Ketoacidosis

NIDDM is a much more common disease than IDDM, accounting for about 85—90% of all cases of diabetes meUitus. Whereas NIDDM may be present at any age, the incidence increases dramatically with advanced age over 10% of the population reaching 70 years of age has NIDDM. Patients with NIDDM do not require insulin treatment to maintain life or prevent the spontaneous occurrence of diabetic ketoacidosis. Therefore, NIDDM is frequendy asymptomatic and unrecognized, and diagnosis requires screening for elevations in blood or urinary sugar. Most forms of NIDDM are associated with a family history of the disease, and NIDDM is commonly associated with and exacerbated by obesity. The causes of NIDDM are not well understood and there may be many molecular defects which lead to NIDDM. 

Insulin is necessary for controlling type 1 diabetes mellitus that is caused by a marked decrease in the amount of insulin produced by die pancreas. Insulin is also used to control the more severe and complicated forms of type 2 diabetes mellitus. However, many patients can control type 2 diabetes with diet and exercise alone or with diet, exercise, and an oral antidiabetic drug (see section Oral Antidiabetic Dmgp ). Insulin may also be used in the treatment of severe diabetic ketoacidosis (DKA) or diabetic coma. Insulin is also used in combination with glucose to treat hypokalemia by producing a shift of potassium from die blood and into die cells. 

SYMPTOMS HYPOGLYCEMIA (INSUUN REACTION) HYPERGLYCEMIA (DIABETIC COM A, KETOACIDOSIS)... 

Urine testing can play a role in identifying ketone excretion in patients prone to ketoacidosis. If urine testing is done, it is usually recommended tiiat the nurse use the second voided specimen (ie, fresh urine collected 30 minutes after the initial voiding) to check glucose or acetone levels, ratiier than die first specimen obtained. 

Metformin is contraindicated in patients with heart failure, renal disease, hypersensitivity to metformin, and acute or chronic metabolic acidosis, including ketoacidosis. The drug is also contraindicated in patients older than 80 years and during pregnancy (Pregnancy Category B) and lactation. 

The a-glucosidase inhibitors are contraindicated in patients with a hypersensitivity to the drug, diabetic ketoacidosis, cirrhosis, inflammatory bowel disease, colonic ulceration, partial intestinal obstruction or predisposition to intestinal obstruction, or chronic intestinal diseases. Acarbose and miglitol are used cautiously in patients with renal impairment or pre-existing gastrointestinal (GI) problems such as irritable... 

MANAGING HYPERGLYCEMIA AND KETOACIDOSIS. Capillary blood specimens are obtained and tested in the same manner as for insulin (see Fhtient and Family Teaching Checklist, p. 497). The nurse notifies the health care provider if blood sugar levels are elevated... 

Increased fatty acid oxidation is a characteristic of starvation and of diabetes meUims, leading to ketone body production by the Ever (ketosis). Ketone bodies are acidic and when produced in excess over long periods, as in diabetes, cause ketoacidosis, which is ultimately fatal. Because gluconeogenesis is dependent upon fatty acid oxidation, any impairment in fatty acid oxidation leads to hypoglycemia. This occurs in various states of carnitine deficiency or deficiency of essential enzymes in fatty acid oxidation, eg, carnitine palmitoyltransferase, or inhibition of fatty acid oxidation by poisons, eg, hypoglycin. 

Higher than normal quantities of ketone bodies present in the blood or urine constitute ketonemia (hyperke-tonemia) or ketonuria, respectively. The overall condition is called ketosis. Acetoacetic and 3-hydroxybutyric acids are both moderately strong acids and are buffered when present in blood or other tissues. However, their continual excretion in quantity progressively depletes the alkah reserve, causing ketoacidosis. This may be fatal in uncontrolled diabetes mellitus. 

If hypoglycemia develops in the setting of continued ketoacidosis, lower the insulin infusion and administer glucose infusions to maintain euglycemia. Do not stop the insulin infusion... 

Convert to insulin glargine (Lantus ) or NPH SQ insulin (several methods depending on style) once ketoacidosis has resolved and the patient is eating... 

It is important to realize that the serum HCO, concentration may be affected by the presence of unmeasured endogenous acids (lactic acidosis or ketoacidosis). Bicarbonate will attempt to buffer these acids, resulting in a 1 mEq loss of serum HCO, for each 1 mEq of acid titrated. Because the cation side of the equation is not affected by this transaction, the loss of serum HC03 results in an increase in the calculated anion gap. Identification of an increased anion gap is very important for identifying the etiology of the acid-base disorder. The concept of the increased anion gap will be applied later in the case studies section. 

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