Acute Diabetic Ketoacidosis Research Articles

PDB7 DIABETIC COMPLICATIONS ASSOCIATED WITH SGLT2 AND DPP4 INHIBITORS: A REAL-WORLD APPROACH

Prior studies have shown an association between use of sodium glucose cotransporter 2 (SGLT2) inhibitors with serious adverse events (SAEs), including lower limb amputation, acute kidney injury, diabetic keto-acidosis and acute pancreatitis. This study aims to investigate whether there is any difference in the risk for these SAEs when comparing sodium glucose cotransporter 2 (SGLT2) inhibitors, to dipeptidyl peptidase-4 (DPP4) inhibitors in a real world setting. Real world data, composed of electronic medical records, pharmacy records and insurance claims from approximately 190 million U.S. patients were analyzed using TriNetX Analytics. Type 2 diabetes patients were defined with the ICD-10 code, E11. The index event was defined as initiation of either SGLT2 or DPP4 inhibitors for type 2 diabetes. ICD-10, LOINC and CPT codes were used to define primary outcomes, which included acidosis (E87.2, 9021, 11558-4), acute kidney failure (N17, N18, N19), acute pancreatitis (K85.9) and lower limb amputation (1005524, 1005529, 1005298, 1014590, 28820, 27880, 28810, 1005146, 1014580, 27590, 28825, 1005525, 28805, 27882, 27886, Z89.4, Z89.5, Z89.6), with an observation period between 7 days to 5 years after medication initiation. Risk ratios (RR) were calculated and propensity score matching used to balance cohorts and adjust for 22 most likely confounders. Propensity scores matched 1:1 using a nearest neighbor greedy matching algorithm with a caliper of 0.25 times the standard deviation. In the balanced cohort of 10,538 patients, use of SGLT2 inhibitors, compared to DPP4 inhibitors was associated with a lower risk for acidosis RR 0.51 (p<0.0001), amputation RR 0.56 (p<0.0001), acute kidney failure RR 0.28 (p<0.0001), but not with acute pancreatitis RR 1.5 (p=0.13). In this real world analysis, use of SGLT2 inhibitors was associated with a lower risk for acidosis, acute kidney injury and lower limb amputation, but not acute pancreatitis as compared with DPP4 inhibitors.

Non Traumatic Acute Abdominal pain (100 days study in Emergency Department)

Background: Abdominal symptoms are possibly the most frequent of all symptoms encountered in surgical practice. Pain is the most common of all abdominal symptoms. Causes of acute abdominal pain include both medical and surgical. Most symptoms arise from intra-abdominal organs or systems while some may originate extra abdominally and are then referred to the abdomen. Medical causes of abdominal pain are encountered more frequently.&#x0D; Objective: To study the causes of acute abdominal pain in patients attending emergency department in Al- Imamain Al- Kadhimain Medical City.&#x0D; Type of the study: A prospective cross sectional study&#x0D; Methods: The patients attending Emergency Department in Al- Imamain Al- Kadhimain Medical City over the period from April-2014 to April 2016. There was a one day call duty per week managed by the same surgical team (total one hundred days study). Onlypatients above 12 years old with acute non-traumatic abdominal pain were included in this study.&#x0D; Results: The total number was 1217 patients over hundred days study. Their age ranges from 12-83 years; average age was 36.18 ±17 year. There was slight female predominance, 638 (52.42%) female patients and 579 (47.58%) male patients. The most common cause of abdominal pain was acute appendicitis 252 (20.70%), followed by ureteric colic 251 (20.62%), and acute cholecystitis249 (20.46%). Conservative management was done for 836 (68.69%) patients, while operative management done for 379 (31.14%) patients. Postoperative mortality was 8 (2.11%) patients.Medical causes of acute abdominal pain were found in 48 (5.74%) patients.&#x0D; Conclusion: Not all the patients attending surgical emergency department needs operations. Causes of acute abdominal pain include both medical and surgical diseases, some of the medical diseases are very serious like acute viral hepatitis, myocardial infarction , and diabetic ketoacidosis; and should not submit those patients to unnecessary operations with serious and may be fatal postoperative complications. General urine examination is a must in all patients with acute abdominal pain. Electrocardiography (ECG) may be needed in old patients.

SUN-276 Acute Pancreatitis and Diabetic Ketoacidosis in an 8-Year-Old Following Induction Therapy for Pre-B Acute Lymphocytic Leukemia

Introduction Peg-Asparaginase and Dexamethasone are both used in the induction therapy for pre-B Acute Lymphocytic Leukemia (ALL) and have overlapping adverse effects. Peg-Asparaginase is an enzyme that causes depletion of asparagine which is an essential amino acid for leukemia cells. Dexamethasone is a long-acting glucocorticoid with a 30-fold increase in anti-inflammatory activity relative to Hydrocortisone. Hyperglycemia and acute pancreatitis are both adverse reactions of Peg-asparaginase and glucocorticoids. Clinical case An 8-year-old male with obesity presented with acute pancreatitis and diabetic ketoacidosis (DKA) following induction therapy for pre-B ALL. The patient was euglycemic at the time of diagnosis. On day 1 induction chemotherapy was administered which included IV vincristine, IT cytarabine and PO dexamethasone (4 mg BID daily). On day 2, patient developed hyperglycemia (167 mg/dL). On day 4 he received IV Peg-Asparaginase (3,800 IU). On day 8 patient returned with back pain, fatigue, polydipsia, polyuria, and Kussmaul breathing. Labs revealed hyperglycemia (1,118 mg/dL), metabolic acidosis with an elevated anion gap (pH 7.14, pCO2 < 17 mmHg, HCO3 4.6 mmol/L, anion gap 36), elevated lipase (2,256 IU/L), mild transaminitis, and elevated creatinine and BUN. Pancreatic ultrasound was consistent with pancreatitis. The patient was admitted to the pediatric ICU for insulin drip and management of pancreatitis. On day 10 he was transitioned to SQ glargine insulin. Chemotherapy was restarted with dexamethasone and vincristine. Patient had persistent hyperglycemia requiring lispro insulin to cover meals and to correct hyperglycemia. His glucose normalized on this treatment and insulin was tapered down to be discontinued 9 days after initially started. His HbA1c was 7.5% (normal <5.6%) and he had negative T1DM-related antibodies. A CT of the abdomen showed pancreatic inflammation but no fluid collection or necrosis. At the time of discharge, patient was euglycemic. In the following months, in the absence of glucocorticoids and asparaginase, the patient had multiple admissions for recurrent pancreatitis with development of a pseudocyst. No further episodes of hyperglycemia were documented. Conclusion DKA can develop as side effect of treatment with Peg-Asparaginase and glucocorticoids. Patients treated with these medications need to be closely monitored to identify and treat hyperglycemia and pancreatitis as early as it develops.

MON-151 Hypertriglyceridemia and Acute Pancreatitis Leading to Ketoacidosis in a Patient with Type 2 Diabetes

Introduction: We describe a case of type 2 diabetes presenting with acute pancreatitis (AP), hypertriglyceridemia, and diabetic ketoacidosis (DKA). Clinical Case: A 34-year-old Caucasian male presented to the emergency room with worsening intractable nausea and vomiting for 2 days. Medical problems included obesity, hypertension, hyperlipidemia, and fatty liver disease. He had a history of polysubstance use (denied recent alcohol intake) and noncompliance with self-care and was a known carrier for hemochromatosis. He gave a history of 30-lb weight loss over the past 6 weeks with associated polydipsia, polyuria, and abdominal pain. Six days prior to admission, the patient had been seen by his primary care physician for headache, nausea and vomiting, found to have a hemoglobin A1c of 13.5% (n=4.2-5.8%) and was started on metformin for newly-diagnosed T2DM. Physical exam revealed him to be afebrile, tachycardic (heart rate 145 bpm), and with a BP of 146/98 mmHg. Laboratory tests were significant for sodium 125 mmol/L (n=135-145mmol/L), potassium 4.0 mmol/L (n=3.5-5.1 mmol/L), anion gap 25 mmol/L (n=2-14 mmol/L), glucose 330 mg/dL (n=70-99 mg/dL), creatinine 1.5 mg/dL (n=0.5-1.3 mg/dL), lipase 268 U/L (n=8-78 U/L), triglyceride 1619 mg/dl (n<150 mg/dL), and negative alcohol and cardiac markers. Urine testing was positive for ketones with a negative drug screen. Arterial blood gas showed a pH of 7.27 (n=7.35-7.45), pCO2 19 mmHg (n= 35-45 mmHg), and pO2 111 mmHg (n=80-100 mmHg). CT of the abdomen revealed inflammation surrounding the pancreatic head, consistent with pancreatitis. The patient was admitted to the intensive-care unit for DKA and AP. He was treated with intravenous fluids and required an insulin drip for 72 hours before transitioning to subcutaneous insulin with resumption of oral nutrition as the pancreatic inflammation and gastrointestinal symptoms resolved. He was discharged on basal-bolus insulin therapy and lipid-lowering medications. Conclusion: Both DKA and AP are serious medical conditions with a high mortality rate when these two disorders occur simultaneously. Treatment requires aggressive fluid resuscitation with replacement of electrolytes and initiation of insulin. Identifying the potential trigger is key to preventing future occurrences. In the case presented, it is likely that primary hypertriglyceridemia, worsened by elevated glucose levels, was the etiologic factor for the onset of AP, which in turn precipitated DKA. However, it is also possible, though less likely, that uncontrolled hyperglycemia, glucose toxicity, and relative insulin deficiency led to increased production of very-low-density lipoprotein (VLDL) in the liver and its reduced clearance from the plasma, thus predisposing to hypertriglyceridemia. Close monitoring and appropriate therapy are required to control the latter and prevent future recurrences of AP and possibly DKA.

Barriers to and facilitators of the development and utilization of context appropriate evidence based clinical algorithms to optimize clinical care and patient outcomes in the Tikur\xa0Anbessa emergency department: a multi-component qualitative study

BackgroundEvidence-based clinical algorithms (EBCA) are knowledge tools to promote evidence use by codifying evidence into action plans to facilitate appropriate care. However, their impact on process and outcomes of care varies considerably across practice settings and providers, highlighting the need for tailoring of both these knowledge tools and their implementation strategies to target end users and the setting in which EBCAs are to be employed.Leadership at the Tikur Anbessa Specialized Hospital emergency department (TASH-ED) in Addis Ababa, Ethiopia identified a need for context-appropriate EBCAs to improve evidence uptake to mitigate care gaps in this high volume, high acuity setting. We aimed to identify barriers and facilitators to utilization of EBCAs in the TASH-ED, to identify priority targets for development of EBCAs tailored for the TASH-ED context and to understand the process of care in the TASH-ED to inform implementation planning.MethodsWe employed a multi-component qualitative design including: semi-structured interviews with TASH-ED clinical, administrative and support services staff, and Toronto EM physicians who had worked in the TASH-ED; direct observation of the process of care in TASH-ED; document review.ResultsAlthough most TASH-ED participants reported an awareness of EBCAs, they noted little or no experience using them, primarily due to the poor fit of many EBCAs to their practice setting. All participants felt that context-appropriate EBCAs were needed to ensure standardized and evidence-based care and improve patient outcomes for common ED presentations. Trauma, sepsis, acute cardiac conditions, hypertensive emergencies, and diabetic keto-acidosis were most commonly identified as priorities for EBCA development. Lack of medication, equipment and human resources were identified as the primary barriers to use of EBCAs in the TASH-ED. Support from leadership and engagement of stakeholders outside the ED where EBCAs were believed to be less well accepted were identified as essential facilitators to implementation of EBCAs in the TASH-ED.ConclusionsThis study found a perceived need for EBCAs tailored to the TASH-ED setting to support uptake of evidence-based care into routine practice for common clinical presentations. Barriers and facilitators provide information essential to development of both context-appropriate EBCAs and plans for their implementation in the TASH-ED.

Sudden Death in a Patient with Undiagnosed Diabetes, Acute Pancreatitis and Acute Adrenalitis

It has been well documented that acute pancreatitis and diabetic ketoacidosis (DKA) co-occur, and both of them present either as a cause or result of the other [1] [2]. Recently, hypertriglyceridemia has been reported to co-occur as well [3] [4]; the involvement of acute adrenalitis in the setting of acute pancreatitis and DKA has not been reported. We report a case of sudden death due to diabetic ketoacidosis, acute pancreatitis and acute adrenalitis in a 37-year-old female. She was found unresponsive and breathless in bed by her mother at their residence. At the time of the autopsy, both lungs were expanded and sigmoid diverticulosis was discovered on gross examination. Histology of the pancreas and the adrenal glands revealed acute inflammation despite appearing normal upon gross examination. The postmortem toxicology report showed high levels of acetone (12 mg/dL) in the postmortem blood and extremely high levels of glucose (>500 mg/dL) in the postmortem vitreous fluid. This is the first reported case of fatal diabetic ketoacidosis co-occurring with acute pancreatitis and acute adrenalitis.

Caffeine Toxicity Following Ingestion of an Exercise Supplement by a Patient with Type 1 Diabetes.

We report the case of a patient with type 1 diabetes who developed acute severe diabetic ketoacidosis following ingestion of an energy supplement containing caffeine. Some 95% of the US adult population consume caffeine, and the general perception is that there are no negative consequences for health. The upper limit of safe consumption is less than 400 mg per day. However, acute ingestion of high doses of caffeine may cause significant metabolic changes that can be fatal. Here the patient consumed a toxic dose of caffeine causing unpleasant and puzzling symptoms, vomiting and, following omission of his long-acting basal insulin, severe diabetic ketoacidosis. As the sports nutrition market continues to expand, providers and manufacturers have a responsibility to give clear and accurate dosing instructions as well as side effect profiles for their products, particularly for diabetic patients.LEARNING POINTSThe impact of caffeine on blood glucose levels has implications for people with diabetes who may be thinking of consuming supplements containing caffeine.Providers of sports supplements have a responsibility to provide an accurate description of the side effects with a clear warning for diabetic patientsLegislators should review protocols for regulating the sports and nutritional supplements industry.

Etiological analysis, morbidities and mortality that affect the young and middle aged admitted with altered mental status in a general hospital

Background: Authors conducted this study to find the profile of causes and diseases that affect patients of younger age group in altered sensorium admitted in a general hospital associated with Government Medical College Srinagar, in India.Methods: Authors conducted present study over a period of eight months. The patients of young and middle age who were admitted in their hospital ward with altered mental status were included. The study subjects were divided into two groups: group A included patients of age upto 30 years, and group B with patients in age group 31-50 years. The patients were studied for their diagnoses, comorbidities, gender distribution, duration of stay in hospital and mortality patterns.Results: Authors had a total of 112 patients of young and middle age admitted in their hospital ward with altered mental status during the study period. In group A, there were 42 patients or 37.5% (20 males and 22 females). In group B, there were 70 patients or 62.5% (30 males and 40 females). The most common cause of admission in these patients was infection (29.46%) followed by seizures (17.85%) and cardioembolic strokes (11.60%).The most common comorbidities in studied patients were underlying seizure disorder, psychiatric disease in the form of bipolar affective disorder or schizophrenia, hypertension, type 2 diabetes and chronic kidney disease.There were 14 deaths in group A and 30 deaths in group B. The most common cause of death was infections followed by seizures, Acute respiratory distress syndrome (ARDS) and severe diabetic ketoacidosis (DKA).Conclusions: The most common cause of admission in young and middle-aged patients in authors’ hospital was infection followed by seizures and cardioembolic strokes. The most common cause of death was again infections followed by seizures, acute respiratory distress syndrome and severe diabetic ketoacidosis.

Experiential Learning: Integrating Simulation in Teaching Undergraduate Medical Physiology

INTRODUCTIONMany medical students struggle to connect the fundamental knowledge from didactic lectures with clinical aspects of patient care. Experiential learning, which can be effectively achieved by simulation, is an active process during which the learner constructs knowledge by linking new information and novel experiences with existing knowledge and understanding. Accordingly, we have introduced multiple activities within the first year undergraduate medical physiology curriculum intended to develop student's diagnostic reasoning skills.METHODSThe first step in the sequential approach involves teaching point‐of‐care ultrasound (POCUS) assessment of anatomical structure with the eventual objective of identifying pathological presentations. This involves interactive sessions in which students perform imaging of each of the major organ systems in Standardized Patients. We build upon this foundation with simulated patient encounters using high‐fidelity manikins to demonstrate compensatory physiological mechanisms evoked in response to disease. The initial encounters are straight forward (e.g., trauma with blood loss or tension pneumothorax). However, a progressive increase in realism and clinical relevance is achieved by introducing progressively more complex cases. Pertinent examples include acute pancreatitis and diabetic ketoacidosis. Patient interactions/examinations are challenging skills for pre‐clerkship students to master. However, medical simulation allows the acquisition of clinical skills through deliberate practice rather than relying on the traditional apprentice style of learning. Practicing assessment of patients relying on history and physical examination, ordering relevant diagnostic laboratory testing and obtaining POCUS images facilitates students analyzing the potential differential diagnoses to arrive at the correct diagnosis and treatment plan.RESULTSThe use of clinical simulations of increasing complexity followed by debriefing has allowed us to substantially reduce the number of formal lecture hours over the last 5 years without compromising students' performance on either in‐house or standardized examinations. We have refined the delivery of content to routinely require as few as 4 facilitators for 196 students. The students then participate in a simulation debrief where important aspects of clinical decision making are addressed.CONCLUSIONSWe have found that integrating patient history and physical examination with imaging and laboratory test results into clinical simulation scenarios to be a useful adjunct to traditional methods of teaching physiology to pre‐clinical medical students. A distinct advantage of this innovative experiential approach to teaching is simulation serves as an alternative to learning on real patients. Thus, a trainee can make mistakes and learn from them without the possibility of harming the patient. This approach encourages students to become facile at integrating diagnostic imaging and clinical pathology as part of their assessment in order to reach a definitive diagnosis. Moreover, it contributes to providing our students with a solid foundation in clinical reasoning.

Steroid-Induced Diabetic Ketoacidosis in a Patient with Type 2 Diabetes Mellitus

ABSTRACT Objective: Diabetic ketoacidosis (DKA) is usually associated with type 1 diabetes mellitus; however, it is increasingly being recognized in patients with type 2 diabetes mellitus (T2DM). Triggering factors usually involve infections and poor medication adherence. Other potential triggers are myocardial infarction, antipsychotic drug usage, malignancy, and cerebrovascular accidents. No case of steroid-induced DKA in a patient with T2DM has been reported in the literature. Methods: Clinical and laboratory data are presented. Results: We present a case of a middle-aged patient with a history of well-controlled T2DM via metformin. The patient was started on oral prednisone for lumbar disc herniation, and then presented with acute DKA. No other trigger for DKA but steroid initiation was found. Conclusion: We conclude that patients with diabetes who receive glucocorticoids should be monitored carefully, as steroids can precipitate DKA. This may occur in the absence of any other triggering factor, and e...

Molecular Detection of Scrub Typhus Using Nested PCR Analysis in Chennai: A Case Report

Scrub typhus is a mite-borne rickettsial zoonosis caused by Orientia tsutsugamushi. We report a case of scrub typhus with Acute Respiratory Distress Syndrome (ARDS) and Diabetic ketoacidosis (DKA) in an adult diabetic male in Chennai. The diagnosis was made initially by serology and subsequently confirmed by detection of the 56 kDa gene.

Evaluation of serum neutrophil gelatinase-associated lipocalin in predicting acute kidney injury in critically ill patients.

ObjectiveThis investigation evaluated the real-time point-of-care testing (RT-POCT) of neutrophil gelatinase-associated lipocalin (NGAL) for detecting acute kidney injury (AKI) and prognosis of critically ill patients.MethodsA total of 249 critically ill patients in the emergency department (ED), who were diagnosed with acute decompensated heart failure, sepsis or diabetic ketoacidosis were enrolled in this study. All enrolled patients were followed up for 28 days or to death and the mortalities were recorded. Serum creatinine (sCr) and NGAL were measured.Results40.6% enrolled patients deteriorated to AKI during the observation period. The NGAL level was significantly higher in the AKI versus non-AKI group. The NGAL levels in the non-survivors group at 7-day and 28-day were significantly higher than in the survivors group. NGAL was detected as an independent risk factor of AKI, and 7-day and 28-day morality. The receiver operating characteristic curve of NGAL was calculated for diagnosing AKI; the area under the curve (AUC) was significantly higher than that of 1-day eGFR.ConclusionsNGAL is an independent predictor of AKI, and 7-day and 28-day mortality in critically ill ED patients, and can be an early alert for AKI and useful for determining prognosis.

Histological and cognitive alterations in adult diabetic rats following an episode of juvenile diabetic ketoacidosis: Evidence of permanent cerebral injury

Evidence suggests that diabetic ketoacidosis (DKA) may cause subtle cognitive alterations in children but the mechanisms are poorly understood. Acute DKA is associated with reactive astrogliosis and microglial activation in a rat model. Whether these inflammatory changes permanently alter brain histology is unknown. We aimed to determine whether DKA results in permanent alterations in brain histology and whether these changes are associated with cognitive deficits in a rat model. We induced diabetes in juvenile rats with streptozotocin at 4 weeks of age. We induced DKA in one group (n=21) at 5 weeks of age and compared this group to rats with diabetes without DKA episodes (n=13). Beginning at 7 weeks, rats underwent a series of cognitive tests to evaluate memory. At 15 weeks, rat brains were harvested and examined using immunohistochemistry (IHC). In tests of novel object recognition and social recognition, both groups performed similarly, however, the DKA group performed more poorly in object-place recognition tests, suggesting alterations in hippocampal function. IHC studies demonstrated increased glial fibrillary acidic protein staining intensity in the hippocampus of DKA rats suggesting astrogliosis, and decreased NeuN positive cell counts in the cortex suggesting neuron loss. These studies demonstrate that DKA results in permanent alterations in brain microstructure in a rat diabetes model. These structural changes are associated with deficits in hippocampal function.

Elevated Leukocyte Azurophilic Enzymes in Human Diabetic Ketoacidosis Plasma Degrade Cerebrovascular Endothelial Junctional Proteins.

Diabetic ketoacidosis in children is associated with vasogenic cerebral edema, possibly due to the release of destructive polymorphonuclear neutrophil azurophilic enzymes. Our objectives were to measure plasma azurophilic enzyme levels in children with diabetic ketoacidosis, to correlate plasma azurophilic enzyme levels with diabetic ketoacidosis severity, and to determine whether azurophilic enzymes disrupt the blood-brain barrier in vitro. Prospective clinical and laboratory study. The Children's Hospital, London Health Sciences Centre. Pediatric type 1 diabetes patients; acute diabetic ketoacidosis or age-/sex-matched insulin-controlled. Acute diabetic ketoacidosis in children was associated with elevated polymorphonuclear neutrophils. Plasma azurophilic enzymes were elevated in diabetic ketoacidosis patients, including human leukocyte elastase (p < 0.001), proteinase-3 (p < 0.01), and myeloperoxidase (p < 0.001). A leukocyte origin of human leukocyte elastase and proteinase-3 in diabetic ketoacidosis was confirmed with buffy coat quantitative real-time polymerase chain reaction (p < 0.01). Of the three azurophilic enzymes elevated, only proteinase-3 levels correlated with diabetic ketoacidosis severity (p = 0.002). Recombinant proteinase-3 applied to human brain microvascular endothelial cells degraded both the tight junction protein occludin (p < 0.05) and the adherens junction protein VE-cadherin (p < 0.05). Permeability of human brain microvascular endothelial cell monolayers was increased by recombinant proteinase-3 application (p = 0.010). Our results indicate that diabetic ketoacidosis is associated with systemic polymorphonuclear neutrophil activation and degranulation. Of all the polymorphonuclear neutrophil azurophilic enzymes examined, only proteinase-3 correlated with diabetic ketoacidosis severity and potently degraded the blood-brain barrier in vitro. Proteinase-3 might mediate vasogenic edema during diabetic ketoacidosis, and selective proteinase-3 antagonists may offer future vascular- and neuroprotection.

Neuroimaging findings in acute pediatric diabetic ketoacidosis

Diabetic ketoacidosis (DKA) is a state of severe insulin deficiency and a serious complication in children with diabetes mellitus type 1. In a small number of children, DKA is complicated by injury of the central nervous system. These children have a significant mortality and high long-term neurological morbidity. Cerebral edema is the most common neuroimaging finding in children with DKA and may cause brain herniation. Ischemic or hemorrhagic stroke during the acute DKA episode is less common and accounts for approximately 10% of intracerebral complications of DKA. Here we present the neuroimaging findings of two children with DKA and brain injury. Familiarity with the spectrum of neuroimaging findings seen in pediatric DKA is important to allow early detection as well as initiation of therapy and, hence, prevent complications of the central nervous system.

Acute pancreatitis and diabetic ketoacidosis in non-diabetic psychotic patient

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Medical Emergencies in Pediatric Dentistry.

Medical emergencies that are life threatening can occur in dental practice. Complications may arise because of an underlying disease or a reaction to medication. Reactions to medications may be allergic and toxic. The most common reactions are toxic reactions to local anesthetics, whereas allergies occur mainly as a consequence of the application of antibiotics, usually penicillin. In response to stress, vasovagal syncope typically occurs. Other causes may be related to an underlying disease-specific pathology (such as acute asthma attack, diabetic ketoacidosis, hypoglycemia, or seizures) or accidents (aspiration of a foreign body causing obstruction of the respiratory system). For all the above conditions, guidelines have been established that need to be known. If complications occur or necessary measures are not taken, it can lead to cardiac and respiratory arrest. Therefore, cardiopulmonary resuscitation is needed. All procedures and dosages should be adapted to the age of the child.

Examining the "Killer K" of Diabetic Ketoacidosis at a Tertiary Care Hospital: An Exploratory Study.

Hypokalemia, a frequently cited complication of diabetic ketoacidosis (DKA) treatment, can have critical implications, including arrhythmias and death. We assessed the prevalence of hypokalemia and its associated factors in patients with DKA at our tertiary-care centre and identified opportunities to improve care. We conducted a retrospective chart review to establish the prevalence of hypokalemia in patients diagnosed with DKA between July 2012 and July 2013. A focused root-cause analysis was subsequently performed to identify Canadian Diabetes Association DKA clinical practice guideline deviations and preventable errors that resulted in significant hypokalemia (K<3.3 mmol/L) during the first 48 hours of management. Clinical and management details were reviewed to determine the type, preventability and root cause(s) of each error. We identified 40 cases of DKA during the study period. The overall prevalence of hypokalemia during DKA treatment was 38% (15/40), with 25% in type 1 and 56% in type 2 diabetes. Males were more likely to experience hypokalemia (87%), and 47% of hypokalemic incidents occurred in the first presentation of diabetes. All 10 cases of significant hypokalemia were reviewed. We identified 23 errors in 6 (60%) cases, of which 87% were deemed to be preventable. The most common errors were noncessation of insulin infusion during hypokalemia (60%), inadequate potassium supplementation (50%) and infrequent biochemical monitoring (50%). Hypokalemia occurs frequently during acute DKA management and is often preventable. Our findings suggest that interventions targeted at enhancing awareness of guidelines may reduce hypokalemia rates.

Severe hypercalcemia and hypernatremia in a patient treated with canagliflozin.

SummaryDrugs that inhibit the sodium-glucose co-transporter-2 (SGLT2) are an exciting novel, insulin-independent treatment for diabetes that block glucose reabsorption from the proximal tubules of the kidney, leading to increased glucose excretion and lower blood glucose levels. Inhibition of SGLT2 activity also reduces sodium reabsorption, which together with glycosuria produces a mild diuretic effect with the potential for dehydration and hyperkalemia. We report on a 60-year-old man with uncontrolled type 2 diabetes treated with insulin, glimepiride, metformin and canagliflozin, who was admitted with altered mental status after a syncopal episode. He had a 1-week history of ingestion of Tums for heartburn followed by poor appetite and lethargy. Laboratory work-up showed acute kidney injury, diabetic ketoacidosis (DKA), and parathyroid hormone-independent severe hypercalcemia of 17.4 mg/dl. DKA resolved with insulin treatment, and saline hydration led to improvement in hypercalcemia and renal function over 48 h, but was accompanied by a rapid increase in the serum sodium concentration from 129 to 162 mmol/l despite changing fluids to 0.45% saline. Urine studies were consistent with osmotic diuresis. Hypernatremia was slowly corrected with hypotonic fluids, with improvement in his mental status over the next 2 days. This is the first report of hypercalcemia associated with the use of a SLGT2 inhibitor. Although the exact mechanism is unknown, canagliflozin may predispose to hypercalcemia in patients ingesting excessive calcium because of dehydration from osmotic diuresis, with reduced calcium excretion and possible increased intestinal calcium absorption. Saline therapy and osmotic diuresis may lead to hypernatremia from electrolyte-free water loss.Learning points Canagliflozin, an SGLT2 inhibitor, may cause hypercalcemia in susceptible patients.Although the exact mechanisms are unknown, dehydration from osmotic diuresis and increased intestinal calcium absorption play a role.Close monitoring of serum calcium levels is recommended in patients treated with SGLT2 inhibitors who are elderly, have established hypercalcemia, or take oral calcium supplements.Saline therapy and osmotic diuresis may lead to hypernatremia from electrolyte-free water loss in susceptible patients.

Diabetic Ketoacidosis Alters Plasma Levels of Matrix Metalloproteinases and PMN‐Specific Elastase in Children

IntroductionDiabetic ketoacidosis (DKA) is associated with cerebrovascular complications in children such as vasogenic edema. Circulating matrix metalloproteinases (MMPs), their endogenous inhibitors (TIMPs), and other proteases may contribute to loss of cerebrovascular endothelial cell junctional integrity. Our aim was to determine the effects of acute DKA on systemic MMP/TIMP levels, as well as polymorphonuclear neutrophil(PMN)‐specific elastase.MethodsPlasma was obtained from children ages 4‐17 years old, with type‐1 diabetes, either in an acute DKA state or insulin‐controlled (CON). DKA and CON samples were age‐ and sex‐matched for all experiments. Gelatin zymography was used to assess gelatinolytic activity. ELISA‐based methods were used to assess plasma concentration of proteins.ResultsDKA plasma showed significantly increased MMP‐9 activity(P&lt;0.01) and decreased MMP‐2 activity(P&lt;0.001), compared to CON plasma. MMP‐9 activity in DKA plasma was inversely correlated with pH(P&lt;0.05). DKA plasma had increased circulating levels of MMP‐3(P&lt;0.05), MMP‐8(P&lt;0.001) and TIMP‐4(P&lt;0.01). In addition, a significant increase in circulating levels of PMN elastase(P&lt;0.001) was detected in DKA plasma.SummaryDKA is associated with dynamic changes in plasma levels of MMP‐2, MMP‐3, MMP‐8, MMP‐9 and TIMP‐4, as well as PMN elastase, which may contribute to loss of blood‐brain barrier integrity.