A RARE CASE MORTALITY OF DIABETIC KETOACIDOSIS- CEREBRAL EDEMA WITH TONSILLAR HERNIATION- A CONTRADICTORY OPINION.IS SODIUM BICARBONATE A REAL CULPRIT?

2021 ◽  
pp. 8-10
Author(s):  
Sruthi P ◽  
Manzoor Sharieff M ◽  
Prasanth Kumar P ◽  
Vishnu priya V ◽  
Nagarajan N ◽  
...  
Keyword(s):  
Diabetic Ketoacidosis ◽  
Cerebral Edema ◽  
Hydrogen Exchange ◽  
Ketone Bodies ◽  
Acetoacetic Acid ◽  
Tonsillar Herniation ◽  
Sodium Hydrogen ◽  
Uncontrolled Diabetes ◽  
Case Mortality

Diabetic ketoacidosis (DKA) is the most common complication seen in uncontrolled diabetes mellitus. DKA is most commonly seen with patients of type 1 diabetes. Depletion of Insulin leads to high blood sugars which in turn leads osmotic diuresis, production of ketone bodies i.e, βhydroxybutyric acid and acetoacetic acid, dysregulation of sodium hydrogen exchange mechanism[2]. As a consequence to the above stated mechanisms, cerebral edema has been documented as a fatal complication in DKA. Mortality documented due to cerebral edema is 21-25%[4].

scholarly journals Simulated diabetic ketoacidosis therapy in vitro elicits brain cell swelling via sodium-hydrogen exchange and anion transport

2015 ◽  
Vol 309 (4) ◽  
pp. E370-E379 ◽  
Author(s):  
Keeley L. Rose ◽  
Andrew J. Watson ◽  
Thomas A. Drysdale ◽  
Gediminas Cepinskas ◽  
Melissa Chan ◽  
...  
Keyword(s):  
Diabetic Ketoacidosis ◽  
Hydrogen Exchange ◽  
Brain Slices ◽  
Anion Transport ◽  
Brain Cell ◽  
Cell Swelling ◽  
Sodium Hydrogen ◽  
Disulphonic Acid

A common complication of type 1 diabetes mellitus is diabetic ketoacidosis (DKA), a state of severe insulin deficiency. A potentially harmful consequence of DKA therapy in children is cerebral edema (DKA-CE); however, the mechanisms of therapy-induced DKA-CE are unknown. Our aims were to identify the DKA treatment factors and membrane mechanisms that might contribute specifically to brain cell swelling. To this end, DKA was induced in juvenile mice with the administration of the pancreatic toxins streptozocin and alloxan. Brain slices were prepared and exposed to DKA-like conditions in vitro. Cell volume changes were imaged in response to simulated DKA therapy. Our experiments showed that cell swelling was elicited with isolated DKA treatment components, including alkalinization, insulin/alkalinization, and rapid reductions in osmolality. Methyl-isobutyl-amiloride, a nonselective inhibitor of sodium-hydrogen exchangers (NHEs), reduced cell swelling in brain slices elicited with simulated DKA therapy (in vitro) and decreased brain water content in juvenile DKA mice administered insulin and rehydration therapy (in vivo). Specific pharmacological inhibition of the NHE1 isoform with cariporide also inhibited cell swelling, but only in the presence of the anion transport (AT) inhibitor 4,4′-diisothiocyanatostilbene-2,2′-disulphonic acid. DKA did not alter brain NHE1 isoform expression, suggesting that the cell swelling attributed to the NHE1 was activity dependent. In conclusion, our data raise the possibility that brain cell swelling can be elicited by DKA treatment factors and that it is mediated by NHEs and/or coactivation of NHE1 and AT.

Synthesis of a Sodium–Hydrogen Exchange Type 1 Inhibitor: An Efficient Cu-Catalyzed Conjugated Addition of a Grignard Reagent to an Acetyl Pyridinium Salt

2013 ◽  
Vol 17 (3) ◽  
pp. 382-389 ◽  
Author(s):  
Wenjun Tang ◽  
Nitinchandra D. Patel ◽  
Xudong Wei ◽  
Denis Byrne ◽  
Ashish Chitroda ◽  
...  
Keyword(s):  
Grignard Reagent ◽  
Hydrogen Exchange ◽  
Pyridinium Salt ◽  
Sodium Hydrogen

scholarly journals A Pediatric Diabetic Ketoacidosis Patient with Multisystem Complications and a Prolonged Course

2019 ◽  
Vol 12 (3) ◽  
pp. 89-90
Author(s):  
John Henry Carson ◽  
Lindall E. Smith ◽  
Poornima Pandiyan ◽  
Priyank J Yagnik
Keyword(s):  
Diabetes Mellitus ◽  
Acute Pancreatitis ◽  
Diabetic Ketoacidosis ◽  
Cerebral Edema ◽  
Unique Case ◽  
Vein Thrombosis ◽  
Life Threatening ◽  
Life Threatening Complication ◽  
Deep Vein

The prevalence of diabetic ketoacidosis (DKA) in children with type 1 diabetes mellitus (T1DM) is 30% at the time of diagnosis.1 Cerebral edema is a rare, but life-threatening complication of DKA, occurring in only 0.3 - 1% of cases.2 Deep vein thrombosis and acute pancreatitis are other rare complications of DKA. Supraventricular tachycardia (SVT) as a complication of pediatric DKA has been reported.3 A unique case of a pediatric patient who had multiple rare complications of DKA including cerebral edema, venous thrombosis, and hypertriglyceridemia associated acute pancreatitis is presented.The SVT episode encountered during the admission was due to complications arising from a procedure and not due to DKA itself.

Treatment of Diabetic Ketoacidosis (DKA) with 2 Different Regimens Regarding Fluid Substitution and Insulin Dosage (0.025 vs. 0.1 units/kg/h)

2012 ◽  
Vol 120 (05) ◽  
pp. 273-276 ◽  
Author(s):  
T. Kapellen ◽  
C. Vogel ◽  
D. Telleis ◽  
M. Siekmeyer ◽  
W. Kiess
Keyword(s):  
Type 1 Diabetes ◽  
Blood Glucose ◽  
Diabetic Ketoacidosis ◽  
Cerebral Edema ◽  
Standard Dose ◽  
Insulin Dose ◽  
Neurological Status ◽  
Insulin Dosage ◽  
Pediatric Diabetes

AbstractDiabetic ketoacidosis (DKA) is still the most dangerous acute complication in type 1 diabetes. The aim of this study was to compare treatment of DKA with a regimen of a low insulin dose (0.025 units/kg/h) vs. a standard insulin dose (0.1 units/kg/h).We retrospectively analysed all cases of children and adolescents (age 0–18 years) with type 1 diabetes and DKA who needed treatment in the ICU in the time period of 1998–2005 in 2 pediatric diabetes centers. In a chart review of the first 48 h after onset of DKA the following parameters where evaluated: pH, blood glucose, sodium, potassium, and ketones in urine. Consciousness, neurological status and complications such as cerebral edema, hypoglycaemia or hypokalemia were also recorded.23 children were treated in center A (low insulin dose) whereas 41 where treated in center B (standard insulin dose). Mean age of the patients was 8.9 (range 1.58–17.7) and 13.5 years (1.25–17.7) respectively (p=0.134). Mean pH was 7.1 and HCO3 was 9.05 and 7.79 respectively (p=0.122). Initial blood glucose was 26 mmol/l (no difference between the 2 centres). Treatment with the standard insulin dose resulted in a slightly shorter duration of acidosis (8 h in center A, 6.5 h in center B) and a significantly faster normalization of blood glucose (18 h in A, vs. 10.5 h in B) (p<0.005). During the first day we found similar and very low rates of hypoglycaemia. In center B one case of suspected cerebral edema and cerebral infarction occurred.Low dose insulin substitution is as safe as the recommended standard dose in respect to the occurrence of acute complications. Acidosis is broken slightly earlier with the standard dose. Implications of this earlier normalisation of pH remain unclear.

Synthesis of a Sodium-Hydrogen Exchange Type 1 Inhibitor

Synfacts ◽  
2013 ◽  
Vol 9 (06) ◽  
pp. 0591-0591
Keyword(s):  
Hydrogen Exchange ◽  
Sodium Hydrogen

scholarly journals Sodium, Hydrogen exchange type 1 and bile ductular secretory activity in the guinea pig

Hepatology ◽  
2000 ◽  
Vol 31 (3) ◽  
pp. 562-571 ◽  
Author(s):  
Christian Hübner ◽  
Wolfgang Stremmel ◽  
Christoph Elsing
Keyword(s):  
Guinea Pig ◽  
Hydrogen Exchange ◽  
Secretory Activity ◽  
Sodium Hydrogen

Infantile cerebral infarction caused by severe diabetic ketoacidosis in new-onset type 1 diabetes mellitus

2019 ◽  
Vol 32 (12) ◽  
pp. 1391-1394
Author(s):  
Junichi Suzuki ◽  
Tatsuo Fuchigami ◽  
Kengo Kawamura ◽  
Masako Aoki ◽  
Tatsuhiko Urakami ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Cerebral Infarction ◽  
Type 1 Diabetes Mellitus ◽  
Diabetic Ketoacidosis ◽  
Cerebral Edema ◽  
Rare Complication ◽  
Case Presentation ◽  
New Onset

Abstract Background Diabetic ketoacidosis (DKA) is a common complication of type 1 diabetes mellitus (T1DM). Infants and children with new-onset T1DM may present with DKA, and the risk of cerebral edema is high in infantile DKA. What is new? Neurological deterioration during an episode of DKA is usually attributed to cerebral edema and cerebrovascular accidents. However, cerebral infarction is a very rare complication in infantile DKA. Case presentation We describe a rare case of infantile cerebral infarction caused by severe DKA in a patient with new-onset T1DM. Conclusions Cerebral infarction is an important intracranial complication in infantile DKA. Careful observation and treatment for DKA during the first 24 h of therapy are necessary in infants with new-onset T1DM because the risk of cerebral infarction is highest during this timeframe.

Diabetologische Notfälle: Ketoazidose und hyperglykämes Koma

2018 ◽  
Vol 143 (06) ◽  
pp. 384-391 ◽  
Author(s):  
Christina Schumann ◽  
Michael Faust
Keyword(s):  
Diabetic Ketoacidosis ◽  
Professional Education ◽  
Ketone Bodies ◽  
Insulin Deficiency ◽  
Laboratory Findings ◽  
Metabolic Complications ◽  
Hyperosmolar Hyperglycemic State ◽  
Electrolyte Abnormalities ◽  
Healthcare Professional Education

Abstract Background Diabetic ketoacidosis and the hyperosmolar hyperglycemic state are the most serious diabetic emergencies. Before the discovery of insulin in 1921 by Banting and Best the diagnosis of type 1 diabetes was fatal ending in diabetic ketoacidosis equivalent to a torturous death. Today, mortality from diabetic ketoacidosis is low at approximately 2 %. But each death from these two acute metabolic complications of diabetes is potentially avoidable by improved patient and healthcare professional education. Therefore, there is a need to raise awareness of hyperglycemic crisis and its management amongst physicians. Pathogenesis Insulin deficiency or resistence and increased concentrations of counterreulatory hormones (glucagon, catecholamines, cortisol and growth hormone) are responsible for the development of diabetic ketoacidosis and the hyperosmolar hyperglycemic state. Hyperglycemia develops as a result of increased gluconeogenesis and accelerated glyconeogenesis. In DKA, the absolute insulin deficiency additionally leads to increased lipolysis and production of ketone bodies and resulting metabolic acidosis. Diagnosis Both DKA and HHS require prompt recognition and management. The diagnosis can be suspected by clinical features and confirmed by laboratory findings. Treatment The treatment of DKA and HHS is similar, including correction of fluid and electrolyte abnormalities and the administration of insulin.

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