Abstract: Diabeticketoacidosis (DKA) is a rare yet potentially fatal hyperglycemic crisis that can occur in patients with both type 1 and 2 diabetes mellitus. Due to its increasing incidence and economic impact related to the treatment and associated morbidity, effective management and prevention is key. Elements of management include making the appropriate diagnosis using current laboratory tools and clinical criteria and coordinating fluid resuscitation, insulin therapy, and electrolyte replacement through feedback obtained from timely patient monitoring and knowledge of resolution criteria. In addition, awareness of special populations such as patients with renal disease presenting with DKA is important. During the DKA therapy, complications may arise and appropriate strategies to prevent these complications are required. DKA prevention strategies including patient and provider education are important. This review aims to provide a brief overview of DKA from its pathophysiology to clinical presentation with in depth focus on up-to-date therapeutic management.
In the 7 episodes of non-diabeticketoacidosis reported here, insulin administration could successfully correct acidosis. One patient (case 1, Table 2) who was not treated with insulin infusion took the longest time in re- covering from acidosis, despite the patient receiving the highest amount of bicarbonate infusion. The most severe case of acidosis (case 5, 2nd episode, Tables 1 and 2, serum bicarbonate <3 mmol/L) had received moderate amounts of bicarbonate infusion but prolonged insulin administration. He had relatively short recovery time from acidosis. This suggests the efficacy of insulin treatment in non-diabeticketoacidosis. However, use of insulin can lead to hypoglycemia. In children with non- diabeticketoacidosis, their blood glucose levels are usually low or normal (Table 1). Insulin should be administered together with glucose in a ratio of 4–6 g glucose for every 1 unit of insulin, with frequent blood glucose monitoring, in order to maintain a high-normal glucose value, since patients with non-diabetic ketoaci- dosis had high risk for hypoglycemia .
This is to certify that this dissertation work titled “ A STUDY OF PREDICTORS AND FACTORS AFFECTING OUTCOME IN DIABETICKETOACIDOSIS ” of the candidate DR. SHAARON.S with registration Number 201511209 for the award of M.D in the branch of General Medicine. I personally verified the urkund.com website for the purpose of plagiarism Check. I found that the uploaded thesis file contains from introduction to conclusion pages and result shows 4% of plagiarism in the dissertation.
Hypokalaemiaatpresentationofdiabeticketoacidosisisuncommonasinsulindeficiencyandmetabolicacidosis shifts potassium extracellularly. However, hypokalaemia is a recognised complication of the management of diabeticketoacidosis as insulin administration and correction of metabolic acidosis shifts potassium intracellularly. We describe the case of a 9-year-old girl with newly diagnosed type 1 diabetes mellitus presenting in diabeticketoacidosis, with severe hypokalaemia at presentation due to severe and prolonged emesis. After commencing management for her diabeticketoacidosis, her serum sodium and osmolality increased rapidly. However, despite maximal potassium concentrations running through peripheral access, and multiple intravenous potassium ‘corrections’, her hypokalaemia persisted. Seventy two hours after presentation, she became drowsy and confused, with imaging demonstrating central pontine myelinolysis – a rare entity seldom seen in diabeticketoacidosis management in children despite rapid shifts in serum sodium and osmolality. We review the literature associating central pontine myelinolysis with hypokalaemia and hypothesise as to how the hypokalaemia may have contributed to the development of central pontine myelinolysis. We also recommend an approach to the management of a child in diabeticketoacidosis with hypokalaemia at presentation.
We describe two cases of SGLT2i-induced euglycaemic diabeticketoacidosis, which took longer than we anticipated to treat despite initiation of our DKA protocol. Both patients had an unequivocal diagnosis of type 2 diabetes, had poor glycaemic control with a history of metformin intolerance and presented with relatively vague symptoms post-operatively. Neither patient had stopped their SGLT2i pre-operatively, but ought to have by current treatment guidelines.
Diabeticketoacidosis (DKA)is a life-threatening acute metabolic complication of diabetes mellitus caused by complete lack of insulin in type 1diabetes mellitus or inadequate insulin levels associated with stress or severe illness either in type 1 or type 2 diabetes mellitus. The onset of diabeticketoacidosis varies considerably (between 15% and 67%) from one country to another. DKA is responsible for more than 500,000 hospital days per year at an estimated annual direct medical expense and indirect cost of 2.4 billion USD. Severe depletion of water and electrolytes from intra- and extracellular fluid compartments characterizes DKA. The key diagnostic feature in DKA is the elevation in circulating total blood ketone concentration. Treatment includes fluid replacement, insulin therapy, potassium replacement, bicarbonate therapy and phosphate therapy.As diabetes mellitus is increasing rapidly; more awareness is needed to care diabetic’s complications such as DKA. Of diabetic complications, sudden deaths are mostly caused by DKA. In the past few decades standardized care and studies decreased the mortality of DKA. The prevention of DKA will require further study as well as patient education.The aim of this review is to find the cause, symptoms and treatment ofDKA, also to make aware of DKA. Keywords: Diabeticketoacidosis (DKA), insulin therapy, ketone concentration, cerebral edema, counter regulatory hormones, glycogenolysis and gluconeogenesis
A 10-year-old girl presented with diabeticketoacidosis, shock, and se- vere abdominal pain. She was found to have acute pancreatitis and acute kidney injury after shock resuscitation and severe persistent hypertriglyceridemia. The severe hypertriglyceridemia was treated with 1 course of plasmapheresis, which corrected the triglyceride level and was temporally associated with improvement of the abdominal pain and renal dysfunction. Diabetes is known to contribute to an el- evated triglyceride level, especially in the setting of an underlying lipid disorder. However, no such disorders were found in this patient. To the best of our knowledge, this is the ﬁ rst report of a pediatric patient presenting with the triad of severe hypertriglyceridemia, diabeticketoacidosis, and pancreatitis treated successfully with plasmaphere- sis. Pediatrics 2012;129:e195 – e198
Dr Baumer-Mouradian conceptualized and designed the study, conducted the initial interventions, coordinated and supervised data collection, analyzed the data, drafted the initial manuscript, and reviewed and revised the manuscript; Dr Gray assisted in the study design, data analysis, and statistical analysis and reviewed and revised the manuscript; Dr Wolfgram provided expert opinion on diabeticketoacidosis management, assisted in the study design and data analysis, and critically reviewed the manuscript for important intellectual content; Mr Kopetsky designed the data collection instruments, conducted data analysis, and critically reviewed the manuscript for intellectual content; Dr Chang and Mr Frenkel assisted in the study design, conducted initial interventions and data collection, and critically reviewed the manuscript; Drs Brousseau and Ferguson assisted in the study design and analysis of data and critically reviewed the manuscript for important intellectual content; and all authors approved the ﬁ nal version of the manuscript as submitted.
In the case outlined above there are also nutritional factors which may have increased the risk of brain in- jury. Folic acid deficiency has been linked to cognitive impairment with behavioural disturbance in young adults . Non-ketotic hyperglycaemia (NKH) can result in multiple neurological consequences such as seizures, hemichorea and hemianopia. In NKH, hyperglycaemia-induced blood brain barrier perme- ability contributes to epileptogenesis . Therefore, we may hypothesize that recurrent hyperglycaemia and subsequent blood brain barrier permeability may have contributed to epileptogenesis and indeed brain injury in this case. Moreover, multiple sclerosis re- lated blood-brain barrier permeability, although not the primary pathology in MS, may have contributed to reduced neuroprotection and increased risk of en- cephalopathy . Factors such as nutritional defi- ciency, alcohol excess, cannabis use, depression and multiple sclerosis may have contributed to this pa- tient’s susceptibility to encephalopathy however meta- bolic encephalopathy secondary to diabeticketoacidosis was the most likely diagnosis.
Diabeticketoacidosis (DKA) is an acute metabolic disorder characterized by markedly increased circulating ketone bodies e.g. beta-hydroxybutyrate, aceto-acetate and acetone in the presence of hyperglycemia. DKA is a serious and potentially life-threatening metabolic complication of diabetes mellitus. Some well-known precipitants of DKA include new-onset T1DM, insulin withdrawal and acute illness. In this report, we present a subject who presented with DKA as an initial manifestation of Cushing’s disease secondary to ACTH-producing pituitary adenoma.
Diabeticketoacidosis (DKA) is an acute and life-threa- tening complication of diabetes mellitus (DM) and con- sists of the biochemical triad of hyperglycemia, ketonemia, and metabolic acidosis . Even in reference centers, 15 to 67% of diabetic patients still present DKA as the first manifestation of type 1 diabetes, mainly in children under 5 years old and in populations with diffi- cult access to health services for socioeconomic reasons [2,3]. In Brazil, recent studies have shown that DKA was present in 32,8 to 41% of the patients at the time of diagnosis of type 1 DM [4-7], in agreement with inter- national data. DKA is the most frequent cause of hospi- talization and mortality among type 1 diabetes children and adolescents, and it accounts for approximately 50% of all deaths of DM individuals up to 24 years of age
Aim: We aimed to evaluate the clinical utility of blood ketone measurement and to test the performance of the diagnostic criteria for diabeticketoacidosis (DKA) issued by the American Diabetes Association, the Joint British Diabetes Societies, and the American Association of Clinical Endocrinologists and the American College of Endocrinology. Methods: This retrospective analysis included 278 patients with suspected DKA who were hospitalized at 4 university hospitals and aged ≥ 16 years with a blood glucose level of >200 mg/dL and a blood ketone level of ≥ 1.0 mmol/L as well as other biochemical data. The patients were categorized into four subgroups (ketosis, typical DKA, atypical DKA, and DKA + lactic acidosis). Atypical DKA in each analysis was de ﬁ ned by our supplementary criteria if the biochemical data did not meet each set of diagnostic criteria from the aforementioned societies. Results: Blood ketone levels in patients with diabetic ketosis and those with DKA varied widely, 1.05 – 5.13 mmol/L and 1.02 – 15.9 mmol/L, respectively. Additionally, there were signi ﬁ cant discrepancies between the guidelines in the diagnosis of DKA. Thus, the propor- tion of patients with atypical DKA ranged from 16.5% to 42.4%. Notably, the in-hospital mortality was comparable between patients with typical and atypical DKA, with a very high mortality in patients with DKA + lactic acidosis (blood lactate >5 mmol/L).
Five days following the 3rd cycle of nivolumab, a monoclonal antibody, which acts as immune checkpoint inhibitor against the programmed cell death protein-1, for metastatic lung adenocarcinoma, a 56-year-old woman presented at the hospital critically ill. On admission, she had severe diabeticketoacidosis (DKA), as evidenced by venous glucose of 47 mmol/L, blood ketones of 7.5 mmol/L, pH of 6.95 and bicarbonate of 6.6 mmol/L. She has had no personal or family history of diabetes mellitus (DM), while random venous glucose, measured 1 week prior to hospitalisation, was 6.1 mmol/L. On admission, her HbA1c was 8.2% and anti-GAD antibodies were 12 kIU/L (0–5 kU/L), while islet cell antibodies and serum C-peptide were undetectable. Nivolumab was recommenced without the development of other immune-mediated phenomena until 6 months later, when she developed hypothyroidism with TSH 18 U/L and low free T4. She remains insulin dependent and has required levothyroxine replacement, while she has maintained good radiological and clinical response to immunotherapy. This case is notable for the rapidity of onset and profound nature of DKA at presentation, which occurred two months following commencement of immunotherapy. Despite the association of nivolumab with immune-mediated endocrinopathies, only a very small number of patients developing type 1 DM has been reported to date. Patients should be closely monitored for hyperglycaemia and thyroid dysfunction prior to and periodically during immunotherapy.
In the tropics where the prevalence of sickle cell anaemia (SCA) is high, reports of concurrence of sickle cell anaemia and diabetes mellitus are rare with diabeticketoacidosis (DKA), being rarer. In this case report, we present the cases of two Nigerian adolescents (one male and one female) with homozygous SCA who presented in DKA. Sickle cell anaemia was diagnosed eight and nine months respectively prior to their presentation with DKA. There was no history of previous multiple blood transfusions. Neither of the two cases had positive family history of diabetes mellitus. The diagnosis of DKA in each case was based on the presence of hyperglycaemia, ketonuria and acidosis. The families of these two patients were of low socio-economic status.
diagnosis of myxedema coma can be made with a patient who has a history of thyroid disease or thyroidectomy with altered mental status or hypothermia. However, it can be misdiagnosed due to various clinical conditions that can present several manifestations similar to those of myxedema coma, such as sepsis, heart failure, cere- brovascular disease, drug use, or metabolic disorder . Here we report the case of a 43-year-old man with un- diagnosed diabetes mellitus who showed atypical clinical presentation of myxedema coma precipitated by diabeticketoacidosis (DKA). Study approvals were obtained from the Institutional Review Board (IRB) of Seoul St. Mary’s Hospital (No. IRB; KC18ZESI0785).
There are several reports on patients with diabeticketoacidosis in whom the serum glucose level is not elevated. The pathophysiologic basis of this condition has been extensively discussed in the literature, but the exact mechanism is yet to be determined. Many newer findings, including the observation that EuDKA may be seen in diabetic patients taking SGLT2 inhibitors, have helped us understand the possible mechanisms behind this disease. In summary, depletion of glycogen stores in the liver following starvation or urinary loss of glucose, slows the hyperglycemic phase of diabetic ketoacidois, while lipolysis and production of the ketone bodies continues. This results in a state of ketoacidosis without marked hyperglycemia. Diagnosis of EuDKA requires a high index of suspicion on the clinician’s side and measurement of the presence of ketones in the plasma and urine. EuDKA is principally a diagnosis of exclusion and several conditions should also be considered. These include AKA and SKA. SKA may overlap with EuDKA. History, physical examination, and laboratory values may help differentiate these disease states. While diagnosed, treatment should be instituted promptly and meticulously.
Diabeticketoacidosis (DKA) is a preventable but serious complication of type 1 diabetes and carries a mortality rate of 0.3 – 0.5% in developed economies and much higher in developing economies (about 10%). 1,2 It occurs due to an interplay between insulin (de ﬁ ciency) and counter-regulatory hormones (excess). The former leads to hyperglycemia and ketosis, while the latter (epinephrine, cortisol and growth hormone) released in response to stress, aggravates hyperglycemia by blocking the action of insulin and enhancing glycogenolysis in the liver. 3 When blood glucose levels exceed the renal threshold (180mg/dL), glycosuria occurs. The resultant osmotic diuresis leads to volume depletion and dehydration, which activates the renin-angiotensin-aldoster- one axis and also triggers the release of counter-regulatory hormones. These hormones act towards preserving the intravascular volume. Vomiting, due to stimulation of chemoreceptor trigger zone by hydrogen ions and ketones, further aggravates volume loss and dehydration leading to a vicious cycle.
Children with DKA seen in non-pediatric community hospital’s EDs are often managed by adult trained emer- gency physicians. Guidelines for the management of adult diabeticketoacidosis still include administration of IV insulin bolus and sodium bicarbonate . Because referring facilities treat a higher percentage of adults than children, it may be speculated that this is the rea- son that IV insulin and sodium bicarbonate was admin- istered to pediatric patients referred to the PICU. From the statistical analyses performed, there did not appear to be any factors that increased the likelihood that all guideline parameters would be met.