The diagnostic work-up for HHS is identical to that for DKA. The findings are somewhat different, however. On presentation, the patient with HHS has glucosuria and no or minimal ketonuria and ketonemia. A mild metabolic acidosis may be present in these patients.
Laboratory criteria used to diagnose DKA include a glucose level greater than 250 mg/dL, a pH less than 7.35, a serum bicarbonate of 12-15 mEq/dL, a high anion gap, and positive ketones. (Occasionally DKA can occur with a normal glucose level when there is vomiting, reduced intake of carbohydrate, and continued insulin therapy.) (See also Table 6.)
A serum glucose determination should always be obtained, but most management can be done with bedside glucose testing. Suspect DKA when the glucose is greater than 250 mg/dL.48 However, normoglycemia may be seen in patients who received insulin before being seen in the ED, were fasting, or who have impaired gluconeogenesis from liver failure.
The massive diuresis may contribute significantly to the electrolyte abnormalities seen in DKA. Free water, sodium, potassium, magnesium, and phosphate are excreted into the urine along with the glucose. Ketoacids act as nonresorbable ions in the kidney and are excreted as potassium and sodium salts. Because urine contains about 70-80 mEq/L of cations, most of which are sodium and potassium, massive total body deficiencies in sodium and potassium may result.
Despite this urinary potassium loss and total body deficits of potassium, most patients will have an elevated potassium at initial laboratory evaluation.47 This is due to the lack of insulin, acidosis, and the increased osmolality. Loss of insulin will cause a shift in intracellular potassium into the serum. Acidosis and movement of water from the intracellular space to the extracellular space will further move potassium into the extracellular fluid.
The sodium should be corrected for the high glucose seen in the patient with HHS. The effects of a very elevated glucose on the sodium may be greater than the usual correction. There is some controversy about the method of correction to be used.113 See Table 6 for the usually accepted correction.
Complete Blood Count
The complete blood count often shows a leukocytosis. This may be in part due to the hemoconcentration from dehydration. White blood cell counts of 20,000 cells/mm3 are not uncommon. If the patient has an elevated band count (bandemia) on peripheral smear, then an infectious process is likely.67
An arterial blood gas or venous gas should be sent early in the evaluation of the patient considered to have DKA.68,69 (The correlation between arterial and venous pH is quite close, and the two can be used interchangably for the evaluation of DKA patients.) This will help determine the degree of acidosis and bicarbonate loss. When the pH is less than 7.35 and a low HCO3 - is found, then the diagnosis of DKA should be seriously considered.
Blood Urea Nitrogen And Creatinine
The patient will often have some elevation of the blood urea nitrogen due to dehydration. The clinician should carefully consider the po ssibility of chronic renal failure. The patient with both diabetes and renal failure may be quite difficult to manage. Fluid losses may be smaller than when the patienthas normal renal function, and fluid replacement must bemuch more conservative. Therapeutic emphasis will switchto insulin, careful monitoring of potassium, and considerationof dialysis.
Urinalysis And Urine Culture
Check the urine on every patient who presents with a possible diagnosis of DKA in order to identify possible urosepsis causing the DKA. Likewise, in females of childbearing age, a urine pregnancy test is equally important.
ketone testing may not correlate with the degree of ketoacidosis.
Beta-hydroxybutyric acid is the major ketoacid produced
in DKA. It does not react with nitroprusside, so urine
or blood testing for ketones may be negative or only slightly
During the treatment of DKA, beta-hydroxybutyric acid will be converted to acetoacetic acid. The resultant increase in acetoacetic acid may make the serum or urine testing for ketones more positive, despite clinical improvement and an increasing pH and decreasing anion gap. While some literature has suggested that urine ketones can be used to rule out DKA, serum ketones are mo re accurate and should be used instead.
Because biological membranes are readily permeable to water molecules, there is a continuing movement or exchange of water between various fluid compartments.
The forces governing the movement of water are both hydrostatic and osmotic pressures. The osmotic pressures greatly exceed hydrostatic pressures in the body.
pressure is a property of solutions that depends
on the number of osmotically active molecules in solution.
It does not depend on the ionic charge, the size of the
molecule, or the chemical properties of the molecule. One
gram-molecular weight (1 mole) of a compound is also termed
1 osmole (osmol or Osm). Most biological concentrations are
expressed in milliosmolar (mOsm) or microosmolar
(μOsm) concentrations. Ionized molecules such
as sodium chloride will dissociate in solution, and each ion
exerts its own osmotic force. (This means that 1 mOsm of
NaCl exerts 2 mOsm of osmotic pressure.) Osmolality is the
expression of this quantity of osmotically active particles per
1000 grams of water or solvent. The more common term, osmolarity,
expresses the number of osmotically active particles
per liter of solvent. The difference between osmolarity
and osmolality is due to protein and fat, which comprise
about 6%-8% of the solutes in plasma.
Hyperosmolality in diabetes is largely due to hyperglycemia.
Lumbar puncture is indicated in patients with an acute alteration of consciousness and clinical features suggestive of possible central nervous system infection.
Hemoglobin A1c Determination
Glycosylated hemoglobin measurement is not needed for the emergent management of the patientís diabetes. The hemoglobin A1c will give the clinician some idea of the duration or degree of control of the patientís diabetes prior to the emergency.