pallor, tremor, anxiety, tachycardia, palpitations, diaphoresis, headache, dizziness, irritability, fatigue, poor judgment, confusion, visual disturbances, hunger, seizures, and coma Kussmaul respirations (hyperventilation in an attempt to compensate for the acidosis), postural dizziness, central nervous system depression, lethargy, ketonuria, anorexia/weight loss, nausea, abdominal pain, thirst, dry mouth, polyuria, and a fruity or acetone odor on the breath. Less profound insulin deficiency, more profound fluid deficiency, a serum glucose level >600 mg/dl, a serum pH >7.30, a serum bicarbonate level >15 mg/dl, a serum osmolarity >320 mOsm/L, and either absent or small numbers of ketones in the urine and serum. Glucose levels are considerably higher in HHNKS than in DKA because of volume depletion. Clinical manifestations include severe dehydration, polyuria, thirst, tachycardia, hypoperfusion; loss of electrolytes, including potassium; weakness, nausea, vomiting, abdominal pain; and neurologic changes, such as stupor, coma, and seizures. Tissues that do not require insulin for glucose transport, such as kidney, red blood cells (RBCs), blood vessels, eye lens, and nerves, cannot down-regulate the cellular uptake of glucose; consequently, intracellular glucose is shunted into an alternate metabolic pathway, known as the polyol pathway. Overactivation of the polyol pathway results in two processes that may contribute to the complications of diabetes. One is the excessive accumulation of sorbitol (a six-carbon sugar alcohol, or polyol), which causes cataracts and interferes with nerve conduction and perfusion. Activation of the polyol pathway also reduces the level of glutathione, an important antioxidant, and consequently there is oxidative injury in cells and tissues.