Alternative Management Of Diabetic Ketoacidosis In A Brazilian Pediatric Emergency Department
Go to: DKA is a severe metabolic derangement characterized by dehydration, loss of electrolytes, hyperglycemia, hyperketonemia, acidosis and progressive loss of consciousness that results from severe insulin deficiency combined with the effects of increased levels of counterregulatory hormones (catecholamines, glucagon, cortisol, growth hormone). The biochemical criteria for diagnosis are: blood glucose > 200 mg/dl, venous pH <7.3 or bicarbonate <15 mEq/L, ketonemia >3 mmol/L and presence of ketonuria. A patient with DKA must be managed in an emergency ward by an experienced staff or in an intensive care unit (ICU), in order to provide an intensive monitoring of the vital and neurological signs, and of the patient's clinical and biochemical response to treatment. DKA treatment guidelines include: restoration of circulating volume and electrolyte replacement; correction of insulin deficiency aiming at the resolution of metabolic acidosis and ketosis; reduction of risk of cerebral edema; avoidance of other complications of therapy (hypoglycemia, hypokalemia, hyperkalemia, hyperchloremic acidosis); identification and treatment of precipitating events. In Brazil, there are few pediatric ICU beds in public hospitals, so an alternative protocol was designed to abbreviate the time on intravenous infusion lines in order to facilitate DKA management in general emergency wards. The main differences between this protocol and the international guidelines are: intravenous fluid will be stopped when oral fluids are well tolerated and total deficit will be replaced orally; if potassium analysis still indicate need for replacement, it will be given orally; subcutaneous rapid-acting insulin analog is administered at 0.15 U/kg dose every 2-3 hours until resolution of metabolic acidosis; Continue reading >>
Respiratory Failure In Diabetic Ketoacidosis
Go to: INTRODUCTION Ketoacidosis in subjects with type 1, or less frequently, type 2 diabetes mellitus remains a potentially life-threatening diabetic manifestation. The subject has justifiably attracted attention in the literature. Sequential reviews[1-9] have documented important changes in the clinical concepts that are related to diabetic ketoacidosis (DKA) and its management. A large number of case series of DKA have addressed various aspects of its clinical presentation and management. For this review, we selected representative studies focused on management, outcome, age differences, gender differences, associated morbid conditions, ethnicity and prominent clinical and laboratory features[10-35]. In recognition of the complexity of treatment, the recommendation to provide this care in intensive care units was made more than 50 years ago. Severe DKA is treated in intensive care units today. Evidence-based guidelines for the diagnosis and management of DKA have been published and frequently revised in North America[37,38] and Europe. Losses of fluids and electrolytes, which are important causes of morbidity and mortality in DKA, vary greatly between patients. Quantitative methods estimating individual losses and guiding their replacement have also been reported[40,41]. The outcomes of DKA have improved with new methods of insulin administration and adherence to guidelines[43-46]. The aim of treatment is to minimize mortality and prevent sequelae. One study documented that the target of zero mortality is feasible. However, mortality from DKA, although reduced progressively in the early decades after the employment of insulin treatment, remains high. Up to fifty plus years ago, mortality from DKA was between 3% and 10%[1,16]. A recent review re Continue reading >>
Cerebral Edema In Children With Diabetic Ketoacidosis
Abstract Cerebral edema is the most frequent serious complication of diabetic ketoacidosis (DKA) in children, occurring in 1% to 5% of DKA episodes. The rates of mortality and permanent neurologic morbidity from this complication are high. The pathophysiologic mechanisms underlying DKA-related cerebral edema are unclear. A number of past and more recent studies have investigated biochemical and therapeutic risk factors for the development of cerebral edema. Recent studies have shown that a higher initial serum urea nitrogen concentration and lower initial partial pressure of carbon dioxide are associated with the development of cerebral edema. This and other information suggests that the pathophysiology of DKA-related cerebral edema may involve cerebral ischemia. Preview Unable to display preview. Download preview PDF. Continue reading >>
Vbg Versus Abg
OVERVIEW Venous blood gases (VBG) are widely used in the emergency setting in preference to arterial blood gases (ABG) as a result of research published since 2001 The weight of data suggests that venous pH has sufficient agreement with arterial pH for it to be an acceptable alternative in clinical practice for most patients Nevertheless acceptance of this strategy has been limited by some specialties and maybe inappropriate in some settings; for instance there is no data to confirm that this level of agreement is maintained in shock states or mixed acid-base disturbances Clinically acceptable limits of agreement for blood gas parameters remains poorly defined ARTERIAL BLOOD GAS PROS AND CONS Advantages gold standard test for determining the arterial metabolic millieu (pH, PaCO2, HCO3) can determine PaO2 Disadvantages pH, PCO2 (if normocapnic), HCO3 and base excess from a VBG are usually adequate for clinical decision making SpO2 is usually sufficient for clinical decision making unless pulse oximetry is unreliable for other reasons (e.g. shock state, poor pick up) painful (should be performed with local anaesthetic in conscious patients) increased risk of bleeding and hematoma risk of pseudo aneurysm and AV fistula infection nerve injury digital ischemia injury to staff delays in care serial exams may be needed venous sampling may better represent the tissue milieu CORRELATION BETWEEN VBG AND ABG pH Good correlation pooled mean difference: +0.035 pH units pCO2 good correlation in normocapnia non-correlative in severe shock 100% sensitive in detecting arterial hypercarbia in COPD exacerbations using cutoff of PaCO2 45 mmHg and laboratory based testing (McCanny et al, 2012), i.e. if VBG PCO2 is normal then hypercapnia ruled out (PaCO2 will be normal), though this conflic Continue reading >>
Beta-hydroxybutirate Levels As A Determinant For The Success Of Diabetic Ketoacidosis Management.
Abstract AIM: To obtain a greater understanding of the diagnosis and evaluation of success in diabetic ketoacidosis management. METHODS: A prospective observational study was performed on patients with diabetic ketoacidosis at the Emergency Unit of Cipto Mangunkusumo General Hospital. All patients that were admitted were had their blood glucose, beta-hydroxybutirate, acetoacetate, pH, pCO2, HCO3, anion gap and consciousness levels serially monitored on upon admittance (0 hour) and the 2nd, 6th, 12th, 18th and 24(th) hours. The correlation coefficient of each examination was also calculated. The benefit of serial examination of each variable was also determined for each ketoacidosis undergoing the study. RESULTS: Out of the 19 available samples, a strong negative correlation was found between beta-hydroxybutirate and pH with a value of r>0.5 (from -0.524 to -0.833 with p<0.05) for 24 hours, compared to acetoacetate with the lowest r of -0.515 to -0.731 lasting up to 12 hours. Blood glucose and pH is correlated only at 0 hour, the same with the correlation between beta-hydroxybutirate and HCO(3). pCO2 and anion gap is better compared to that of blood glucose and acetoacetate. There is no correlation between the three and the level of consciousness. Significant serial examinations to perform are blood glucose, beta-hydroxybutirate, and HCO(3). CONCLUSION: beta-Hydroxybutirate has a stronger correlation compared to blood glucose and or acetoacetate towards pH, pCO2, HCO(3), and anion gap. Patients with ketoacidosis are recommended to undergo blood beta-hydroxybutirate examination. Serial examination should be performed for blood glucose, beta-hydroxybutirate, and bicarbonate. Continue reading >>
- Diabetes management 3: the pathogenesis and management of diabetic foot ulcers
- World's first diabetes app will be able to check glucose levels without drawing a drop of blood and will be able to reveal what a can of coke REALLY does to sugar levels
- PredictBGL is a diabetes management app predicting fluctuations in blood sugar levels
Blood Gas Measurements In Dka: Are We Searching For A Unicorn?
Introduction Recently there have been numerous publications and discussions about whether VBGs can replace ABGs in DKA. The growing consensus is that VBGs are indeed adequate. Eliminating painful, time-consuming arterial blood draws is a huge step in the right direction. However, the ABG vs. VBG debate overlooks a larger point: neither ABG nor VBG measurements are usually helpful. It is widely recommended to routinely obtain an ABG or VBG, for example by both American and British guidelines. Why? Is it helping our patients, or is it something that we do out of a sense of habit or obligation? Diagnosis of DKA: Blood gas doesn’t help These are the diagnostic criteria for DKA from the America Diabetes Association. They utilize either pH or bicarbonate in a redundant fashion to quantify the severity of acidosis. It is unclear what independent information the pH adds beyond what is provided by the bicarbonate. Practically speaking, the blood gas doesn’t help diagnose DKA. This diagnosis should be based on analysis of the metabolic derangements in the acid-base status (e.g. anion gap, beta-hydroxybutyrate level). The addition of a blood gas to serum chemistries only adds information about the respiratory status, which does not help determine if the patient has ketoacidosis. Management: Does the pH help? It is debatable whether knowing or attempting to directly “treat” the pH is helpful. The pH will often be very low, usually lower than would be expected by looking at the patient. This may induce panic. However, it is actually a useful reminder that acidemia itself doesn't necessarily cause instability (e.g. healthy young rowers may experience lactic acidosis with a pH <7 during athletic exertion; Volianitis 2001). A question often arises regarding whether bicarbonate Continue reading >>
Is A Vbg Just As Good As An Abg?
Faculty Peer Reviewed A rapid response is called overhead. As white-coated residents rush to the patient’s bedside, the medical consult starts to shout out orders to organize the chaos. “What’s the one-liner?” “Whose patient is this?” And of course, “Who’s drawing the labs?” Usually, at this point, the intern proceeds to collect the butterfly needle, assorted colored tubes, and the arterial blood gas (ABG) syringe. If lucky, there’s a strong pulse. The intern pauses, directs the needle, and hopes for that pulsatile jet of bright red blood to come through the clear tubing. If successful, a sigh of relief. If not, a wave of defeat and more butterfly needles are scattered across the bed as multiple residents attempt to get the elusive arterial blood. Obtaining the ABG is considered almost a rite of passage for the medicine intern. However in ill patients with thready pulses, it can be difficult to obtain. Also, getting the ABG is not without its complications. Significant pain, hematoma, aneurysm formation, thrombosis or embolization, and needlestick injuries are all risks . Given these risks, the question is whether we are subjecting our patients to undue pain and potential complications when a venous blood gas (VBG) would suffice. An ABG provides important data including the pH, arterial oxygen tension (PaO2), carbon dioxide tension (PaCO2), arterial oxyhemoglobin saturation (SaO2), lactate, and electrolytes. In certain instances, an ABG is considered unequivocal. In order to calculate an A-a gradient, the ABG is necessary. To assess whether that HIV patient with PCP pneumonia needs steroids, we use the A-a gradient to help guide out treatment plan . However, are there other patient populations in which the VBG is just as good as the ABG? Brande Continue reading >>
- Kris Jenner Says Rob Kardashian Wants to Return to KUWTK Following Diabetes Diagnosis: ''He Just Wants to Feel Good''
- Type 2 diabetes can be reversed in just four months, trial shows
- Type 2 diabetes IS reversible: Eating just 600 calories a day for 8 weeks can save the lives of millions of sufferers
Mary Ann Liebert, Inc. - Home
Introduction: Diabetic ketoacidosis (DKA) affects many children with type 1 diabetes. Insulin treatment of DKA is traditionally guided by changes in the blood glucose levels and blood gases, whereas β-hydroxybutyrate (β-OHB)—the main ketoacid causing acidosis—is rarely measured. The purpose of this study was to evaluate if bedside monitoring of blood β-OHB levels can simplify management of DKA through elimination of superfluous laboratory monitoring. Methods: Our emergency department treated 68 children with DKA using a standard protocol with monitoring of venous pH, partial pressure of CO2 (pCO2), bicarbonate, glucose, blood urea nitrogen, and electrolytes (two to 10 time points per patient). Venous β-OHB levels were measured using the Precision Xtra™ meter (MediSense/Abbott Diabetes Care, Abbott Park, IL) and, on duplicate batched serum samples, using a reference laboratory method (Cobas Mira Plus; Roche Diagnostics, Indianapolis, IN). Correlations between bedside meter β-OHB and other parameters were evaluated in a series of general linear models with a time series covariance structure fit using spatial power law. Results: The bedside meter β-OHB levels were significantly correlated with pH (r = –0.63; P <0.0001), bicarbonate (r = –0.74; P <0.0001), and pCO2 (r = –0.55; P <0.0001) at all points of measurement during the treatment (unadjusted Pearson correlations). The pH, bicarbonate, and pCO2 were entered into separate time series analysis models with treatment duration as a measure of time. The results confirmed that bedside levels of β-OHB correlated very closely with time-dependent levels of venous pH, bicarbonate, and pCO2. Good agreement between the two methods of β-OHB measurement (r = 0.92; P <0.0001) was confirmed using the Bland-Altman p Continue reading >>
Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus. Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness. A person's breath may develop a specific smell. Onset of symptoms is usually rapid. In some cases people may not realize they previously had diabetes. DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances. Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids. DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies. DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine. The primary treatment of DKA is with intravenous fluids and insulin. Depending on the severity, insulin may be given intravenously or by injection under the skin. Usually potassium is also needed to prevent the development of low blood potassium. Throughout treatment blood sugar and potassium levels should be regularly checked. Antibiotics may be required in those with an underlying infection. In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended. Rates of DKA vary around the world. In the United Kingdom, about 4% of people with type 1 diabetes develop DKA each year, while in Malaysia the condition affects about 25% a year. DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost univ Continue reading >>
Diabetic Ketoacidosis Workup
Approach Considerations Diabetic ketoacidosis is typically characterized by hyperglycemia over 250 mg/dL, a bicarbonate level less than 18 mEq/L, and a pH less than 7.30, with ketonemia and ketonuria. While definitions vary, mild DKA can be categorized by a pH level of 7.25-7.3 and a serum bicarbonate level between 15-18 mEq/L; moderate DKA can be categorized by a pH between 7.0-7.24 and a serum bicarbonate level of 10 to less than 15 mEq/L; and severe DKA has a pH less than 7.0 and bicarbonate less than 10 mEq/L.  In mild DKA, anion gap is greater than 10 and in moderate or severe DKA the anion gap is greater than 12. These figures differentiate DKA from HHS where blood glucose is greater than 600 mg/dL but pH is greater than 7.3 and serum bicarbonate greater than 15 mEq/L. Laboratory studies for diabetic ketoacidosis (DKA) should be scheduled as follows: Repeat laboratory tests are critical, including potassium, glucose, electrolytes, and, if necessary, phosphorus. Initial workup should include aggressive volume, glucose, and electrolyte management. It is important to be aware that high serum glucose levels may lead to dilutional hyponatremia; high triglyceride levels may lead to factitious low glucose levels; and high levels of ketone bodies may lead to factitious elevation of creatinine levels. Continue reading >>
Management Of Diabetic Ketoacidosis In Extreme Insulin Resistance
Abstract: Background: Management of diabetic ketoacidosis (DKA) in extreme insulin resistance (IR) is not well-described in the literature. Clinical case: The patient is an 18-year old young man with extreme IR due to Rabson-Mendenhall Syndrome (mutation of the insulin receptor). Two weeks prior to a routine visit at the National Institutes of Health (NIH), he underwent a root canal for an abscessed tooth, and did not take prescribed antibiotics. At NIH, labs showed A1c 14%, bicarbonate 26-30, and chronic glucosuria and ketonuria. He continued his home insulin regimen of 1500 units/day of U-500. Antibiotics were initiated; he was discharged in hemodynamically stable condition. Two days later, he was admitted to another hospital with DKA, pH 7.08, pCO2 27, bicarbonate 8, and worsened jaw pain. Insulin drip was started at 100 U/hr, increased on day 1 to 1000 U/hr, and 2000 U/hr on day 2 without resolution of acidosis. CT showed a dental abscess extending to adjacent soft tissue, the likely trigger for DKA. Due to lack of improvement despite IV antibiotics, bicarbonate was given, and dental extraction was performed, after which the patient developed septic shock requiring pressor support for 24 hrs. He improved thereafter, and was transitioned back to subcutaneous insulin. Conclusion: This case demonstrates the complexity of managing DKA in a patient with extreme IR. Routine diabetes care in extreme IR requires high-dose insulin, typically >200 U/day. Despite high-dose insulin, good glycemic control is often not achieved. DKA management in extreme IR is a major challenge due to the unusually high doses of insulin required, raising major safety concerns for providers not experienced with extreme IR. As seen in this case, insulin as high as 2000 U/hr can be safely administer Continue reading >>
Arterial Blood Gases (blood Gases), Acidosis And Alkalosis
Sample The better choice is the Radial artery. The sample may be taken from the femoral artery or brachial. The tests are done immediately because oxygen and carbon dioxide are unstable. Arterial blood is better than the venous blood. For arterial blood don't use the tourniquet and no pull on the syringe plunger. For venous blood syringe or tubes are completely filled and apply a tourniquet for few seconds. Arterial VS Venous blood Arterial blood gives good mixture of blood from various areas of the body. Venous blood gives information of the local area from where the blood sample is taken. Metabolism of the extremity varies from area to area. Arterial blood measurement gives the better status of the lung oxygenating the blood. Arterial blood gives information about the ability of the lung to regulate the acid-base balance through retention or release of CO2. Precautions for the collection of blood Avoid pain and anxiety to the patient which will lead to hyperventilation. Hyperventilation due to any cause leads to decreased CO2 and increased pH. Keep blood cool during transit. Don't clench finger or fist. This will leads to lower CO2 and increased acid metabolites. pCO2 values are lower in the sitting or standing position in comparison with the supine position. Don't delay the performance of the test. Avoid air bubbles in the syringe. Excess of heparin decreases the pCO2 may be 40% less. Not proper mixing of the blood before running the test. Purpose of the test This test is done on the mostly hospitalized patient. Mostly the patients are on ventilator or unconscious. For patients in pulmonary distress. To assess the metabolic (renal) acid-base and electrolytes imbalance. Its primary use is to monitor arterial blood gases and pH of blood. Also used to monitor oxygenatio Continue reading >>
- Diagnostic accuracy of resting systolic toe pressure for diagnosis of peripheral arterial disease in people with and without diabetes: a cross-sectional retrospective case-control study
- Drinking Red Wine With Type 2 Diabetes: Resveratrol Benefits Heart Health By Reducing Arterial Stiffness
- Lower Blood Sugar Naturally to Prevent High Blood Sugar from Leading to Diabetes
About Diabetic ketoacidosis must be managed with a defined well documented and communicated plan It is seen in new presentations and Type 1 diabetics with intercurrent illness and poor control Patients need education on not to stop insulin when unwell and to seek medical help There is a severe deficit of Fluid, Insulin and Potassium Aetiology Glucose and K+ usually enter cells through the actions of Insulin In DKA the Insulin deficit leads to cell starvation and a switch to burning fatty acids The beta-oxidation of fats creates acid byproducts which lower the pH At the same time there is a profound osmotic diuresis due to the severe hyperglycaemia Vomiting can compound the fluid losses Clinical Recent thirst, polyuria and polydipsia, vomiting and breathlessness Severe hyperventilating Kussmaul's respiration to blow off CO2 Smell of acetone "nail varnish" on the breath (not all of us can smell it) Profound dehydration and volume loss from polyuria due to glycosuria Sunken eyes, reduced skin turgor, hypotensive, tachycardia, oliguric Possibly sepsis - chest and urine or elsewhere Investigations Ketonuria 3+ and glycosuria and Raised [glucose] There is a low bicarbonate < 15 mmols/l FBC - elevated WCC and CRP may suggest infection U&E - may show mild uraemia and hypernatraemia. Initially raised K+ due to acidosis but potassium levels fall with Insulin administration as it oves into the intracellular space so U&E needs repeated monitoring Glucose - high usually > 20 mmol/L Arterial Blood gas There is an increased Anion gap CXR if chest disease eg pneumonia suspected CT scan if comatose to exclude other diagnoses Management In a nutshell is careful replacement of Insulin, Fluid, Potassium. Involve Endocrinology and ITU support early. Ensure treatment plans well documented. E Continue reading >>
Cc: Test 3 - Dka And Hhns Case Study
Sort DKA Case Study Mr. Jones, a 65 year old male, is admitted to the Emergency Department in an unconscious state. His family tells you he has a history of IDDM. Mr. Jones' daughter says that he had had the flu and has been unable to eat or drink very much for several days. She is not sure whether he has taken insulin in the last 24 hours. On admission, his vital signs are: Temperature 101.8 degrees F. Pulse 120/minute, weak and thready Respiration 22/minute deep (with fruity breath odor) Blood pressure 64/42 mmHg A basic metabolic profile, complete blood counts, and arterial blood gases are drawn. The nurse initiates an IV infusion of normal saline. ... Does insulin Stimulate or Inhibit each of the following processes? ____ glucose uptake by the cells ____ glycogenolysis ____ gluconeogenesis ____ glycogenesis ____ lipolysis ____ protein catabolism Stimulate Inhibit Inhibit List 5 counterregulatory hormones and their impact on this diabetic emergency. Blood glucose- Serum osmolality- BUN- Potassium- Arterial pH- Arterial pCO2- glucagon - glucagon is a hormone produced by the pancreas that, along with insulin, controls the level of glucose in the blood. Glucagon has the opposite effect of insulin. It increases the glucose levels in blood. Glucagon, the drug, is a synthetic (man-made) version of human glucagon and is manufactured by genetic engineering using the bacteria Escherichia coli. Glucagon is used to increase the blood glucose level in severe hypoglycemia (low blood glucose). Glucagon is a glucose-elevating drug. epinephrine - cortisol - one major function of cortisol is the regulation of glucose concentration. It increases blood glucose through stimulation of hepatic glucogenesis (conversion of amino acids to glucose) and inhibiting protein synthesis norepinephr Continue reading >>
- NZ case study; A citizen scientist controls autoimmune diabetes without insulin, with a low carb diet, a glucose meter, and metformin.
- Diagnostic accuracy of resting systolic toe pressure for diagnosis of peripheral arterial disease in people with and without diabetes: a cross-sectional retrospective case-control study
- Maternal obesity as a risk factor for early childhood type 1 diabetes: a nationwide, prospective, population-based case–control study
Exam Shows Diffuse Abdominal Tenderness With Guarding.
A 14 y/o female is brought to the emergency department by her mother after being found unresponsive at home. She had been ill the day before with nausea and vomiting, but was not running a fever. Her parents had kept her home from school that day. When her mother came home at lunchtime to check on her, she was very lethargic and not responding coherently. By the time she arrived at the hospital, she had to be brought in to the ED on a gurney. Initial evaluation showed O2 sat 100% on room air, pulse 126, respirations 30, BP 92/68, temperature 101.2 F. She appears pale, mucous membranes are dry and she only responds to painful stimuli. Exam shows diffuse abdominal tenderness with guarding. Differential diagnosis? What initial treatment would you suggest? What labs would you order? Any xrays or additional studies? CBC WBC 23,500 Hgb 14.2 g/dL Hct 45% Platelets 425,000 BMP Sodium 126 Potassium 5.2 Chloride 87 CO2 <5 BUN 32 Creatinine 1.5 Glucose 1,376 Arterial Blood Gases pH 7.19 Po2 100 mm Hg HCO3 7.5 mmo/L Pco2 20 mm Hg Sao2 98% (room air) Urine Specific gravity 1.015 Ketones 4+ Leukocytes few Glucose 4+ Nitrates 0 RBCs many Diabetic ketoacidosis (DKA) is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. DKA occurs mostly in type 1 diabetics. It causes nausea, vomiting, and abdominal pain and can progress to cerebral edema, coma, and death. DKA is diagnosed by detection of hyperketonemia and anion gap metabolic acidosis in the presence of hyperglycemia. Treatment involves volume expansion, insulin replacement, and prevention of hypokalemia. Symptoms and signs of DKA Nausea & vomiting Abdominal pain--particularly in children Lethargy and somnolence Kussmaul respirations Hypotension Tachycardia Fruity breath Continue reading >>