Diabetic Ketoacidosis and Hyperosmolar Coma

Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) are

acute complications of diabetes mellitus (DM). DKA is seen primarily in individuals withtype 1 DM and HHS in individuals withtype 2 DM. Both disorders

are associated withabsolute or relative insulin deficiency, volume depletion,

and altered mental status. The metabolic similarities and differences in

DKA and HHS are summarized in Table 24-1.

DIABETIC KETOACIDOSIS

ETIOLOGY DKA results from insulin deficiency witha relative or absolute

increase in glucagon and may be caused by inadequate insulin administration,

infection (pneumonia, UTI, gastroenteritis, sepsis), infarction (cerebral,

coronary, mesenteric, peripheral), surgery, drugs (cocaine), or pregnancy.

CLINICAL FEATURES The initial symptoms of DKA include anorexia,

nausea, vomiting, polyuria, and thirst. Abdominal pain, altered mental function,

or frank coma may ensue. Classic signs of DKA include Kussmaul respirations

and an acetone odor on the pt’s breath. Volume depletion can lead to dry mucous

membranes, tachycardia, and hypotension. Fever and abdominal tenderness may

also be present. Laboratory evaluation reveals hyperglycemia, ketosis (_-hydroxybutyrate _ acetoacetate), and metabolic acidosis (arterial pH 6.8–7.3)

withan increased anion gap (Table 24-1). The fluid deficit is often 3–5 L.

Despite a total-body potassium deficit, the serum potassium at presentation may be normal or mildly high as a result of acidosis. Leukocytosis, hypertriglyceridemia,

and hyperlipoproteinemia are common. Hyperamylasemia is usually of

salivary origin but may suggest a diagnosis of pancreatitis. The measured serum

sodium is reduced as a consequence of hyperglycemia (1.6-meq reduction for

each100-mg/dL rise in the serum glucose).

TREATMENT

The management of DKA is outlined in Table 24-2.

HYPERGLYCEMIC HYPEROSMOLAR STATE

ETIOLOGY Relative insulin deficiency and inadequate fluid intake are

the underlying causes of HHS. Hyperglycemia induces an osmotic diuresis that leads to profound intravascular volume depletion. HHS is often precipitated by

a serious, concurrent illness suchas myocardial infarction or sepsis and compounded by conditions that impede access to water.

CLINICAL FEATURES Presenting symptoms include polyuria, thirst,

and altered mental state, ranging from lethargy to coma. Notably absent are

symptoms of nausea, vomiting, and abdominal pain and the Kussmaul respirations

characteristic of DKA. The prototypical pt is an elderly individual with

a several week history of polyuria, weight loss, and diminished oral intake. The

laboratory features are summarized in Table 24-1. In contrast to DKA, acidosis

and ketonemia are usually not found; however, a small anion gap may be due

to lactic acidosis, and moderate ketonuria may occur from starvation. Though

the measured serum sodium may be normal or slightly low, the corrected serum

sodium is usually increased (add 1.6 meq to measured sodium for each100-

mg/dL rise in the serum glucose).

TREATMENT

The precipitating problem should be sought and treated. Sufficient IV fluids

(1–3 L of 0.9% normal saline over the first 2–3 h) must be given to stabilize

the hemodynamic status. The calculated free water deficit (usually 8–10 L)

should be reversed over the next 1–2 days, using 0.45% saline initially then

5% dextrose in water. Potassium repletion is usually necessary. The plasma

glucose may drop precipitously with hydration alone, though insulin therapy

withan intravenous bolus of 5–10 units followed by a constant infusion rate

(3–7 units/h) is usually required. Glucose should be added to intravenous

fluid when the plasma glucose falls to 13.9 mmol/L (250 mg/dL). The insulin

infusion should be continued until the patient has resumed eating and can be

transitioned to a subcutaneous insulin regimen.

Table 24-2

Management of Diabetic Ketoacidosis

1. Confirm diagnosis (qplasma glucose, positive serum ketones, metabolic

acidosis).

2. Admit to hospital; intensive-care setting may be necessary for frequent

monitoring or if pH _ 7.00 or unconscious.

3. Assess: Serum electrolytes (K_, Na_, Mg2_, Cl_, bicarbonate, phosphate)

Acid-base status—pH, HCO3

_, PCO , _-hydroxybutyrate 2

Renal function (creatinine, urine output)

4. Replace fluids: 2–3 L of 0.9% saline over first 1–3 h(5 –10 mL/kg per

hour); 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 14 mmol/

L, (250 mg/dL).

5. Administer regular insulin: IV (0.1 units/kg) or IM (0.4 units/kg), then 0.1

units/kg per hour by continuous IV infusion; increase 2- to 10-fold if no

response by 2–4 h. If initial serum potassium is _ 3.3 mmol/L (3.3 meq/

L), do not administer insulin until the potassium is corrected to_3.3 mmol/

L (3.3.meq/L).

6. Assess patient: What precipitated the episode (noncompliance, infection,

trauma, infarction, cocaine)? Initiate appropriate workup for precipitating

event (cultures, CXR, ECG).

7. Measure capillary glucose every 1–2 h; measure electrolytes (especially

K_, bicarbonate, phosphate) and anion gap every 4 h for first 24 h.

8. Monitor blood pressure, pulse, respirations, mental status, fluid intake and

output every 1–4 h.

9. Replace K_: 10 meq/hwh en plasma K_ _ 5.5 meq/L, ECG normal, urine

flow and normal creatinine documented; administer 40–80 meq/hwh en

plasma K_ _3.5 meq/L or if bicarbonate is given.

10. Continue above until patient is stable, glucose goal is 150–250 mg/dL, and

acidosis is resolved. Insulin infusion may be decreased to 0.05–0.1 units/

kg per hour.

11. Administer intermediate or long-acting insulin as soon as patient is eating.

Allow for overlap in insulin infusion and subcutaneous insulin injection.