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Neurological Complications Of Dka

Diabetic Ketoacidosis: Evaluation And Treatment

Diabetic Ketoacidosis: Evaluation And Treatment

Diabetic ketoacidosis is characterized by a serum glucose level greater than 250 mg per dL, a pH less than 7.3, a serum bicarbonate level less than 18 mEq per L, an elevated serum ketone level, and dehydration. Insulin deficiency is the main precipitating factor. Diabetic ketoacidosis can occur in persons of all ages, with 14 percent of cases occurring in persons older than 70 years, 23 percent in persons 51 to 70 years of age, 27 percent in persons 30 to 50 years of age, and 36 percent in persons younger than 30 years. The case fatality rate is 1 to 5 percent. About one-third of all cases are in persons without a history of diabetes mellitus. Common symptoms include polyuria with polydipsia (98 percent), weight loss (81 percent), fatigue (62 percent), dyspnea (57 percent), vomiting (46 percent), preceding febrile illness (40 percent), abdominal pain (32 percent), and polyphagia (23 percent). Measurement of A1C, blood urea nitrogen, creatinine, serum glucose, electrolytes, pH, and serum ketones; complete blood count; urinalysis; electrocardiography; and calculation of anion gap and osmolar gap can differentiate diabetic ketoacidosis from hyperosmolar hyperglycemic state, gastroenteritis, starvation ketosis, and other metabolic syndromes, and can assist in diagnosing comorbid conditions. Appropriate treatment includes administering intravenous fluids and insulin, and monitoring glucose and electrolyte levels. Cerebral edema is a rare but severe complication that occurs predominantly in children. Physicians should recognize the signs of diabetic ketoacidosis for prompt diagnosis, and identify early symptoms to prevent it. Patient education should include information on how to adjust insulin during times of illness and how to monitor glucose and ketone levels, as well as i Continue reading >>

How Does Ketoacidosis Affect The Human Brain?

How Does Ketoacidosis Affect The Human Brain?

Diabetic Ketoacidosis (DKA) is the body’s emergency reaction to glucose starvation in the absence of insulin. It is a disastrous reaction — in general, it makes things worse rather than better, and starts a vicious cycle of blood acidity, rising blood glucose, dehydration, and blood hyperosmolality (high concentration of dissolved stuff) that can be hard to break. One of the hardest-hit organs in DKA is the brain, due to the dehydration and acidic blood entering that sensitive organ. Severe DKA may lead to brain swelling (edema) which is life-threatening. But recent studies have shown that even a short, apparently fully-recovered stint of DKA leads to measurable brain injury. Diabetic Ketoacidosis (DKA) is a life–threatening consequence of diabetes. DKA occurs when there is a lack of insulin in the body causing hyperglycemia. As a result of the inability of glucose to enter the cells, the body must find other means to obtain energy. As such, fat breakdown occurs resulting in the accumulation of fatty acids. The fatty acids are metabolized to ketones that cause the blood to become acidotic (pH less than7.3). Because glucose remains in the blood, there is an increase in thirst and drinking to eliminate the solute load of glucose, which also results in increased urination (polyuria and polydipsia). Thus, the combination of increased serum acidity, weight loss, polyuria, and polydipsia may lead to extreme dehydration, coma, or brain damage. Without a doubt, the most severe acute complication of DKA is cerebral edema. Many cases of new onset type 1 diabetes present DKA (15-70 percent depending on age and geographic region, according to multiple studies), hence the importance of an early diagnosis of diabetes in order to avoid potential consequences. Much research is be Continue reading >>

2017/18 Icd-10-cm Codes E13*: Other Specified Diabetes Mellitus

2017/18 Icd-10-cm Codes E13*: Other Specified Diabetes Mellitus

E10.1 Type 1 diabetes mellitus with ketoacidosis E10.10 Type 1 diabetes mellitus with ketoacidosis wi... E10.11 Type 1 diabetes mellitus with ketoacidosis wi... E10.2 Type 1 diabetes mellitus with kidney complica... E10.21 Type 1 diabetes mellitus with diabetic nephro... E10.22 Type 1 diabetes mellitus with diabetic chroni... E10.29 Type 1 diabetes mellitus with other diabetic ... E10.3 Type 1 diabetes mellitus with ophthalmic comp... E10.31 Type 1 diabetes mellitus with unspecified dia... E10.311 Type 1 diabetes mellitus with unspecified dia... E10.319 Type 1 diabetes mellitus with unspecified dia... E10.32 Type 1 diabetes mellitus with mild nonprolife... E10.321 Type 1 diabetes mellitus with mild nonprolife... E10.3211 Type 1 diabetes mellitus with mild nonprolife... E10.3212 Type 1 diabetes mellitus with mild nonprolife... E10.3213 Type 1 diabetes mellitus with mild nonprolife... E10.3219 Type 1 diabetes mellitus with mild nonprolife... E10.329 Type 1 diabetes mellitus with mild nonprolife... E10.3291 Type 1 diabetes mellitus with mild nonprolife... E10.3292 Type 1 diabetes mellitus with mild nonprolife... E10.3293 Type 1 diabetes mellitus with mild nonprolife... E10.3299 Type 1 diabetes mellitus with mild nonprolife... E10.33 Type 1 diabetes mellitus with moderate nonpro... E10.331 Type 1 diabetes mellitus with moderate nonpro... E10.3311 Type 1 diabetes mellitus with moderate nonpro... E10.3312 Type 1 diabetes mellitus with moderate nonpro... E10.3313 Type 1 diabetes mellitus with moderate nonpro... E10.3319 Type 1 diabetes mellitus with moderate nonpro... E10.339 Type 1 diabetes mellitus with moderate nonpro... E10.3391 Type 1 diabetes mellitus with moderate nonpro... E10.3392 Type 1 diabetes mellitus with moderate nonpro... E10.3393 Type 1 diabetes mellitus with Continue reading >>

Cerebral Edema And Diabetic Ketoacidosis

Cerebral Edema And Diabetic Ketoacidosis

Cerebral edema is the most feared emergent complication of pediatric diabetic ketoacidosis. Fortunately, it is relatively rare, but the rarity can lead to some confusion when it comes to its management. We recently discussed the use of mannitol and hypertonic saline for pediatric traumatic brain injury, but when should we consider these medications for the patient presenting with DKA? Cerebral Edema is a relatively rare. Incidence <1% of patients with DKA. Overall tends to occur in the newly diagnosed diabetic patient (4.3% vs 1.2%). While rare, it is a devastating complication. 1990 study showed case fatality rate was 64%. Those treated BEFORE respiratory failure had lower rate of mortality (30%). Lesson = treat early! The exact mechanism is not known… and may be varied between individual patients. Signs and Symptoms develop in: 66% within the first 7 hours of treatment (these tend to be younger). 33% within 10-24 hours of treatment. The diagnosis is clinical! ~40% of initial brain imaging of kids with cerebral edema are NORMAL! This is the area that often leads to finger pointing… most often those fingers being pointed toward the Emergency Physician who was initially caring for the kid. Much of the literature focused on interventions, but: Administration of Bicarb Sodium Bicarb was shown to be associated with Cerebral Edema in one study… Unfortunately, this study did not adjust for illness severity. Type of IV Fluids Generally, there is an absence of evidence that associates volume, tonicity, or rate change in serum glucose with Cerebral Edema development. There are cases presenting with cerebral edema prior to any therapies. Risk Factors that seem to stay consistent: Kids < 5 years of age More likely to have delayed diagnosis More severely ill at presentation S Continue reading >>

Complications Of Diabetes Mellitus

Complications Of Diabetes Mellitus

Natural History Of Diabetic Nephropathy In Persons With Insulin The 1982 publication of The Prevention and Treatment of FiveComplications of Diabetes: A Guide for Primary Care Practitionerswas an initial attempt to provide straightforward and practicalinformation that primary care practitioners could immediately applyin their practice in the diagnosis and prevention of complicationsof diabetes. In the eight years since that publication wasreleased, over 200,000 copies have been distributed. The emphasison early application of currently available preventive measures ortreatments has resulted in the widespread use of the document. The scope of the present revised edition has been broadened tocover nine complications of diabetes, and the recommendations forthe previous five. We anticipate continued widespread use of thisguide in assisting practitioners in the care of their patients withdiabetes. The recommendations are clear, practical, and based uponscientific evidence, and they can be generally implemented in anoffice practice. We believe that they are conceptually consistentwith the American Medical Association's new emphasis on practiceparameters. Although this publication is meant to provide freestanding andpractical assistance in an office practice, the most appropriateuse is in continuing education programs and workshops. In thesesettings, the practical application of the recommendations can bediscussed and barriers to their application in individual practicesovercome. We congratulate the Centers for Disease Control in its efforts to updatethis guide and wish it the same success as the previous edition. This publication is designed to help the primary carepractitioner in the day-to-day management of patients withdiabetes. The recommendations relate to the preventio Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a serious metabolic disorder that can occur in patients with diabetes mellitus (DM).1,2 Veterinary technicians play an integral role in managing and treating patients with this life-threatening condition. In addition to recognizing the clinical signs of this disorder and evaluating the patient’s response to therapy, technicians should understand how this disorder occurs. Technicians must also educate owners about the long-term care of diabetic pets. DM is caused by a relative or absolute lack of insulin production by the pancreatic β cells or by inactivity or loss of insulin receptors, which are usually found on membranes of skeletal muscle, fat, and liver cells.1,3 In dogs and cats, DM is classified as either type I (insulin dependent; the body is unable to produce sufficient insulin) or type II (non–insulin dependent; the body produces insulin, but the body’s tissues are resistant to insulin).4 Most dogs that develop DM have insulin deficiency, while cats that develop DM tend to have insulin resistance.5 DKA occurs when the body cannot use glucose for energy because of a lack of, or resistance to, insulin. When this happens, the body uses alternative energy sources, resulting in ketone production and subsequent acidosis.1 Insulin has many functions, including the enhancement of glucose uptake by the cells for energy.1 Without insulin, cells cannot use glucose, causing them to starve.2 The unused glucose remains in the circulation, resulting in hyperglycemia. To provide cells with an alternative energy source, the body breaks down adipocytes, releasing free fatty acids (FFAs) into the bloodstream. The liver subsequently converts FFAs to triglycerides and ketone bodies. These ketone bodies (i.e., acetone, acetoacetic acid, β-hydrox Continue reading >>

Cerebrovascular Complications Of Diabetic Ketoacidosis In Children

Cerebrovascular Complications Of Diabetic Ketoacidosis In Children

CLINICAL CASE REPORT Complicações cerebrovasculares da cetoacidose diabética em crianças Luis Felipe Mendonça de Siqueira Hospital das Clínicas, Universidade Federal de Minas Gerais (UFMG); Department of Pediatrics, Faculty of Medicine, UFMG, Belo Horizonte, MG, Brazil SUMMARY Neurological deterioration in children with diabetic ketoacidosis (DKA) is commonly caused by cerebral edema. However, subtle cerebral injuries including strokes should also be suspected, since children with hyperglycemia and DKA are prone to thrombosis. In this paper, a case involving a 2 month-old patient that presented cerebral edema and stroke as complications of DKA is reported. In the discussion, the literature on neurological complications of DKA in children is briefly reviewed, emphasizing the prothrombotic tendency of these patients. SUMÁRIO Alterações neurológicas em crianças com cetoacidose diabética (CAD) são comuns, sobretudo em decorrência de edema cerebral. Contudo, lesões cerebrais agudas, como acidente vascular cerebral (AVC), também devem ser investigadas, já que as crianças com hiperglicemia e cetoacidose têm maior chance de apresentar essa complicação. Neste relato, descreve-se a história de um paciente de 2 meses de idade que apresentou edema cerebral e AVC como complicações de um quadro de cetoacidose diabética. Durante a discussão, será feita uma breve revisão da literatura sobre as complicações neurológicas da CAD nos pacientes pediátricos enfatizando sua tendência pró-trombótica. INTRODUCTION Children with new onset type 1 diabetes mellitus (T1DM) frequently have diabetic ketoacidosis (DKA) as their initial presentation, a disorder that is associated with significant morbidity and mortality. In this context, neurological complications, in Continue reading >>

Risk Factors For Cerebral Edema In Children With Diabetic Ketoacidosis

Risk Factors For Cerebral Edema In Children With Diabetic Ketoacidosis

Cerebral edema is an uncommon but devastating complication of diabetic ketoacidosis in children. Risk factors for this complication have not been clearly defined. In this multicenter study, we identified 61 children who had been hospitalized for diabetic ketoacidosis within a 15-year period and in whom cerebral edema had developed. Two additional groups of children with diabetic ketoacidosis but without cerebral edema were also identified: 181 randomly selected children and 174 children matched to those in the cerebral-edema group with respect to age at presentation, onset of diabetes (established vs. newly diagnosed disease), initial serum glucose concentration, and initial venous pH. Using logistic regression, we compared the three groups with respect to demographic characteristics and biochemical variables at presentation and compared the matched groups with respect to therapeutic interventions and changes in biochemical values during treatment. A comparison of the children in the cerebral-edema group with those in the random control group showed that cerebral edema was significantly associated with lower initial partial pressures of arterial carbon dioxide (relative risk of cerebral edema for each decrease of 7.8 mm Hg [representing 1 SD], 3.4; 95 percent confidence interval, 1.9 to 6.3; P<0.001) and higher initial serum urea nitrogen concentrations (relative risk of cerebral edema for each increase of 9 mg per deciliter [3.2 mmol per liter] [representing 1 SD], 1.7; 95 percent confidence interval, 1.2 to 2.5; P=0.003). A comparison of the children with cerebral edema with those in the matched control group also showed that cerebral edema was associated with lower partial pressures of arterial carbon dioxide and higher serum urea nitrogen concentrations. Of the ther Continue reading >>

Risk Factors For Cerebral Oedema In Children And Adolescents With Diabetic Ketoacidosis

Risk Factors For Cerebral Oedema In Children And Adolescents With Diabetic Ketoacidosis

Cerebral oedema (CO) is a rare life-threatening complication of diabetic ketoacidosis (DKA) in children. We analysed the biochemical and therapeutic risk factors for CO in DKA by a retrospective review of 256 children hospitalized for DKA between February 2003 and March 2015. The demographic characteristics, biochemical variables and therapeutic interventions were compared between the patients with and without CO. CO was observed in 22 (8.6%) of the 256 subjects included in the study. One of these patients (5%) had a fatal outcome and two patients (9%) survived with neurological consequences. CO was significantly associated with severe DKA: lower initial venous pH (p < 0.001) and bicarbonate (p < 0.001), higher initial blood glucose (p < 0.01), urea level (p < 0.05) and baseline serum osmolality (р < 0.05). During the treatment of DKA, low serum phosphate level was found to be significantly associated with CO (p < 0.05). We also found significant dependence between the development of CO and the initiation of treatment for DKA in another facility before hospitalization in our hospital (p < 0.05), bicarbonate application (p < 0.001), higher fluid volume infused initially (p < 0.01) and delayed potassium substitution (p < 0.01). Severe ketoacidosis, hyperglycaemia and dehydration at presentation, and low serum phosphate during treatment are significantly related to CO formation in children with DKA. The initial severe acidosis and hyperglycaemia probably cause brain injury which progresses into CO in the course of developing hypophosphatemia and cerebral hypervolemia. Continue reading >>

Neurological Consequences Of Diabetic Ketoacidosis At Initial Presentation Of Type 1 Diabetes In A Prospective Cohort Study Of Children

Neurological Consequences Of Diabetic Ketoacidosis At Initial Presentation Of Type 1 Diabetes In A Prospective Cohort Study Of Children

Go to: To investigate the impact of new-onset diabetic ketoacidosis (DKA) during childhood on brain morphology and function. Patients aged 6–18 years with and without DKA at diagnosis were studied at four time points: <48 h, 5 days, 28 days, and 6 months postdiagnosis. Patients underwent magnetic resonance imaging (MRI) and spectroscopy with cognitive assessment at each time point. Relationships between clinical characteristics at presentation and MRI and neurologic outcomes were examined using multiple linear regression, repeated-measures, and ANCOVA analyses. Thirty-six DKA and 59 non-DKA patients were recruited between 2004 and 2009. With DKA, cerebral white matter showed the greatest alterations with increased total white matter volume and higher mean diffusivity in the frontal, temporal, and parietal white matter. Total white matter volume decreased over the first 6 months. For gray matter in DKA patients, total volume was lower at baseline and increased over 6 months. Lower levels of N-acetylaspartate were noted at baseline in the frontal gray matter and basal ganglia. Mental state scores were lower at baseline and at 5 days. Of note, although changes in total and regional brain volumes over the first 5 days resolved, they were associated with poorer delayed memory recall and poorer sustained and divided attention at 6 months. Age at time of presentation and pH level were predictors of neuroimaging and functional outcomes. DKA at type 1 diabetes diagnosis results in morphologic and functional brain changes. These changes are associated with adverse neurocognitive outcomes in the medium term. Continue reading >>

Neurological Complications In Diabetic Ketoacidosis- Before And After Insulin Therapy

Neurological Complications In Diabetic Ketoacidosis- Before And After Insulin Therapy

Original Research Manmohan Krishna Pandey, Purnima Mittra, Jitendra Doneria, Pradeep Kumar Maheshwari. Abstract Background: Neurological complications in DKA may present before, during and after the therapy. Present study was designed to evaluate neurological complication in DKA and effects of insulin therapy. Aims & Objective: To compare neurological complications of DKA before and after insulin therapy. Material and Methods: This was Cross-Sectional Study with sample size of 40. 40 cases of diabetes mellitus in DKA were given standard treatment with intravenous insulin infusion and fluids. Patients were compared with the symptoms and signs of DKA before and 12 hours of insulin therapy. Result were analyzed with Graph Pad Software with paired t-test and discussed in terms of p-value. Results: The general symptoms like pain in abdomen, thirst, nausea and vomiting and general signs of DKA like tachycardia, hypotension dry mucous membrane, dehydration and Kussmaul’s respiration showed clinically significant improvement and statistically very significant with p-value less than 0.05 after insulin infusion therapy. The CNS symptoms like headache, altered mentation, unconsciousness and abnormal verbal/motor response to pain increased after 12 hours of insulin infusion therapy and intravenous fluids and results were statistically significant with p-value 0.0221 and CNS signs of DKA i.e. bradycardia, extensor planter response, papilledema and third cranial nerve palsy showed clinically significant results but statistically not significant with p-value 0.0911 after insulin infusion therapy. Conclusion: CNS manifestation of DKA may aggravate symptoms and signs with insulin infusion therapy. Patient should be monitored for CNS manifestations during therapy along with oxygen Continue reading >>

Dka Final

Dka Final

1. Diabetic Ketoacidosis EPU Team (Dr. Uko P., Dr. Eke E.P., Dr. Jemide O., Dr. Osang S.) FMC Keffi 28th of May, 2014 2. Outline  Overview of Diabetic Mellitus  Diabetic Ketoacidosis: Introduction  Epidemiology  Physiology  Pathophysiology  Clinical Presentation  Diagnosis  Complications  Treatment/Monitoring  Prevention  Conclusion  References 2 3. Overview of Diabetes Mellitus Diabetes mellitus is a group of metabolic diseases characterized by chronic hyperglycaemia resulting from defects in insulin secretion, insulin action or both. 4. Criteria for diagnosis Symptoms of DM and casual plasma glucose conc. > 11.1mmol/L(200mg/dl) (10 for venous) Fasting Plasma Glucose > 7.0mmol/L (126mg/dl) (6.3 for venous and capillary) 2hr post load of glucose >11.1mmol/L during an OGTT 5. Types of DM 1. Type 1 Diabetes Mellitus (T1DM):- β cell destruction leading to absolute insulin deficiency. Immune mediated, idiopathic 2. Type 2 Diabetes Mellitus (T2DM):- insulin resistance with relative insulin deficiency 3. Other types  Gestational DM 6. Genetic defects of ◦ β cell function ◦ Insulin action Diseases of the pancreas Endocrinopathies Infections Drug or chemical induced Genetic syndromes Uncommon forms of immune related 7. TYPE 1 DM Type 1 DM is the most common endocrine metabolic disorder of childhood and adolescence. Autoimmune mechanisms are factors in the genesis of T1DM. • Most cases are primarily due to T-cell mediated pancreatic islet β-cell destruction. 8. Serological markers of an autoimmune pathologic process, including islet cell, glutamic acid decarboxylase (GAD), islet antigen (IA)-2, IA-2b, or insulin autoantibodies (IAAs), are present in 85– 90% of individuals when fasting hyp Continue reading >>

Complications Of Diabetes Mellitus

Complications Of Diabetes Mellitus

The complications of diabetes mellitus are far less common and less severe in people who have well-controlled blood sugar levels. Acute complications include hypoglycemia and hyperglycemia, diabetic coma and nonketotic hyperosmolar coma. Chronic complications occur due to a mix of microangiopathy, macrovascular disease and immune dysfunction in the form of autoimmune disease or poor immune response, most of which are difficult to manage. Microangiopathy can affect all vital organs, kidneys, heart and brain, as well as eyes, nerves, lungs and locally gums and feet. Macrovascular problems can lead to cardiovascular disease including erectile dysfunction. Female infertility may be due to endocrine dysfunction with impaired signalling on a molecular level. Other health problems compound the chronic complications of diabetes such as smoking, obesity, high blood pressure, elevated cholesterol levels, and lack of regular exercise which are accessible to management as they are modifiable. Non-modifiable risk factors of diabetic complications are type of diabetes, age of onset, and genetic factors, both protective and predisposing have been found. Overview[edit] Complications of diabetes mellitus are acute and chronic. Risk factors for them can be modifiable or not modifiable. Overall, complications are far less common and less severe in people with well-controlled blood sugar levels.[1][2][3] However, (non-modifiable) risk factors such as age at diabetes onset, type of diabetes, gender and genetics play a role. Some genes appear to provide protection against diabetic complications, as seen in a subset of long-term diabetes type 1 survivors without complications .[4][5] Statistics[edit] As of 2010, there were about 675,000 diabetes-related emergency department (ED) visits in the Continue reading >>

Diabetic Coma Recovery: What You Need To Know

Diabetic Coma Recovery: What You Need To Know

In people with diabetes, a diabetic coma occurs when severe levels of either high or low uncontrolled blood sugar are not corrected. If treated quickly, a person will make a rapid recovery from a diabetic coma. However, diabetic coma can be fatal or result in brain damage. It is important for people with diabetes to control their blood sugars and know what to do when their blood sugar levels are not within their target range. The severe symptoms of uncontrolled blood sugar that can come before a diabetic coma include vomiting, difficulty breathing, confusion, weakness, and dizziness. Recovery from diabetic coma If a diabetic coma is not treated within a couple of hours of it developing, it can cause irreversible brain damage. If no treatment is received, a diabetic coma will be fatal. In addition, having blood sugar levels that continue to be too low or too high can be bad for long-term health. This remains true even if they do not develop into diabetic coma. Recognizing the early signs of low or high blood sugar levels and regular monitoring can help people with diabetes keep their blood sugar levels within the healthy range. Doing so will also reduce the risk of associated complications and diabetic coma. What is diabetes? Diabetes is a long-term condition in which the body is unable to control the level of a sugar called glucose in the blood. Diabetes is caused by either a lack of insulin, the body's inability to use insulin correctly, or both. In people who don't have diabetes, insulin usually ensures that excess glucose is removed from the bloodstream. It does this by stimulating cells to absorb the glucose they need for energy from the blood. Insulin also causes any remaining glucose to be stored in the liver as a substance called glycogen. The production of insul Continue reading >>

Diabetic Ketoacidosis

Diabetic 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 the Pre-diabetes (Impaired Glucose Tolerance) article more useful, or one of our other health articles. See also the separate Childhood Ketoacidosis article. Diabetic ketoacidosis (DKA) is a medical emergency with a significant morbidity and mortality. It should be diagnosed promptly and managed intensively. DKA is characterised by hyperglycaemia, acidosis and ketonaemia:[1] Ketonaemia (3 mmol/L and over), or significant ketonuria (more than 2+ on standard urine sticks). Blood glucose over 11 mmol/L or known diabetes mellitus (the degree of hyperglycaemia is not a reliable indicator of DKA and the blood glucose may rarely be normal or only slightly elevated in DKA). Bicarbonate below 15 mmol/L and/or venous pH less than 7.3. However, hyperglycaemia may not always be present and low blood ketone levels (<3 mmol/L) do not always exclude DKA.[2] Epidemiology DKA is normally seen in people with type 1 diabetes. Data from the UK National Diabetes Audit show a crude one-year incidence of 3.6% among people with type 1 diabetes. In the UK nearly 4% of people with type 1 diabetes experience DKA each year. About 6% of cases of DKA occur in adults newly presenting with type 1 diabetes. About 8% of episodes occur in hospital patients who did not primarily present with DKA.[2] However, DKA may also occur in people with type 2 diabetes, although people with type 2 diabetes are much more likely to have a hyperosmolar hyperglycaemic state. Ketosis-prone type 2 diabetes tends to be more common in older, overweight, non-white people with type 2 diabetes, and DKA may be their Continue reading >>

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