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Neurological Complications Of Dka

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 >>

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 >>

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 >>

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 >>

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 >>

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 >>

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 >>

Understanding Diabetic Ketoacidosis - Wsava2005 - Vin

Understanding Diabetic Ketoacidosis - Wsava2005 - Vin

World Small Animal Veterinary Association World Congress Proceedings, 2005 Assistant Professor of Small Animal Medicine Diabetic ketoacidosis (DKA) is a complication of unregulated diabetes mellitus (DM) that produces marked hyperglycemia, profound metabolic acidosis, and hyperketonemia in severely affected patients. DKA is often discussed as a condition that is separate from uncomplicated diabetes mellitus but, in fact, diabetes mellitus is a spectrum of disorders that ranges from non-ketotic hyperosmolar diabetes mellitus on one end to diabetic ketoacidosis on the other end. It is important to remember that most complicated diabetics have another medical problem. Thus, management of DKA must be performed in the context of any concurrent disorder. DKA can be precipitated by factors such as inadequate insulin therapy, physiologic stress, drugs that affect insulin production or action, bacterial infection, and decreased fluid intake. Concurrent illness is common in animals with DKA. In one study, about half of cats with DKA had azotemia on admission; azotemia was moderate to severe in 20% of those cats. Other concurrent disorders found in that same group of cats included: inflammatory bowel disease, asthma, pancreatitis, hyperthyroidism, urinary tract infection, neoplasm, and corticosteroid therapy. In dogs, concurrent disorders include: urinary tract infection, neoplasia, pneumonia, pyometra, prostatitis, renal failure, hyperadrenocorticism, heart failure, and drug therapy (corticosteroids or progestins), among others. Signalment: There is no characteristic or specific signalment for animals with DM or those likely to develop complicated DM. Gender. Middle-aged and older female dogs have an increased risk for the development of diabetes mellitus when compared to males. Continue reading >>

Fluid Therapy And Cerebral Injury In Pediatric Diabetic Ketoacidosis

Fluid Therapy And Cerebral Injury In Pediatric Diabetic Ketoacidosis

DESCRIPTION (provided by applicant): Cerebral edema is the most frequent and most feared serious complication of diabetic ketoacidosis (DKA) in children. Furthermore, it is the most important cause of death in this vulnerable pediatric population with a common chronic illness. Overt, symptomatic cerebral edema occurs in approximately 1% of pediatric DKA episodes, but recent data suggest that mild, or even apparently asymptomatic, cerebral edema occurs more frequently, likely in most children with DKA. Furthermore, recent pilot data suggest that even apparently uncomplicated DKA may result in subtle cerebral injury and long-term neurocognitive alterations. The relationship of fluid therapy for DKA and risk of cerebral injury and cerebral edema is not well understood and has been debated for decades. Some investigators have suggested that cerebral edema might be caused by rapid administration of intravenous fluids resulting in a rapid decline in serum osmolality and osmotically-mediated cell swelling. Recent data from our group, however, suggest that DKA may be associated with substantial reductions in cerebral blood flow and that DKA-related cerebral edema may be more similar to cerebral edema resulting from stroke or other hypoxic/ischemic cerebral injuries than to osmotically-mediated edema. Slower infusion of intravenous fluids has been advocated by some investigators, with the goal of avoiding rapid osmotic change. Conversely, more rapid infusion of fluids may be beneficial if cerebral edema is related to cerebral hypo-perfusion, resulting in more rapid restoration of normal cerebral blood flow. Because of the lack of prospective, appropriately controlled studies investigating the relationship between fluid treatment protocols and risk of cerebral edema, substantial 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 >>

Hyperglycemia

Hyperglycemia

University of California San Francisco, Fresno, California Edited By: David A. Wald Temple University School of Medicine Philadelphia, Pennsylvania Objectives The objectives of this module will be to: Review the classic presentation of a patient with hyperglycemia, including DKA and HHS. Review the diagnostic work up of the hyperglycemic patient. Review the principles of managing a patient with hyperglycemia. Hyperglycemia complicating diabetes ranges from the asymptomatic and benign in patients with mild to moderate uncomplicated hyperglycemia to the life-threatening (i.e. diabetic ketoacidosis (DKA) or hyperosmolar hyperglycemic state (HHS). DKA and HHS represent a spectrum of complications from diabetes and differ mainly in the level of hyperglycemia, extent of dehydration and presence and degree of ketoacidosis. Each condition revolves around insulin deficiency, either absolute or relative. DKA and HHS are the most serious, acute metabolic complications of diabetes. Generally DKA occurs in younger patients (<65 y/o) with Type 1 diabetes and usually evolves rapidly over 24 hours. HHS usually occurs in older patients (>65 y/o) with poorly controlled Type 2 diabetes and evolves over several days. Both disease entities originate from a reduction in insulin and an increase in counter-regulatory stress hormones. In the emergency department hyperglycemia is most often seen as a complication of diabetes (both types 1 and 2). Hyperglycemia is defined as: Fasting Blood Glucose (for 8 hrs) > 90 – 130 mg/dL Postprandial Blood Glucose > 180 mg/dL Initial Actions and Primary Survey In these patients, a thorough history and physical examination should be performed with a focus on trying to identify a precipitating cause of the hyperglycemia. In patients with an incidental findin 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 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 >>

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 >>

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 >>

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