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Recovering From Dka

Recurrent Diabetic Ketoacidosis Raises Mortality Risk In T1d

Recurrent Diabetic Ketoacidosis Raises Mortality Risk In T1d

Recurrent episodes of diabetic ketoacidosis (DKA) were associated with a substantially increased risk of death in patients with type 1 diabetes, according to a retrospective cohort study. Patients with a single hospitalization for DKA during the study period had a 5.2% risk of death, compared with a 23.4% risk of death for patients hospitalized for DKA more than five times (hazard ratio 6.18; P=0.001), reported a research team led by Fraser Gibb, MBChB, PhD, of the Royal Infirmary of Edinburgh in Scotland. Patients with recurrent hospitalizations for DKA tended to be younger, poorer, have higher glycated hemoglobin levels, and to have mental health problems, Gibb and colleagues reported in Diabetologia. "Most strikingly, a greater than one in five risk of death was observed in those with the highest frequency of DKA presentation over a median 2.4 years of follow-up, compared with a one in 20 risk of death in those with a single DKA admission over a median of 4 years. This represents a substantially elevated risk of death when compared with the Scottish type 1 diabetes population," Gibb and colleagues said. "The main implications of the study are that we have identified a significant risk of death in patients with recurrent DKA, many of whom are young," Gibb told MedPage Today via email. "With this in mind, we need to build an evidence base for strategies to help prevent mortality in this at-risk group. I suspect this will focus on community-based, multi-disciplinary care for this group of patients." The deaths almost always occurred at home rather than in the hospital, the investigators noted. "In keeping with other modern cohorts, we found a low rate of inpatient mortality in patients presenting with DKA," they said. "However, the frequency of subsequent sudden death a Continue reading >>

Type 1 Diabetes In Adults: Diagnosis And Management.

Type 1 Diabetes In Adults: Diagnosis And Management.

Go to: 12.1. Ketone monitoring [2015] 12.1.1. Introduction Ketosis and ketonuria reflect a greater degree of insulin deficiency than hyperglycaemia alone. The presence of ketones indicates that insulin concentrations are too low not only to control blood glucose concentrations but also to prevent the breakdown of fat (lipolysis). Because ketones are acid substances, high ketone concentrations in the blood may create acidosis. Diabetic ketoacidosis (DKA) is a medical emergency and in its established state carries a 0.7–5% mortality in adults.459,476,784 High ketones in the blood are associated with high levels of fatty acids and together create insulin resistance. The patient with significant ketonaemia will require more insulin than usual to control the blood glucose. Traditionally, ketonaemia has been assessed by urine testing. This has been applied in three main settings: it is recommended as part of guidance for patient self-management of acute illness at home, when patients are advised to increase their usual corrective insulin doses in the presence of significant ketonuria; in the assessment of patients presenting to emergency services with hyperglycaemia, where presence of ketonuria may influence management decisions, including need for admission and in the management of established DKA, where resolution of ketonuria is an important indication of recovery. However, not all ketone bodies are detected by urine testing. For example, beta-hydroxybutyrate (β-OHB) is not detected with current strip tests and if there is a high β-OHB:acetoacetate ratio, urine testing may give a falsely low estimate of ketosis. Furthermore, after an episode of ketoacidosis, where measurement of blood ketones may provide a more accurate assessment of re-insulinisation than blood glucos Continue reading >>

Cerebral Edema In Diabetic Ketoacidosis: A Look Beyond Rehydration

Cerebral Edema In Diabetic Ketoacidosis: A Look Beyond Rehydration

The Journal of Clinical Endocrinology & Metabolism Cerebral Edema in Diabetic Ketoacidosis: A Look Beyond Rehydration Department of Pediatrics University of Florida Gainesville, Florida 32610 Search for other works by this author on: The Journal of Clinical Endocrinology & Metabolism, Volume 85, Issue 2, 1 February 2000, Pages 509513, Andrew Muir; Cerebral Edema in Diabetic Ketoacidosis: A Look Beyond Rehydration, The Journal of Clinical Endocrinology & Metabolism, Volume 85, Issue 2, 1 February 2000, Pages 509513, INJUDICIOUS fluid resuscitation is frequently suggested as the cause of the cerebral edema that is the most common cause of mortality among pediatric patients with diabetic ketoacidosis (DKA) ( 1 ). The evidence, however, supports the hypothesis that neurological demise in DKA is a multifactorial process that cannot be reliably prevented by cautious rehydration protocols. Mortality and severe morbidity can, however, be reduced when healthcare providers watch vigilantly for and respond rapidly to the sentinel neurological signs and symptoms that precede, often by hours, the dramatic collapse that is typically described in these patients. Children being treated for DKA develop clinically important neurological compromise about 0.21.0% of the time ( 2 ). Subclinical neurological pathology, causing raised intracranial pressure, likely precedes the initiation of therapy in almost all cases of DKA ( 3 5 ). Intracranial hypertension has been considered to be aggravated by therapy of the DKA ( 4 , 6 , 7 ), but in keeping with the physicians perplexity about the problem, even this widely held tenet has recently been challenged ( 8 ). The pathogenic mechanism for this terrifying complication remains unknown. Hypothetical causes of cerebral edema in children with DKA m Continue reading >>

Emergency Management Of Diabetic Ketoacidosis In Adults

Emergency Management Of Diabetic Ketoacidosis In Adults

Diabetic ketoacidosis (DKA) is a potentially fatal metabolic disorder presenting most weeks in most accident and emergency (A&E) departments.1 The disorder can have significant mortality if misdiagnosed or mistreated. Numerous management strategies have been described. Our aim is to describe a regimen that is based, as far as possible, on available evidence but also on our experience in managing patients with DKA in the A&E department and on inpatient wards. A literature search was carried out on Medline and the Cochrane Databases using “diabetic ketoacidosis” as a MeSH heading and as textword. High yield journals were hand searched. Papers identified were appraised in the ways described in the Users’ guide series published in JAMA. We will not be discussing the derangements in intermediary metabolism involved, nor would we suggest extrapolating the proposed regimen to children. Although some of the issues discussed may be considered by some to be outwith the remit of A&E medicine it would seem prudent to ensure that A&E staff were aware of the probable management of such patients in the hours after they leave the A&E department. AETIOLOGY AND DEFINITION DKA may be the first presentation of diabetes. Insulin error (with or without intercurrent illness) is the most common precipitating factor, accounting for nearly two thirds of cases (excluding those where DKA was the first presentation of diabetes mellitus).2 The main features of DKA are hyperglycaemia, metabolic acidosis with a high anion gap and heavy ketonuria (box 1). This contrasts with the other hyperglycaemic diabetic emergency of hyperosmolar non-ketotic hyperglycaemia where there is no acidosis, absent or minimal ketonuria but often very high glucose levels (>33 mM) and very high serum sodium levels (>15 Continue reading >>

Pulmcrit – Four Dka Pearls

Pulmcrit – Four Dka Pearls

Introduction I have a confession to make: I love treating DKA. It’s satisfying to take a patient from severe acidosis, electrolytic disarray, and hypovolemia to normal physiology during an ICU shift. Although it's usually straightforward, there are some pitfalls and a few tricks that may help your patients improve faster.0 Pearl #1: Avoid normal saline A common phenomenon observed when starting a DKA resuscitation with normal saline (NS) is worseningof the patient’s acidosis with decreasing bicarbonate levels (example below). This occurs despite an improvement in the anion gap, and is explained by a hyperchloremic metabolic acidosis caused by bolusing with NS. This could be a real problem for a patient whose initial bicarbonate level is extremely low.1 A while ago I made the switch from NS to lactated ringers (LR) for resuscitation of DKA patients, and have not observed this phenomenon when using LR. Example of the effect of normal saline resuscitation during the initial phase of DKA resuscitation. This patient received approximately 3 liters normal saline between admission labs and the next set of labs as well as an insulin infusion, all textbook management per American Diabetes Association guidelines. The anion gap decreased from 33 mEq/L to 30 mEq/L, indicating improvement of ketoacidosis. However, the bicarbonate decreased from 8 mEq/L to 5 mEq/L due to a hyperchloremic metabolic acidosis caused by the normal saline. Note the increase in chloride over four hours. Failure of the potassium to decrease significantly despite insulin infusion may reflect potassium shifting out of the cells in response to the hyperchloremic metabolic acidosis. There is only one randomized controlled trial comparing NS to LR for resuscitation in DKA (Zyl et al, 2011). These authors fou Continue reading >>

Diabetic Ketoacidosis Treatment & Management

Diabetic Ketoacidosis Treatment & Management

Approach Considerations 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: 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 ultra–short-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 intravenous infusion of insulin at a weight-based fixed rate until ketosis has subsided. Should blood glucose fall below 14 mmol/L (250 mg/dL), 10% glucose should be added to allow for the continuation of fixed-rate insulin infusion. [19, 20] In established patient Continue reading >>

Effect Of Glargine On Recovery Of Patients With Diabetic Ketoacidosis

Effect Of Glargine On Recovery Of Patients With Diabetic Ketoacidosis

Therapy change decreased recovery time, incidence of hypoglycemia and hypokalemia… Diabetes ketoacidosis is an emergency situation caused by acute high blood glucose concentration, which may be correlated with both type 1 and 2 diabetes. The current treatment for diabetic ketoacidosis is injection of rapid-acting regular insulin. The preferred protocol is intravenous infusion. However, intravenous regular insulin has a short half-life and requires an infusion pump. Long-acting insulin, such as glargine, has an onset of action is about an hour and is stable for 24 hours. Given the duration of action of glargine, it seems that adding long-acting insulin to standard therapy improves the recovery of the patients. The aim of the present study was to evaluate the effects of glargine on the recovery of patients with diabetic ketoacidosis. The study was designed as a randomized controlled study, which consisted of 40 patients with diabetic ketoacidosis. Both groups were administered standard therapy for diabetic ketoacidosis. The experimental group received 0.4 units/kg of glargine within three hours of the start of intravenous infusion. The results showed that the average duration of acidosis correction time and recovery from diabetic ketoacidosis was 13.77±6.10 and 16.91±6.49 h in the experimental and control groups, respectively (p=0.123). The average dosage of regular insulin until recovery from diabetic ketoacidosis was 84.8±45.6 in the experimental group and 116.5±91.6 units in control groups (p=0.17). Hypokalemia happened in three patients in the experimental group and four patients in control groups. In 35% of models in the experimental group and 51% in control group blood glucose was greater than 10 mmol/l for 24 h after starting the insulin infusion (p=0.046). T Continue reading >>

Childhood Ketoacidosis

Childhood Ketoacidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find one of our health articles more useful. Diabetic ketoacidosis (DKA) is the leading cause of mortality in childhood diabetes.[1]The primary cause of DKA is absolute or relative insulin deficiency: Absolute - eg, previously undiagnosed type 1 diabetes mellitus or a patient with known type 1 diabetes who does not take their insulin. Relative - stress causes a rise in counter-regulatory hormones with relative insulin deficiency. DKA can be fatal The usual causes of death are: Cerebral oedema - associated with 25% mortality (see 'Cerebral odedema', below). Hypokalaemia - which is preventable with good monitoring. Aspiration pneumonia - thus, use of a nasogastric tube in the semi-conscious or unconscious is advised. Deficiency of insulin. Rise in counter-regulatory hormones, including glucagon, cortisol, growth hormone, and catecholamines. Thus, inappropriate gluconeogenesis and liver glycogenolysis occur compounding the hyperglycaemia, which causes hyperosmolarity and ensuing polyuria, dehydration and loss of electrolytes. Accelerated catabolism from lipolysis of adipose tissue leads to increased free fatty acid circulation, which on hepatic oxidation produces the ketone bodies (acetoacetic acid and beta-hydroxybutyric acid) that cause the metabolic acidosis. A vicious circle is usually set up as vomiting usually occurs compounding the stress and dehydration; the cycle can only be broken by providing insulin and fluids; otherwise, severe acidosis occurs and can be fatal. Biochemical criteria The biochemical criteria required for a diagnosis of DKA to be made are Continue reading >>

Diabetes Complications In Dogs And Cats: Diabetes Ketoacidosis (dka)

Diabetes Complications In Dogs And Cats: Diabetes Ketoacidosis (dka)

Unfortunately, we veterinarians are seeing an increased prevalence of diabetes mellitus in dogs and cats. This is likely due to the growing prevalence of obesity (secondary to inactive lifestyle, a high carbohydrate diet, lack of exercise, etc.). So, if you just had a dog or cat diagnosed with diabetes mellitus, what do you do? First, we encourage you to take a look at these articles for an explanation of the disease: Diabetes Mellitus (Sugar Diabetes) in Dogs Once you have a basic understanding of diabetes mellitus (or if you already had one), this article will teach you about life-threatening complications that can occur as a result of the disease; specifically, I discuss a life-threatening condition called diabetes ketoacidosis (DKA) so that you know how to help prevent it! What is DKA? When diabetes goes undiagnosed, or when it is difficult to control or regulate, the complication of DKA can occur. DKA develops because the body is so lacking in insulin that the sugar can’t get into the cells -- resulting in cell starvation. Cell starvation causes the body to start breaking down fat in an attempt to provide energy (or a fuel source) to the body. Unfortunately, these fat breakdown products, called “ketones,” are also poisonous to the body. Symptoms of DKA Clinical signs of DKA include the following: Weakness Not moving (in cats, hanging out by the water bowl) Not eating to complete anorexia Large urinary clumps in the litter box (my guideline? If it’s bigger than a tennis ball, it’s abnormal) Weight loss (most commonly over the back), despite an overweight body condition Excessively dry or oily skin coat Abnormal breath (typically a sweet “ketotic” odor) In severe cases DKA can also result in more significant signs: Abnormal breathing pattern Jaundice Ab Continue reading >>

Diabetes With Ketone Bodies In Dogs

Diabetes With Ketone Bodies In Dogs

Studies show that female dogs (particularly non-spayed) are more prone to DKA, as are older canines. Diabetic ketoacidosis is best classified through the presence of ketones that exist in the liver, which are directly correlated to the lack of insulin being produced in the body. This is a very serious complication, requiring immediate veterinary intervention. Although a number of dogs can be affected mildly, the majority are very ill. Some dogs will not recover despite treatment, and concurrent disease has been documented in 70% of canines diagnosed with DKA. Diabetes with ketone bodies is also described in veterinary terms as diabetic ketoacidosis or DKA. It is a severe complication of diabetes mellitus. Excess ketone bodies result in acidosis and electrolyte abnormalities, which can lead to a crisis situation for your dog. If left in an untreated state, this condition can and will be fatal. Some dogs who are suffering from diabetic ketoacidosis may present as systemically well. Others will show severe illness. Symptoms may be seen as listed below: Change in appetite (either increase or decrease) Increased thirst Frequent urination Vomiting Abdominal pain Mental dullness Coughing Fatigue or weakness Weight loss Sometimes sweet smelling breath is evident Slow, deep respiration. There may also be other symptoms present that accompany diseases that can trigger DKA, such as hypothyroidism or Cushing’s disease. While some dogs may live fairly normal lives with this condition before it is diagnosed, most canines who become sick will do so within a week of the start of the illness. There are four influences that can bring on DKA: Fasting Insulin deficiency as a result of unknown and untreated diabetes, or insulin deficiency due to an underlying disease that in turn exacerba Continue reading >>

Take Care Of Yourself When Sick Or Under Stress

Take Care Of Yourself When Sick Or Under Stress

When we're stressed, our bodies need extra energy to help us cope and recover. This is true whether bodies are under stress from illness or injury or are dealing with the effects of emotional stress, both good and bad. To meet the demand for more energy, the body responds by releasing into the bloodstream sugar that's been stored in the liver, causing blood sugar levels to rise. In someone without diabetes, the pancreas responds to the rise in blood sugar by releasing enough insulin into the bloodstream to help convert the sugar into energy. This brings blood sugar levels back down to normal. In someone with diabetes, the extra demand usually means needing to take more diabetes medicine (insulin or pills.) To make sure your body is getting enough medicine to help keep your blood sugar levels close to normal, you'll need to test more often when you are: Sick Recovering from surgery Fighting an infection Feeling upset Under more stress than usual Traveling Type 1 Diabetes In people with type 1 diabetes, blood sugar levels rise in response to stress, but the body doesn't have enough insulin to turn the sugar into energy. Instead, the body burns stored fat to meet energy needs. When fat is burned for energy, it creates waste products called ketones. As fat is broken down, ketones start to build up in the bloodstream. High levels of ketones in the blood can lead to a serious condition known as diabetic ketoacidosis (DKA), which can cause a person to lose consciousness and go into a diabetic coma. Type 2 Diabetes In people with type 2 diabetes, the body usually has enough insulin available to turn sugar into energy, so it doesn't need to burn fat. However, stress hormones can cause blood sugar levels to rise to very high and even dangerous levels. People with type 2 diabetes Continue reading >>

How Long Does It Take To Recover From Dka

How Long Does It Take To Recover From Dka

How long does it take to recover from DKA Registration is fast, simple and absolutely free so please,join our community todayto contribute and support the site. This topic is now archived and is closed to further replies. How long does it take to recover from DKA Hi Forum, this is my first post. I am type 1 and have had serious DKA back in July. I was on a drip for a week and altogether it took 8 days in hospital. Now I am ina similar position. I have read some places where keytones are out of the system in a day or two but I am not getting better. Has anyone had DKA and for how long. And how many days to tyou were able to eat again. Thank you for your help. It took me 2 weeks to recover from my DKA but I had pneumonia also. It is different for everyone, but a week to 10 days seems to be average from what I hear. Note my 2 weeks was my first and only DKA in my life so far. Thanks this makes me feel like I have a bit of time to get over this. May I ask - How long before yolu were able to eat? I am a lightweight - only 'normally' 65 Kg's but I have just lost 10KG weight. I can't keep stuff down and hardly want to eat. Did bad control bring it on with Pneumonia or just the infection? Thanks for your help and time. I was diagnosed with diabetes when I got my DKA so I'd say my control was pretty bad. I was able to eat again in 3 to 4 days, but a part of that was due to my colon as well. I hope someone else can chip in with their DKA experiences. Gareth, it really sounds like you should go back to the hospital and have them help you with this until you can eat again, all that weightloss is rather worrying! I've never been in a bad DKA (touch wood) in my 4 years of being T1. I was heading that way when diagnosed though, but i caught my symtoms fairly early so i didn't even go Continue reading >>

Diabetic Ketoacidosis/cerebral Edema

Diabetic Ketoacidosis/cerebral Edema

How can diabetic ketoacidosisrelated cerebral edema be prevented? OVERVIEW: What every practitioner needs to know Are you sure your patient has diabetic ketoacidosisrelated cerebral edema? What are the typical findings for this disease? Cerebral edema is a potentially life-threatening complication of diabetic ketoacidosis (DKA) and is responsible for the majority of diabetes-related deaths in children. Cerebral edema typically occurs after several hours of treatment with insulin and intravenous fluids but can also occur at the time of presentation of DKA before treatment is started. The risk of cerebral edema is related to the severity of acidosis, hypocapnia, and dehydration at the time of presentation of DKA. Although severe, clinically apparent cerebral edema occurs in just 1% of DKA episodes in children, numerous studies have demonstrated that mild cerebral edema, associated with only minimal or no alterations in mental status, is present in the majority of children during DKA treatment. The relationship between intravenous fluid treatment and the risk of DKA-related cerebral edema is frequently debated; however, there are no clear associations between the use of particular fluid treatment protocols and increased risk of DKA-related cerebral edema. At present, whether and how cerebral edema can be prevented is unknown. Treatment for clinically apparent cerebral edema typically involves use of hyperosmolar agents (mannitol or hypertonic saline). DKA-related cerebral edema is a clinical diagnosis. Imaging studies may be helpful but are not always definitive. The most common symptoms of DKA-related cerebral edema include mental status changes (confusion, irritability, obtundation) associated with severe headache, recurrence of vomiting, seizures, hypertension, inappro Continue reading >>

Cardiovascular Complications Of Ketoacidosis

Cardiovascular Complications Of Ketoacidosis

US Pharm. 2016;41(2):39-42. ABSTRACT: Ketoacidosis is a serious medical emergency requiring hospitalization. It is most commonly associated with diabetes and alcoholism, but each type is treated differently. Some treatments for ketoacidosis, such as insulin and potassium, are considered high-alert medications, and others could result in electrolyte imbalances. Several cardiovascular complications are associated with ketoacidosis as a result of electrolyte imbalances, including arrhythmias, ECG changes, ventricular tachycardia, and cardiac arrest, which can be prevented with appropriate initial treatment. Acute myocardial infarction can predispose patients with diabetes to ketoacidosis and worsen their cardiovascular outcomes. Cardiopulmonary complications such as pulmonary edema and respiratory failure have also been seen with ketoacidosis. Overall, the mortality rate of ketoacidosis is low with proper and urgent medical treatment. Hospital pharmacists can help ensure standardization and improve the safety of pharmacotherapy for ketoacidosis. In the outpatient setting, pharmacists can educate patients on prevention of ketoacidosis and when to seek medical attention. Metabolic acidosis occurs as a result of increased endogenous acid production, a decrease in bicarbonate, or a buildup of endogenous acids.1 Ketoacidosis is a metabolic disorder in which regulation of ketones is disrupted, leading to excess secretion, accumulation, and ultimately a decrease in the blood pH.2 Acidosis is defined by a serum pH <7.35, while a pH <6.8 is considered incompatible with life.1,3 Ketone formation occurs by breakdown of fatty acids. Insulin inhibits beta-oxidation of fatty acids; thus, low levels of insulin accelerate ketone formation, which can be seen in patients with diabetes. Extr Continue reading >>

Management Of Diabetic Ketoacidosis

Management Of Diabetic Ketoacidosis

Diabetic ketoacidosis is an emergency medical condition that can be life-threatening if not treated properly. The incidence of this condition may be increasing, and a 1 to 2 percent mortality rate has stubbornly persisted since the 1970s. Diabetic ketoacidosis occurs most often in patients with type 1 diabetes (formerly called insulin-dependent diabetes mellitus); however, its occurrence in patients with type 2 diabetes (formerly called non–insulin-dependent diabetes mellitus), particularly obese black patients, is not as rare as was once thought. The management of patients with diabetic ketoacidosis includes obtaining a thorough but rapid history and performing a physical examination in an attempt to identify possible precipitating factors. The major treatment of this condition is initial rehydration (using isotonic saline) with subsequent potassium replacement and low-dose insulin therapy. The use of bicarbonate is not recommended in most patients. Cerebral edema, one of the most dire complications of diabetic ketoacidosis, occurs more commonly in children and adolescents than in adults. Continuous follow-up of patients using treatment algorithms and flow sheets can help to minimize adverse outcomes. Preventive measures include patient education and instructions for the patient to contact the physician early during an illness. Diabetic ketoacidosis is a triad of hyperglycemia, ketonemia and acidemia, each of which may be caused by other conditions (Figure 1).1 Although diabetic ketoacidosis most often occurs in patients with type 1 diabetes (formerly called insulin-dependent diabetes mellitus), more recent studies suggest that it can sometimes be the presenting condition in obese black patients with newly diagnosed type 2 diabetes (formerly called non–insulin-depe Continue reading >>

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