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Neurological Complications Of Dka

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 >>

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 (dka)

Diabetic Ketoacidosis (dka)

Diabetic ketoacidosis is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. Hyperglycemia causes an osmotic diuresis with significant fluid and electrolyte loss. DKA occurs mostly in type 1 diabetes mellitus (DM). It causes nausea, vomiting, and abdominal pain and can progress to cerebral edema, coma, and death. DKA is diagnosed by detection of hyperketonemia and anion gap metabolic acidosis in the presence of hyperglycemia. Treatment involves volume expansion, insulin replacement, and prevention of hypokalemia. Diabetic ketoacidosis (DKA) is most common among patients with type 1 diabetes mellitus and develops when insulin levels are insufficient to meet the body’s basic metabolic requirements. DKA is the first manifestation of type 1 DM in a minority of patients. Insulin deficiency can be absolute (eg, during lapses in the administration of exogenous insulin) or relative (eg, when usual insulin doses do not meet metabolic needs during physiologic stress). Common physiologic stresses that can trigger DKA include Some drugs implicated in causing DKA include DKA is less common in type 2 diabetes mellitus, but it may occur in situations of unusual physiologic stress. Ketosis-prone type 2 diabetes is a variant of type 2 diabetes, which is sometimes seen in obese individuals, often of African (including African-American or Afro-Caribbean) origin. People with ketosis-prone diabetes (also referred to as Flatbush diabetes) can have significant impairment of beta cell function with hyperglycemia, and are therefore more likely to develop DKA in the setting of significant hyperglycemia. SGLT-2 inhibitors have been implicated in causing DKA in both type 1 and type 2 DM. 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 >>

Department Of Emergency Medicine

Department Of Emergency Medicine

Lehigh Valley Health Network LVHN Scholarly Works Department of Emergency Medicine Continued Confusion After Resolution of Diabetic Ketoacidosis Ryan Rogers DO Lehigh Valley Health Network, [email protected] Gretchen A. Perilli MD Lehigh Valley Health Network, [email protected] Philip Dunn DO Lehigh Valley Health Network, [email protected] Follow this and additional works at: Part of the Emergency Medicine Commons, and the Endocrinology, Diabetes, and Metabolism Commons This Poster is brought to you for free and open access by LVHN Scholarly Works. It has been accepted for inclusion in LVHN Scholarly Works by an authorized administrator. For more information, please contact [email protected] Published In/Presented At Rogers, R., Perilli, G., Dunn, P. (2015, April 30). Continued Confusion After Resolution of Diabetic Ketoacidosis. Poster presented at: POMA Annual Clinical Assembly, King of Prussia, PA. Lehigh Valley Health Network, Allentown, Pennsylvania Continued Confusion After Resolution of Diabetic Ketoacidosis Ryan Rogers, DO, Gretchen Perilli, MD, and Philip Dunn, DO Introduction Case Presentation Diabetic Ketoacidosis (DKA) is a complication of an uncontrolled type I diabetic. After resolution of the ketosis, the polyuria, polydipsia, nausea and encephalopathy usually subside. DKA poses risks for developing several cerebral complications including cerebral edema, seizure activity and CVA but intracranial hemorrhages (ICH) have been reported in rare case among children. Discussion: © 2015 Lehigh Valley Health Network References: 1. Levin, Daniel L., MD. “Cerebral Edema in Diabetic Ketoacidosis.†Pediatric Critical Care Medicine 9.3 (2008): 320-26 2. Hatun, Sukru, Filiz Cizmecioglu, and Demet Toprak. “Cerebral Complication 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 >>

Diabetes Mellitus And The Nervous System

Diabetes Mellitus And The Nervous System

Classification The division of diabetes into two major types has long been known. The current classification1 (table 1) distinguishes type 1 (otherwise known as insulin dependent diabetes mellitus, IDDM) and type 2 (non-insulin dependent diabetes mellitus, NIDDM). This classification is important because the two types are distinct both in causation and management and is thus of direct clinical relevance. In Western Europe, type 1 diabetes accounts for perhaps 10%-20% of all patients, although in the world at large there seems to be an extraordinary increase in type 2 diabetes from an estimated 124 million at present to a predicted 221 million by the year 2010 with only 3% of all patients with type 1 diabetes. The many other types of diabetes, either secondary to other causes or specific genetic syndromes, account for only a small proportion of patients (table 1). MITOCHONDRIAL DISORDERS Mitochondria possess their own DNA (mtDNA), which is arranged as a discrete circular molecule encoding for a proportion of the peptides required for the components of the respiratory chain. MtDNA is passed exclusively down the maternal line of inheritance. There are several reported mutations in the tRNA Leu(UUR) gene, the one most often found occurring at position 3243.2 3 These mutations are associated with maternally inherited diabetes combined with sensorineural deafness (MIDD) and accounts for around two type 2 diabetic patients in every 1000 and less than half that number among type 1 patients. Diabetes has also been reported in patients with the same mutation causing the MELAS syndrome—that is, patients with associated myopathy, encephalopathy, lactic acidosis, and stroke-like episodes, and in the Kearns-Sayre syndrome. Mitochondrial related diabetes usually presents at between 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 >>

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 >>

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 >>

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 >>

Pediatric Diabetic Ketoacidosis

Pediatric Diabetic Ketoacidosis

Practice Essentials Diabetic ketoacidosis, in pediatric and adult cases, is a metabolic derangement caused by the absolute or relative deficiency of the anabolic hormone insulin. Together with the major complication of cerebral edema, it is the most important cause of mortality and severe morbidity in children with diabetes. Signs and symptoms Symptoms of acidosis and dehydration include the following: Symptoms of hyperglycemia, a consequence of insulin deficiency, include the following: Patients with diabetic ketoacidosis may also have the following signs and symptoms: Cerebral edema Most cases of cerebral edema occur 4-12 hours after initiation of treatment. Diagnostic criteria of cerebral edema include the following: Major criteria include the following: Minor criteria include the following: See Clinical Presentation for more detail. Laboratory studies The following lab studies are indicated in patients with diabetic ketoacidosis: Imaging studies Head computed tomography (CT) scanning - If coma is present or develops Chest radiography - If clinically indicated Electrocardiography Electrocardiography (ECG) is a useful adjunct to monitor potassium status. Characteristic changes appear with extremes of potassium status. See the images below. Consciousness Check the patient’s consciousness level hourly for up to 12 hours, especially in a young child with a first presentation of diabetes. The Glasgow coma scale is recommended for this purpose. See Workup for more detail. Management Replacement of the following is essential in the treatment of diabetic ketoacidosis: Insulin - Continuous, low-dose, intravenous (IV) insulin infusion is generally considered the safest and most effective insulin delivery method for diabetic ketoacidosis Potassium - After initial resuscitatio Continue reading >>

Diabetic Ketoacidosis Symptoms

Diabetic Ketoacidosis Symptoms

What is diabetic ketoacidosis? Diabetic ketoacidosis, also referred to as simply ketoacidosis or DKA, is a serious and even life-threatening complication of type 1 diabetes. DKA is rare in people with type 2 diabetes. DKA is caused when insulin levels are low and not enough glucose can get into the body's cells. Without glucose for energy, the body starts to burn fat for energy. Ketones are products that are created when the body burns fat. The buildup of ketones causes the blood to become more acidic. The high levels of blood glucose in DKA cause the kidneys to excrete glucose and water, leading to dehydration and imbalances in body electrolyte levels. Diabetic ketoacidosis most commonly develops either due to an interruption in insulin treatment or a severe illness, including the flu. What are the symptoms and signs of diabetic ketoacidosis? The development of DKA is usually a slow process. However, if vomiting develops, the symptoms can progress more rapidly due to the more rapid loss of body fluid. Excessive urination, which occurs because the kidneys try to rid the body of excess glucose, and water is excreted along with the glucose High blood glucose (sugar) levels The presence of ketones in the urine Other signs and symptoms of ketoacidosis occur as the condition progresses: These include: Fatigue, which can be severe Flushing of the skin Fruity odor to the breath, caused by ketones Difficulty breathing Type 2 Diabetes Diagnosis, Treatment, Medication What should I do if I think I may have, or someone I know may diabetic ketoacidosis? You should test your urine for ketones if you suspect you have early symptoms or warning signs of ketoacidosis. Call your health-care professional if your urine shows high levels of ketones. High levels of ketones and high blood sug 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 >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis is a state of insulin deficiency, characterised by rapid onset, extreme metabolic acidosis, a generally intact sensorium, and only mild hyperglycaemia. DKA comes up frequently in the CICM SAQs, but usually as an ABG interpretation exercise. This chapter focuses on the medical side of DKA, including its causes, manifestations, complications, and management strategies. Questions which have required such thinking have included the following: Question 1 from the second paper of 2016 (differences between HONK and DKA) Question 17 from the first paper of 2014 (differences between HONK and DKA) Question 2 from the second paper of 2009 (general approach to management) Question 15 from the second paper of 2000 (whether or not saline is appropriate) Definition of diabetic ketoacidosis How does one discriminate between DKA and HONK even when in about 30% of instances the two disorders coexist? Arbitrary definitions exist, proposed by the American Diabetes Association. In summary: DKA presents with acidosis as the major feature HONK presents with hyperglycaemia as the major feature Discriminating Between HONK and DKA Domain Features suggestive of DKA Features suggestive of HONK Demographic Young Known Type 1 diabetic Elderly Known Type 2 diabetic History Rapid clinical course History of noncompliance with insulin Abdominal pain Shortness of breath Prolonged course History of noncompliance with oral antihyperglycaemic agents and insulin Polydipsia, polyuria, weight loss Neurological symptoms Examination Tachypnoea Normal level of consciousness, or only slightly decreased Coma Seizures Biochemistry Severe acidosis Severe ketosis Mild hyperglycaemia Renal function normalises rapidly Mild acidosis Little ketosis; mainly lactate is raised Severe hyperglycaemia Esta Continue reading >>

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