{"id":5154,"date":"2011-07-14T20:23:58","date_gmt":"2011-07-14T20:23:58","guid":{"rendered":"http:\/\/crashtext.org\/misc\/5154.htm\/"},"modified":"2013-07-15T16:38:29","modified_gmt":"2013-07-15T20:38:29","slug":"diabetes-mellitus-hypertonic-hyperglycemic-syndrome","status":"publish","type":"post","link":"https:\/\/crashingpatient.com\/medical-surgical\/metabolic-disorders\/diabetes-mellitus-hypertonic-hyperglycemic-syndrome.htm\/","title":{"rendered":"Diabetes Mellitus and Hypertonic Hyperglycemic Syndrome"},"content":{"rendered":"<h4><a href=\"\/wp-content\/pdf\/DKA%20Data%20Sheet.pdf\">DKA Flow Sheet<\/a><\/h4>\n<h4><a href=\"https:\/\/crashingpatient.com\/medical-surgical\/ada-guidelines-for-hyperglycemic-crisis.htm\/\">Summary of ADA Guidelines<\/a><\/h4>\n<h4><a href=\"https:\/\/crashingpatient.com\/medical-surgical\/diabetes-mellitus-hypertonic-hyperglycemic-syndrome.htm\/attachment\/british-dka-guidelines\/\" rel=\"attachment wp-att-8950\">British Guidlines (Fantastic)<\/a><\/h4>\n<h4><a href=\"\/toxicology\/141a-hypoglycemics.htm\">Insulin Preparations<\/a><\/h4>\n<p><a href=\"http:\/\/www.obfocus.com\/calculators\/HemoglobinA1C.htm\">A1C to average sugar<\/a><\/p>\n<p>&nbsp;<\/p>\n<h2><span class=\"ez-toc-section\" id=\"Bicarb_Doesnt_Help_with_Even_Severe_Acidosis\"><\/span>Bicarb Doesn&#8217;t Help with Even Severe Acidosis<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p>Ann Pharmacother. 2013 Jul;47(7-8):970-5.<\/p>\n<p>&nbsp;<\/p>\n<h4>ADA Treatment Guidelines (Diabetes Care, Volume 27, Supplement 1, January 2004)<\/h4>\n<p>DKA had similar responsiveness to IM or IV infusion insulin (Ann Intern Med 1979;90(1):36)<\/p>\n<h3><span class=\"ez-toc-section\" id=\"Classification_of_DM\"><\/span>Classification of DM<span class=\"ez-toc-section-end\"><\/span><\/h3>\n<h4>Type I<\/h4>\n<p>autoimmune b-cell destruction<\/p>\n<h4>Type II<\/h4>\n<p>insulin resistance and relative b-cell secretory deficiency\u00a0 Can now be seen in the pediatric population thanks to rising obesity<\/p>\n<h4>Atypical diabetes of African Americans<\/h4>\n<p>AA adults or teens who present with DKA with transient insulin deficiency.\u00a0 72% will regain at least partial b-cell function and can be switched to oral agents<\/p>\n<h4>Latent Autoimmune Diabetes of Adults<\/h4>\n<p>type I autoimmune diabetes presenting in patients &gt;25 y\/o<\/p>\n<p>&nbsp;<\/p>\n<h3><span class=\"ez-toc-section\" id=\"Classification_of_Decompensated_Diabetic_Emergencies\"><\/span><strong>Classification of Decompensated Diabetic Emergencies<\/strong><span class=\"ez-toc-section-end\"><\/span><\/h3>\n<p><strong>\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 <\/strong> <strong>DKA<\/strong> <strong>HHNC<\/strong> <strong>Mixed<\/strong> <strong>Glucose<\/strong> &gt;250 &gt;600 &gt;600 <strong>Arterial pH<\/strong> &lt;7.3 &gt;7.3 &lt;7.3 <strong>Bicarb<\/strong> &lt;18 &gt;18 &lt;18 <strong>Osm<\/strong> &lt;320 &gt;320 &gt;320 <strong>Ketones<\/strong> Present Absent Present <strong>Dehydration<\/strong>Mild Extreme Mild<\/p>\n<p>&nbsp;<\/p>\n<h2><span class=\"ez-toc-section\" id=\"DKA_Diabetic_Ketoacidosis\"><\/span>DKA (Diabetic Ketoacidosis)<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p>Labs:\u00a0 UA, Urine Cx, ABG or VBG, Lytes, CBC, PT\/PTT, Acetone, Osmolality, Phosphorous, Mg, Lactate, LFTs, EKG<\/p>\n<p>LFTs, Amylase, lipase, and CPK can all be elevated<\/p>\n<p>Creatinine is falsely high b\/c of interference with assay by AcAc<\/p>\n<p>&nbsp;<\/p>\n<p>Correct Sodium:<\/p>\n<p>old correction was add\u00a0 1.6 per 100 glucose over 100<\/p>\n<p>new correction is 2.4 (Am J of Medicine 1999;106:399)<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>Urine Ketones do not measure beta-hydroxybutyrate, Urine dipstick has sensitivity of 95% and predictive value negative of 98% for diagnosis of DKA and DK. (Ann Emerg Med 34(3) 1999)<\/p>\n<p>&nbsp;<\/p>\n<p>In acutely acidotic patients, ratio of b-hydroxybutyrate to acetoacetate may be 30:1 instead of the normal ratio of 3:1 Both serum and dipstick measurements are based on acetoacetate.<\/p>\n<p>&nbsp;<\/p>\n<p>Venous pH=Arterial, so after initial abg, you can use venous blood<\/p>\n<p>Corrected K-subtract .6 for every .1 decrease in pH.<\/p>\n<p>Replace K (Down 200-500 mEq total) and Mg (maybe phosphorous, if you do, oral if possible.\u00a0 &gt;1.0 don\u0092t worry about it)<\/p>\n<p>Insulin-Give bolus of 10 units, then .1 u\/kg\/hr, when glucose is less than &lt;300, give d51\/2 NS<\/p>\n<p>No initial bolus is necessary (Journal of Emergency Medicine.\u00a0 2010 May; 38(4):422-7.\u00a0\u00a0 Diabetes Care.\u00a0 2008 Nov; 31(11):2081-5)<\/p>\n<p>Aim to Correct sugar by 50-75 an hour, if not getting this rate, double the infusion rate<\/p>\n<p>Correct pH to 7.1<\/p>\n<p>Insulin sticks to plastic tubing, flush with 10 u first<\/p>\n<p>Nitroprusside only measures acetoacetate and acetate not beta-hydroxybutyrate, so may actually rise with treatment.\u00a0 If you get a urine test negative for ketones, but want to make sure.\u00a0 Add a drop of hydrogen peroxide to the urine and retest c dipstick.\u00a0 Will convert b-hydroxybutyrate to acetoacetate so should test +.<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>Osmolality Calc 2Na + BUN\/2.8 + Glucose\/18 (Normal 280-295)<\/p>\n<p>Levels &gt;320 are associated with altered mental status<\/p>\n<p>&nbsp;<\/p>\n<p>After 3 L of NS switch to 1\/2NS<\/p>\n<p>&nbsp;<\/p>\n<p>ABD pain is very common as a result of the acidosis, but if it persists despite resolution of near normal pH, consider searching for an intra-abdominal cause of the initial decompensation into DKA. The increase in circulating prostaglandins &#8211; one of the metabolic derangements associated with DKA &#8211; is felt to be the cause of the nausea, vomiting, and abdominal pain (JEM, Vol. 39, pg. 449).<\/p>\n<p>&nbsp;<\/p>\n<ul>\n<li>Maintain Plasma Osm&gt;285 for the first 12 hours<\/li>\n<li>If Na&gt;150, switch to 1\/2 NS, when glucose&lt;300, add D5W at 100-200 cc\/hr (5-10 g hr)<\/li>\n<li>10-30 meq K\/hr if good urine output and K&lt;5.5<\/li>\n<\/ul>\n<p>Giving Bicarb will exacerbate hypokalemia and increase intracellular acidosis.<\/p>\n<p>However, the glycolytic enzyme phosphofructokinase is inactivated by decreasing pH and, thus, the glucose utilizationin brain cells is impaired.\u00a0 This can result in coma or death. Consider Bicarb only when pH is &lt;7.0-7.1.\u00a0 7.1 number came from French studies where it was found that resp compensation actually decreased beyond this pH.<\/p>\n<p>If cerebral edema is suspected, give Mannitol Infusion 0.5-2 g\/kg<\/p>\n<p>&nbsp;<\/p>\n<p>Patients withmild DKA should first receive a &#8220;priming&#8221; dose of regular insulinof 0.4\u00960.6 units\/kg body wt, half as an intravenous bolusand half as a subcutaneous or intramuscular injection.Thereafter, 0.1 unit \u00b7 kg\/ hof regular insulin should be given subcutaneously or intramuscularly<\/p>\n<p>Electrolytes<\/p>\n<p>Potassium<\/p>\n<p>&nbsp;<\/p>\n<p>increased WBC is common up to 20000, if bandemia is present, then an infectious process may be present<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>Phosphate<\/p>\n<p>Do not replace unless &lt;1.0 with CV dysfunction or respiratory distress.<\/p>\n<p>&nbsp;<\/p>\n<p>initial bolus is unnecessary (The Journal of Emergency Medicine Volume 38, Issue 4, May 2010, Pages 422-427)<\/p>\n<h3><span class=\"ez-toc-section\" id=\"Criteria_for_resolution_of_DKA\"><\/span>Criteria for resolution of DKA<span class=\"ez-toc-section-end\"><\/span><\/h3>\n<p>glucose &lt;200 mg\/dl,serum bicarbonate 18 mEq\/l, and a venous pH of &gt;7.3.<\/p>\n<p>OnceDKA is resolved, if the patient is NPO, continue intravenousinsulin and fluid replacement and supplement with subcutaneousregular insulin as needed every 4 h. In adult patients, thiscan be given in 5-unit increments for every 50 mg\/dl increasein blood glucose above 150 mg\/dl for up to 20 units for bloodglucose of 300 mg\/dl. When the patient is able to eat, a multiple-doseschedule should be started that uses a combination of short-or rapid-acting and intermediate- or long-acting insulin asneeded to control plasma glucose. Continue intravenous insulininfusion for 1\u00962 h after the split-mixed regimen is begunto ensure adequate plasma insulin levels. An abrupt discontinuationof intravenous insulin coupled with a delayed onset of a subcutaneousinsulin regimen may lead to worsened control; therefore, someoverlap should occur in intravenous insulin therapy and initiationof the subcutaneous insulin regimen. Patients with known diabetesmay be given insulin at the dose they were receiving beforethe onset of DKA or HHS and further adjusted as needed for control.In patients with newly diagnosed diabetes, the initial totalinsulin dose should be 0.5\u00961.0 units \u00b7 kg -1 \u00b7day-1, divided into at least two doses in a regimen includingshort- and long-acting insulin until an optimal dose is established.<\/p>\n<p>&nbsp;<\/p>\n<p>for each 100 mg\/dl glucose &gt;100 mg\/dl, add 1.6 mEq to sodium value for corrected serum sodium value<\/p>\n<p>Acetone will go up with resolving DKA so monitor anion gap instead.<\/p>\n<p>AG&gt;25 or Gluc&gt;800 buys a unit bed<\/p>\n<p>If signs of cerebral edema, drowsiness, HA, papilledema, seizures, give mannitol .25-1 g per kilo<\/p>\n<p>&nbsp;<\/p>\n<p>Since acetone is highly lipid soluble, it will continue to be released from tissues for ~48 hours and will cause a positive urine ketone test.<\/p>\n<p>Increase in the anion gap should equal the decrease in bicarb unless a mixed picture is present.<\/p>\n<p>&nbsp;<\/p>\n<h2><span class=\"ez-toc-section\" id=\"Fluid_Choices\"><\/span>Fluid Choices<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p>balanced solutions (p-lyte) led to lower Cl and higher bicarb (Am J Emerg Med 2010 PBP Mahler SA) and (J Crit Care , 27:138\u2013145, 2012)<\/p>\n<h3><span class=\"ez-toc-section\" id=\"Screening_for_DKA\"><\/span>Screening for DKA<span class=\"ez-toc-section-end\"><\/span><\/h3>\n<p>Urine ketone dip test as a screen for ketonemia in diabetic ketoacidosis and ketosis in the emergency department.<\/p>\n<p>The sensitivity of the UKDT for the detection of ketonemia in all patients with DKA or DK was 97% (95% CI, 94% to 99%). In the subgroup of patients with DKA, the sensitivity of the UK was 97% (95% CI, 92% to 99%). For patients with DK, the sensitivity of the UK was 98% (95% CI, 89% to 99%). (Ann Emerg Med. 1997 Jun;29(6):735-8)<\/p>\n<p>&nbsp;<\/p>\n<p>Screening for ketonemia in patients with diabetes.<\/p>\n<p>RESULTS: The study group comprised 697 patients, including 98 patients with diabetic ketoacidosis (DKA) and 88 with diabetic ketosis (DK). The sensitivity, specificity, positive, and nega tive predictive values of the urine ketone dip test for the detection of DKA were 99% (95% CI 97% to 100%), 69% (95% CI 66% to 73%), 35% (95% CI 29% to 41%), and 100% (95% CI 99% to 100%), respectively. For DKA and DK, the sensitivity, specificity, positive, and negative predictive values of the urine ketone dip test were 95% (95% CI 90% to 97%), 80% (95% CI 76% to 83%), 63% (95% CI 57% to 69%) and 98% (95% CI 96% to 99%). The anion gap and serum bicarbonate level were less sensitive but more specific than the urine ketone dip test for the detection of DKA and DK. Ann Emerg Med. 1999 Sep;34(3):342-6.<\/p>\n<p>&nbsp;<\/p>\n<h3><span class=\"ez-toc-section\" id=\"DKA_in_Type_II_Diabetics_or_New_Onset_Adults\"><\/span>DKA in Type II Diabetics or New Onset Adults<span class=\"ez-toc-section-end\"><\/span><\/h3>\n<p>The occurrence of diabetic ketoacidosis in non-insulin-dependent diabetes and newly diagnosed diabetic adults. (Am J Med &#8211; 01-JUL-1996; 101(1): 19-24)\u00a0 RESULTS: Two hundred twenty-six patients were included in the study; 106 (47%) were classified as type I and 58 (26%) as type II from data available in the medical record, and 62 (27%) had DKA as the initial manifestation of the disease. Nineteen percent of the patients in whom diabetes was a new diagnosis and 52% of the patients who had a prior history of NIDDM were &gt; or = 40 years old. Of patients with follow-up of at least 12 months, about 24% of the newly diagnosed and 8% of those with a history of NIDDM were not taking insulin. CONCLUSION: DKA occurs in patients with type II diabetes. Older patients may present with clinically apparent type I diabetes. Some adults who present with DKA do not remain insulin dependent.<\/p>\n<h3><span class=\"ez-toc-section\" id=\"Amylase_and_Lipase\"><\/span>Amylase and Lipase<span class=\"ez-toc-section-end\"><\/span><\/h3>\n<p>Nonspecific hyperamylasemia and hyperlipasemia in diabetic ketoacidosis: incidence and correlation with biochemical abnormalities. Yadav D &#8211; Am J Gastroenterol &#8211; 01-NOV-2000; 95(11): 3123-8 RESULTS: Elevated amylase and lipase levels ranged from 111 to 1257 IU\/L (normal 30-110 IU\/L) and 25-529 IU\/dl (normal &lt; 24 IU\/dl) (CT-proven AP = 16, excluded). Nonspecific amylase elevation (CNSA + PNSA) = 25 (16.6%) cases, CNSA in 10 (6.6% of all DKA or 27% of amylase elevations), and PNSA in 15 (10% of all DKA or 41% of amylase elevations). Nonspecific lipase elevation (CNSL + PNSL) = 36 (24%), CNSL in 23 (15.3% of all DKA or 47% of all lipase elevations), and PNSL in 13 (8.7% of all DKA or 26.5% of all lipase elevations). Multiple regression analyses showed significant correlation of pH and serum osmolality with amylase elevation. Lipase elevation showed positive correlation with serum osmolality alone. CONCLUSIONS: In DKA nonspecific elevations of amylase and lipase occur in 16-25% of cases. Amylase elevation is correlated with pH and serum osmolality, but lipase elevation is correlated with serum osmolality alone. Diagnosis of AP based solely on elevated amylase or lipase, even &gt; 3 times normal, is not justifiable.<\/p>\n<h3><span class=\"ez-toc-section\" id=\"Abdominal_pain\"><\/span>Abdominal pain<span class=\"ez-toc-section-end\"><\/span><\/h3>\n<p>Abdominal pain in patients with hyperglycemic crises. Umpierrez G &#8211; J Crit Care &#8211; 01-MAR-2002; 17(1): 63-7 RESULTS: Abdominal pain occurred in 86 of 189 patients with DKA (46%). In 30 patients, the cause of abdominal pain was considered to be secondary to the precipitating cause of metabolic decompensation. Five of them required surgical intervention including 1 patient with Fournier&#8217;s necrotizing fasciitis, 1 with cholecystitis, 1 with acute appendicitis, and 2 patients with perineal abscess.The presence of abdominal pain was not related to the severity of hyperglycemia or dehydration; however, a strong association was observed between abdominal pain and metabolic acidosis. In DKA patients with abdominal pain, the mean serum bicarbonate (9 +\/- 1 mmol\/L) and blood pH (7.12 +\/- 0.02) were lower than in patients without pain (15 +\/- 1 mmol\/L and 7.24 +\/- 0.09, respectively, both P &lt;.001). Abdominal pain was present in 86% of patients with serum bicarbonate less than 5 mmol\/L, in 66% of patients with levels of 5 to less than 10 mmol\/L, in 36% of patients with levels 10 to less than 15 mmol\/L, and in 13% of patients with bicarbonate levels 15 to 18 mmol\/L. Patients with DKA and abdominal pain had a more frequent history of alcohol (51%) and cocaine abuse (13%) than those without abdominal pain (24% and 2%, respectively, both P &lt;.001). One patient with HHS reported nausea and vomiting on admission, but abdominal pain was not reported in any patient with HHS. CONCLUSIONS: Gastrointestinal manifestations including abdominal pain are common in patients with DKA and are associated with severe metabolic acidosis and with a history of alcohol or cocaine abuse, but not with the severity of hyperglycemia or dehydration. Our study indicates that investigation of the etiology of abdominal pain in DKA should be reserved for patients without severe metabolic acidosis or if the pain persists after the resolution of ketoacidosis.<\/p>\n<h3><span class=\"ez-toc-section\" id=\"Fulminant_Type_1_Diabetes\"><\/span>Fulminant Type 1 Diabetes<span class=\"ez-toc-section-end\"><\/span><\/h3>\n<p>A nationwide survey in Japan. Diabetes Care. 26(8):2345-2352, August 2003 Inclusion criteria for fulminant type 1 diabetes in this study were 1) ketosis or ketoacidosis within a week after the onset of hyperglycemic symptoms; 2) urinary C-peptide excretion &lt;10 \u00b5g\/day, fasting serum C-peptide &lt;0.3 ng\/ml (0.1 nmol\/l), or serum C-peptide &lt;0.5 ng\/ml (0.17 nmol\/l) after glucagon injection or meal load soon after disease onset; and 3) HbA1c &lt;8.5% on the first visit. These criteria were determined based on the data from the first 11 patients diagnosed with fulminant diabetes, as reported by Imagawa et al. The mean age at onset of type 1 diabetes was 39.1 years in fulminant type 1 diabetic patients and was significantly older than age at onset in autoimmune type 1 diabetic patients. The age at onset of male fulminant patients was 42.8 \u00b1 14.8 years (mean \u00b1 SD) and significantly higher than that of female fulminant patients (35.1 \u00b1 15.8) (P = 0.002). The age at onset of fulminant diabetes ranged from 1 year to 80 years. A proposal of three distinct subtypes of type 1 diabetes mellitus based on clinical and pathological evidence. Annals of Medicine. 32(8):539-543, November 2000.<\/p>\n<p><a href=\"\/wp-content\/images\/part1\/fulminantdiabetes.jpg\"> <img decoding=\"async\" alt=\"\" src=\"\/wp-content\/images\/part1\/fulminantdiabetes_small.jpg\" \/><\/a><\/p>\n<p>&nbsp;<\/p>\n<h3><span class=\"ez-toc-section\" id=\"Type_II_Diabetes_from_DKA\"><\/span>Type II Diabetes from DKA<span class=\"ez-toc-section-end\"><\/span><\/h3>\n<p>Type 2 Diabetes Presenting as DKA Adults not infrequently present to the ED with new-onset diabetes, which is almost always type 2 diabetes. These patients are frequently dehydrated and exhibit a metabolic acidosis. Emergency Physicians must not reflexively attribute the acidosis to dehydration, lactic acidosis, or another cause and must recognize that patients with type 2 diabetes may present with DKA. Type 2 diabetes is by far the most common type of diabetes, and is characterized by variable degrees of insulin deficiency and resistance; it occurs in people over age 40 who are likely to be obese. However, it is occasionally difficult to distinguish between type 1 and atypical presentations of type 2 diabetes. DKA can occur in the presence of partial (but not complete) insulin deficiency, and therefore cannot be relied upon as an absolute indicator that the patient has type 1 diabetes. Typically, the stress of infection causes increased secretion of counterregulatory hormones and an increase in insulin resistance. The already impaired insulin secretion is unable to respond to the increased demand, leading to hyperglycemia. Recently, increasing attention has been focused on a condition, often termed &#8220;Flatbush diabetes,&#8221; or &#8220;ketosis-prone type 2 diabetes mellitus (KPD)&#8221; in which patients, usually obese, present with DKA as their first manifestation of diabetes but are subsequently found to have type 2 diabetes. These patients typically are African-Americans, or are of African, Hispanic or Caribbean descent. KPD has been reported to account for up to 60% of cases of new onset-diabetes with DKA in US African-American and Hispanic patients (3). Hospital therapy for DKA in type 2 diabetes is the same as for type 1 diabetes. References: (1) Kitabchi AE. Ketosis-prone diabetes &#8211; a new subgroup of patients with atypical type 1 and type 2 diabetes? J Clin Endocrinol Metab 2003; 88: 5087-9. (2) Wittlesey CD. Case Study: Diabetic Ketoacidosis Complications in Type 2 Diabetes Clinical Diabetes 2000;18: 88. (3) Umpierrez, GE, et al. Narrative review: ketosis-prone type 2 diabetes mellitus Ann Intern Med 2006;144: 350. Go to source&gt;&gt;<\/p>\n<h3><span class=\"ez-toc-section\" id=\"Sub-Q_Insulin_rather_than_Drip\"><\/span>Sub-Q Insulin rather than Drip<span class=\"ez-toc-section-end\"><\/span><\/h3>\n<p>Annals EM Review of Lit (Annals of Emergency Medicine Volume 53, Issue 2, February 2009, Pages 259-263)<\/p>\n<p>&nbsp;<\/p>\n<p>EFFICACY OF SUBCUTANEOUS INSULIN LISPRO VERSUS CONTINUOUS INTRAVENOUS REGULAR INSULIN FOR THE TREATMENT OF PATIENTS WITH DIABETIC KETOACIDOSIS Click here to hear the Reviewer&#8217;s comments via MP3.Umpierrez, G.E., et al, Am J Med 117:291, September 1, 2004 BACKGROUND: Recently introduced analogues of human insulin such as insulin lispro (Humalog) and aspart (Novolog) have a rapid onset of action when given subcutaneously (10-20 minutes) and might be suitable for the treatment of DKA outside of the ICU setting. METHODS: This prospective study, from the University of Tennessee and Atlanta (GA) Medical Center, compared outcomes in 40 adults with uncomplicated DKA who were randomized to subcutaneous insulin lispro (0.3u\/kg, followed by 0.1u\/kg per hour until the blood sugar decreased to 250mg\/dL, and then 0.05u\/kg per hour until resolution of DKA) or IV infusion of regular insulin (a 0.1u\/kg bolus followed by 0.1u\/kg\/hour until blood sugar decreased to 250mg\/dl, and then 0.05u\/kg\/hour until resolution of DKA). By hospital policy, the IV insulin group was managed in the ICU while the alternate group was managed in a step-down unit or general medicine floor. RESULTS: There were no significant differences between the groups in baseline characteristics, or in the rate of decline of the plasma glucose level, correction of acid-base parameters, duration of insulin treatment or hospital stay, or amount of insulin given until DKA was resolved. One patient in each group developed mild hypoglycemia. The mean charges for DKA treatment were significantly reduced in the insulin lispro group ($8,801 vs. $14,429). CONCLUSIONS: In stable adults with uncomplicated DKA, administration of subcutaneous insulin lispro was as safe and effective as infusion of regular insulin, but did not require ICU admission and was associated with a significant reduction in the costs of care. 35 references (<a href=\"mailto:geumpie@emory.edu\">geumpie@emory.edu<\/a>)<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<blockquote><p>Treatment Protocol for Diabetic Ketoacidosis<\/p>\n<p>Intravenous fluids \u0095 0.9% saline at 500 to 1000 mL\/h for 2 hours \u0095 0.45% saline at 250 to 500 mL\/h until blood glucose levels &lt;250 mg\/dL (13.9 mmol\/L) \u0095 Dextrose 5% in 0.45% saline at 150 to 250 mL\/h until resolution of diabetic ketoacidosis Potassium replacement \u0095 If serum K+ levels &gt;5.5 mEq\/L, do not give K+ but check serum levels every 2 hours \u0095 K+ levels = 4 to 5.5 mEq\/L, add 20 mmol of KCl to each liter of intravenous fluid \u0095 K+ levels = 3 to &lt;4 mEq\/L, add 40 mmol of KCl to each liter of intravenous fluid \u0095 K+ levels = &lt;3 mEq\/L, give 10 to 20 mmol of KCl per hour until serum levels &gt;3 mEq\/L, then add 40 mmol of KCl to each liter of intravenous fluid Insulin therapy Subcutaneous lispro every hour \u0095 Initial dose subcutaneously: 0.3 unit\/kg of body weight, followed by \u0095 Subcutaneous lispro insulin at 0.1 unit\/kg\/h \u0095 When blood glucose levels &lt;250 mg\/dL, change intravenous fluids to dextrose 5% in 0.45% saline and reduce rate to 0.05 unit\/kg\/h to keep glucose levels 200 mg\/dL (11.1 mmol\/L) until resolution of diabetic ketoacidosis Intravenous regular insulin \u00a0a) Initial intravenous bolus: 0.1 unit\/kg body weight, followed by \u00a0b) Continuous insulin infusion at 0.1 unit\/kg\/h \u0095 When blood glucose levels &lt;250 mg\/dL, change intravenous fluids to dextrose 5% in 0.45% saline and reduce rate to 0.05 unit\/kg\/h to keep glucose levels 200 mg\/dL (11.1 mmol\/L) until resolution of diabetic ketoacidosis Laboratory \u0095 Admission: cell blood count with differential, complete metabolic profile, venous pH, and serum \u03b2-hydroxybutyrate \u0095 During treatment: basic metabolic profile (glucose, bicarbonate, potassium, chloride, urea, and creatinine), venous pH, phosphorus, and \u03b2-hydroxybutyrate at 2 hours, 4 hours, and every 4 hours until resolution of diabetic ketoacidosis \u0095 Glucose by finger stick: check glucose every hour in patients receiving hourly insulin lispro injections and every 2 hours in patients receiving intravenous insulin<\/p><\/blockquote>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>As per the ADA, sub-q is fine in mild DKA (Diabetes Care 2004 27: S94-102.)<\/p>\n<p><a href=\"file:\/\/\/C:\/Documents%20and%20Settings\/Scott\/My%20Documents\/My%20Webs\/book\/065-132\/summaryADAguidelines.htm\"> Summary<\/a><\/p>\n<p>DKA<\/p>\n<hr \/>\n<p>Mild Plasma glucose (mg\/dl) &gt;250 Arterial pH 7.25\u00967.30 Serum bicarbonate (mEq\/l) 15\u009618 Urine ketones Positive Serum ketones Positive Effective serum osmolality (mOsm\/kg) Variable Anion gap &gt;10 Alteration in sensoria or mental obtundation Alert<\/p>\n<p>With mildDKA, regular insulin given either subcutaneously or intramuscularlyevery hour is as effective as intravenous administration inlowering blood glucose and ketone bodies (<a href=\"#R27\">27<\/a>). Patients withmild DKA should first receive a &#8220;priming&#8221; dose of regular insulinof 0.4\u00960.6 units\/kg body wt, half as an intravenous bolusand half as a subcutaneous or intramuscular injection (<a href=\"#R22\">22<\/a>).Thereafter, 0.1 unit \u00b7 kg-1 \u00b7 h-1 of regular insulinshould be given subcutaneously or intramuscularly.<\/p>\n<p>&nbsp;<\/p>\n<p>22 Kitabchi AE, Sacks HS, Young RT, Morris L: Diabetic ketoacidosis: reappraisal of therapeutic approach. Ann Rev Med 30:339\u0096357, 1979[Medline] 27 Fisher JN, Shahshahani MN, Kitabchi AE: Diabetic ketoacidosis: low dose insulin therapy by various routes. N Engl J Med 297:238\u0096247, 1977[Abstract]<\/p>\n<p>&nbsp;<\/p>\n<p>The diagnosis of diabetic ketoacidosis was established in the emergency department using a plasma glucose level &gt;250 mg\/dL (13.9 mmol\/L), a serum bicarbonate level &lt;15 mEq\/L, a blood pH &lt;7.3, a positive serum ketone level at a dilution \u22651:4 by the nitroprusside reaction, and a serum \u03b2-hydroxybutyrate level &gt;31 mg\/dL (&gt;3 mmol\/L). We excluded patients who had persistent hypotension (systolic blood pressure &lt;80 mm Hg) after the administration of 1 liter of normal saline, comatose state (loss of consciousness), acute myocardial ischemia, heart failure, end-stage renal disease, anasarca, dementia, or pregnancy.<\/p>\n<p>&nbsp;<\/p>\n<p>Ketoacidosis was considered resolved when serum bicarbonate levels were \u226518 mEq\/L and venous pH was &gt;7.3 (<a href=\"#bib2\">2<\/a>). When these occurred, intravenous insulin infusion or subcutaneous lispro was discontinued 1 hour after the administration of patients\u0094 maintenance dose of regular and intermediate-acting insulin. Patients with newly diagnosed diabetes received an initial insulin dose of 0.6 unit\/kg of body weight per day; two thirds in the morning and one third in the evening.<\/p>\n<p>&nbsp;<\/p>\n<h2><span class=\"ez-toc-section\" id=\"Order_Set\"><\/span>Order Set<span class=\"ez-toc-section-end\"><\/span><\/h2>\n<p>Diabetic ketoacidosis order set\u00a0 (Crit Care Med 2007;35(1):41) Phase 1. Occurs in the emergency department<\/p>\n<p>1.1. Monitoring<\/p>\n<p>* Assess volume status by checking mentation, orthostatic blood pressure and pulse (if possible and unless the patient has hypotension and\/or tachycardia when supine), and by urine output<\/p>\n<p>* Insert two large-bore intravenous catheters<\/p>\n<p>* STAT measurement of complete blood count, electrolytes, glucose, blood urea nitrogen, creatinine, calcium, magnesium, phosphate<\/p>\n<p>* STAT urine analysis<\/p>\n<p>1.2. Intravenous fluids<\/p>\n<p>* Infuse 2-4 L of normal saline (NS) in first hour (reduced for patients in congestive heart failure, those with end-stage liver or renal disease, those &gt;65 yrs of age, or those with hypoxemia)<\/p>\n<p>1.3. Potassium repletion<\/p>\n<p>* Normal renal function<\/p>\n<p>* Decreased renal function: call physician (MD)<\/p>\n<p>1.4. Insulin<\/p>\n<p>* Do not initiate until potassium is &gt;3.2 mEq\/L, or is being corrected<\/p>\n<p>* If blood glucose is 150-300 mg\/dL: 5 units regular insulin intravenously, then 3 units\/hr<\/p>\n<p>* If blood glucose is &gt;300 mg\/dL: 10 units regular insulin intravenously, then 6 units\/hr<\/p>\n<p>Phase 2. Occurs in the intensive care unit after completing phase 1<\/p>\n<p>2.1. Monitoring<\/p>\n<p>* Measure blood glucose every hour 0\u00972, then every 2 hrs<\/p>\n<p>* Measure blood ketones every 4 hrs until negative<\/p>\n<p>* Measure blood chemistry every 4 hrs until anion gap is closed AND electrolytes have normalized<\/p>\n<p>* Urine analysis, complete blood count, chemistry panel, calcium, magnesium, phosphorus if not sent from ED<\/p>\n<p>* Measure arterial blood gases if serum bicarbonate is &lt;6 mEq\/L<\/p>\n<p>* Measure orthostatic blood pressure and pulse at arrival in intensive care unit (if possible and unless the patient has hypotension and\/or tachycardia when supine)<\/p>\n<p>2.2. Volume resuscitation (through intravenous catheter 1). Volume assessment by MD using level of mentation and orthostatic changes in vital signs (Note: patient MAY require continued high-rate volume infusion)<\/p>\n<p>* NS, 500 mL\/hr intravenously 0\u00972 hrs, then 250 mL\/hr \u00c3\u0083\u00978 hrs, then \u00c3\u0082\u00c2\u00bd \u00c2\u00bd NS at 125 mL\/hr, or<\/p>\n<p>* NS, 250 mL\/hr intravenously 0\u00972 hrs, then 125 mL\/hr \u00c3\u0083\u00978 hrs, then CALL MD for orders<\/p>\n<p>* Add 20 mEq KCl\/L for first 2 L only (further KCl repletion per <a href=\"http:\/\/mail.google.com\/mail\/?view=page&amp;name=gp&amp;ver=sh3fib53pgpk#TTA2\"> Table 2<\/a>)<\/p>\n<p>* Other rate ________ INDICATION: _______<\/p>\n<p>2.3. Insulin and glucose (through intravenous catheter 2). Note: 5% dextrose in H2O (D5W) is initiated at blood sugar of &lt;350 mg\/dL<\/p>\n<p><a href=\"http:\/\/mail.google.com\/mail\/?view=page&amp;name=gp&amp;ver=sh3fib53pgpk#toc\">\u00a0<\/a><\/p>\n<p>&nbsp;<\/p>\n<p>* Once adequate volume resuscitation, MD may cap intravenous catheter 1 and change from D5W\/NS to D5\/\u00c3\u0082\u00c2\u00bdNS<\/p>\n<p>* Adjust insulin and D5W rates based on blood glucose and CURRENT insulin rate (see Appendix <a href=\"http:\/\/mail.google.com\/mail\/?view=page&amp;name=gp&amp;ver=sh3fib53pgpk#TTA1\"> Table<\/a> below)<\/p>\n<p>*\u00a0Mix regular insulin as follows: 1 unit\/mL (100 units\/100 mL)<\/p>\n<p>* D5W must be \u00c3\u00a2\u0080\u00ac\u009cpiggybacked\u00c3\u00a2\u0080\u00c2\u009d into insulin catheter (intravenous c catheter 2) to avoid iatrogenic hypoglycemia or hyperglycemia<\/p>\n<p>* Once the patient is euvolemic, has a blood sugar between 90 and 140 mg\/dL, and has cleared their blood ketones, insulin should be administered subcutaneously and intravenous insulin should be discontinued 30 mins later<\/p>\n<p>2.4. Potassium repletion<\/p>\n<p><a href=\"http:\/\/mail.google.com\/mail\/?view=page&amp;name=gp&amp;ver=sh3fib53pgpk#toc\">\u00a0<\/a><\/p>\n<p>&nbsp;<\/p>\n<p>* Select one:<\/p>\n<p>[white square] Normal renal function. Replete potassium as follows:(Note: Do not give the additional 20 mEq intravenous KCl if already added to NS)<\/p>\n<p>[white square] or KCl: ___<\/p>\n<p>[white square] Replete phosphorus if &lt;1.5 mg\/dL with two 500-mg tablets of potassium phosphate neutral or 20 mmol potassium phosphate intravenously over 6 hrs if not taking orally. If phosphorus is &lt;1.0 mg\/dL, give a single dose of 0.24 mmol\/kg<\/p>\n<p>[white square] Replete magnesium if &lt;1.5 with 2 g of magnesium sulfate intravenously<\/p>\n<p>Modifications<\/p>\n<p>&nbsp;<\/p>\n<p>* For severe chronic heart failure or end-stage renal disease: administer 10% of the above volume using D50W (e.g., if blood glucose is 91\u00c3\u00a2\u0080&#8221;140 mg\/dL, give D50W at 200 mL\/hr through a central catheter)<\/p>\n<p>* For other conditions requiring volume restriction (e.g., left ventricular diastolic dysfunction, end-stage liver disease), give 50% of volume using D10W (e.g., if blood glucose is 91\u00c3\u00a2\u0080&#8221;140 give D110W at 100 mL\/hr)<\/p>\n<p>Other orders:<\/p>\n<p>* Call MD if pH &lt;6.9 for 2 hrs for consideration of sodium bicarbonate drip<\/p>\n<p>* Additional labs now:<\/p>\n<p>* Hemoglobin A1C<\/p>\n<p>* Fasting lipids<\/p>\n<p>* Other ______<\/p>\n<p>* Morning labs: _______<\/p>\n<p>* Diet: increase diet as tolerated once nausea\/vomiting have resolved<\/p>\n<p>* Other ____<\/p>\n<p>* Call MD for discontinuation of intravenous insulin protocol and initiation of subcutaneous insulin once diabetic ketoacidosis and nausea\/vomiting have resolved<\/p>\n<p><a href=\"\/wp-content\/images\/part1\/insulin%20drip.jpg\"> <img decoding=\"async\" alt=\"\" src=\"\/wp-content\/images\/part1\/insulin%20drip_small.jpg\" \/><\/a><a href=\"\/wp-content\/images\/part1\/kcl.jpg\"><img decoding=\"async\" alt=\"\" src=\"\/wp-content\/images\/part1\/kcl_small.jpg\" \/><\/a><\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>HHS<\/p>\n<p>No dilantin for seizures, inhibits insulin release<\/p>\n<p>20-25% fluid deficit c total body sodium deficit.\u00a0 Replete c at least 3 liters in the first two hours.\u00a0 Insulin Drip at .1 U\/kg\/hr as sugar is maintaining osmals<\/p>\n<p>Will have serum osm&gt;315<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>Late complications-nephropathy, retinopathy, neuropathy<\/p>\n<p>&nbsp;<\/p>\n<p>can also be a cause of hemiballism (doi:10.1016\/j.ajem.2004.12.01)<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>Related Articles, Links Effect of 50 milliliters of 50% dextrose in water administration on the blood sugar of euglycemic volunteers. Balentine JR, Gaeta TJ, Kessler D, Bagiella E, Lee T. Department of Emergency Medicine, St. Barnabas Hospital, Bronx, NY 10457, USA. jbalentine@pol.net OBJECTIVE: To evaluate the effect of administration of 1 ampule of 50% dextrose in water solution (D50W) on serum glucose levels in healthy adult volunteers, the authors set out to determine whether a pre-D50W serum glucose level can be predicted from the ED sample. METHODS: This was a prospective, interventional study conducted from the ED of an urban, university-affiliated hospital. All subjects were healthy employee volunteers between 25 and 40 years of age. Baseline serum glucose levels were determined and all subjects were given an i.v. bolus of 25 grams of 50% dextrose solution. The main outcome measures were post-D50W serum glucose levels (observed) at 5 predetermined time intervals (5 min, 15 min, 30 min, 1 hr, and 2 hr). An expected change in serum glucose was calculated using the volume of distribution formula for glucose. RESULTS: Twenty-five volunteers (17 males and 8 females) participated in the study. The mean baseline serum glucose was 82.3 +\/- 13.5 mg\/dL. The mean post-infusion levels were: 244.4 +\/- 44.6 mg\/dL (5 min), 145.8 +\/- 52.3 mg\/dL (15 min), 88.1 +\/- 28.8 mg\/dL (30 min), 77.6 +\/- 13.6 mg\/dL (60 min), and 83.2 +\/- 11.4 mg\/dL (120 min). Using a mixed-effect regression model, statistically significant increases in serum glucose levels were found at 5 minutes (p &lt; 0.001) and 15 minutes (p &lt; 00001) following administration of D50W. There was a return to baseline serum glucose by 30 minutes. The expected change based on the volume of distribution formula (53.7 +\/- 34.9) did not correlate with the observed changes at any measured time interval. CONCLUSION: Without pre-intervention blood drawing by emergency medical services, it is not possible to accurately predict pre-D50W serum glucose levels based on post-D50W glucose levels. The diagnosis of hypoglycemia as the etiology of altered mental status must therefore remain a diagnosis of exclusion. In addition, the return of serum glucose to baseline after 30 minutes suggests the duration of the effect of 1 ampule of D50W. Frequent re-evaluation of the serum glucose levels of suspected or proven hypoglycemic patients after administration of D50W should be considered. Go to source: Entrez PubMed<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>Hi, If truly we can send insulin drip patients to regular floors, then I agree we should drip all of our DKAs. \u00a0I am glad you will be pursuing this with the nursing staff. \u00a0In all of my dealings with MARs and admitting teams, this did not seem to be a possibility with a regular floor admit. I have never found hourly sc insulin dosing to be burdensome. I just write my order as fingerstick q 1hr, if sugar &gt;250, insulin 0.1 units\/kg sc, if sugar &lt;250 please notify MD. \u00a0Of course, \u00a0I would still give the insulin if the sugar is &lt;250 assuming a gap still exists, this just allows me to be notified when fluids must be changed to D5w and allows me to reassess the patient. \u00a0This is not burdensome to the nurses as they have to do my fingerstick at that time anyway. \u00a0I don&#8217;t believe that the SC prick is really that burdensome for the patient either. \u00a0The advantage of this is that it insures that the insulin infusion will not be continued without an hourly fingerstick. \u00a0I have seen instances where the infusion just runs despite no fingerstick for hours, especially when our ED nurses are overwhelmed. \u00a0This seems an especially dangerous situation in the mild cases of DKA where resolution occurs more quickly. Titration with sc hourly dosing is easy, just adjust the amount given sc, insulin drips are not titrated more frequently than q 1 hour. I think the ideal forum to discuss these issues would be the monthly IM\/EM morning report. \u00a0Perhaps you could speak to the folks scheduled to present it next month (this month was an EM case choice, so I believe next month is IM.) \u00a0Even if you can not find a perfect actual, case, let&#8217;s just make up a case of a mild dka and see the differing views on management. Scott At 11:48 AM 2\/25\/2004, you wrote:<\/p>\n<blockquote><p>Hey, thanks for the response. \u00a0I&#8217;m glad you sent along the ADA guidelines &#8211; we actually had a noon conference recently by Mona Shimshi using the same guidelines so I&#8217;m glad we&#8217;re all on the same page. I would say that, while it is acceptable in mild DKA to use hourly sq insulin with hourly iv boluses for high sugars, it is pretty burdensome for physicians, nurses and rather painful for the patients. \u00a0Especially in the ER, where new patients are constantly coming in and needing immediate attention, it&#8217;s easy to fall behind and miss a dose. \u00a0There&#8217;s no downside to a drip for these patients and it seems to me a significantly reduced burden on staff and patients. \u00a0That&#8217;s the main reason we do it, in addition to the ease of being able to titrate doses quickly. We do occasionally use insulin drips on 10W (at least, I remember doing so as a resident), especially when we don&#8217;t anticipate having to do so for lengthy periods of time &#8211; i.e. for mild DKA &#8211; so starting a drip does not force an upgrade to the stepdown. \u00a0I will, however, check this out with the nursing staff. Would you like to have an interdepartmental conference, or do you want to hold off until we identify a problemmatic case? Leora Content-type: multipart\/alternative; boundary=&#8221;Boundary_(ID_z+UvcqAlTYU8GEyQs8WzUw)&#8221; &#8211;Boundary_(ID_z+UvcqAlTYU8GEyQs8WzUw) Content-type: text\/plain; charset=us-ascii; format=flowed Hi Leora, JD was kind enough to forward me your e-mail regarding the management of DKA in the ED. \u00a0It is interesting that this has been brought up as an issue, because there does seem to be a difference in perspective between the ED management of DKA and the strategy of most of the IM residents. True DKA presents with various levels of severity. \u00a0Patients who come in with moderate to severe DKA are easy from the insulin perspective, I think everybody is in agreement that an insulin drip is needed, with or without an initial bolus. \u00a0These patients need a high level of care in either a unit or a stepdown bed. I think most of the confusion and discrepancies lie in the area of mild cases of DKA. \u00a0I have always used the severity scale provided by the American Diabetes Assoc. \u00a0I have attached a copy of the most recent iteration of their policy statement for the management of hyperglycemic emergencies. If a patient fits into the mild severity criteria, i.e. pH&gt;7.25, Bicarb &gt;15, with fully alert mental status, then they do not require an insulin drip. \u00a0I think a significant portion of our dka admits fall into this category. \u00a0Of course, if there is a suspicion of coexistent metabolic alkalosis, it is worth calculating the \u00a0delta gap. \u00a0Insulin can be given by sc or im route. \u00a0Some clinicians would even give half of the initial insulin dose IV followed by half IM or SC in these patients. \u00a0This strategy is spoken about in the attached guidelines. \u00a0Personally, I give these patients their initial dose IM to counter any decreased absorption from volume loss, then subsequent doses SC. I use this strategy only at Sinai, at Elmhurst, the increased availability of CCA beds makes these extra sticks to the patient unnecessary. At Sinai, with only 4 stepdown beds, it does not seem to make sense to start an insulin drip in mild cases of DKA. \u00a0If the nurses on the floor could be convinced that an insulin drip is a fairly benign infusion and these patients could be admitted to a regular teaching bed (which is what is done at many hospitals,) then I would have no problem dripping all true DKA patients. If you have any cases where patients are being managed solely with IV insulin boluses, I would appreciate it if you brought them to our attention so that we may refer the cases for QA. \u00a0Using just iv bolus insulin is obviously unacceptable. In short, from my perspective, trending the anion gap is quite useful to guide continuing therapy, but the presence of a gap alone is not an indication for an insulin drip, though certainly an indication for hourly insulin and a trending of the gap for resolution. As to sugar levels, \u00a0DKA is absolutely possible at sugar levels &lt;200, but I think it behooves \u00a0the treating physician to consider other causes of anion gap acidosis in these patients before falling back on DKA as a diagnosis. \u00a0Because we do not have quantitative ketone measurements which can be evaluated to see if they fully account for the anion gap, other sources for the acidosis must be sought first. It would be great to get together and discuss these issues further as it seems an area ripe for the creation of interdepartmental guidelines for the better care of these patients. \u00a0Please send me any comments on the above. Regards, Scott Scott Weingart, MD Chief Resident Department of Emergency Medicine Mount Sinai School of Medicine &gt; &gt;&gt;&gt;Joanna and I spent some time this afternoon trying &gt;to put together a short but useful guide to DKA and &gt;realized it was best taught orally. \u00a0We wondered &gt;whether it would be possible to co-opt one of your &gt;Wednesday teaching sessions &#8211; either ourselves, or to &gt;bring in an endocrinologist. \u00a0The major problems we &gt;have encountered (and these have been consistent over &gt;the past few years, nothing special recently) relate &gt;to true DKA and insulin drips. \u00a0Generally we find the &gt;ER underestimates the importance of anion gaps (which &gt;are the chief way we decide whether a patient needs an &gt;insulin drip) and overestimates the value of insulin &gt;iv pushes (which only last a few minutes and should &gt;never be used without initiating a drip). \u00a0We also &gt;find the ER places undue importance on glucose levels &gt;(which can certainly be in the 100s or 200s in true &gt;type one DKA), thus missing some important cases of &gt;DKA.&lt;&lt;&lt; &#8211;Boundary_(ID_z+UvcqAlTYU8GEyQs8WzUw) Content-type: text\/html; charset=us-ascii Hi Leora, JD was kind enough to forward me your e-mail regarding the management of DKA in the ED. \u00a0It is interesting that this has been brought up as an issue, because there does seem to be a difference in perspective between the ED management of DKA and the strategy of most of the IM residents. True DKA presents with various levels of severity. \u00a0Patients who come in with moderate to severe DKA are easy from the insulin perspective, I think everybody is in agreement that an insulin drip is needed, with or without an initial bolus. \u00a0These patients need a high level of care in either a unit or a stepdown bed. I think most of the confusion and discrepancies lie in the area of mild cases of DKA. \u00a0I have always used the severity scale provided by the American Diabetes Assoc. \u00a0I have attached a copy of the most recent iteration of their policy statement for the management of hyperglycemic emergencies. If a patient fits into the mild severity criteria, i.e. pH&gt;7.25, Bicarb &gt;15, with fully alert mental status, then they do not require an insulin drip. \u00a0I think a significant portion of our dka admits fall into this category. \u00a0Of course, if there is a suspicion of coexistent metabolic alkalosis, it is worth calculating the \u00a0delta gap. \u00a0Insulin can be given by sc or im route. \u00a0Some clinicians would even give half of the initial insulin dose IV followed by half IM or SC in these patients. \u00a0This strategy is spoken about in the attached guidelines. \u00a0Personally, I give these patients their initial dose IM to counter any decreased absorption from volume loss, then subsequent doses SC. I use this strategy only at Sinai, at Elmhurst, the increased availability of CCA beds makes these extra sticks to the patient unnecessary. At Sinai, with only 4 stepdown beds, it does not seem to make sense to start an insulin drip in mild cases of DKA. \u00a0If the nurses on the floor could be convinced that an insulin drip is a fairly benign infusion and these patients could be admitted to a regular teaching bed (which is what is done at many hospitals,) then I would have no problem dripping all true DKA patients. If you have any cases where patients are being managed solely with IV insulin boluses, I would appreciate it if you brought them to our attention so that we may refer the cases for QA. \u00a0Using just iv bolus insulin is obviously unacceptable. In short, from my perspective, trending the anion gap is quite useful to guide continuing therapy, but the presence of a gap alone is not an indication for an insulin drip, though certainly an indication for hourly insulin and a trending of the gap for resolution. As to sugar levels, \u00a0DKA is absolutely possible at sugar levels &lt;200, but I think it behooves \u00a0the treating physician to consider other causes of anion gap acidosis in these patients before falling back on DKA as a diagnosis. \u00a0Because we do not have quantitative ketone measurements which can be evaluated to see if they fully account for the anion gap, other sources for the acidosis must be sought first. It would be great to get together and discuss these issues further as it seems an area ripe for the creation of interdepartmental guidelines for the better care of these patients. \u00a0Please send me any comments on the above. Regards, Scott Scott Weingart, MD Chief Resident Department of Emergency Medicine Mount Sinai School of Medicine<\/p>\n<blockquote><p>&gt;&gt;&gt;Joanna and I spent some time this afternoon trying to put together a short but useful guide to DKA and realized it was best taught orally. \u00a0We wondered whether it would be possible to co-opt one of your Wednesday teaching sessions &#8211; either ourselves, or to bring in an endocrinologist. \u00a0The major problems we have encountered (and these have been consistent over the past few years, nothing special recently) relate to true DKA and insulin drips. \u00a0Generally we find the ER underestimates the importance of anion gaps (which are the chief way we decide whether a patient needs an insulin drip) and overestimates the value of insulin iv pushes (which only last a few minutes and should never be used without initiating a drip). \u00a0We also find the ER places undue importance on glucose levels (which can certainly be in the 100s or 200s in true type one DKA), thus missing some important cases of DKA.&lt;&lt;&lt;<\/p><\/blockquote>\n<\/blockquote>\n<p><img decoding=\"async\" alt=\"\" src=\"\/wp-content\/images\/part1\/hyperglycemia%20and%20renal%20fx.png\" \/><\/p>\n<p>(UTDOL.com)<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>Metformin for treatment of diabetics we&#8217;re going to send home<\/p>\n<p>Cr &lt;1.4 in men &lt;1.5 in women???<\/p>\n<p>&nbsp;<\/p>\n<h3><span class=\"ez-toc-section\" id=\"_Hyperglycemia_in_the_HD_patient\"><\/span>\u00a0<a href=\"\/wp-content\/pdf\/hyperglycemia%20in%20hd%20pts.pdf\">Hyperglycemia in the HD patient<\/a><span class=\"ez-toc-section-end\"><\/span><\/h3>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>|\u00a0\u00a0 \u00a0\u00a0 |\u00a0\u00a0 \u00a0\u00a0 |<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Array<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_genesis_hide_title":false,"_genesis_hide_breadcrumbs":false,"_genesis_hide_singular_image":false,"_genesis_hide_footer_widgets":false,"_genesis_custom_body_class":"","_genesis_custom_post_class":"","_genesis_layout":"","footnotes":""},"categories":[24],"tags":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v22.5 - 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