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Diabetic Ketoacidosis Treatment Protocol

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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 Continue reading >>

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  1. NinaC

    Janine,
    Bolusing the patient with 2 Liters of NS is a common order for DKA basically to dilute the glucose. It is what is ordered commonly in the ER. If the attending had questions about the order and did not want to listen to your explanation, then you should have reffered her to the ER doctor or perhaps you could have asked the attending why the patient should not be bolused with the saline over that period of time.

  2. CEN35

    first you did nothing wrong............ second............clearly the attending/admitting doc was a moron. unless.........this person had a hx of chf/pulmonary edema, a-fib/flutter or recent cabg.
    let's start with many of the needed results and hx to treat properly. i'll answer tomorrow sometime.
    #1 - blood glucose initially was?
    #2 - etoh use?
    #3 - hx of dm yes or no?
    #4 - abg's - if his bs was really high and a true dka, then ph is crucial.
    #5 - the remainder of the chemistries +amylase+lipase+hfp are important, with a cbccdiff, chest x-ray, and ekg also.
    assuming he is/was a true healthy dka......the nss bolus is fine no problem there. it's not to dilute the bs, it's to rehydrate the intervascular system......because these people are severely dehydrated, from polyuria, secondary to the kidneys attempt to spill glucose.
    thiamine 100mg im or iv........because thiamine is a co-enzyme that allows the brain to use glucose.....if they are thiamine deficient anything else you do is futile. if the person is an excessive user of etoh, and may be the cause of this event...you may need to add an amp of mvi to the bag also. make sure nothing is given im if you think it is etoh related. if it is etoh related you want to avoid any im injections, if the liver is screwed up a little im shot could cause a large bleeding problem.
    then most like to start an insulin drip at 10 units per hour. some also like to give 10 units iv push, prior to starting the drip. why 10 units? the liver can only metabolize about 10 units an hour. anything more than that, is just asking for the patients blood sugar to take a dive to "0", after the drip is stopped. it dont get any worse than that!
    keep and eye on the one touches/accu-checks........stop the drip when it hits about 250. the other thing you want to do........is make sure you get the potasium checked when it hits about 250.......of course it also depends where it is initially. with most dka's > 700 you can expect the k to be between 5.5 and 7.9. as the glucose drops........so does the k. if they are at 750 glucose and 5.5 k, the risk is for the k to drop too about 2.8-3.2 or maybe lower when the glucose hits 250, so you need to compensate for that. of course......usually the k is going to be high......depending on the glucose say 750-1000 probably the k will be about 6.8 to 7.9.
    the good side of this.....is by the time they hit a glucose of 250.....they should have a k about 4.5 -5.8, which is good.
    outside of that stuff.............the only other things needed, are to keep the body temperature up......which can drop (i've seen them as low as 31.7c in a 72 degree house, and watch for arrhythmias and the b/p if they are acidodic.
    once the glucose is about 250........then they can go ahead with the d51/2nss to get the rest of the tissues hydrated.....and keep him from bottoming out.......and your home free!!!

  3. TI2Grr

    Janine Looks as if you did wonderfully.. The big thing here is making sure that you don't shift to quickly the patient is in acidosis and the most important thing is insuring his Ph changes occur slowly, thus you want to keep giving dextrose and maintain the blood glucose preferably above 200 or 250 so he/she doesn't crash on you, then presenting more problems. The important thing is watching Ph, and also Ketones in urine.. Hence you will be giving quite a lot of bolus, normally in a couple of different IV solutions, one probably being NS, and the other being a dextrose solution, and watching the shift occur from acidosis to a normal baseline.
    An important thing to realize here is that different strokes for different folks -- referring to Doc's here, and this shift can occur in a couple of different manners, initial phase of getting this person stabilized was done as normally seen by a lot of different facilities and also patients. Sounds like the intern didn't know what the heck was going on or didn't explain something else due to something seen in the patients lab values..
    Don't get frustrated.. You did well..

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What is DIABETIC KETOACIDOSIS? What does DIABETIC KETOACIDOSIS mean? DIABETIC KETOACIDOSIS meaning - DIABETIC KETOACIDOSIS definition - DIABETIC KETOACIDOSIS explanation. Source: Wikipedia.org article, adapted under https://creativecommons.org/licenses/... license. SUBSCRIBE to our Google Earth flights channel - https://www.youtube.com/channel/UC6Uu... Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus. Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness. A person's breath may develop a specific smell. Onset of symptoms is usually rapid. In some cases people may not realize they previously had diabetes. DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances. Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids. DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies. DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine. The primary treatment of DKA is with intravenous fluids and insulin. Depending on the severity, insulin may be given intravenously or by injection under the skin. Usually potassium is also needed to prevent the development of low blood potassium. Throughout treatment blood sugar and potassium levels should be regularly checked. Antibiotics may be required in those with an underlying infection. In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended. Rates of DKA vary around the world. About 4% of people with type 1 diabetes in United Kingdom develop DKA a year, while in Malaysia the condition affects about 25% a year. DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost universally fatal. The risk of death with adequate and timely treatment is currently around 1–4%. Up to 1% of children with DKA develop a complication known as cerebral edema. The symptoms of an episode of diabetic ketoacidosis usually evolve over a period of about 24 hours. Predominant symptoms are nausea and vomiting, pronounced thirst, excessive urine production and abdominal pain that may be severe. Those who measure their glucose levels themselves may notice hyperglycemia (high blood sugar levels). In severe DKA, breathing becomes labored and of a deep, gasping character (a state referred to as "Kussmaul respiration"). The abdomen may be tender to the point that an acute abdomen may be suspected, such as acute pancreatitis, appendicitis or gastrointestinal perforation. Coffee ground vomiting (vomiting of altered blood) occurs in a minority of people; this tends to originate from erosion of the esophagus. In severe DKA, there may be confusion, lethargy, stupor or even coma (a marked decrease in the level of consciousness). On physical examination there is usually clinical evidence of dehydration, such as a dry mouth and decreased skin turgor. If the dehydration is profound enough to cause a decrease in the circulating blood volume, tachycardia (a fast heart rate) and low blood pressure may be observed. Often, a "ketotic" odor is present, which is often described as "fruity", often compared to the smell of pear drops whose scent is a ketone. If Kussmaul respiration is present, this is reflected in an increased respiratory rate.....

952: Evaluation Of A Diabetic Ketoacidosis Treatment Protocol Using Subcutaneous Insulin Aspart

Introduction:Insulin therapy is one aspect of managing diabetic ketoacidosis (DKA), and the American Diabetes Association recommends regular insulin by continuous IV infusion as the treatment of choice for all but mild cases of DKA. Several studies, each enrolling a small number of patients, have examined rapid-acting subcutaneous insulin analogs for DKA treatment. Patients in these studies who received subcutaneous insulin analogs were treated outside of the ICU. Hypothesis:A DKA treatment protocol that uses subcutaneous insulin aspart, with weight-based doses administered every two hours, is safe and effective. Methods:This study was a retrospective chart review. Adult patients who received insulin aspart for treatment of DKA at Rush University Medical Center between January 2008 and December 2011 were eligible for study inclusion. Efficacy outcomes included time to resolution of DKA-associated laboratory abnormalities, length of stay, time to initiation of basal insulin, and amount of insulin received. The primary safety outcome was hypoglycemic events. Subgroup analyses were conducted for type 1 vs. type 2 diabetes, DKA severity, and whether or not patients received concomitan Continue reading >>

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  1. nurseprnRN

    The hypokalemia comes when the patient gets treated with insulin, driving the glucose and K+ into the cells. The kidneys can't (and won't) move so much out through urine with the excess glucose to make for hypokalemia.

  2. Esme12

    There can be a brief period of hypoglycemia in the early stages of an elevated blood sugar (polyuria)....but by the time "ketoacidosis" sets in the Serum potassium is elevated but the cellular potassium is depleted (all that shifting that goes on)
    Diabetic ketoacidosis

  3. April2152

    So pretty much what we would observe clinically is hyperkalemia because the osmotic duiresis does not move serum potassium significantly?

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University Of Zagreb

SCHOOL OF MEDICINE Mohammad Imran Khan Malik A review of the efficacy of the Milwaukee protocol in the treatment of ketoacidosis in pediatric Intensive Care Unit patients at Rebro hospital between 2009-2014. GRADUATE THESIS Zagreb, 2014 UNIVERSITY OF ZAGREB SCHOOL OF MEDICINE Mohammad Imran Khan Malik A review of the efficacy of the Milwaukee protocol in the treatment of ketoacidosis in pediatric Intensive Care Unit patients at Rebro hospital between 2009-2014. GRADUATE THESIS Zagreb, 2014 This graduation paper has been completed at the Department of Paediatrics at the University Hospital Centre Zagreb (Rebro hospital) under the supervision of Dr. sc. Mario Ćuk and was submitted for evaluation during the academic year 2013 /2014. LIST OF TABLES Table 1: DKA laboratory diagnosis criteria Table 2: Classification of DKA. Modified from Kliegman et al. Nelson Textbook of Pediatrics, 2011. Table 3: Table 3: Summary of key data of patients admitted to pediatric ICU at Rebro hospital. LIST OF FIGURES Figure 1: DKA pathogenesis. Figure 2: Ketone bodies: showing formation of negatively charged conjugate bases of the ketoacids. The conjugate bases cause the increased anion gap in DKA meta Continue reading >>

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  1. Michael Simpson

    Diabetic ketoacidosis (the formal name, and the one most diabetics use, abbreviating it as DKA) can happen in Type 2 diabetics, but as you implied it is rare.
    Type 1 diabetics totally lack or have insufficient amounts of insulin. So the body produces the antagonistic hormone, glucagon, because there's no insulin, which to the body means there's low glucose. Glucagon then induces the liver to use fat as energy, producing ketone bodies while also forcing the liver to convert glycogen to glucose. Unfortunately, the blood glucose levels are high because the Type 1 Diabetic has no insulin. This causes the blood osmolarity to skyrocket, and the kidneys try to compensate by removing ketones and glucose from the blood.
    Since the kidneys have a maximum capacity to clear excess glucose from the blood, the blood becomes more acidotic and ketone bodies rise at the same time. And that leads to more serious issues like coma and death.
    The feedback systems are all broken, so the body spins out of control. It is often the first sign of Type 1 diabetes.
    So the one difference between Type 1 and Type 2 diabetics is that Type 1 has no insulin, but Type 2 generally has insulin in the blood to suppress the release of glucagon. And this is why it's rare in Type 2 diabetics.

  2. Liang-Hai Sie

    We need insulin to be able to utilize glucose, type 2 has some insulin, not enough because of the insulin resistance, type 1 don't, so in type one ketosis can develop because the lack of insulin causes the body to burn fat that forms ketones if no inslin is administered. I knew a man who every time he was arrested by intent "forgot" to inject his insulin so ended in hospital with a keto-aciditic diabetic coma, out of jail.

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