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Neurological Complications Of Dka

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 >>

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 >>

Get Your Full Text Copy In Pdf

Get Your Full Text Copy In Pdf

Joyce A. Akwe, Gloria E Westney, Tatah S Fongeh Background: Pancreatic encephalopathy is a rare complication of acute pancreatitis. Acute pancreatitis is associated with a variety of complications that can involve the CNS, with altered mental status (AMS), Pulmonary, Cardiac, Renal, Hematology, Gastrointestinal systems with various clinical manifestations. Pancreatic encephalopathy (PE) could be a contributing factor to the persistence of altered mental status in patients presenting with AMS and acute pancreatitis with persistence of AMS even after the resolution of metabolic changes in this patient. Case Report: We describe a case of altered mental status in a patient with acute pancreatitis and diabetic ketoacidosis, presenting with persistent neurological symptoms which Persisted even after complete resolution of metabolic changes. Conclusions: Pancreatic encephalopathy is a main contributor to persistent neurological changes in patients with acute pancreatitis. It is frequently under-diagnosed. Look for other causes of AMS in patients with acute pancreatitis presenting with AMS that does not resolve with the resolution of metabolic changes . This paper has been published under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) allowing to download articles and share them with others as long as they credit the authors and the publisher, but without permission to change them in any way or use them commercially. 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 >>

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 >>

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 >>

Racgp - A Sugary Problem

Racgp - A Sugary Problem

Sarah, 20 years of age, is a student who presented to her family doctor with a one-day history of vertigo and occipital headache. She denied photophobia, neck stiffness, or altered vision or hearing. Sarah had been admitted to a general hospital ward one week earlier with a diagnosis of viral gastroenteritis complicated by diabetic ketoacidosis (DKA). At her presentation one week earlier, her initial pH was 7.28, bicarbonate was 13 mmol/L and ketones were 4.4 mmol/L. She had an uncomplicated recovery with standard care, including fluid rehydration and an insulin infusion. Sarahs medical history included type 1 diabetes mellitus, diagnosed at 8 years of age, with no previous DKA episodes or vascular complications. A recent glycated haemoglobin (HbA1c) measurement was 62 mmol/mol (7.8%). She self-administered insulin detemir twice daily and insulin aspart with meals. Sarah was not on any other regular medication, and there was no other significant personal or family medical history. She denied smoking cigarettes, use of alcohol or recreational drugs, including no cocaine or amphetamine use. On examination, Sarahs blood pressure was 130/70 mmHg, and she had a pulse rate of 70 beats per minute and regular. Neurological examination revealed subtle right beating nystagmus in all directions of gaze. Skew deviation and head thrust testings were unremarkable. Cerebellar testing revealed subtle dysdiadochokinesia and Sarah was unable to perform tandem gait. However, there was no dysmetria and ataxia, and Rombergs test was negative. There were no other significant findings on the remainder of the neurological or physical examinations. Her family doctor ordered cerebral magnetic resonance imaging (MRI), and a representative image is shown in Figure 1. Sarah was referred to the neu Continue reading >>

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

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

, Volume 34, Issue4 , pp 701705 | Cite as 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 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 patients headache and vision disturbance subsided within 1week. Subsequent MR scans demonstrated that the lesion in the spinal cord had decreased significantly in 10days, and the large patchy lesions in the brain disappeared completely in 2months. Her paraplegia improved gradually without obvious sequela 3months 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. Posterior reversible encephalopath 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 >>

Diabetic Ketoacidosis-associated Stroke In Children And Youth

Diabetic Ketoacidosis-associated Stroke In Children And Youth

Copyright © 2011 Jennifer Ruth Foster et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Diabetic ketoacidosis (DKA) is a state of severe insulin deficiency, either absolute or relative, resulting in hyperglycemia and ketonemia. Although possibly underappreciated, up to 10% of cases of intracerebral complications associated with an episode of DKA, and/or its treatment, in children and youth are due to hemorrhage or ischemic brain infarction. Systemic inflammation is present in DKA, with resultant vascular endothelial perturbation that may result in coagulopathy and increased hemorrhagic risk. Thrombotic risk during DKA is elevated by abnormalities in coagulation factors, platelet activation, blood volume and flow, and vascular reactivity. DKA-associated cerebral edema may also predispose to ischemic injury and hemorrhage, though cases of stroke without concomitant cerebral edema have been identified. We review the current literature regarding the pathogenesis of stroke during an episode of DKA in children and youth. 1. Introduction Type 1 diabetes mellitus (T1DM) is a common autoimmune condition that often presents in childhood and may be complicated by episodes of diabetic ketoacidosis (DKA). DKA is a state of severe insulin deficiency, either absolute or relative, resulting in hyperglycemia, ketonemia, acidemia, and systemic inflammation. Compared with adults, episodes of DKA in children carry a higher risk of morbidity and mortality. This is predominantly attributable to intracerebral complications [1–5], which occur in 3–10 pediatric patients per 1000 cases of DKA [6]. The most common Continue reading >>

Complications Of Diabetic Ketoacidosis Essay Examples

Complications Of Diabetic Ketoacidosis Essay Examples

Complications of Diabetic Ketoacidosis Essay examples Complications of Diabetic Ketoacidosis Essay examples Length: 1018 words (2.9 double-spaced pages) Diabetic Ketoacidosis (DKA) is a serious disease with complications that may have fatal results in some cases. DKA is defined as an insulin deficiency that occurs when glucose fails to enter insulin into muscles such as: liver and adipose tissue. When there is an accumulation of ketones, it leads to metabolic acidosis which causes nausea and vomiting, as a result fluid and electrolytes are loss (Gibbs). There are many complications of diabetic ketoacidosis, some of the most prevalent are: Cerebral Edema, Hypolglycemia, and Acute Pancreatitis. Cerebral Edema is a rare but fatal complication of diabetic ketoacidosis. To thoroughly describe the clinical signs of cerebral edema is characterized by deterioration in the level of consciouness, with lethargy, decrease in arousal and headache. The timing of the development of cerebral edema is variable, with most cases occurring 4 to 12 hours after starting treatment. Several case reports showed presence of cerebral edema before the itntiation of therapy. A method of clinical diagnosis based on bedside evaluation of a neurological state in DKA have been developed. (Pandey) Primarly, cerebral edema occurs in children. Studies show that the largest reported cases are 95% with patients younger than 20 years of age. One third of these cases occur in patients younger than 5 years of age. Generally, after the initiation of therapy, within 3-12 hours it occur in children who seem to be metabolically returning to normal. (Pandey) Insulin was discovered in 1922, prior to, the moratality due to DKA was virtually 100%. With the discovery of insulin, antiboiotics, intravenous potassium rep 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 >>

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 >>

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