Glycosuria occurs when the serum glucose concentrationexceeds the renal threshold for glucose reabsorption (from 160to 190 mg/dL). Glycosuria causes an osmotic diuresis (includingobligate loss of sodium, potassium, and other electrolytes), leading to dehydration. Polydipsia occurs as the patient attempts tocompensate for the excess fluid losses. Weight loss results fromthe persistent catabolic state and the loss of calories through glycosuria and ketonuria. The classic presentation of DM1 includespolyuria, polydipsia, polyphagia, and weight loss.
If the clinical features of new-onset DM1 are not detected, diabetic ketoacidosis (DKA) will occur. DKA may also occur in patients with known DM1 if insulin injections are omitted 0 50 100 Beta cell mass (% of max) 0 Time (y) Progressive Impairment In Insulin Release Overt Diabetes “Honeymoon” Period Release Birth Figure 171-1 Schematic representation of the autoimmune evolution of diabetes in genetically predisposed individuals.
or during an intercurrent illness when greater insulin requirements are unmet in the presence of elevated concentrations of the counter-regulatory and stress hormones (glucagon, growth hormone [GH], cortisol, and catecholamines). DKA can be considered to be present if (1) the arterial pH is below 7.3, (2) the serum bicarbonate level is below 15 mEq/L, and (3) ketones are elevated in serum or urine.
In the absence of adequate insulin secretion, persistent partialhepatic oxidation of fatty acids to ketone bodies occurs. Twoof these three ketone bodies are organic acids and lead to metabolic acidosis with an elevated anion gap. Lactic acid maycontribute to the acidosis when severe dehydration results indecreased tissue perfusion. Hyperglycemia causes an osmoticdiuresis that is initially compensated for by increased fluidintake. As the hyperglycemia and diuresis worsen, most patients are unable to maintain the large fluid intake, anddehydration occurs. Vomiting, as a result of increasing acidosis, and increased insensible water losses caused by tachypneacan worsen the dehydration. Electrolyte abnormalities occurthrough a loss of electrolytes in the urine and transmembrane alterations resulting from acidosis. As hydrogen ionsaccumulate as a result of ketoacidosis, intracellular potassium is exchanged for hydrogen ions. Serum concentrationsof potassium increase initially with acidosis then decrease asserum potassium is cleared by the kidney. Depending on theduration of ketoacidosis, serum potassium concentrations at diagnosis may be increased, normal, or decreased, but intracellular potassium concentrations are depleted. A decreasedserum potassium concentration is an ominous sign of totalbody potassium depletion. Phosphate depletion also can occur as a result of the increased renal phosphate excretion required for elimination of excess hydrogen ions. Sodiumdepletion is also common ketoacidosis, resulting from renallosses of sodium caused by osmotic diuresis and from gastrointestinal losses from vomiting (Fig. 171-2).
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