Criteria and classification of diabetic ketoacidosis (DKA)
Common causes: infection, pancreatitis, cardiac event (i.e., MI), pregnancy, noncompliance with medication or inadequate insulin administration, new-onset diabetes, or cocaine use.
Signs and symptoms: dehydration, abdominal pain, nausea/vomiting, polydipsia, polyuria, and confusion. Often the patient can have a “ketotic” odor or “fruity” smell to their breath. Since the body is overwhelmed by the rising acidosis, the body tries to compensate via hyperventilation, which is why you may see the patient taking deep gasping breathing (Kussmaul respirations).
Initial lab tests: in order to make the diagnosis, the following are necessary – basic metabolic panel, serum osmolality, ß-hydroxybutyrate or urinalysis (to indicate ketones in the urine), CBC, and venous blood gas to get the pH.
Goals of treatment:
Resuscitate the patient – average adult in DKA has a total body water shortage of about 6 L in addition to shortages of multiple electrolytes, such as sodium, potassium, chloride, phosphate, magnesium, and calcium . Replace the fluid deficit within the first 24–36 h with the goal of 50 % of volume replacement within the first 12 h.
Close the gap and normalize acidosis – this is primarily done with fluid hydration and starting an insulin drip:
Insulin drip: the potassium level should be >3.3 mEq/L before initiating insulin therapy. A Common form of practice is to start an intravenous regular insulin drip at 0.1 units/kg per hour. Blood glucose levels should be checked hourly, and when levels fall below 250 mg/dL, it may be appropriate to decrease the inulin infusion rate to 0.05 units/kg per hour and add dextrose (5–10 %) to the IV fluids running. The insulin drip should be continued until the anion gap is closed, at which point the IV insulin should continue for 2 h more after initiation of subcutaneous insulin for people who are able to eat.
Bicarbonate use in DKA remains controversial. Prospective randomized studies have failed to show either beneficial or deleterious changes in morbidity or mortality with bicarbonate therapy in DKA patients with pH between 6.9 and 7.1 . Current recommendations state no bicarbonate is necessary if pH is >7.0. However, if the pH remains <7.0 after the initial hour of hydration, it seems prudent to administer 1–2 mEq/kg sodium bicarbonate over the course of 1 h .
Resolution of DKA – plasma glucose <200 mg/dL, serum HCO3 >18 mEq/L, venous blood pH >7.3, and anion gap <12 
Hypoglycemia and hypokalemia – most frequent complications that can be prevented with insulin dose adjustment and frequent monitoring of glucose (hourly point of care glucose checks) and potassium levels (every 2–3 h).
Cerebral edema – it is the most dangerous complication seen from over-vigorous fluid resuscitation and is most commonly seen in children. Likely due to a combination of factors, dehydration, severe acidosis, and low carbon dioxide levels along with the increased level of inflammation and coagulation may, together with these factors, lead to decreased blood flow. The brain swells once fluid replacement has been started causing an increase in intracranial pressure and ultimately death .
Pulmonary edema – can develop from excessive fluid replacement, particularly in those with chronic kidney disease (CKD) or congestive heart failure (CHF).
Non-anion gap hyperchloremic acidosis – likely secondary to intensive administration of chloride-containing fluids (NaCl) and low plasma bicarbonate. This normally resolves and doesn’t affect treatment course.
Hyperosmolar hyperglycemic state (HHS) – also known as hyperosmolar hyperglycemic nonketotic coma (HHNC). It is much less common than DKA, but confers a greater mortality (~15 %) . Prognosis is substantially worsened at the extremes of age and in the presence of coma and hypotension. More common in T2DM patients and process likely evolves over several days to weeks. Identified by marked elevation of blood glucose, hyperosmolarity secondary to high blood sugars causing severe dehydration, and little or no ketosis . This is secondary to the fact that plasma insulin concentrations are inadequate to facilitate glucose utilization by insulin-insensitive tissues but adequate to prevent lipolysis and subsequent ketogenesis .
Diagnosis: blood glucose >600 mg/dL, pH >7.30, serum bicarb >15 mEq/L, small urine ketones, normal or slightly elevated ß-hydroxybutyrate, and serum osmolality >320 mEq/L; anion gap is variable. There are also several electrolyte losses: sodium, chloride, potassium, phosphate, calcium, and magnesium .
Causes: underlying infections are the most common, but other causes include noncompliance with medications, certain drugs that affect carbohydrate metabolism (i.e., corticosteroids, thiazides, and sympathomimetic agents like dobutamine or terbutaline), undiagnosed diabetes, substance abuse, and coexisting disease .
Signs and symptoms – polyuria, polydipsia, vomiting, dehydration, weakness, hypothermic secondary to vasodilation, clouding of sensoria, and finally coma . Hypothermia and hypotension are poor prognostic signs.
Treatment – goals of treatment and management are the same as DKA listed above in regard to fluid resuscitation and insulin infusion. Patients in HHS have profound dehydration, up to an average of 9 L fluid deficit; however, frequent reevaluations need to be done in patients with either cardiac or renal compromise as to prevent iatrogenic fluid overload. In HHS, insulin therapy is continued with glucose levels being maintained around 250–300 mg/dL until mental obtundation and hyperosmolarity are resolved:
Complications of treatment – include hypokalemia, hypoglycemia, and cerebral edema
Hypoglycemia – from physiological point of view, a detectable impairment of higher cerebral function has been demonstrated at plasma glucose levels of 54 mg/dL or less; however, counterregulatory responses to hypoglycemia have been described at plasma levels between 65 and 70 mg/dL acting within a few minutes . Hypoglycemia occurs when insulin deficiency in diabetics is overcorrected.
Components of these counterregulatory responses: suppression of insulin secretion from pancreatic B-cells, increase in glucagon secretion from pancreatic a-cells, increase in adrenomedullary epinephrine secretion, and increase in growth hormone and adrenocorticotropin secretion from the anterior pituitary .
In diabetic patients, these counterregulatory responses are decreased leading to more frequent episodes of hypoglycemia particularly in the setting of exogenous insulin administration.
Hypoglycemia is a more common problem in T1DM compared to T2DM secondary to impairment of the first and second counterregulatory mechanisms . In T2DM, the counterregulatory mechanisms are preserved except for in the elderly (>65 years), it may be reduced, and thereby these patients are also more susceptible to hypoglycemia .
Insulin overdose: most insulin overdoses are intentional, but many are accidental. Symptoms include diaphoresis, chills, lightheadedness/dizziness, tachycardia, tremors, blurred vision, and tingling around the lips/mouth . More severe symptoms include change in mental status, seizures, unconsciousness, and death. Initial emergency response is to inject glucagon (D50) and to have close/strict monitoring over glucose levels. If levels continue to drop, pt can be placed on a D5 infusion.
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American Diabetes Association (ADA) recommendations:
Goals of treatmen t – HgA1C <7.0 for many nonpregnant adult: recommendation based on pathophysiologic reasoning, expert opinion, and the reduction in microvascular complications shown in the UK Prospective Diabetes Study (UKPDS):
Recommends HgA1C <6.5 is reasonable for patients with a short duration of diabetes, a long life expectancy, and no significant cardiovascular disease.
More stringent control of HgA1C <6.0 may be appropriate in T1DM and during pregnancy.
Recommends HgA1C <7.5–8 is appropriate for patients with a short life expectancy, cardiovascular disease, two or more cardiovascular disease risk factors, or duration of disease of 10 years or more because of a lack of benefit and the potential for increased risk of mortality.
The ADA recommends starting therapy with metformin first-line therapy to reduce microvascular complications, assist in weight management, reduce the risk of cardiovascular events, and reduce the risk of mortality in patients with type 2 diabetes mellitus.
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