Dka Icu

Management Of Diabetic Ketoacidosis And Other Hyperglycemic Emergencies

Understand the management of patients with diabetic ketoacidosis and other hyperglycemic emergencies. The acute onset of hyperglycemia with attendant metabolic derangements is a common presentation in all forms of diabetes mellitus. The most current data from the National Diabetes Surveillance Program of the Centers for Disease Control and Prevention estimate that during 2005-2006, at least 120,000 hospital discharges for diabetic ketoacidosis (DKA) occurred in the United States,(1) with an unknown number of discharges related to hyperosmolar hyperglycemic state (HHS). The clinical presentations of DKA and HHS can overlap, but they are usually separately characterized by the presence of ketoacidosis and the degree of hyperglycemia and hyperosmolarity, though HHS will occasionally have some mild degree of ketosis. DKA is defined by a plasma glucose level >250 mg/dL, arterial pH <7.3, the presence of serum ketones, a serum bicarbonate measure <18 mEq/L, and a high anion gap metabolic acidosis. The level of normal anion gap may vary slightly by individual institutional standards. The anion gap also needs to be corrected in the presence of hypoalbuminemia, a common condition in the critically ill. Adjusted anion gap = observed anion gap + 0.25 * ([normal albumin]-[observed albumin]), where the given albumin concentrations are in g/L; if given in g/dL, the correction factor is 2.5.(3) HHS is defined by a plasma glucose level >600 mg/dL, with an effective serum osmolality >320 mOsm/kg. HHS was originally named hyperosmolar hyperglycemic nonketotic coma; however, this name was changed because relatively few patients exhibit coma-like symptoms. Effective serum osmolality = 2*([Na] + [K]) + glucose (mg/dL)/18.(2) Urea is freely diffusible across cell membranes, thus it will Continue reading >>

Diabetic Ketoacidosis: “sneaky” Triggers And Clinical Pearls

Authors: Catherine Reynolds, MD (EM Resident Physician, UT Houston), Kathryn Fisher, MD (EM Resident Physician, UT Houston), and Hilary Fairbrother, MD (EM Attending Physician, UT Houston) // Edited by: Alex Koyfman, MD (@EMHighAK) and Brit Long, MD (@long_brit) Clinical Case #1: The patient is a 45-year-old male with history of type 2 DM and HTN who presents to the emergency department with diffuse abdominal pain, nausea, and vomiting for two days. The patient reports that he was recently started on Invokana (canagliflozin) about two weeks ago for his diabetes, and prior to that he was managing his sugars with diet and exercise alone. The patient has had difficulty keeping any food down over the last two days, but denies shortness of breath, chest pain, or fever. He reports his vomit is non-bilious and non-bloody. His initial finger stick is 84 mg/dL, and your intern states that he “knows that this is not DKA” as the serum glucose is normal. Vital signs showed RR 28, HR 110, BP 152/86, SpO2 98% on room air, T 98.4 F. Labs on presentation reveal a Na of 132 mmol/L, K of 5 mmol/L, Cl of 98 mmol/L, bicarbonate of 10 mmol/L, glucose of 84 mg/dL, and venous pH of 7.1. Venous lactate is within normal limits, and serum beta-hydroxybutyrate is positive. The patient is started on dextrose-containing fluids, an insulin drip, and admitted to the ICU for DKA. What was the cause of the patient’s euglycemic DKA? Clinical Case #2: The patient is a 62-year-old male with a history of DM, CAD, HTN, HLD, an NSTEMI, and 2 subsequent cardiac stents. He presents to the ED with diffuse abdominal pain, nausea, vomiting, and diarrhea for two days. The patient is on Humalog and Lantus but he hasn’t taken the medications over the last two days because he hasn’t been eating. He denies s Continue reading >>

Dka Without The Icu

As we discussed yesterday, the treatment algorithm for DKA is fairly straightforward with a few subtleties we rarely appreciate, until now. Yesterday we focused on fluids, today we move on to the insulin. Can we offer the patient anything else beside an insulin drip? Obviously the answer is yes, or else this pearl wouldn’t exist. In 2004, Umpierrez et al conducted an RCT of 20 patients comparing subcutaneous lispro (0.3U/kg bolus followed by 0.1U/kg/h) vs. an IV insulin (0.1 u/kg bolus followed by 0.1 U/kg/h drip). They found that there was no difference in time to correction of hyperglycemia, time to resolution of DKA, length of hospital stay, or rates of hypoglycemia. Later that year, they conducted a second study of 45 patients comparing doses of 0.1U/kg/h subcutaneous insulin to 0.2U/kg/h subcutaneous insulin to standard therapy. Not surprisingly, they showed that no protocol was more efficacious than another, however they did show a 39% high hospitalization charges in the IV insulin group due to the ICU setting necessary to manage the insulin drip. Since then the Cochrane collaborative has addressed the same question. They reviewed 5 trials including 201 total patients (some children). They found “low to very low-quality evidence that there are neither advantages nor disadvantages when comparing the effects of subcutaneous rapid-acting insulin analogues vs. IV regular insulin when treating mild to moderate DKA.” As long as the nurses are comfortable with q1 fingersticks, its something to consider next time you treat DKA. References Andrade-Castellanos CA, Colunga-Lozano LE, Delgado-Figueroa N, Gonzalez-Padilla DA. Subcutaneous rapid-acting insulin analogues for diabetic ketoacidosis. Cochrane Database of Systematic Reviews 2016, Issue 1. Art. No.: CD011281. D Continue reading >>

Diabetic Ketoacidosis

OVERVIEW potentially life-threatening complication of diabetes melitus resulting from the consequences of insulin deficiency Diagnostic criteria pH < 7.3 ketosis (ketonemia or ketonuria) HCO3 <15 mmol/L due to high anion gap metabolic acidosis (HAGMA) hyperglycemia (may be mild; euglycemic DKA can occur) PATHOGENESIS increased glucagon, cortisol, catcholamines, GH decreased insulin -> hyperglycaemia -> hyperosmolality + glycosuria -> electrolyte loss -> ketone production from metabolism of TG -> acidosis HISTORY dry, abdominal pain, polyuria, weight loss, coma risk factors: non-compliance, illness, newly diagnosed ROS to rule find out possible precipitant (infection, MI, pneumonia, GI illness) normal insulin regime diabetic control previous DKA’s/admissions previous ICU admissions EXAMINATION volume assessment signs of cause e.g. (infection) GCS work of breathing INVESTIGATIONS ABG electrolytes osmolality urinalysis: ketones pregnancy test standard investigations to rule out cause: FBC, ECG, CXR MANAGEMENT Goals (1) establish precipitant and treat (2) assess severity of metabolic derangement (3) cautious fluid resuscitation with replacement of body H2O (4) provision of insulin (5) replacement of electrolytes Resuscitate intubation for airway protection if required O2 as required IV access fluid boluses (20mL/kg boluses of NS/HMN) urinary catheter Acid-base and Electrolyte abnormalities will have a severe metabolic acidosis with probable incomplete respiratory compensation K+ may be normal but patient will have a whole body K+ deficiency -> needs to be replaced once < 5mmol/L -> use KH2PO4 Na+ may be deranged acidaemia rarely requires HCO3- therapy and will respond to other treatments Specific therapy start insulin infusion (avoid bolus) 0.1u/kg/hr aim to lower glucose Continue reading >>

Diabetic Ketoacidosis: Treatment In The Intensive Care Unit Or General Medical/surgical Ward?

Go to: INTRODUCTION Patients with diabetes mellitus (DM) have health care costs 2.3 times higher than others without this diagnosis[1]. In a prevalence-based study, by the American Diabetes Association, in the United States in 2012, the total cost for diagnosed DM was $245 billion United States dollars, and of it, $176 billion was used for direct medical care costs[1]. In addition, and even more concerning, is the fact that hospitalizations for patients with DM have being increasing[2]. The National Surveillance of Diabetes Public Health Resources, reported that diabetic ketoacidosis (DKA) admissions increased from 80000/year in 1988 to 140000/year in 2009[2]. DKA causes an acute metabolic disorder, which is primarily characterized by an increased presence of circulating ketone bodies, and the development of severe ketoacidosis in the presence of prolonged uncontrolled hyperglycemia, usually due to insulin deficiency[3]. It is more commonly seen in patients with insulin-dependent diabetes mellitus (IDDM), especially among children and young adults. Occasionally, patients with insulin resistant DM can present this complication; especially those that are noncompliant with insulin therapy or who present severe infection[3]. DKA has arbitrarily been classified by some as mild, moderate and severe, according to the initial diagnostic criteria (which includes plasma glucose, arterial pH, serum bicarbonate, urine and serum ketones, serum osmolality and anion gap; and the alteration in the mental status)[4]. Continue reading >>

5 Months... From Icu/dka To Top Of A Mountain

Diabetes Forum The Global Diabetes Community This site uses cookies. By continuing to use this site, you are agreeing to our use of cookies. Learn More. Get the Diabetes Forum App for your phone - available on iOS and Android . Find support, ask questions and share your experiences. Join the community 5 Months... From ICU/DKA to top of a mountain Just a bit of a positive story from me this weekend. I was meaning to try and climb a famous mountain in Ireland for a long time, but decided it was something I wanted to aim for after diagnosis. Didn't think I would get it done so soon after being in Intensive Care with DKA on diagnosis, but my good friend asked me would I give it a go yesterday and we headed off early. I found it incredibly difficult, thinking of quitting nearly half way up, but thanks to some pure thickness in me and my friend pushing me on, I made it. Managed it on no carbs in the morning, but 7 jelly babies along the way...! Very proud of myself to get this done in 5 months. Probed to myself I don't give up. Hopefully it gives some of you a confidence boost. Rachox Type 2 (in remission!) Moderator Lovely story. Very encouraging, thank you. well done joe you are an inspiration and its nice to read a positive post from a fellow type 1 What a beautiful story to read on Easter Sunday, @JoeT1 , and a magnificent achievement. Well done! And thank you for posting those gorgeous photo, especially the second one - that is breath-taking. Fabulous to see, especially on a very rainy weekend (although we have a bit of sun at the moment)! Fantastic! Both your achievement and the views. Hopefully good for your mental health too. Fairygodmother Type 1 Well-Known Member Beautiful pictures @JoeT1 ! What a glorious view! And what a stupendous achievement, well done! Just a Continue reading >>

Infection As A Trigger Of Diabetic Ketoacidosis In Intensive Care—unit Patients

Together with hyperglycemic coma, diabetic ketoacidosis (DKA) is the most severe acute metabolic complication of diabetes mellitus [ 1 ]. Defined by the triad hyperglycemia, acidosis, and ketonuria, DKA can be inaugural or complicate known diabetes [ 2 ]. Although DKA is evidence of poor metabolic control and usually indicates an absolute or relative imbalance between the patient's requirements and the treatment, DKA-related mortality is low among patients who receive standardized treatment, which includes administration of insulin, correction of hydroelectrolytic disorders, and management of the triggering factor (which is often cessation of insulin therapy, an infection, or a myocardial infarction) [ 3–8 ]. Although there is no proof that diabetics are more susceptible to infection, they seem to have more difficulty handling infection once it occurs [ 9 , 10 ]. Indeed, several aspects of immunity are altered in diabetic patients: polymorphonuclear leukocyte function is depressed, particularly when acidosis is present, and leukocyte adherence, chemotaxis, phagocytosis, and bactericidal activity may also be impaired [ 11–15 ]. Joshi et al. [ 10 ] reported recently on the lack of clinical evidence that diabetics are more susceptible to infection than nondiabetic patients. Nevertheless, infection is a well-recognized trigger of DKA. Earlier studies have investigated the prevalence of infection as a trigger of DKA and the impact of antimicrobial treatment [ 2 , 15–18 ]. However, none of these studies were of intensive care unit (ICU) patients only. Furthermore, most were descriptive, included small numbers of patients, used univariate analysis only, and did not designate infection as the sole outcome variable of interest. Efforts to identify correlates of infection h Continue reading >>

Diabetic Ketoacidosistreatment & Management

Diabetic KetoacidosisTreatment & Management Author: Osama Hamdy, MD, PhD; Chief Editor: Romesh Khardori, MD, PhD, FACP more... Managing diabetic ketoacidosis (DKA) in an intensive care unit during the first 24-48 hours always is advisable. When treating patients with DKA, the following points must be considered and closely monitored: Correction of fluid loss with intravenous fluids Correction of electrolyte disturbances, particularly potassium loss Treatment of concurrent infection, if present It is essential to maintain extreme vigilance for any concomitant process, such as infection, cerebrovascular accident, myocardial infarction, sepsis, or deep venous thrombosis . It is important to pay close attention to the correction of fluid and electrolyte loss during the first hour of treatment. This always should be followed by gradual correction of hyperglycemia and acidosis. Correction of fluid loss makes the clinical picture clearer and may be sufficient to correct acidosis. The presence of even mild signs of dehydration indicates that at least 3 L of fluid has already been lost. Patients usually are not discharged from the hospital unless they have been able to switch back to their daily insulin regimen without a recurrence of ketosis. When the condition is stable, pH exceeds 7.3, and bicarbonate is greater than 18 mEq/L, the patient is allowed to eat a meal preceded by a subcutaneous (SC) dose of regular insulin. Insulin infusion can be discontinued 30 minutes later. If the patient is still nauseated and cannot eat, dextrose infusion should be continued and regular or ultrashort-acting insulin should be administered SC every 4 hours, according to blood glucose level, while trying to maintain blood glucose values at 100-180 mg/dL. The 2011 JBDS guideline recommends the Continue reading >>

Predictors Of Intensive Care Unit And Hospital Length Of Stay In Diabetic Ketoacidosis

Volume 17, Issue 4 , December 2002, Pages 207-211 Predictors of intensive care unit and hospital length of stay in diabetic ketoacidosis Author links open overlay panel Amado X.Freireabcd Get rights and content Objective: To detemine the predictive value for prolonged intensive care unit (ICU) and hospital length of stay (LOS) in patients with diabetic ketoacidosis (DKA) of the Acute Physiology and Chronic Health Evaluation II (APACHE II) score and Logistic Organ Dysfunction System (LODS), and to identify associated characteristics. Design: Prospective cohort, 18-month observation. Subjects and Setting: All admissions to a 12-bed, inner-city, university-affiliated hospital, medical ICU from July 1999 to December 2000. Measurements: Data for APACHE II and LODS scoring systems were collected within 24 hours of admission. Lengths of ICU and hospital stay were the primary outcomes. Prolonged ICU and hospital LOS were defined as 3 or more and 6 or more days. Results: A total of 584 patients, mean age 49, 56% men, 82% African American were admitted to the ICU. At admission they had (mean SD) APACHE II (18 10), LODS (54), and predicted mortality of 32% 29%. DKA was the admitting diagnosis in 42 (7.6%) patients; they had lower APACHE II (126), LODS (21), and predicted mortality 5%5% than the general ICU population (all, P<.001). Hospital mortality in non-DKA patients was 18%; there were no deaths in patients with DKA. Among DKA patients, those with insulin noncompliance had a shorter hospital stay (2.8 1 d) than those with an underlying illness as the DKA trigger (4.83, P=02). Between patients with DKA, regardless of the LOS, there were no significant differences in APACHE II, LODS, or predicted mortality. Conclusions: ICU-admitted patients with DKA are less ill, and have lowe Continue reading >>

Incidence And Outcome Of Adults With Diabetic Ketoacidosis Admitted To Icus In Australia And New Zealand

Abstract Over the last two decades, there have been several improvements in the management of diabetes. Whether this has impacted on the epidemiology and outcome of diabetic ketoacidosis (DKA) requiring intensive care unit (ICU) admission is unknown. This was a retrospective study of 8533 patients with the diagnosis of DKA admitted to 171 ICUs in Australia and New Zealand between 2000–2013 with separate independent analysis of those on established insulin (Group I) or not on insulin (Group NI) at the time of hospitalisation. Of the 8553 patients, 2344 (27 %) were identified as NI. The incidence of ICU admission with DKA progressively increased fivefold from 0.97/100,000 (95 % CI 0.84–1.10) in 2000 to 5.3/100,000 (95 % CI 4.98–5.53) in 2013 (P < 0.0001), with the proportions between I and NI remaining stable. Rising incidences were observed mainly in rural and metropolitan hospitals (P < 0.01). In the first 24 hours in the ICU, mean worst pH increased over the study period from 7.20 ± 0.02 to 7.24 ± 0.01 (P < 0.0001), and mean lowest plasma bicarbonate from 12.1 ± 6.6 to 13.8 ± 6.6 mmol/L (P < 0.0001). In contrast, mean highest plasma glucose decreased from 26.3 ± 14 to 23.2 ± 13.1 mmol/L (P < 0.0001). Hospital mortality was significantly greater in NI as compared to I (2.4 % vs 1.1 %, P > 0.0001). Elevated plasma urea in the first 24 hours (≥25 mmol/L, adjusted odds ratio 20.6 (6.54–65.7), P < 0.0001) was the strongest individual predictor of mortality. The incidence of ICU admission of patients with DKA in Australia and New Zealand has increased fivefold over the last decade, with a significant proportion of patients not on insulin at presentation. Overall physiological status in the first 24 hours of ICU admission has progressively improved and mortali Continue reading >>

Management Of Diabetic Ketoacidosis In The Picu

DKA - A common PICU diagnosis Incidence 4.6 â€“ 8 per 1000 person years among people with diabetes Pediatric mortality rate is 1-2% DKA causes profound dehydration Hyperglycemia leads to osmotic diuresis Often 10-15% down from baseline weight Profound urinary free water and electrolyte loss Free water follows glucose into urine Electrolytes follow free water into urine Electrolyte abnormalities Pseudo-hyponatremia with hyperglycemia Sodium should rise with correction of glucose Profound total-body K+ depletion Urinary loss, decreased intake, emesis Initial K+ may be high due to acidosis, low insulin Aggressive K+ replacement necessary to prevent arrhythmias Phosphate, magnesium, calcium require replacement Initial DKA management - ED Resuscitation aimed at shock reversal Begin with 10-20 mL/kg NS bolus, may repeat if signs of shock persist Bolus fluids only necessary if signs of shock present Avoid overly-aggressive fluid resuscitation Concern for inciting cerebral edema, though no clear data Initial DKA management - ED NEVER give bicarbonate Increases risk of cerebral edema Begin insulin infusion at 0.1 units/kg/hr Should be initiated prior to leaving ED SQ or bolus insulin not indicated Pre-PICU arrival Order several bags of dextrose-containing and non-dextrose-containing IVF pre-PICU arrival Often takes pharmacy 1 hour to custom-make IVF No dextrose-containing fluids stocked in PICU Fluid Management - PICU 3 components to replacement fluids Deficit (often 10-15% total body water deficit) Ongoing losses (polyuria, emesis) Maintenance Possible to calculate the above, or give: 1.5X maintenance if moderately dehydrated 2X maintenance if severely dehydrated Isotonic fluid with potassium NS + 20 mEq/L KCl + 20 mEq/L KPhos Start with 40 mEq/L of potassium if K+ < 5 K+ Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic ketoacidosis is a condition that results from when the body is deprived of the ability to use glucose as an energy source. Usually this is due to a lack of insulin. Insulin is used to uptake glucose into the cells to be used for energy. If there is no insulin or the cells are resistant to insulin, the blood sugar levels increase to dangerous levels for the patient. It seems counter intuitive that the patient wouldn't have energy with such high levels of glucose, but this glucose is essentially unusable without insulin. Because your body needs energy to survive, it starts turning to alternative fuel sources (fat). Fat cells start breaking down and, as a result, release ketones (which are acidic) into the bloodstream. Hence the name: diabetic ketoacidosis. “High levels of ketones can poison the body. When levels get too high, you can develop DKA. DKA may happen to anyone with diabetes, though it is rare in people with type 2. Treatment for DKA usually takes place in the hospital. But you can help prevent it by learning the warning signs and checking your urine and blood regularly.” Causes The most common causes of DKA are not getting enough insulin, having a severe infection, becoming dehydrated, or a combination of these issues. It seems like it occurs mainly in patients with type one diabetes. Symptoms Some of the symptoms that people experience with DKA include the following: Excessive thirst and urination (more water is pulled into the urine as a result of high ketone loss in the urine) Lethargy Breathing very quickly (patients have a very high level of acids in their bloodstream and they try to "blow" off carbon dioxide by breathing quickly) A fruity odor on their breath (ketones have a fruity smell) Nausea and vomiting (the body tries to get rid of acid Continue reading >>

Diabetic Ketoacidosis In The Pediatric Icu

... Effective serum osmolality, which is computed by ignoring the contribution of freely diffusible urea to total osmolality, is often between 300 and 350 mOsm/L and correlates well with abnormalities in mental status [17, 26]. Leukocytosis with leftward shift is common in DKA due to release of cytokines and catecholamines, and does not necessarily indicate infection [27] BUN blood urea nitrogen a Estimates of capillary blood glucose by glucometer must be cross-checked against laboratory venous glucose since the former may be inaccurate in the presence of poor peripheral circulation and acidosis and lack of glucometer calibration b Other researchers have proposed a correction factor of 2.4 instead of 1.6 [15, 16] (fall of >90 mg/ dl/ h), fluid containing 5% dextrose and with tonicity between 0.45% saline to NS should be used . However, if serum sodium is low (<132 mEq/L) and does not rise with fall in blood glucose, NS can be used for subsequent fluid replacement [29]. ... ... This water transcellular shift also generates an extracellular efflux of potassium, further aggravated by metabolic acidosis, causing a high intracellular potassium deficit [12,15,16]. The total-body potassium deficit occurs mainly due to vomiting and osmotic diuresis; however, despite the total depletion, serum potassium levels at diagnosis may be increased, normal or decreased [12, . Hyperglycemia is the determining factor of serum hyperosmolality, responsible for the osmotic flux of water to extracellular space, which may cause dilutional hyponatremia; it is estimated that for each 100 mg/dl blood glucose concentration above the limit of 100 mg/ dl, there is a 1.6 mEq/L reduction in serum sodium. ... Continue reading >>

Children's Hospital Of Philadelphia

If you have questions about any of the clinical pathways or about the process of creating a clinical pathway please contact us. ©2017 by Children's Hospital of Philadelphia, all rights reserved. Use of this site is subject to the Terms of Use. The clinical pathways are based upon publicly available medical evidence and/or a consensus of medical practitioners at The Children’s Hospital of Philadelphia (“CHOP”) and are current at the time of publication. These clinical pathways are intended to be a guide for practitioners and may need to be adapted for each specific patient based on the practitioner’s professional judgment, consideration of any unique circumstances, the needs of each patient and their family, and/or the availability of various resources at the health care institution where the patient is located. Accordingly, these clinical pathways are not intended to constitute medical advice or treatment, or to create a doctor-patient relationship between/among The Children’s Hospital of Philadelphia (“CHOP”), its physicians and the individual patients in question. CHOP does not represent or warrant that the clinical pathways are in every respect accurate or complete, or that one or more of them apply to a particular patient or medical condition. CHOP is not responsible for any errors or omissions in the clinical pathways, or for any outcomes a patient might experience where a clinician consulted one or more such pathways in connection with providing care for that patient. Continue reading >>

The Scary Experience Of Diabetic Ketoacidosis

Today, we’re excited to share with you another guest blog from Katie Janowiak, who works for the Medtronic Foundation, our company’s philanthropic arm. When she first told me her story about food poisoning and Diabetic Ketoacidosis (DKA), I knew others could benefit from hearing it as well. Thanks Katie for your openness and allowing us to share your scary story so that the LOOP community can learn from it. Throughout this past year, I’ve had the honor of sharing with you, the amazing LOOP community, my personal journey and the often humorous sequence of events that is my life with T1. Humor is, after all, the best (and cheapest) therapy. Allow me to pause today to share with you the down and dirty of what it feels like to have something that is not the slightest bit humorous: diabetic ketoacidosis.You are hot. You are freezing. You are confused. You are blacked out but coherent. You go to talk but words fail you. Time flies and goes in slow motion simultaneously. You will likely smell and look like death. In my instance, this was brought on by the combination of excessive vomiting and dehydration caused by food poisoning and the diabetic ketoacidosis that followed after my body had gone through so much. In hindsight, I was lucky, my husband knew that I had food poisoning because I began vomiting after our meal. But I had never prepped him on diabetic ketoacidosis and the symptoms (because DKA was for those other diabetics.) Upon finding me in our living room with a bowl of blood and bile by my side (no, I am not exaggerating), he got me into the car and took me to emergency care. It was 5:30 p.m. – and I thought it was 11:00 a.m. The series of events that led up to my stay in the ICU began innocently enough. It was a warm summer night and my husband and I walke Continue reading >>