Checking your ketones at home is simple. You should also test for ketones if you have any of the symptoms of DKA. Call your doctor if your ketones are moderate or high. Elevated ketones are a sign of DKA, which is a medical emergency and needs to be treated immediately. Your treatment will likely include:. DSMES services are a vital tool to help you manage and live well with diabetes while protecting your health.
Skip directly to site content Skip directly to page options Skip directly to A-Z link. Section Navigation. Facebook Twitter LinkedIn Syndicate. Administer priming insulin bolus at 0. Measure bedside glucose every 1 hour to adjust the insulin infusion rate. With a number of DKA guidelines and technical reviews in the field published by several societies, 3 , 8 , 36 , 37 there is a call to efficiently deliver current knowledge to the bedside.
One approach to delivering best clinical practices is development of inpatient standardized protocols for DKA management. Studies have shown that protocol-directed care of patients with hyperglycemic crises is both safe and efficient, as highlighted by significant decreases in length of stay without increases in the rate of iatrogenic complications.
Outcomes of protocol-based care have differed in other institutions. One retrospective case review study conducted in the United Kingdom revealed that, though providers were aware of the existence of a universal protocol, this did not translate into protocol adherence for a number of reasons, including patient- and clinician-related factors.
The greatest benefit was observed during the first few hours of early DKA management, where intravenous access was gained appropriately, initial fluid resuscitation was started, and initial laboratory testing was completed. Following early care, variations in adherence to protocol increased, as less than one-half of patients received appropriate fluid therapy or repeat laboratory studies or were referred to the appropriate care unit. The care of patients with DKA should be a collaborative effort that includes the expertise of endocrinology, intensive care, medical pharmacy, and nursing specialists.
Hypoglycemia is the most frequent complication of DKA and can be prevented by timely adjustment of insulin dose and frequent monitoring of blood glucose levels. When DKA is resolved, strategies to manage hypoglycemia will depend on whether or not the patient is able to maintain oral intake. Non-anion gap hyperchloremic metabolic acidosis frequently develops during DKA treatment and is believed to occur due to urinary losses of ketoanions, which are needed for bicarbonate regeneration, and preferential reabsorption of chloride in proximal renal tubule secondary to intensive administration of chloride-containing fluids.
This acidosis usually resolves spontaneously in a few days and should not affect the treatment course. Cerebral edema due to rapid reduction in serum osmolality has been reported in young adult patients. Mannitol infusion and mechanical ventilation should be used to treat this condition. Rhabdomyolysis is another possible complication due to hyperosmolality and hypoperfusion. Pulmonary edema can develop from excessive fluid replacement in patients with chronic kidney disease or congestive heart failure.
Discharge planning should include diabetes education, selection of an appropriate insulin regimen that is understood by and affordable for the patient, and preparation of supplies for the initial insulin administration at home. Many cases of DKA can be prevented by better access to medical care, proper education, and effective communication with a health care provider during an intercurrent illness. Sick-day management should be reviewed with all patients and include specific information on 1 when to contact the health care provider, 2 blood glucose goals and the use of supplemental short-acting insulin during illness, 3 insulin use during fever and infection, and 4 initiation of an easily digestible liquid diet containing carbohydrates and electrolytes.
Most importantly, the patient should be advised to never discontinue insulin and to seek professional advice early in the course of the illness. Advances in technology have provided more efficient means of monitoring diabetes and maintaining glycemic control in an outpatient setting. The use of real-time continuous glucose monitoring in adult patients with type 1 diabetes has been shown to significantly lower hemoglobin A 1c.
Real-time continuous glucose monitoring also has the advantage of signaling to patients the early detection of glucose abnormalities, allowing for prompt intervention. Pathophysiology-driven DKA management is complex and requires careful selection of approaches aimed at restoring deficiencies in insulin, fluids, and electrolytes. Available clinical practice recommendations and guidelines offer solid foundations for achieving successful DKA resolution.
However, we advise that individualized decisions should be made, as DKA patients may have unique clinical and biochemical characteristics. Recent studies showing clinical benefits and safety of subcutaneous insulin administration in patients with mild DKA and utility of protocol-driven care offer new pathways to reducing the cost of DKA care while maintaining quality of clinical outcomes.
Also, resources should be directed toward the education of primary care providers and patients and their families so that they can identify signs and symptoms of uncontrolled diabetes earlier. With the increasing focus on health disparities, access to medical care is a major focus in determining better care in diabetes, which would ultimately contribute to decreasing the occurrence of hyperglycemic crises of diabetes. National Center for Biotechnology Information , U.
Diabetes Metab Syndr Obes. Published online Jun Author information Copyright and License information Disclaimer. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. This article has been cited by other articles in PMC.
Abstract Diabetic ketoacidosis DKA is a rare yet potentially fatal hyperglycemic crisis that can occur in patients with both type 1 and 2 diabetes mellitus. Introduction In , there were , hospitalizations for diabetic ketoacidosis DKA with an average length of stay of 3. Pathophysiology Insulin deficiency, increased insulin counter-regulatory hormones cortisol, glucagon, growth hormone, and catecholamines , and peripheral insulin resistance lead to hyperglycemia, dehydration, ketosis, and electrolyte imbalance, which underlie the pathophysiology of DKA.
Treatment The therapeutic goals of DKA management include optimization of 1 volume status; 2 hyperglycemia and ketoacidosis; 3 electrolyte abnormalities; and 4 potential precipitating factors. Several important steps should be followed in the early stages of DKA management: collect blood for metabolic profile before initiation of intravenous fluids; infuse 1 L of 0.
Open in a separate window. Figure 1. Workflow of management of adult DKA. Table 1 Checklist of DKA management milestones. Insulin therapy Treatment of DKA with intravenous insulin Insulin administration is essential in DKA treatment because it promotes glucose utilization by peripheral tissues, diminishes glycogenolysis and gluconeogenesis, and suppresses ketogenesis.
Treatment of DKA with subcutaneous insulin Early investigations assessing optimal insulin doses and administration route in the treatment of DKA demonstrated that subcutaneous delivery of regular insulin is effective but inferior to the intravenous insulin infusion. Potassium, bicarbonate, and phosphate therapy Serum potassium should be closely monitored during DKA treatment.
Metabolic treatment targets Serial measurements every 2—4 hours of metabolic parameters are required to monitor therapy and then confirm resolution of DKA. Insulin therapy after resolution of DKA When the patient is able to tolerate oral intake and DKA is resolved, transition to subcutaneous insulin must be initiated. Table 2 Pharmacokinetics and pharmacodynamics of subcutaneous insulin preparations. Insulin Onset of action Time to peak Duration Timing of dose Regular 30—60 min 2—3 h 8—10 h 30—45 min before meal Aspart 5—15 min 30—90 min 4—6 h 15 min before meal Glulisine 5—15 min 30—90 min 5.
Key DKA management points Start intravenous fluids before insulin therapy. Transition to subcutaneous insulin only when DKA resolution is established. DKA management protocols in clinical care With a number of DKA guidelines and technical reviews in the field published by several societies, 3 , 8 , 36 , 37 there is a call to efficiently deliver current knowledge to the bedside. Complications Hypoglycemia is the most frequent complication of DKA and can be prevented by timely adjustment of insulin dose and frequent monitoring of blood glucose levels.
Prevention Discharge planning should include diabetes education, selection of an appropriate insulin regimen that is understood by and affordable for the patient, and preparation of supplies for the initial insulin administration at home. Conclusion Pathophysiology-driven DKA management is complex and requires careful selection of approaches aimed at restoring deficiencies in insulin, fluids, and electrolytes.
Footnotes Disclosure The authors report no conflicts of interest in this report. References 1. Diabetic ketoacidosis. Philadelphia, PA: Elsevier Saunders; Hyperglycemic crises in adult patients with diabetes. Diabetes Care. Hyperglycemic crises in diabetes mellitus: diabetic ketoacidosis and hyperglycemic hyperosmolar state. Endocrinol Metab Clin North Am. Recurrent diabetic ketoacidosis in inner-city minority patients: behavioral, socioeconomic, and psychosocial factors.
Narrative review: ketosis-prone type 2 diabetes mellitus. Ann Intern Med. Impaired expression and insulin-stimulated phosphorylation of Akt-2 in muscle of obese patients with atypical diabetes. Am J Physiol Endocrinol Metab. Hyperglycemic crises in adult patients with diabetes: a consensus statement from the American Diabetes Association.
Can serum beta-hydroxybutyrate be used to diagnose diabetic ketoacidosis? Evidence-based management of hyperglycemic emergencies in diabetes mellitus. Diabetes Res Clin Pract.
Hydration in diabetic ketoacidosis. What is the effect of the infusion rate? Medicina B Aires ; 57 1 — Effect of normal saline and half normal saline on serum electrolytes during recovery phase of diabetic ketoacidosis.
The initial priority in the treatment of diabetic ketoacidosis is the restoration of extra-cellular fluid volume through the intravenous administration of a normal saline 0. This step will restore intravascular volume, decrease counterregulatory hormones and lower the blood glucose level. In patients with mild to moderate volume depletion, infusion rates of 7 mL per kg per hour have been as efficacious as infusion rates of 14 mL per kg per hour.
When the blood glucose concentration is approximately mg per dL This allows continued insulin administration until ketonemia is controlled and also helps to avoid iatrogenic hypoglycemia.
Another important aspect of rehydration therapy in patients with diabetic ketoacidosis is the replacement of ongoing urinary losses. Modern management of diabetic ketoacidosis has emphasized the use of lower doses of insulin. This has been shown to be the most efficacious treatment in both children and adults with diabetic ketoacidosis.
It is prudent to withhold insulin therapy until the serum potassium concentration has been determined. In the rare patient who presents with hypokalemia, insulin therapy may worsen the hypokalemia and precipitate life-threatening cardiac arrhythmias. Standard low-dose insulin therapy consists of an initial intravenous bolus of 0. In clinical situations in which continuous intravenous insulin cannot be administered, the recommended initial insulin dose is 0.
Subsequently, regular insulin should be given in a dosage of 0. If the blood glucose concentration does not fall by 50 to 70 mg per dL 2. Either of these treatments should be continued until the blood glucose level falls by 50 to 70 mg per dL. Low-dose insulin therapy typically produces a linear fall in the glucose concentration of 50 to 70 mg per dL per hour. More rapid correction of hyperglycemia should be avoided because it may increase the risk of cerebral edema.
This dreaded treatment complication occurs in approximately 1 percent of children with diabetic ketoacidosis. Cerebral edema is associated with a mortality rate of up to 70 percent. When a blood glucose concentration of mg per dL has been achieved, the continuous or hourly insulin dosage can be reduced to 0.
The insulin and fluid regimens are continued until ketoacidosis is controlled. This requires the achievement of at least two of these acid-base parameters: a serum bicarbonate concentration of greater than 18 mEq per L, a venous pH of 7. Although the typical potassium deficit in diabetic ketoacidosis is to mEq to mmol , most patients are hyperkalemic at the time of diagnosis because of the effects of insulinopenia, hyperosmolality and acidemia. One protocol entails using insulin and intravenous fluids until the serum potassium concentration is less than 5.
At this time, potassium chloride is added to intravenous fluids in the amount of 20 to 40 mEq per L. The exact amount of potassium that is administered depends on the serum potassium concentration. When the serum potassium level is less than 3. If the serum potassium is greater than 3. The goal is to maintain the serum potassium concentration in the range of 4 to 5 mEq per L 4 to 5 mmol per L.
In general, supplemental bicarbonate therapy is no longer recommended for patients with diabetic ketoacidosis, because the plasma bicarbonate concentration increases with insulin therapy. Retrospective reviews and prospective randomized studies have failed to identify changes in morbidity or mortality with sodium bicarbonate therapy in patients who presented with a pH of 6.
Therefore, the use of bicarbonate in a patient with a pH greater than 7. Furthermore, bicarbonate therapy carries some risks, including hypokalemia with overly rapid administration, paradoxic cerebrospinal fluid acidosis and hypoxia. Some authorities, however, recommend bicarbonate administration when the pH is less than 7.
If bicarbonate is used, it should be given as a nearly isotonic solution, which can be approximated by the addition of one ampule of sodium bicarbonate in mL of sterile water. The bicarbonate solution is administered over a one-hour period. A small percentage of patients who have diabetic ketoacidosis present with metabolic acidosis and a normal anion gap. Therefore, they have fewer ketones available for the regeneration of bicarbonate during insulin administration.
Osmotic diuresis leads to increased urinary phosphate losses. During insulin therapy, phosphate reenters the intracellular compartment, leading to mild to moderate reductions in the serum phosphate concentration. Adverse complications of hypophosphatemia are uncommon and occur primarily in patients with severe hypophosphatemia a serum phosphate concentration of less than 1. Prospective studies have indicated no clinical benefit for phosphate replacement in the treatment of diabetic ketoacidosis, and excessive phosphate replacement may contribute to hypocalcemia and soft tissue metastatic calcification.
One protocol is to administer two thirds of the potassium as potassium chloride and one third as potassium phosphate. The use of phosphate for this purpose reduces the chloride load that might contribute to hyperchloremic acidosis and decreases the likelihood that the patient will develop severe hypophosphatemia during insulin therapy. When diabetic ketoacidosis has been controlled, subcutaneous insulin therapy can be started.
The half-life of regular insulin is less than 10 minutes. Therefore, to avoid relapse of diabetic ketoacidosis, the first subcutaneous dose of regular insulin should be given at least one hour before intravenous insulin is discontinued. In patients who are unable to eat, 5 percent dextrose in hypotonic saline solution is continued at a rate of to mL per hour.
Blood glucose levels are monitored every four hours, and regular insulin is given subcutaneously every four hours using a sliding scale Figure 2. When patients are able to eat, multidose subcutaneous therapy with both regular short-acting and intermediate-acting insulin may be given. In patients with newly diagnosed diabetes, an initial total insulin dosage of 0. A typical regimen is two thirds of the total daily dosage before breakfast and one third of the total daily dosage before dinner, with the insulin doses consisting of two-thirds NPH intermediate-acting insulin and one-third regular short-acting insulin.
Patients with known diabetes can typically be given the dosage they were receiving before the onset of diabetic ketoacidosis. Symptomatic cerebral edema occurs primarily in pediatric patients, particularly those with newly diagnosed diabetes. No single factor predictive for cerebral edema has yet been identified. As noted previously, however, overly rapid rehydration or overcorrection of hyperglycemia appears to increase the risk of cerebral edema.
Onset of headache or mental status changes during therapy should lead to consideration of this complication. Intravenous mannitol in a dosage of 1 to 2 g per kg given over 15 minutes is the mainstay of therapy.
Prompt involvement of a critical care specialist is prudent. Adult respiratory distress syndrome ARDS is a rare but potentially fatal complication of the treatment of diabetic ketoacidosis. Patients with an increased alveolar to arterial oxygen gradient AaO2 and patients with pulmonary rales on physical examination may be at increased risk for ARDS. Monitoring of oxygen saturation with pulse oximetry may assist in the management of such patients.
Hyperchloremic metabolic acidosis with a normal anion gap typically persists after the resolution of ketonemia. This acidosis has no adverse clinical effects and is gradually corrected over the subsequent 24 to 48 hours by enhanced renal acid excretion. No randomized prospective studies have evaluated the optimal site of care for patients with diabetic ketoacidosis. The response to initial therapy in the emergency department can be used as a guideline for choosing the most appropriate hospital site i.
Admission to a step-down or intensive care unit should be considered for patients with hypotension or oliguria refractory to initial rehydration and for patients with mental obtundation or coma with hyperosmolality total osmolality of greater than mOsm per kg of water.
Most patients can be treated in step-down units or on general medical wards in which staff members have been trained in on-site blood glucose monitoring and continuous intravenous insulin administration. Milder forms of diabetic ketoacidosis can be treated in the emergency department using the same treatment guidelines described in this review.
Successful outpatient therapy requires the absence of severe intercurrent illness, an alert patient who is able to resume oral intake and the presence of mild diabetic ketoacidosis pH of greater than 7.
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