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Neurological Complications Of Dka

Diabetic Ketoacidosis And Cerebral Edema

Diabetic Ketoacidosis And Cerebral Edema

Elliot J. Krane, M.D. Departments of Pediatrics and Anesthesiology Stanford University Medical Center Introduction In 1922 Banting and Best introduced insulin into clinical practice. A decade later the first reported case of cerebral edema complicating diabetic ketoacidosis (DKA) was reported by Dillon, Riggs and Dyer writing in the pathology literature. While the syndrome of cerebral edema complicating DKA was either not seen, ignored, or was unrecognized by the medical community until 3 decades later when the complication was again reported by Young and Bradley at the Joslin Clinic, there has since been a flurry of case reports in the 1960's and 1970's and basic and clinical research from the 1970's to the 1990's leading to our present day acceptance of this as a known complication of DKA, or of the management of DKA. In fact, we now recognize that the cerebral complications of DKA (including much less frequent cerebral arterial infarctions, venous sinus thrombosis, and central nervous system infections) are the most common cause of diabetic-related death of young diabetic patients (1), accounting for 31% of deaths associated with DKA and 20% of all diabetic deaths, having surpassed aspiration, electrolyte imbalance, myocardial infarction, etc. Furthermore, diabetes mellitus remains an important cause of hospitalization of young children. The prevalence rate of diabetes continues to grow in all Western developed nations, nearly doubling every decade, resulting in 22,000 hospital admissions in children under 15 years of age for diabetes in the United States in 1994, the majority of which were due to ketoacidosis. With approximately 4 hospital admissions of children for DKA per 100,000 population per year (2), every PICU located in a major metropolitan center will conti Continue reading >>

Severe Diabetic Ketoacidosis In A Newly Diagnosed Child With Type 2 Diabetes Mellitus: A Case Report

Severe Diabetic Ketoacidosis In A Newly Diagnosed Child With Type 2 Diabetes Mellitus: A Case Report

Abdulmoein E Al-Agha1* and Mohammed A Al-Agha2 1Department of Pediatric Endocrinology, King Abdul-Aziz University Hospital, Saudi Arabia 2Faculty of Medicine, King Abdul-Aziz University, Saudi Arabia Citation: Abdulmoein E Al-Agha1, Mohammed A Al-Agha (2017) Severe Diabetic ketoacidosis in a Newly Diagnosed Child with Type 2 Diabetes Mellitus: A Case Report. J Diabetes Metab 8:724. doi:10.4172/2155-6156.1000724 Copyright: © 2017 Al-Agha AE, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Visit for more related articles at Journal of Diabetes & Metabolism Abstract Background: Diabetes ketoacidosis (DKA) is an acute complication of both type 1 and type 2 diabetes mellitus (DM). DKA is characterized by the presence of hyperglycemia, ketosis, ketonuria, and metabolic acidosis. Cerebral edema is a rare but rather a serious complication of DKA. Case presentation: An obese 12-year-old, Egyptian boy, previously medically free, presented to the emergency room (ER) of King Abdulaziz university hospital, with two weeks' histories of dizziness, shortness of breath, polyuria, polydipsia & nocturia. His symptoms were deteriorating with a change in sensorial and cognitive functions at the time of presentation. He was diagnosed with type 2 DM based upon clinical background, namely the presence of obesity (weight+7.57 Standard Deviation Score (SDS), height+1.4 SDS, and body mass index (BMI) of 34.77 kg/m2 (+3.97SDS) together with the presence of Acanthosis nigricans and biochemically based on, normal level of serum insulin, normal serum level of connecting peptide and negative autoantibodies. H 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 >>

Cerebral Accidents In Pediatric Diabetic Ketoacidosis: Different Complications And Different Evolutions

Cerebral Accidents In Pediatric Diabetic Ketoacidosis: Different Complications And Different Evolutions

Cerebral Accidents in Pediatric Diabetic Ketoacidosis: Different Complications and Different Evolutions Mozzillo E.a D'Amico A.b Fattorusso V.a Carotenuto B.b Buono P.a De Nitto E.a Falco M.a Franzese A. a I have read the Karger Terms and Conditions and agree. I have read the Karger Terms and Conditions and agree. Buy a Karger Article Bundle (KAB) and profit from a discount! If you would like to redeem your KAB credit, please log in . Save over 20% compared to the individual article price. Buy Cloud Access for unlimited viewing via different devices Access to all articles of the subscribed year(s) guaranteed for 5 years Unlimited re-access via Subscriber Login or MyKarger Unrestricted printing, no saving restrictions for personal use * The final prices may differ from the prices shown due to specifics of VAT rules. For additional information: Diabetic ketoacidosis (DKA) may be associated with neurologic complications: the most common is cerebral edema while the risk of venous and arterial stroke is rare. There is a pathogenetic link between DKA, hypercoagulability and stroke, whose risk is underestimated by clinicians. Our cases present a wide spectrum of cerebral accidents during DKA, the first one being diffuse cerebral edema, the second one venous stroke after 5 days of DKA resolution, while the third one multifocal edema suspected to be extrapontine myelinolysis although without electrolyte imbalance. Our cases suggest that DKA requires very accurate treatment, particularly at an early age, and it can be complicated by cerebral accidents even with appropriate medical care. Ho J, Mah JK, Pacaud D: Pediatric stroke associated with new onset type 1 diabetes mellitus: case reports and review of the literature. Pediatr Diabetes 2006;7:116-121. ISPAD Clinical Practice Co Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

INTRODUCTION Diabetic ketoacidosis (DKA) is a very serious complication of diabetes mellitus, a metabolic disorder that is characterized by hyperglycemia, metabolic acidosis, and increased body ketone concentrations. The most common causes of DKA are infection and poor compliance with medication regimens. Other causes include undiagnosed diabetes, alcohol abuse, and a multitude of medical conditions such as cerebrovascular accident (CVA), complicated pregnancy, myocardial infarction, pancreatitis, and stress. Diabetic ketoacidosis is a complicated pathology. Early recognition of DKA, a good understanding of the pathological processes of DKA, and aggressive treatment are the keys to successful treatment. With good care, DKA can be managed and the patient will survive. OBJECTIVES When the student has finished studying this module, he/she will be able to: 1. Identify the correct definition of DKA. 2. Identify a basic function of insulin. 3. Identify the insulin derangements of types I and II diabetes. 4. Identify the basic cause of DKA. 5. Identify two specific causes of DKA. 6. Identify the two pathogenic mechanisms that produce the signs/symptoms of DKA. 7. Identify metabolic consequences of increased hormone concentrations in DKA. 8. Identify the criteria used to diagnose DKA. 9. Identify common signs and symptoms of DKA. 10. Identify laboratory abnormalities seen in DKA. 11. Identify complications of DKA. 12. Identify the three most important therapies for treating DKA. 13. Identify the correct roles of sodium bicarbonate and phosphate in treating DKA. 14. Identify an important rule for using potassium replacement in DKA. 15. Identify an important rule for switching from IV to subcutaneous insulin. EPIDEMIOLOGY Most cases of DKA are seen in patients with type I diabete Continue reading >>

Diabetic Ketoacidosis And Brain Function

Diabetic Ketoacidosis And Brain Function

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 being conducted to predict the development of severe complications of DKA, most notably on brain herniation, the swelling of the brain that causes it to push towards the spinal cord, as well as other neurological consequences. Fulminant cerebral edema, or swelling of the brain, is relatively rare and has an incidence rate of 0.5-0.9 percent. However, what about the subtler, less severe alterations in brain functions that occur after DKA? Indeed, a recent paper published in Diabetes Care 2014; 37: 1554-1562by Cameron, Scratch, Nadebaum, Northum, Koves, Jennings, Finney, Neil, Wellard, Mackay, and Inder on behalf of the DKA Brain Injury Study Group entitled "Neurological Consequences of 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 >>

Diabetic Ketoacidosis With Cerebral Hemorrhage And Alpha Coma In An Adolescent Female

Diabetic Ketoacidosis With Cerebral Hemorrhage And Alpha Coma In An Adolescent Female

Abstract: Background: Diabetic ketoacidosis (DKA) is one of the most common complications of type 1 diabetes in children. Neurological complications including seizures and coma can be secondary to cerebral edema, hemorrhagic, or ischemic events. Alpha coma (AC), an alpha-frequency EEG rhythm, is a rare finding in comatose patients and is generally associated with a poor prognosis. We report an adolescent with severe DKA, intraparenchymal cerebral hemorrhage, and AC, who had rapid resolution of neurological symptoms. Clinical Case: A 17-year old female with a 4-year history of poorly controlled type 1 diabetes was seen in the ED for change in mental status. At presentation she was unresponsive and severely dehydrated with Kussmaul respirations. She experienced a 3-second seizure upon arrival and another 2-minute seizure which was treated with lorazepam and fosphenytoin, and she required intubation. IV fluid and mannitol were administered and an insulin drip started. She remained unresponsive to pain with absent oculocephalic reflexes but reactive pupils. Initial laboratory findings included pH 6.69, sodium 131 mmol/L, potassium 10.9 mmol/L, chloride 88 mmol/L, carbon dioxide 3 mmol/L, glucose 1622 mg/dL, calcium 8.6 mg/dL, phosphate 18.5 mg/dL. CT of the brain showed acute intraparenchymal hemorrhage in the right parietal cortex and left pineal region with extension into the adjacent quadrigeminal plate cistern, but no cerebral edema. EEG showed diffuse alpha frequency of 8-12 Hz with an amplitude of 20-30 µV with frontal predominance. Within 24 hours the DKA and electrolyte abnormalities resolved, she regained consciousness and was extubated. Twenty-four hours after the initial event MRI and MRA of the brain demonstrated multiple 1-2 cm hemorrhages in various areas of 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 >>

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 >>

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 >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

A 12 year old boy, previously healthy, is admitted to the hospital after 2 days of polyuria, polyphagia, nausea, vomiting and abdominal pain. Vital signs are: Temp 37C, BP 103/63 mmHg, HR 112, RR 30. Physical exam shows a lethargic boy. Labs are notable forWBC 16,000,Glucose 534, K 5.9, pH 7.13, PCO2 is 20 mmHg, PO2 is 90 mmHg. result of insulin, glucagon, growth hormone, catecholamine increased tidal volume and rate as a result of metabolic acidosis due to gluconeogenesis and glycogenolysis tissues unable to use the high glucose as it is unable to enter cells anion gap due to ketoacidosis, lactic acidosis consumed in an attempt to buffer the increased acid glucose acts as an osmotic agent and draws water from ICF to ECF acidosis results in ICF/ECF exchange of H+ for K+ depletion of total body potassium due to cellular shift and losses through urine -hydroxybutyrate not detected with normal ketone body tests due to in capillary lipoprotein lipase activity H2PO4- is increased in urine, as it is titratable acid used to buffer the excess H+ that is being excreted must prevent resultant hypokalemia and hypophosphatemia labs may show pseudo-hyperkalemia prior to administartion of fluid and insulin due to transcellular shift of potassium out of the cells to balance the H+ being transfered into the cells Upon administration of insulin, potassium will shift intracellularly, possibly resulting in dangerous hypokalemia give phosphatesupplementation to prevent respiratory paralysis (M1.EC.31) A 17-year-old male presents to your office complaining of polyuria, polydipsia, and unintentional weight loss of 12 pounds over the past 3 months. On physical examination, the patient is tachypneic with labored breathing. Which of the following electrolyte abnormalities would you most likely Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a serious problem that can occur in people with diabetes if their body starts to run out of insulin. This causes harmful substances called ketones to build up in the body, which can be life-threatening if not spotted and treated quickly. DKA mainly affects people with type 1 diabetes, but can sometimes occur in people with type 2 diabetes. If you have diabetes, it's important to be aware of the risk and know what to do if DKA occurs. Symptoms of diabetic ketoacidosis Signs of DKA include: needing to pee more than usual being sick breath that smells fruity (like pear drop sweets or nail varnish) deep or fast breathing feeling very tired or sleepy passing out DKA can also cause high blood sugar (hyperglycaemia) and a high level of ketones in your blood or urine, which you can check for using home-testing kits. Symptoms usually develop over 24 hours, but can come on faster. Check your blood sugar and ketone levels Check your blood sugar level if you have symptoms of DKA. If your blood sugar is 11mmol/L or over and you have a blood or urine ketone testing kit, check your ketone level. If you do a blood ketone test: lower than 0.6mmol/L is a normal reading 0.6 to 1.5mmol/L means you're at a slightly increased risk of DKA and should test again in a couple of hours 1.6 to 2.9mmol/L means you're at an increased risk of DKA and should contact your diabetes team or GP as soon as possible 3mmol/L or over means you have a very high risk of DKA and should get medical help immediately If you do a urine ketone test, a result of more than 2+ means there's a high chance you have DKA. When to get medical help Go to your nearest accident and emergency (A&E) department straight away if you think you have DKA, especially if you have a high level of ketones in 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 >>

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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