative DKA symptoms) should be considered:

  • Cerebrovascular accident (altered mental status)
  • Brainstem hemorrhage (hyperventilation, glucosuria)
  • Hypoglycemia (altered mental status, tachycardia)
  • Metabolic acidosis (hyperventilation, anion-gap acidosis):
    • Uremia
    • Salicylates
    • Methanol
    • Ethylene glycol
  • Gastroenteritis (nausea, vomiting, abdominal pain)
  • Pneumonia (hyperventilation).
Laboratory Evaluation 

Initial laboratory values are shown in Table 14.2.

Treatment 

Although aggressive therapy is not usually necessary in Type 2 diabetes, the following treatment strategies are for severe cases and for true Type 1 diabetes misdiagnosed as Type 2 diabetes 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.
DCMS15EdelmanTab14-1
DCMS15EdelmanTab14-2

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 Type 2 diabetes. The following treatment guidelines provide an overview for managing DKA. It is not unusual that patients with Type 2 diabetes can be treated adequately in a general hospital ward and not in an intensive care unit.

Fluid and Electrolyte Replacement
  • 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.
  • Most adults require IV fluid administration with normal (0.9%) or half-normal (0.45%) saline (normal saline should be used when intravascular volume depletion is extreme, and half-normal saline, when plasma volume contraction is more moderate).
  • One liter of fluid should be given per hour for the first 2 hours; the rate can be decreased to 500 mL per hour when signs of intravascular volume depletion have subsided.
  • 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 Therapy
  • Most patients with Type 2 diabetes can be treated successfully with frequent (every 2 to 3 hours) injections of Humalog or Novolog insulin subcutaneously (5 to 15 units).
  • A low dose of regular insulin can be administered via IV infusion at a rate of approximately 5 units per hour.
  • 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 can be discontinued and intermediate-acting NPH insulin can be started when HCO3 is >15 mEq/L and the patient can drink and eat light foods.
  • The major mistake with severe DKA is premature discontinuation of aggressive fluid and insulin therapy. Ketogenesis must be curtailed and requires insulin therapy. Serum glucose levels are not reflective of ketone body generation.

Potassium Replacement 

  • Not usually necessary in patients with Type 2 diabetes
  • May be necessary after fluid and insulin therapy has been started because all modes of therapy reduce the serum [K].
  • The goal is to maintain the serum [K] within the normal range.
  • An electrocardiogram (ECG) should be done as soon as possible. Potassium replacement is withheld if the patient is anuric or if the T waves are abnormally tall and peaked or have a high-normal configuration. If the T waves are normal, 20 mEq of potassium (with appropriate anion) is added to the first liter of replacement fluid. Low or flat T waves require the addition of 40 mEq of potassium.
  • An ECG should be done every 1 to 2 hours to evaluate treatment and adjust the potassium replacement regimen. Patients who are able to eat can receive potassium orally via food intake or potassium supplementation (12 to 15 mEq three times daily with meals).
Phosphate Replacement
  • Phosphate levels should be measured initially; some physicians use potassium phosphate for replacement if PO4 is in the low or low-normal range.
Bicarbonate Therapy            
  • This is not necessary in most patients but may be considered under certain circumstances, such as in patients with life-threatening hyperkalemia, lactic acidosis, or severe acidosis (pH <7.0) with shock that does not respond to fluid replacement.
  • When necessary, bicarbonate should be added to 0.45% saline and infused slowly over at least 1 hour; it should never be given in an IV bolus because of the risk of death secondary to hypokalemia.

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 generally is 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.

 

© Copyright 2010. Steven V. Edelman, MD, Robert R. Henry, MD, Professional Communications, Inc. All rights reserved.

Next Week: Hyperosmolar Hyperglycemic Nonketotic Syndrome, Pathophysiology of HHNS, and Hypoglycemia

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