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Neurological Complications Of Dka

Low-dose Vs Standard-dose Insulin In Pediatric Diabetic Ketoacidosisa Randomized Clinical Trial

Low-dose Vs Standard-dose Insulin In Pediatric Diabetic Ketoacidosisa Randomized Clinical Trial

Importance The standard recommended dose (0.1 U/kg per hour) of insulin in diabetic ketoacidosis (DKA) guidelines is not backed by strong clinical evidence. Physiologic dose-effect studies have found that even lower doses could adequately normalize ketonemia and acidosis. Lowering the insulin dose may be advantageous in the initial hours of therapy when a gradual decrease in glucose, electrolytes, and resultant osmolality is desired. Objective To compare the efficacy and safety of low-dose insulin against the standard dose in children with DKA. Design, Setting, and Participants This was a prospective, open-label randomized clinical trial conducted in the pediatric emergency department and intensive care unit of a tertiary care teaching hospital in northern India from November 1, 2011, through December 31, 2012. A total of 50 consecutive children 12 years or younger with a diagnosis of DKA were randomized to low-dose (n = 25) and standard-dose (n = 25) groups. Interventions Low-dose (0.05 U/kg per hour) vs standard-dose (0.1 U/kg per hour) insulin infusion. Main Outcomes and Measures The primary outcome was the rate of decrease in blood glucose until a level of 250 mg/dL or less is reached (to convert to millimoles per liter, multiply by 0.0555). The secondary outcomes included time to resolution of acidosis, episodes of treatment failures, and incidences of hypokalemia and hypoglycemia. Results The mean (SD) rate of blood glucose decrease until a level of 250 mg/dL or less is reached (45.1 [17.6] vs 52.2 [23.4] mg/dL/h) and the mean (SD) time taken to achieve this target (6.0 [3.3] vs 6.2 [2.2] hours) were similar in the low- and standard-dose groups, respectively. Mean (SD) length of time to achieve resolution of acidosis (low vs standard dose: 16.5 [7.2] vs 17.2 [7.7] 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 >>

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 >>

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 >>

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 >>

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 >>

Change In Fractional Anisotropy During Treatment Of Diabetic Ketoacidosis In Children

Change In Fractional Anisotropy During Treatment Of Diabetic Ketoacidosis In Children

Change in fractional anisotropy during treatment of diabetic ketoacidosis in children Pediatric Research volume75,pages6266(2014) Cite this article The pathophysiology resulting in cerebral edema in pediatric diabetic ketoacidosis (DKA) is unknown. To investigate the changes in white matter microstructure in this disease, we measured diffusion tensor imaging (DTI) parameters, including apparent diffusion coefficient (ADC), fractional anisotropy (FA), and radial and axial diffusivity in children with DKA at two time points during treatment. A prospective observational study was conducted at Seattle Childrens Hospital, Seattle, WA. Thirty-two children admitted with DKA (pH < 7.3, bicarbonate < 15 mEq/l, glucose > 300 mg/dl, and ketosis; 11.9 3.2 y; and 47% male) were enrolled and underwent two serial paired diffusion magnetic resonance imaging (MRI) scans following hospital admission. Seventeen of the 32 participants had diffusion tensor images of adequate quality for tract-based spatial statistics (TBSS) analysis. TBSS mapping demonstrated main white matter tract areas with a significant increase in FA and areas with a significant decrease in ADC, from the first to the second MRI. Both radial and axial diffusivity terms showed change, with a diffuse pattern of involvement. Consistent DTI changes occurred during DKA treatment over a short time frame. These findings describe widespread water diffusion abnormalities in DKA, supporting an association between clinical illness and DTI markers of microstructural change in white matter. Diabetic ketoacidosis (DKA) is a common acute complication of diabetes in children, occurring in 1567% of the patients with new-onset diabetes ( 1 ), with an average of 8 episodes per 100 patient-years in children with an existing diagnosis ( 2 Continue reading >>

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 >>

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 >>

39. Diabetic Ketoacidosis Flashcards Preview

39. Diabetic Ketoacidosis Flashcards Preview

A diabetic man is in the ED vomiting, delirious, and breathing deeply/rapidly; his breath has a fruity odor. What is the pathophysiology? Diabetic ketoacidosis; increased insulin requirements (e.g., stressors) cause excess lipolysis/ketogenesis, with resultant ketone bodies A diabetic with diabetic ketoacidosis (DKA) has high serum ketone bodies. Which ketone bodies, specifically, is the lab measuring? -Hydroxybutyrate and acetoacetate are the two main ketone bodies found in DKA (-hydroxybutyrate level > acetoacetate level) A patient has Kussmaul respirations. Describe the respirations and what state they are common in. Deep, rapid respirations and air hunger; characteristic of diabetic ketoacidosis You suspect diabetic ketoacidosis in an ED patient. What are the glucose, pH, bicarbonate, and WBC levels? What is the acid-base status? Increased glucose, low pH (increased H+), decreased bicarbonate, increased WBC count (leukocytosis); anion gap metabolic acidosis A diabetic with diabetic ketoacidosis has a potassium level of 5.3 mEq/L, but the attending orders intravenous potassium repletion. Why? Lab value is falsely high (total and intracellular K+ stores are low); acidosis and low insulin levels shift K+ into extracellular space A man with a recent episode of diabetic ketoacidosis presents with an infection over his sinuses. What infection are you worried about? Mucormycosis infection (e.g., Rhizopus fungus), which can be life-threatening 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 >>

Prime Pubmed | Posterior Reversible Encephalopathy Syndrome With Spinal Cord Involvement (pres-sci) As A Rare Complication Of Severe Diabetic Ketoacidosis: A Case Report And Review Of The Literatur

Prime Pubmed | Posterior Reversible Encephalopathy Syndrome With Spinal Cord Involvement (pres-sci) As A Rare Complication Of Severe Diabetic Ketoacidosis: A Case Report And Review Of The Literatur

In addition to diffuse brain oedema, diabetic ketoacidosis (DKA) can lead to ischaemic or haemorrhagic stroke, extrapontine myelinolysis, and sinovenous thrombosis. However, posterior reversible encephalopathy syndrome (PRES) and spinal cord oedema are rarely reported in patients with DKA. We present a case of a 17-year-old-girl who developed headache, blurred vision, and paraplegia after her DKA was controlled. Sequential magnetic resonance (MR) scans of the brain and spinal cord were performed. Brain MR showed large patchy lesions in the bilateral white matter of the parieto-occipital lobes, which had high T2 signal intensity and low T1 signal intensity. MR scanning of the spinal cord showed longitudinal confluent central spinal cord T2 hyperintensity spanning seven thoracic spinal segments. With symptomatic treatment, the patient's headache and vision disturbance subsided within 1 week. Subsequent MR scans demonstrated that the lesion in the spinal cord had decreased significantly in 10 days, and the large patchy lesions in the brain disappeared completely in 2 months. Her paraplegia improved gradually without obvious sequela 3 months later. The evolution of the disease and radiological findings supported the diagnosis of PRES with spinal cord involvement. To the best of our knowledge, this is the first case report describing PRES with spinal cord involvement as a complication of DKA. PRES is a rare complication that should be considered along with other neurological complications of DKA when focal deficits appear. Nao, Jianfei, et al. "Posterior Reversible Encephalopathy Syndrome With Spinal Cord Involvement (PRES-SCI) as a Rare Complication of Severe Diabetic Ketoacidosis: a Case Report and Review of the Literature." Child's Nervous System : ChNS : Official Journa 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 >>

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 >>

Neuroimaging Findings In Acute Pediatric Diabetic Ketoacidosis

Neuroimaging Findings In Acute Pediatric Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a state of severe insulin deficiency and a serious complication in children with diabetes mellitus type 1. In a small number of children, DKA is complicated by injury of the central nervous system. These children have a significant mortality and high long-term neurological morbidity. Cerebral edema is the most common neuroimaging finding in children with DKA and may cause brain herniation. Ischemic or hemorrhagic stroke during the acute DKA episode is less common and accounts for approximately 10% of intracerebral complications of DKA. Here we present the neuroimaging findings of two children with DKA and brain injury. Familiarity with the spectrum of neuroimaging findings seen in pediatric DKA is important to allow early detection as well as initiation of therapy and, hence, prevent complications of the central nervous system. Continue reading >>

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