Assessing Disease Severity
Mental status and pH and serum bicarbonate levels help clinicians determine the extent of disease severity, classifying patients as having mild, moderate, or severe DKA (Table 4).2 Patients at the highest risk for poor outcomes include those at the extremes of age, who have severe comorbidities, who have underlying infection, and who are hypotensive and/or in a comatose state.3
Table 4.
Patients who have HHS are much more likely to present with altered mental status, including coma. There is a linear relationship between osmolality and degree of altered mental status. Thus, diabetic patients with major changes in mental status but without high serum osmolality warrant immediate workup for alternative causes of their altered mental status.3 In addition, seizures, especially focal seizures, are relatively common in severe cases of HHS. Finally, highly abnormal blood pressure, pulse, and respiratory rate can also provide additional clues regarding the severity of hyperglycemic crisis.
Arterial Blood Gas Assessment: To Stick or Not to Stick?
In the past, measuring arterial blood gases (ABG) has been considered a mainstay in the evaluation of patients with DKA. But does an arterial stick, which is associated with some risk, really add essential information? One study by Ma et al6 evaluated whether ABG results significantly alter how physicians manage patients with DKA. In the study, the authors evaluated 200 ED patients and found that ABG analysis only changed diagnosis in 1% of patients, altered treatment in 3.5% of patients, and changed disposition in only 1% of patients. Arterial stick partial pressure of oxygen and partial pressure of carbon dioxide altered treatment and disposition in only 1% of patients. Furthermore, the study results showed venous pH correlated very strongly with arterial pH (r = 0.95).6 These findings demonstrate that ABG measurements rarely affect or alter DKA management, and support the use of venous pH as an adequate substitute for ABG testing.
Euglycemia
Euglycemic DKA has been reported in patients with type 1 diabetes who had been fasting or vomiting or who had received exogenous insulin prior to presentation.1Euglycemia has also been reported in pregnant patients with type I diabetes.1 More recently, sodium glucose cotransporter 2 inhibitors (SGLT2) have been shown to cause euglycemic DKA. While the therapeutic mechanism of this drug class is to inhibit proximal tubular resorption of glucose, they can cause DKA by decreasing renal clearance of ketone bodies and increasing glucagon levels and promoting hepatic ketogenesis. Patients with DKA who are on SGLT2 inhibitors may present with only modestly elevated glucose levels (typically in the 200- to 300-mg/dL range), but have profound wide gap metabolic acidosis due to β-hydroxybutyrate acid and acetoacetate accumulation.7 When evaluating patients on SGLT2 inhibitors for DKA, EPs should not solely rely on glucose values but rather assess the patient’s overall clinical picture, including the physical examination, vital signs, and pH. Additionally, once resuscitation with intravenous (IV) fluids and insulin is initiated, it may take longer for patients who use SGLT2 inhibitors to clear ketoacids than patients with DKA who do not use these medications.8