Re: Chpt 14 of Diagnosis and Management of Diabetes

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awsome article

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Chpt 14 of Diagnosis and Management of Diabetes

Diagnosis_and_Management_of_Type_2_DiabetesSteve V. Edelman, MD

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....

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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 <600 mg/dL; the

glucose concentration is not related to severity of DKA)

* 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.

Next Week: Hyperosmolar Hyperglycemic Nonketotic Syndrome, Pathophysiology

of HHNS, and Hypoglycemia