Management of Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic Syndromes in the Emergency RoomDiabetic Ketoacidosis Acidosis (DKA) and Hyperosmolar Hyperglycemic Syndromes (HHS) remain the most common Endocrine Emergencies see by Physicians in the ER today. (3) Between 4.6-8 episodes of DKA occur per 1000 diabetics annually whereas the incidence of HHS is much lower at <1%.(1,2) At present over 2 million Canadians are living with Diabetes, a rate that is expected to climb annually. The overall cost of managing DKA and HHS is staggering. In Canada over 9 billion dollars goes into the care of Diabetes and its associated complications. Mortality rate tend to be higher in HHS (>15%) because of age and preexisting illness, whereas the human cost in DKA remains less than 5%. Prognosis for both groups is worse in the extremes of age, and when the initial condition on presentation is coma or hypotension. (4,5) Approximately 90% of DKA occurs in Type 1 diabetics. A disturbing trend toward the development DKA has been identified however, in a subset of Type 2 Diabetics with high Insulin resistance. The majority of theses patients are young pre-teens of native descent where obesity, genetics, inactivity, diet and cigarette smoking appear to correlate with disease development.(6,7,8) Briefly the fundamental deficiency of DKA and HHS is a low circulating level of effective insulin, which results in a corresponding increase in counter regulatory hormones such as glucagon, catecholamines, and growth hormone in an attempt to compensate for the perceived "hypoglycemic state". Because glucose cannot enter insulin-sensitive tissue (muscle, liver, adipose tissue) the body attempts to find other sources of glucose in the liver and adipose tissue further elevating serum glucose. The rising serum glucose generates an osmotic diuresis seen in both DKA and HHS, that results in a substantial loss of water (up to 6-8L/day if the patient has normal renal function), electrolytes (potassium losses up to 300MEq/L/d, sodium, chloride, phosphate), glucose (up to 20g/day) and ketones.(1,2) In the early stages the osmotic diuresis is beneficial to the diabetic because it controls the elevation of serum glucose, but only if the patient continues to drink fluids. In DKA the combined insulin deficiency and rise in counter regulatory hormones gives rise to ketogenesis and the production of ketone bodies, which are responsible for the high anion gap metabolic acidosis. As ketone bodies rise the diabetic begins to experience non-specific abdominal pain, nausea and ileus limiting the ability to drink. With HHS, the insulin levels are adequate enough to prevent lipolysis and subsequent ketogenesis, therefore clinical deterioration may not occur for days to weeks if patient's are able to keep up with their fluid losses. Serum glucose however tends to be much higher on presentation as does the magnitude of dehydration.(9) With DKA and HHS it is often the physical finding of progressive dehydration that triggers the ER staff to the possibility of a hyperglycemic crisis. A bedside glucometer reading, urine ketones and a capillary gas is all that is needed to initiate treatment in the ER, with further serum testing, in particular serum potassium to follow shortly thereafter.(10,11,16) The current diagnostic criteria for DKA include an elevated serum glucose, pH<7.3, high anion gap, serum bicarbonate <18 and ketonemia or ketonuria. (1,2,3,4) The management of DKA and HHS in the Emergency room can be daunting. Over zealous treatment often results in significant complications with hypoglycemia and hypokalemia. Standardized intervention protocols help physicians avoid these pitfalls and have been shown to improve outcome regardless of who cares for the patient in the ER. (1,2). In November 2001 the American Diabetic Association developed a four pillar approach to the management of DKA and HHS in the ER, and invited physicians to adopt these protocols and flow charts when managing patients. To check out the ADA recommendations and treatment guidelines go to http://www.care.diabetesjournal.org/cgi/content/full/25/suppl_1/s100. Recently our institution developed a set of treatment protocols based on the ADA guidelines. (See the accompanying articles). The treatment goals include the restoration of normal hydration, eliminating ketone production, correcting hyperglycemia and electrolyte abnormalities, and identifying and treating the precipitating event. Management of DKA and HHS in the ER start with the ABC's of resuscitation. The initial screening should include temperature, heart rate, respiration, blood pressure, oxygen saturation and glucometer reading. Screening blood work would include an arterial blood gas, serum glucose and electrolytes and preferably serum ketones or urine ketones and anion gap. You must also consider investigations that help sort out the precipitating event. Follow the patient's capillary gases, glucometer readings and potassium to monitor the response to therapy. The pillars of management in DKA and HHS are intravenous fluids, potassium, insulin and bicarbonate. Fluid resuscitation is the most important pillar and should be the focus of the attending physician in the early hours of management. Often deficits in patients with normal renal function are large and can be up to 5-10L in adults and 100ml/kg in children.(1,2,3) Start with 0.9% normal saline to replace the intravascular volume loss. The amount needed will depend on the corrected serum sodium and the patients renal function. Pseudohyponatremia is common due to the dilutional effect of a high glucose and triglyceride levels in these patients. It is best to follow the corrected serum sodium and to keep the corrected sodium on the high side during fluid resuscitation. In children often small boluses of 5-10cc/kg are given initially to stabilize vital signs, while the average adult may require up to 3L in the first few hours. As patients vital signs normalize and they begin to make urine the physician can anticipate that the intravascular volume has been replenished and a switch can be made to 0.45%. (1,2) The intracellular volume deficits can be replaced at a much slower rate. Once the serum glucose reaches approximately 20mmol/L consider switching the fluid to 0.45% NaCl with D5W and maintaining the glucose between 10-15mmol/L to continue the clearing of ketones,(which often lags behind glucose) and to ensure that ketogenesis has stopped. The second pillar of therapy is the use of IV Insulin. Depending on the clinical situation some patients can be started on SC insulin but for simplicity we will address IV insulin only. The trend appears to be moving away from insulin boluses and they are no longer recommended in children.(14) Randomized control trials comparing fluids alone, versus insulin and fluids, in the first four hours of therapy demonstrated no differences in outcome between the two groups. (3,4,5) Once serum glucose levels get to around 20mmol/L it is important to slow insulin rates down to avoid hypoglycemia. Maintain the glucose level between 10-15mmol/L. The average starting insulin dose is 0.1U/kg/h and rates can vary from 1-5U/hr. Physicians can double the insulin rate if glucose is not dropping by 2-4 mmol/L/hr. Increased Insulin rates may be needed in patients with high insulin resistance or if the there is an underlining sepsis.(1,2) When switching from IV to SC insulin overlap the two by approximately 90 minutes to account for the short serum halflife of IV Insulin. Patients can slip back into DKA if the IV rate stops too quickly. It is also essential to bolus the IV tubing with the Insulin-saline mixture prior to setting the infusion rate. Insulin will stick to the sides of the tubing and not get to the patient. When switching from IV to SC Insulin wait until the patient can eat regular meals and is free from abdominal pain. Potassium is the third pillar of therapy. The majority of individuals with DKA or HHS have potassium stores that are markedly depleted. Once fluid resuscitation starts, serum potassium levels drops even lower. Be wary of the patient with normal or low initial potassium as their total body potassium deficits will be high and they may need aggressive replacement therapy prior to the initiation of an Insulin drip. To avoid hypokalemia do not start your Insulin drip until the patient's serum potassium and renal function are known. The controversy surrounding the use of bicarbonate in the resuscitation of DKA is ongoing. Bicarbonate replacement in the severely acidotic patient has been a routine practice by physicians, despite any clear science to support its use.(1,2,18) At present the American Pediatric Association (APA) and the ADA do not recommend the use of bicarbonate in the pediatric patient and there is a movement away from the use of bicarbonate in the adult patient regardless of the pH on presentation in clinical practice. The ADA however at this time recommends bicarbonate still be used in adult patients with severe acidemia. (1,2) Treatment of the adult patient with HHS is similar to DKA however the physician needs to be aware that total body fluid losses may be large unless the patients has underlying renal failure. These patients are often much sicker on presentation because of co-morbidity and pronounced electrolyte disturbances. Sugars are often higher on initial presentation and the mental status is more often altered. (4,5) It is important to consider Dialysis in the patient with HHS and renal failure. The patient can be considered to be out of DKA when the serum glucose is <15mmol/L, the bicarbonate is >16-18, Venous pH is >7.3 and the Anion Gap is <12. (1, 2) In summary, the development of a standardize intervention strategy to the approach of DKA and HHS in the Emergency room improves treatment related outcomes. It is important to develop this strategy with the significant players who will be managing the care in your institution once the patient leaves the emergency room. Do not be in a hurry to start an insulin drip until you have the renal function and serum potassium back. At present the trend is to moving away from IV insulin boluses in the adult patient and not to use them at all in the pediatric age group. Be sure to bolus the IV tubing prior to running the IV drip and wait until the patient is eating and drinking before starting him/her on SC insulin. Be sure to overlap the IV and SC insulin by approximately 90 minutes and don't forget to look for the precipitating event for the hyperglycemic crisis and insure that treatment is initiated. Use bicarbonate conservatively and not at all in the pediatric population. The majority of patients will correct their acidosis with IV fluids and insulin alone. Thanks to Dr. Leo Pereira, Deptartment of Internal Medicine, St. Martha's Regional Hospital in Antigonish Nova Scotia for reviewing the draft copy of this article. References:
You can search for abstracts of the above references by following this link: PubMed Return to Archives Page ] [ Berries Home Page |