DOCSLIB.ORG

Hyperosmolar Hyperglycemic State (HHS) Is the Most Serious Acute Hypergly- Cemic Emergency in Patients with Type 2 Diabetes

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Hyperosmolar Hyperglycemic State (HHS) Is the Most Serious Acute Hypergly- Cemic Emergency in Patients with Type 2 Diabetes 3124 Diabetes Care Volume 37, November 2014 Francisco J. Pasquel and Hyperosmolar Hyperglycemic Guillermo E. Umpierrez State: A Historic Review of the Clinical Presentation, Diagnosis, and Treatment Diabetes Care 2014;37:3124–3131 | DOI: 10.2337/dc14-0984 The hyperosmolar hyperglycemic state (HHS) is the most serious acute hypergly- cemic emergency in patients with type 2 diabetes. von Frerichs and Dreschfeld described the first cases of HHS in the 1880s in patients with an “unusual diabetic coma” characterized by severe hyperglycemia and glycosuria in the absence of Kussmaul breathing, with a fruity breath odor or positive acetone test in the urine. Current diagnostic HHS criteria include a plasma glucose level >600 mg/dL and increased effective plasma osmolality >320 mOsm/kg in the absence of ketoacidosis. The incidence of HHS is estimated to be <1% of hospital admissions of patients with diabetes. The reported mortality is between 10 and 20%, which is about 10 times higher than the mortality rate in patients with diabetic ketoacidosis (DKA). Despite the severity of this condition, no prospective, randomized studies have determined best REVIEW treatment strategies in patients with HHS, and its management has largely been extrapolated from studies of patients with DKA. There are many unresolved questions that need to be addressed in prospective clinical trials regarding the pathogenesis and treatment of pediatric and adult patients with HHS. The hyperosmolar hyperglycemic state (HHS) is a syndrome characterized by severe hyperglycemia, hyperosmolality, and dehydration in the absence of ketoacidosis. The exact incidence of HHS is not known, but it is estimated to account for ,1% of hospital admissions in patients with diabetes (1). Most cases of HHS are seen in elderly patients with type 2 diabetes; however, it has also been reported in children and young adults (2). The overall mortality rate is estimated to be as high as 20%, which is about 10 times higher than the mortality in patients with diabetic keto- acidosis (DKA) (3–5). The prognosis is determined by the severity of dehydration, presence of comorbidities, and advanced age (4,6,7). Treatment of HHS is directed at replacing volume deficit and correcting hyperosmolality, hyperglycemia, and electrolyte disturbances, as well as management of the underlying illness that pre- cipitated the metabolic decompensation. Low-dose insulin infusion protocols de- signed for treating DKA appear to be effective; however, no prospective randomized Division of Endocrinology, Department of Med- studies have determined best treatment strategies for the management of patients icine, Emory University School of Medicine, Atlanta, GA with HHS. Herein, we present an extensive review of the literature on diabetic coma Corresponding author: Guillermo E. Umpierrez, and HHS to provide a historical perspective on the clinical presentation, diagnosis, [email protected]. and management of this serious complication of diabetes. Received 18 April 2014 and accepted 6 July 2014. © 2014 by the American Diabetes Association. History of Diabetic Coma and HHS Readers may use this article as long as the work In 1828, in the textbook Versuch einer Pathologie und Therapie des Diabetes Mellitus, is properly cited, the use is educational and not August W. von Stosch gave the first detailed clinical description of diabetic coma in an for profit, and the work is not altered. care.diabetesjournals.org Pasquel and Umpierrez 3125 adult patient with severe polydipsia, of patients with diabetic coma, noting (glycogenolysis) and by inadequate use polyuria, and a large amount of glucose that not all cases presented with the char- of glucose by peripheral tissues, pri- in the urine followed by progressive acteristic Kussmaul respiration or positive marily muscle. From the quantitative decline in mental status and death (8). urine acetone or diacetic acid (22–26). standpoint, increased hepatic glucose Several case reports followed this publi- These reports created confusion and production represents the major patho- cation, describing patients with newly di- weretakenwithskepticism,asthe genic disturbance responsible for hyper- agnosed or previously known diabetes source of ketone bodies and the role of glycemia in DKA (34). As the glucose presenting with drowsiness or coma, acetoacetic acid in the pathogenesis of concentration and osmolality of extra- most of them with a peculiar breath diabetic coma were not known at the cellular fluid increase, an osmolar gra- odor resembling acetone (9). In 1857, time. Many physicians were against ac- dient is created that draws water out of Petters (10) detected a substance in cepting that adult patients could prog- the cells. Glomerular filtration is ini- the urine of a fatal case of diabetic ress to diabetic coma in the absence of tially increased, which leads to glucosu- coma that resembled acetone in its reac- ketonuria. For example, in the 1930s, ria and osmotic diuresis. The initial tion with sulfuric acid and caustic alkalis Elliot P. Joslin (17) and others (27) glucosuria prevents the development and was later recognized as acetoacetic stated that the presence of acetone or of severe hyperglycemia as long as the acid, also called diacetic acid (11,12). Ac- diacetic acid in the urine was requisite glomerular filtration rate is normal. etone was then recognized as an impor- for the diagnosis of diabetic coma. It However, with continued osmotic di- tant outcome marker warning physicians was later hypothesized that diabetic uresis, hypovolemia eventually occurs, about serious diseases, including diabe- coma with negative urinary ketones which leads to a progressive decline in tes (13,14). In 1874, Kussmaul reported was the result of impaired renal excre- glomerular filtration rate and worsen- several fatal cases of diabetic coma pre- tion, liver dysfunction, and the presence ing hyperglycemia. ceded and accompanied by severe dys- of other acids, such as b-hydroxybutyric Higher hepatic and circulating insulin pnea (15,16). Kussmaul breathing, as this acid, rather than diacetic acid or ace- concentration as well as lower glucagon condition came to be known, quickly be- tone (25,26,28). are present in HHS compared with pa- came one of the hallmarks in the diagno- HHS syndrome received little atten- tients with ketoacidosis (32,33). The sis of diabetic coma, along with the tion and remained poorly understood higher circulating ratio of insulin/glu- presence of positive urine ketones until the reports by de Graeff and Lips cagoninpatientswithHHSprevents (14,17). In the 1880s, Stadelmann (18), (29) and Sament and Schwartz (30) in ketogenesis and the development of Kulz¨ (19), and Minkowski (20) reported 1957. They reported that severe hyper- ketoacidosis. This concept is supported that the urine of most patients with di- glycemia resulted in osmotic diuresis, by clinical studies both in animals and in abetic coma contained, in addition to polyuria, and progressive water deficit. humans, which have shown that the acetoacetic or diacetic acid, the pres- They discussed the relevance of measur- half-maximal concentration of insulin ence of considerable quantities of ing sodium and chloride levels to esti- for antilipolysis is lower than for glucose b-oxybutyric acid (Table 1). The discov- mate extracellular hypertonicity and use by peripheral tissues (35). Finally, a ery of high concentrations of acetoace- cellular dehydration, and they proposed direct role of hyperosmolarity by inhib- tic acid and b-hydroxybutyric acid led that patients with severe hyperglycemia iting lipolysis and free fatty acid release clinicians and researchers in the late and diabetic coma should be treated from adipose tissue has been shown in 1890s to conclude that diabetic coma with large quantities of water (29). experimental animals (36). was a “self-intoxication” due to an ex- Sament and Schwartz (30) suggested Severe hyperglycemia is associated cess of acids in the body (12,13). that some comatose patients with se- with a severe inflammatory state char- The first reports of HHS are attributed vere hyperglycemia and negative or acterized by an elevation of proinflam- to von Frerichs (21) and Dreschfeld (14). trace ketonuria could be treated suc- matory cytokines (tumor necrosis In the 1880s, they reported patients pre- cessfully with the administration of flu- factor-a, interleukin (IL)b,IL6,andIL8) senting with an unusual type of diabetic ids and lower amounts of insulin and reactive oxygen species, with insulin coma characterized by severe hyper- compared with regular acidotic patients secretion and action. Hyperglycemia glycemia and glycosuria but without with diabetic coma. causes an increase in oxidative stress Kussmaul breathing, fruity breath markers such as membrane lipid perox- odor, or a positive urine acetone test. Pathophysiology idation (37). The degree of lipid perox- Dreschfeld (14) described a case series HHS is characterized by extreme eleva- idation is directly proportional to the of patients with “diabetic collapse” pre- tions in serum glucose concentrations glucose concentrations in diabetic pa- senting after age 40 years, who were and hyperosmolality without significant tients. This is thought to occur via several well nourished at the time of the attack, ketosis (Fig. 1). These metabolic de- well-studied mechanisms, including in- andwithfattyinfiltration of the liver rangements result from synergistic fac- creased polyol pathway flux, increased and the heart. Shortly after these re- tors including
Load more

Recommended publications
  • Living with Diabetes in the Family Iabetes Affects All Members of the Family, Fat Diet and the Twice-Daily Insulin Injections
    SA JOURNAL OF DIABETES & VASCULAR DISEASE REVIEW References 10. Hattersley A, Bruining J, Shield J, Njolstad P, Donaghue KC. The diagnosis of and management of monogenic diabetes in children and adolescents. Pediat Diabetes 1. Neel J. Diabetes mellitus: a geneticist’s nightmare. In: Creutzfeldt W, Kobberling 2009; 10(suppl 12): 33–42. J, Neel JV, eds. The Genetics of Diabetes Mellitus. Berlin: Springer-Verlag, 1976: 11. Slingerland AS. Monogenic diabetes in children and adults: Challenges for 1–11. researcher, clinician and patient. Rev Endocr Metab Disord 2006; 7: 171–185. 2. Keen H. The genetics of diabetes: from nightmare to headache. Br Med J 1987; 12. Barrett TG. Differential diagnosis of type 1 diabetes: which genetic syndromes 294: 917–919. need to be considered? Pediat Diabetes 2007; 8(suppl 6): 15–23. 3. Rotter JI. The modes of inheritance of insulin-dependent diabetes mellitus or the 13. Clinical genetics and genetic counseling. In: Jorde LB, et al., eds. Medical genetics of IDDM, no longer a nightmare but still a headache. Am J Hum Genet Genetics, 2nd edn. St Louis: Mosby, 1999: 292. 1981; 33: 835–851. 14. The National Society of Genetic Counselor’s Task Force: Resta R, et al. A new 4. Craig ME, Hattersley A, Donaghue KC. Definition, epidemiology and classification definition of genetic counselling: National Society of Genetic Counselor’s Task of diabetes in children and adolescents. Pediat Diabetes 2009; 10(suppl 12): 3–12 Force report. J Genet Couns 2006; 15(2): 77–83. 5. Jahromi MM, Eisenbarth GS. Cellular and molecular pathogenesis of type 1A 15.
    [Show full text]
  • Hyperosmolar Hyperglycemic State (HHS) Erica Kretchman DO October 19 2018 Speaker for Valeritas, Medtronic, Astrazenica, Boehringer Ingelheim
    Hyperosmolar Hyperglycemic State (HHS) Erica Kretchman DO October 19 2018 Speaker for Valeritas, Medtronic, AstraZenica, Boehringer Ingelheim. These do not influence this presentation Objective • Review and understand diagnosis of Hyperosmolar Hyperglycemic State (HHS) and differentiating from Diabetic Ketoacidosis • Treatment of HHS • Complications of HHS Question 1 • Which of the following is NOT a typical finding in HHS? 1. Blood PH <7.30 2. Dehydration 3. Mental Status Changes 4. Osmotic diuresis Question 2 • Hypertonic fluids, such as 3% saline, are the first line of treatment to correct dehydration in HHS 1. True 2. False Question 3 • Which of the following statements is INCORRECT about Hyperosmolar Hyperglycemic State? 1. HHS occurs mainly in type 2 diabetics. 2. This condition presents without ketones in the urine. 3. Metabolic alkalosis presents in severe HHS. 4. Intravenous Regular insulin is used to treat hyperglycemia. Hyperosmolar Hyperglycemic State (HHS) • HHS and DKA are of two of the most serious complications form Diabetes • Hospital admissions for HHS are lower than the rate for DKA and accounts for less than 1 percent of all primary diabetic admissions • Mortality rate for patients with HHS is between 10 and 20 percent, which is approximately 10 times higher than that for DKA • Declined between 1980 and 2009 • Typically from precipitating illness - rare from HHS itself PRECIPITATING FACTORS • The most common events are infection (often pneumonia or urinary tract infection) and discontinuation of or inadequate insulin
    [Show full text]
  • Diabetic Coma
    University of Nebraska Medical Center DigitalCommons@UNMC MD Theses Special Collections 5-1-1932 Diabetic coma J. Milton Margolin University of Nebraska Medical Center This manuscript is historical in nature and may not reflect current medical research and practice. Search PubMed for current research. Follow this and additional works at: https://digitalcommons.unmc.edu/mdtheses Part of the Medical Education Commons Recommended Citation Margolin, J. Milton, "Diabetic coma" (1932). MD Theses. 218. https://digitalcommons.unmc.edu/mdtheses/218 This Thesis is brought to you for free and open access by the Special Collections at DigitalCommons@UNMC. It has been accepted for inclusion in MD Theses by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. DIAB3TIC COMA J. MIJ/rON 1l1LARGOLIN THE illnVERSITY OF NlsBRASKA COLLEGE OF ~~DICINE -- OMAHA, NEBHASKA 1932 - DIAB3TIG COl£.<\ Diabetic coma is a true medical emergency. It is just as much an emergency as an acute appendicitis or an incarcerated hernia, and as in the latter condition, with every hour that passes without treatment the chances for life decrease. It is early intervention that counts. Therefore, a physician should never let an engagement or any personal desires keep him from the bedside of a patient whom he thinks may be in coma. HISTORY Diabetic coma has been known as a clinical entity since l8bO when a German, Von Dusch and a Scotchman, March firs t de scri bed it. 'l'wen ty years later, Kus smaul publ i shed his classical description of diabetic coma. It is the IlKussmaul breathing, II as described by the author which is the outstanding and characteristic feature of diabetic coma.
    [Show full text]
  • Type 2 Diabetes Mellitus in Children and Adolescents
    CLINICAL Type 2 diabetes mellitus in children and adolescents Kung-Ting Kao, Matthew A Sabin Background ype 2 diabetes mellitus (T2DM), and obesity. Furthermore, treatment previously known as non-insulin options are limited by the lack of licenced The incidence of type 2 diabetes mellitus T dependent diabetes or adult- treatment modalities in the paediatric (T2DM) in children and adolescents is onset diabetes, is a disorder arising from population, and adherence, psychosocial increasing, mirroring the epidemic of insulin resistance and relative (rather than health and wellbeing are often poor.7 paediatric obesity. Early-onset T2DM is absolute) insulin deficiency in the absence Early-onset T2DM is associated with associated with poor long-term outcomes. of autoimmune beta-cell destruction.1 It is significant long-term morbidity and Objectives a polygenic disorder involving interactions mortality. Adolescents diagnosed with between genetic and environmental T2DM are predicted to lose 15 years from In this article, we describe the growing risk factors that result in the underlying their remaining life expectancy when problem of early-onset T2DM in Australia, pathophysiology of hepatic and muscle compared with their peers who do not explore the difference between early- insulin resistance, and subsequent beta-cell have T2DM.8 Complications of diabetes onset and adult-onset T2DM, and review failure.2 Most patients with this disorder are also common and present even earlier the management of T2DM in children and are obese, and T2DM often remains than in adolescents with type 1 diabetes adolescents. undiagnosed for many years while the mellitus (T1DM).9,10 A long-term study patient progresses symptom-free through in Japan found that over a period of 20 Discussion the earlier stages of hyperglycaemia known years, 24% of the 1063 participants were 11 T2DM is difficult to differentiate from the as ‘pre-diabetes’.
    [Show full text]
  • Copyrighted Material
    34_568205 bindex.qxd 5/28/04 11:03 AM Page 365 Index African Americans • A • diabetic kidney disease in, 69 A (alpha) cells, 30, 357 gestational diabetes in, 109 A1c at Home (FlexSite), 131 peripheral vascular disease in, 89 A1c Now (Metrika, Inc.), 131 AGEs (advanced glycated end products), Abbott Laboratories 68, 75, 357 blood glucose meters, 122–123 AIDS medications, 279–280 Web site, 351 albumin, 68–72, 86, 116, 132, 362 acanthosis nigricans, 93, 237 alcohol, 56, 155–156, 240 acarbose, 192–193, 357 aldosterone, 47 accelerated starvation, 106 algorithm, 357 AccuBase A1c Glycohemoglobin alopecia, 92 (Diabetes Technologies), 131 alpha cells, 30, 357 Accu-Chek blood glucose meters alpha lipoic acid, 82–83 (Roche Diagnostics), 124 alpha-blockers, 213 ACE inhibitor, 72, 132, 213, 357 alpha-fetoprotein, 108 acesulfame, 157 alpha-glucosidase inhibitors, 192–193 acetaminophen, 213 alprostadil, 99 acetohexamide, 189 Alzheimer’s disease, 246 acetone, 59, 60, 357 Amaryl, 190, 357 acidosis. See ketoacidosis American Diabetes Association (ADA) acromegaly, 47 diet recommendations, 146 Activa Brand Products (Web site), 352 exchange lists, 335 Activa Corporation (Advanta Jet), 207 membership in, 287 Actos, 195, 357 Web site, 275, 348, 356 ADA. See American Diabetes Association American Discovery Trail, 180 adiponectin, 262–263 American Foundation for the Blind adiposity, central, 85 (AFB), 78–79, 354 adolescents, diabetes in, 238–239 Americans with Disabilities Act, adrenergic symptoms,COPYRIGHTED of hypoglycemia, 255–256 MATERIAL 53, 54 amino acids,
    [Show full text]
  • Postmortem Diagnosis of Diabetes Mellitus and Its Complications 183
    FORENSIC SCIENCE 181 Croat Med J. 2015;56:181-93 doi: 10.3325/cmj.2015.56.181 Postmortem diagnosis of Cristian Palmiere CURML, Centre Universitaire diabetes mellitus and its Romand De Medecine Legale, Lausanne University Hospital, complications Lausanne, Switzerland Diabetes mellitus has become a major cause of death worldwide and diabetic ketoacidosis is the most common cause of death in children and adolescents with type 1 di- abetes. Acute complications of diabetes mellitus as caus- es of death may be difficult to diagnose due to missing characteristic macroscopic and microscopic findings. Bio- chemical analyses, including vitreous glucose, blood (or alternative specimen) beta-hydroxybutyrate, and blood glycated hemoglobin determination, may complement postmortem investigations and provide useful informa- tion for determining the cause of death even in corpses with advanced decompositional changes. In this article, we performed a review of the literature pertaining to the diagnostic performance of classical and novel biochemical parameters that may be used in the forensic casework to identify disorders in glucose metabolism. We also present a review focusing on the usefulness of traditional and alter- native specimens that can be sampled and subsequently analyzed to diagnose acute complications of diabetes mel- litus as causes of death. Received: March 2, 2015 Accepted: May 11, 2015 Correspondence to: Cristian Palmiere CURML, Centre Universitaire Romand De Medecine Legale Chemin de la Vulliette 4 1000 Lausanne 25, Switzerland [email protected] www.cmj.hr 182 FORENSIC SCIENCE Croat Med J. 2015;56:181-93 Diabetes mellitus has become a major cause of death of all deaths from DKA occurs in individuals with no known worldwide in people younger than 60 years.
    [Show full text]
  • Treatment Guide for Diabetes 2016-2017 Edited by Japan Diabetes Society
    Treatment Guide for Diabetes 2016-2017 Edited by Japan Diabetes Society BUNKODO 1 Diabetes mellitus: The disease itself 1 The disease itself The mellitus: Diabetes A What is diabetes mellitus? ▶ Diabetes mellitus (DM) is a group of diseases characterized by chronic ✳ 2 hyperglycemia due to deficiency of insulin action . Diagnosis In type 1 diabetes, deficiency of insulin action is mainly caused by the destruction and loss of β cells in the islets of Langerhans in the pancreas, which produce and secrete insulin (See p.5 : Table 2, Etiological classification of diabetes mellitus and glucose metabolism disorders). Type 2 diabetes arises as a result of genetic factors including those causing reduced 3 insulin secretion and insulin resistance, and a number of environmental factors such as Treatment overeating (especially a high fat diet), lack of exercise, obesity and stress, to which may be added the factor of advancing age. ✳ Insulin is produced and secreted by the β cells of the pancreatic islets of Langerhans. After passing through the portal vein, insulin reaches the liver, and is carried via the hepatic vein to all the tissues 4 of the body. It binds to the insulin receptors in the cell membrane of the liver, muscles, adipose tissue Diet therapy and other tissues that are insulin-sensitive, and promotes the uptake of glucose into the cells, energy usage and storage, protein synthesis, and cell proliferation. ▶ “Insulin action” is used to refer to the metabolic regulatory function exhibited by 5 insulin in the tissues of the body. If a balance between the supply of insulin and the Exercise therapy Exercise insulin requirement of the body is maintained, the metabolism as a whole remains normal, including the plasma glucose level.
    [Show full text]
  • ISPAD Clinical Practice Consensus Guidelines 2018: Diabetic Ketoacidosis and the Hyperglycem
    Received: 11 April 2018 Accepted: 31 May 2018 DOI: 10.1111/pedi.12701 ISPAD CLINICAL PRACTICE CONSENSUS GUIDELINES ISPAD Clinical Practice Consensus Guidelines 2018: Diabetic ketoacidosis and the hyperglycemic hyperosmolar state Joseph I. Wolfsdorf1 | Nicole Glaser2 | Michael Agus1,3 | Maria Fritsch4 | Ragnar Hanas5 | Arleta Rewers6 | Mark A. Sperling7 | Ethel Codner8 1Division of Endocrinology, Boston Children's Hospital, Boston, Massachusetts 2Department of Pediatrics, Section of Endocrinology, University of California, Davis School of Medicine, Sacramento, California 3Division of Critical Care Medicine, Boston Children's Hospital, Boston, Massachusetts 4Department of Pediatric and Adolescent Medicine, Medical University of Vienna, Vienna, Austria 5Department of Pediatrics, NU Hospital Group, Uddevalla and Sahlgrenska Academy, Gothenburg University, Uddevalla, Sweden 6Department of Pediatrics, School of Medicine, University of Colorado, Aurora, Colorado 7Division of Endocrinology, Diabetes and Metabolism, Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, New York 8Institute of Maternal and Child Research, School of Medicine, University of Chile, Santiago, Chile Correspondence Joseph I. Wolfsdorf, Division of Endocrinology, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA. Email: [email protected] 1 | SUMMARY OF WHAT IS Risk factors for DKA in newly diagnosed patients include younger NEW/DIFFERENT age, delayed diagnosis, lower socioeconomic status, and residence in a country with a low prevalence of type 1 diabetes mellitus (T1DM). Recommendations concerning fluid management have been modified Risk factors for DKA in patients with known diabetes include to reflect recent findings from a randomized controlled clinical trial omission of insulin for various reasons, limited access to medical ser- showing no difference in cerebral injury in patients rehydrated at dif- vices, and unrecognized interruption of insulin delivery in patients ferent rates with either 0.45% or 0.9% saline.
    [Show full text]
  • Perioperative Glycaemic Control for Preterm Infant with Transient
    Rattana‑arpa et al. BMC Res Notes (2016) 9:140 DOI 10.1186/s13104-016-1957-y BMC Research Notes CASE REPORT Open Access Perioperative glycaemic control for preterm infant with transient neonatal hyperglycaemia and gastroschisis Sirirat Rattana‑arpa, Saowaphak Lapmahapaisan and Arunotai Siriussawakul* Abstract Background: Neonatal hyperglycaemia is a rare metabolic disorder. There are no reports of an association between neonatal hyperglycaemia and gastroschisis. Case presentation: This report presents preoperative and intraoperative management of blood sugar in a low birth weight Thai preterm neonate with gastroschisis and a diagnosis of neonatal hyperglycaemia. The patient underwent an emergency, multi-staged, surgical repair under general anaesthesia. Conclusion: Anaesthesiologists should be aware of possible perioperative dysglycaemic conditions in these patients. Proper timing of surgery and appropriate preanaesthetic preparation are necessary to reduce the morbidity and mor‑ tality related to hyperglycaemia and gastroschisis. Consent: The patient’s guardian has given consent for the case report to be published. Keywords: Abdominal wall defect, High blood sugar, Prematurity Background fluid loss and infection [3]. Nevertheless, the timing of Dysglycaemia frequently occurs in very low birth weight the surgical correction of the gastroschisis in this par- preterm infants. Deficiency of glycogen stores at birth ticular case was somewhat controversial. This report and defective counter-regulatory hormone responses are demonstrates the challenge of decision-making by a mul- common in prematurity, making hypoglycaemia a more tidisciplinary team that analysed the risks and benefits of frequent occurrence than hyperglycaemia [1]. The inci- promptly going to surgery versus waiting to optimize the dence of neonatal hyperglycaemia has not been clearly patient’s condition.
    [Show full text]
  • Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar Syndrome
    In Brief Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic syndrome (HHS) are two acute complications of diabetes that can result in increased morbidity and mortality if not efficiently and effectively treated. Mortality rates are 2–5% for DKA and 15% for HHS, and mortality is usually a conse- quence of the underlying precipitating cause(s) rather than a result of the metabolic changes of hyperglycemia. Effective standardized treatment proto- cols, as well as prompt identification and treatment of the precipitating cause, are important factors affecting outcome. Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar Syndrome The two most common life-threaten- having type 2 diabetes because 29% ing complications of diabetes mellitus of patients were obese, had measur- include diabetic ketoacidosis (DKA) able insulin secretion, and had a low Guillermo E. Umpierrez, MD, FACP; and hyperglycemic hyperosmolar syn- prevalence of autoimmune markers of Mary Beth Murphy, RN, MS, CDE, drome (HHS). Although there are ␤-cell destruction.4 MBA; and Abbas E. Kitabchi, PhD, important differences in their patho- Treatment of patients with DKA MD, FACP, FACE genesis, the basic underlying mecha- and HHS utilizes significant health nism for both disorders is a reduction care resources. Recently, it was esti- in the net effective concentration of mated that treatment of DKA episodes circulating insulin coupled with a accounts for more than one of every concomitant elevation of counterreg- four health care dollars spent on direct ulatory hormones (glucagon, cate- medical care for adults with type 1 cholamines, cortisol, and growth hor- diabetes, and for one of every two dol- mone). lars for those patients experiencing These hyperglycemic emergencies multiple episodes of DKA.5 continue to be important causes of Despite major advances in their morbidity and mortality among management, recent series have patients with diabetes.
    [Show full text]
  • Perioperative Management of Diabetes Mellitus: a Review
    Perioperative management of Diabetes Mellitus: A review. Dissertação de Mestrado Integrado em Medicina Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto Junho de 2019 Autora: Mariana Raquel Moreira Azevedo Estudante do 6º ano do Mestrado Integrado em Medicina, Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto; Número de aluna: 201303092; Endereço eletrónico: [email protected]. Orientador: Prof. Doutor Humberto José da Silva Machado Assistente Hospitalar Graduado Sénior de Anestesiologia do CHUP; Diretor do Serviço de Anestesiologia do CHUP; Adjunto da Direção Clínica do CHUP; Professor Associado Convidado do ICBAS; Endereço eletrónico: [email protected]. ABSTRACT Introduction: Diabetes Mellitus is frequently observed in surgical patients and relates to an increase in perioperative morbidity and mortality. Disease, anesthesia and surgery result in dysglycemia (hypo and/or hyperglycemia), which is one of the worse prognostic factors. The objective of this work is to review the specific needs of the diabetic surgical patient in the perioperative period, gathering the latest information regarding its optimization. Materials and Methods: This dissertation was elaborated from scientific articles obtained through PubMed, Google Scholar and Google, published between 2008 and 2018 and written in English or Portuguese. In the end, eighty-nine articles were used. Results: Some measures have been proposed in order to reduce perioperative complications in the diabetic. Preoperative period: an
    [Show full text]
  • CDHO Factsheet Diabetes Mellitus
    Disease/Medical Condition DIABETES MELLITUS Date of Publication: May 19, 2015 (also known as “diabetes” or “DM”) Is the initiation of non-invasive dental hygiene procedures* contra-indicated? No Is medical consult advised? ........................................ No, unless previously diagnosed diabetes is thought to be poorly controlled and/or there are significant untreated complications (e.g., infection or renal/cardiovascular disease). Urgent referral (i.e., to the emergency room) should occur if diabetic ketoacidosis1 or significant hypoglycemia is suspected. If diabetes is newly suspected based on the patient/client’s presenting signs/symptoms or history (including history of fasting 2 blood glucose ≥ 7.0 mmol/L [126 mg/dL], 2-hour postprandial blood glucose ≥11.1 mmol/L [200 mg/dL], or hemoglobin A1C ≥ 6.5%), the patient/client should be referred to a physician/nurse practitioner for definitive diagnosis and medical management. Is the initiation of invasive dental hygiene procedures contra-indicated?** Possibly, under certain circumstances of poor diabetes control. See below under “medical clearance”. Is medical consult advised? ........................................ See above. Consultation may also be required for consideration of antibiotic prophylaxis (see below) and for clearance after postponement of treatment. Is medical clearance required? ................................... No, assuming diabetes is well controlled. — Yes, if blood glucose is < 3.9 mmol/L [70 mg/dL] or is > 11.1 mmol/L [200 mg/dL]). Such clearance is particularly important in the presence of various comorbidities3. Blood glucose < 3.9 mmol/L [70 mg/dL] should typically involve prompt administration of carbohydrates. — Yes, if there are any concerns about the patient/client’s suitability for invasive procedures regardless of blood glucose level (including oral infection or infection elsewhere in the body).
    [Show full text]