Description
Management of DKA in critically ill patients requires rapid recognition, hemodynamic stabilization, and correction of metabolic derangements. Initial treatment includes aggressive fluid resuscitation with isotonic saline to restore perfusion, followed by insulin infusion to suppress ketogenesis and normalize glucose. Electrolyte monitoring, especially potassium, is crucial before and during insulin therapy. Bicarbonate therapy is reserved for severe acidosis (pH < 6.9). Frequent monitoring of blood glucose, ketones, electrolytes, and acid-base status is essential in the ICU setting. Early identification of precipitating factors such as infection or myocardial infarction ensures comprehensive management and improves patient outcomes.
Summary Listen
- Diabetic ketoacidosis (DKA) is defined by hyperglycemia, ketosis (blood or urine), and metabolic acidosis. It must be differentiated from hyperglycemic hyperosmolar state (HHS), which involves hyperglycemia and hyperosmolarity but lacks significant ketosis or acidosis. DKA severity is stratified as mild, moderate, or severe based on glucose levels, ketonemia, and acidosis (pH or bicarbonate). Not all criteria must be fulfilled to define a DKA as mild moderate or severe.
- Ketone measurement can be done in blood or urine. It is important to know that reliance on urine ketone testing can underestimate the severity of ketonemia early in the course of diabetic ketoacidosis and overestimate the severity of the ket later in the course. A recent international survey (NIDHI) highlighted that a pH value below 7.20 was a key ICU admission criterion for DKA patients. Intravenous insulin was also a major factor, while ketonemia, glucose, and potassium were less frequently considered.
- DKA's incidence is rising, though mortality remains low (below 1%), but it is no longer decreasing. Precipitating factors, such as new-onset diabetes or insulin omission and infections, are crucial to identify. While both DKA and HHS share an insulin deficiency, DKA involves an absolute deficiency leading to increased glycogenolysis, lipolysis, and ketone production.
- Treatment of DKA involves fluid administration, insulin administration (intravenous or subcutaneous), and management of metabolic disorders, particularly potassium levels. The traditional view that only isotonic saline should be used for fluid replacement is questioned, with balanced crystalloids potentially offering benefits due to lower chloride content and faster DKA resolution in some studies.
- The use of sodium bicarbonate in DKA treatment is controversial, with most current guidelines advising against it unless in cases of very severe acidosis (pH < 7.0). Research indicates no improvement in cardiac function or clinically relevant outcomes with bicarbonate administration, and there's potential for increased risk of cerebral edema.
- Regarding insulin administration, current recommendations advise against a bolus. There is a role for basal-weight dosage intravenous insulin. Intravenous insulin should be continuous until diabetes to acidosis resolution to block lipolizes, even with subcutaneous insulin, which has demonstrated faster DKA resolution and shorter ICU stays in some studies. Insulin should not be started before fluid administration to avoid hypocalemia.
- Potassium and phosphate levels need careful management, with systematic potassium supplementation being standard. Phoshor supplementation is less standard even if the speaker recomendates it in every case. Monitoring involves blood samples. Venuos blood may be sufficient to monitor pH value and becavandate concentration.
- Particular attention should be paid to patients with specific conditions, such as pregnant women or those taking SGLT2 inhibitors, who may present with euglycemic DKA.
Sample Certificate
About the Speakers
Dr. Prof. Mathieu Jozwaik
Intensive Care Medicine University Hospital Center, France
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