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Dka Abg Example

Hyperglycemia: Dka And Hhs

Hyperglycemia: Dka And Hhs

Anne Marie Mattingly Assistant Professor of Medicine Division of Pulmonary and Critical Care Goals of Treatment Accurately diagnose DKA and/or HHS Provide optimal volume resuscitation Use insulin to stop life-threatening metabolic derangements Correct dangerous electrolyte abnormalities Determine the precipitating factors and provide any urgent treatment Points To Learn Normal glucose metabolism Pathophysiology of hyperglycemic syndromes Basic management (and why it works) Fluids Insulin Electrolytes Common precipitating factors Transitioning to SQ insulin (and the floor) *these will parallel the goals of treatment…. 3 DKA, HHS, or neither? 47 year old with DM (on insulin) several days of nausea, vomiting, diarrhea, and abdominal pain missed insulin yesterday labs show: 133 3.5 107 16 34 2.6 407 ABG: pending UA: SpGrav 1.024, 1+ ketones DKA, HHS, or neither? 24 year old with DM (on insulin) several days of nausea, vomiting, diarrhea, and abdominal pain missed insulin yesterday labs show: 136 3.5 95 25 15 1.2 392 ABG: 7.38/38/95/25/99% RA *same symptoms, also missed his insulin *BG still elevated *bicarbonate is 25 and BUN/Cr not as high *pH normal 5 DKA, HHS, or neither? 81 year old SNF resident with DM (diet-controlled), aflutter, CAD, HTN referred to ED from SNF for chest pain, mental status change, and low BP EKG shows rapid a-fib (rate and pain resolve with IVF) labs show: 152 3.6 110 26 65 1.5 916 Lactate 4.0 *not even on insulin *sodium high, but bicarb normal and she has elevated lactate 6 DKA, HHS, or neither? 55 year old SNF resident with DM (on metformin), cerebral palsy, chronic constipation unable to stool for several days, today vomited repeatedly and then aspirated hypotensive and hypoxic labs show: 142 3.1 91 27 16 0.37 499 ABG: 7.47/31/105/22/96% o Continue reading >>

Dka, “answers”

Dka, “answers”

1. When you are suspicious for DKA do you obtain a VBG or an ABG? How good is a VBG for determining acid/base status? Diabetic ketoacidosis (DKA) is defined by five findings: acidosis (pH < 7.30, serum bicarbonate (HCO3) < 18 mEq/L, the presence of ketonuria or ketonemia, an anion gap > 10 mEq/L, and a plasma glucose concentration > 250 mg/dl. It is one of the most serious complications of diabetes seen in the emergency department. The mortality rate of hospitalized DKA patients is estimated to be between 2-10% (Lebovitz, 1995). As a result, its prompt recognition is vital to improving outcomes in these patients. As a result, emergency physicians have long relied on the combination of hyperglycemia and anion gap metabolic acidosis to help point them in the correct diagnostic direction. In the assessment of the level of acidosis in a DKA patient, an arterial blood gas (ABG) has long been thought of as much more accurate than a venous blood gas (VBG) and thus necessary in evaluating a DKA patient’s pH and HCO3 level, two values often used to direct treatment decisions. An ABG is more painful, often time-consuming and labor intensive as it may involve multiple attempts. In addition, ABGs can be complicated by radial artery aneurysms, radial nerve injury and compromised blood supply in patients with peripheral vascular disease or inadequate ulnar circulation. A VBG is less painful, can obtained at the time of IV placement, and is therefore less time consuming. But is it good enough to estimate acid/base status in these patients? Brandenburg, et al. compared arterial and venous blood gas samples in DKA patients taken at the exact same time prior to treatment and found a mean difference in pH between the arterial and venous samples to be only 0.03, with a Pearson’s correl Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find the Pre-diabetes (Impaired Glucose Tolerance) article more useful, or one of our other health articles. See also the separate Childhood Ketoacidosis article. Diabetic ketoacidosis (DKA) is a medical emergency with a significant morbidity and mortality. It should be diagnosed promptly and managed intensively. DKA is characterised by hyperglycaemia, acidosis and ketonaemia:[1] Ketonaemia (3 mmol/L and over), or significant ketonuria (more than 2+ on standard urine sticks). Blood glucose over 11 mmol/L or known diabetes mellitus (the degree of hyperglycaemia is not a reliable indicator of DKA and the blood glucose may rarely be normal or only slightly elevated in DKA). Bicarbonate below 15 mmol/L and/or venous pH less than 7.3. However, hyperglycaemia may not always be present and low blood ketone levels (<3 mmol/L) do not always exclude DKA.[2] Epidemiology DKA is normally seen in people with type 1 diabetes. Data from the UK National Diabetes Audit show a crude one-year incidence of 3.6% among people with type 1 diabetes. In the UK nearly 4% of people with type 1 diabetes experience DKA each year. About 6% of cases of DKA occur in adults newly presenting with type 1 diabetes. About 8% of episodes occur in hospital patients who did not primarily present with DKA.[2] However, DKA may also occur in people with type 2 diabetes, although people with type 2 diabetes are much more likely to have a hyperosmolar hyperglycaemic state. Ketosis-prone type 2 diabetes tends to be more common in older, overweight, non-white people with type 2 diabetes, and DKA may be their Continue reading >>

Blood Gas Measurements In Dka: Are We Searching For A Unicorn?

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 >>

Diabetic Emergencies, Part 5: Dka Case Studies

Diabetic Emergencies, Part 5: Dka Case Studies

Case Study 1 A 32-year-old male with type 1 diabetes since the age of 14 years was taken to the emergency room because of drowsiness, fever, cough, diffuse abdominal pain, and vomiting. Fever and cough started 2 days ago and the patient could not eat or drink water. He has been treated with an intensive insulin regimen (insulin glargine 24 IU at bedtime and a rapid-acting insulin analog before each meal). On examination he was tachypneic, his temperature was 39° C (102.2° F), pulse rate 104 beats per minute, respiratory rate 24 breaths per minute, supine blood pressure 100/70 mmHg; he also had dry mucous membranes, poor skin turgor, and rales in the right lower chest. He was slightly confused. Rapid hematology and biochemical tests showed hematocrit 48%, hemoglobin 14.3 g/dl (143 g/L), white blood cell count 18,000/ μ l, glucose 450 mg/dl (25.0 mmol/L), urea 60 mg/dl (10.2 mmol/L), creatinine 1.4 mg/dl (123.7 μ mol/L), Na+ 152 mEq/L, K+ 5.3 mEq/L, PO4 3−2.3 mEq/L (0.74 mmol/L), and Cl− 110 mmol/L. Arterial pH was 6.9, PO 2 95 mmHg, PCO 2 28 mmHg, HCO 3−9 mEq/L, and O 2 sat 98%. The result of the strip for ketone bodies in urine was strongly positive and the concentration of β-OHB in serum was 3.5 mmol/L. Urinalysis showed glucose 800 mg/dl and specific gravity 1030. What is your diagnosis? The patient has hyperglycemia, ketosis, and metabolic acidosis. Therefore, he has DKA. In addition, because of the pre-existing fever, cough, localized rales on auscultation and high white blood cell count, a respiratory tract infection should be considered. The patient is also dehydrated and has impaired renal function. Do you need more tests to confirm the diagnosis? Determination of the effective serum osmolality and anion gap should be performed in all patients presenti Continue reading >>

Original Article Correlation Between Peripheral Venous And Arterial Blood Gas Measurements In Patients Admitted To The Intensive Care Unit: A Single-center Study

Original Article Correlation Between Peripheral Venous And Arterial Blood Gas Measurements In Patients Admitted To The Intensive Care Unit: A Single-center Study

Introduction The acid–base and respiratory status of critical patients are commonly ascertained by means of arterial blood gas (ABG) analysis. Nevertheless, the test can cause patients to experience discomfort, and its associated complications include arterial injury, thrombosis or embolization, hematoma, aneurysm formation, and reflex sympathetic dystrophy [1,2]. A further drawback for health care providers is the possibility of a needle stick injury when performing an ABG. A comparatively safer procedure is venous blood gas (VBG) analysis, which poses fewer risks to both the patients and health care professionals. VBG may eventually take the place of ABG analysis in determining acid–base status. In contrast to earlier studies, which questioned the precision of VBG values [3–5], more recent evidences indicate a concurrence of ABG and VBG values [6–14]. However, as far as we can determine, the correlation between all parameters typically used in arterial and peripheral VBG samples as found in a broad population of intensive care unit (ICU) patients has not been studied previously. An earlier study investigated whether the similarities between ABG and VBG values are sufficient for the respiratory and dynamic acid–base conditions. For this evaluation, each patient provided multiple paired ABG and VBG samples during the length of their ICU treatment. The purpose of this study was to investigate the correlation of ABG and peripheral VBG samples for all common parameters (bicarbonate, total CO2, pH, and PCO2) in an ICU patient population exhibiting a variety of pathologies. Specific attention was given to the analysis of each patient's multiple paired arterial and venous samples. Methods A single-center, prospective trial was performed from April 2010 to September Continue reading >>

Diabetic Ketoacidosis And Hyperglycaemic Hyperosmolar State

Diabetic Ketoacidosis And Hyperglycaemic Hyperosmolar State

The hallmark of diabetes is a raised plasma glucose resulting from an absolute or relative lack of insulin action. Untreated, this can lead to two distinct yet overlapping life-threatening emergencies. Near-complete lack of insulin will result in diabetic ketoacidosis, which is therefore more characteristic of type 1 diabetes, whereas partial insulin deficiency will suppress hepatic ketogenesis but not hepatic glucose output, resulting in hyperglycaemia and dehydration, and culminating in the hyperglycaemic hyperosmolar state. Hyperglycaemia is characteristic of diabetic ketoacidosis, particularly in the previously undiagnosed, but it is the acidosis and the associated electrolyte disorders that make this a life-threatening condition. Hyperglycaemia is the dominant feature of the hyperglycaemic hyperosmolar state, causing severe polyuria and fluid loss and leading to cellular dehydration. Progression from uncontrolled diabetes to a metabolic emergency may result from unrecognised diabetes, sometimes aggravated by glucose containing drinks, or metabolic stress due to infection or intercurrent illness and associated with increased levels of counter-regulatory hormones. Since diabetic ketoacidosis and the hyperglycaemic hyperosmolar state have a similar underlying pathophysiology the principles of treatment are similar (but not identical), and the conditions may be considered two extremes of a spectrum of disease, with individual patients often showing aspects of both. Pathogenesis of DKA and HHS Insulin is a powerful anabolic hormone which helps nutrients to enter the cells, where these nutrients can be used either as fuel or as building blocks for cell growth and expansion. The complementary action of insulin is to antagonise the breakdown of fuel stores. Thus, the relea Continue reading >>

Blood Gas Interpretation

Blood Gas Interpretation

The body normally controls the pH of blood within a tight range. One must always remember that pH is a logarithmic scale and so a change from 8 to 7 is a ten-fold increase in H+ concentration. A normal intracellular pH is required for the functioning of many enzyme systems. When blood becomes profoundly acidotic (pH<7) then cellular function becomes impossible and death ensues. There are a lot of texts available describing the causes of the respiratory and metabolic acidosis and alkalosis. However the best way to learn how to interpret blood gases is to practice. Normal Blood gas. The only abnormal result here is the pO2, however this is a venous gas and so the pO2 should be low. This is therefore a normal blood gas. It is important to rule out a diabetic ketoacidosis in children with diabetes who are unwell with high blood sugars. The learning point here is that blood gas analysis doesn’t just have to be performed on arterial blood. A lot can be established from venous or capillary samples. Respiratory Acidosis – Respiratory failure (bronchiolitis). This baby has bronchiolitis. There is a respiratory acidosis. Notice the high oxygen secondary to aggressive oxygen therapy. Treatment of bronchiolitis is supportive, ie oxygen and fluids. Respiratory Acidosis – respiratory failure secondary to acute exacerbation of asthma This is a respiratory acidosis. This boy is in respiratory failure secondary to an acute exacerbation of his asthma. A “silent chest” where you can only just hear breath sounds is a very serious clinical sign. This boy will need aggressive treatment and likely intubation and transfer to PICU. Respiratory Acidosis with metabolic compensation– Respiratory failure (pneumonia) This boy has pneumonia associated with respiratory failure. There is a Continue reading >>

The Abcs Of Abgs: Blood Gas Analysis

The Abcs Of Abgs: Blood Gas Analysis

A systematic and step-wise process based upon pH shift is the key to correct interpretation and application of arterial blood gas results In a previous article, “The Pitfalls of Arterial Blood Gases” (RT, April 2013), I described how simple pre-analytical, analytical, and post-analytical errors can produce arterial blood gas test results (ABGs) that are of little or no value, and perhaps even dangerous. In this article, I will assume that we have avoided all of those pitfalls and and will discuss how to interpret valid ABG results. (Some of the foundational information in this article is necessary for those new to interpreting. I encourage more experienced practitioners to bear with me.) This article will not attempt to discuss all of the possible causes or disease states that could relate to the results. Neither will it attempt to go into the interpretation of electrolytes or co-oximetry results. Adequate review of these subjects could require—in fact, have required—whole textbooks, and are beyond the scope of this article. What Is Normal? To interpret ABGs, we first need to know the normal values for the various analytes. Where do these normal values come from? They mostly come from collected results of volunteers or study subjects who appear to have uncompromised lungs and gas exchange. Researchers plotted the results of the various parameters, found the collective center of the bell-shaped curve of data, and declared the results shown in Table 1. Whichever range you and your facility prefer, it is important to think in terms of a normal range, not a single, specific, always “normal” value—except when it comes to pH for interpreting acid-base balance. We will get to why shortly. It is also vital to remember that the aggregate “normal” value is a con Continue reading >>

Respiratory Failure In Diabetic Ketoacidosis

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[36]. Severe DKA is treated in intensive care units today[31]. Evidence-based guidelines for the diagnosis and management of DKA have been published and frequently revised in North America[37,38] and Europe[39]. 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[42] 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[42]. However, mortality from DKA, although reduced progressively in the early decades after the employment of insulin treatment[1], remains high. Up to fifty plus years ago, mortality from DKA was between 3% and 10%[1,16]. A recent review re Continue reading >>

Agreement Between Central Venous And Arterial Blood Gas Measurements In The Intensive Care Unit

Agreement Between Central Venous And Arterial Blood Gas Measurements In The Intensive Care Unit

Go to: Abstract Background and objectives: Venous blood gas (VBG) analysis is a safer procedure than arterial blood gas (ABG) analysis and may be an alternative for determining acid-base status. The objective of this study was to examine the agreement between ABG and central VBG samples for all commonly used parameters in a medical intensive care unit (ICU) population. Design, setting, participants, & measurements: We performed a single-center, prospective trial to assess the agreement between arterial and central VBG measurements in a medical ICU. Adult patients who were admitted to the ICU and required both a central venous line and an arterial line were enrolled. When an ABG was performed, a central venous sample was obtained to examine the agreement among the pH, Pco2, and bicarbonate. Data comparing central and peripheral VBG values were also obtained. Results: The mean arterial minus venous difference for pH, Pco2, and bicarbonate was 0.027, −3.8, and −0.80, respectively. Bland-Altman plots for agreement of pH, Pco2, and bicarbonate showed 95% limits of agreement of −0.028 to 0.081, −12.3 to 4.8, and −4.0 to 2.4, respectively. Regression equations were derived to predict arterial values from venous values as follows: Arterial pH = −0.307 + 1.05 × venous pH, arterial Pco2 = 0.805 + 0.936 × venous Pco2, and arterial bicarbonate = 0.513 + 0.945 × venous bicarbonate. The mean central minus peripheral differences for pH, Pco2, and bicarbonate were not clinically important. Conclusions: Peripheral or central venous pH, Pco2, and bicarbonate can replace their arterial equivalents in many clinical contexts encountered in the ICU. Figure 2. Bland-Altman plot of arterial and central venous blood Pco2 showing the regression line (solid line) and the 95% limits Continue reading >>

Arterial Blood Gases Not Helpful In Ed Management Of Dka

Arterial Blood Gases Not Helpful In Ed Management Of Dka

reviewing Ma OJ et al. Acad Emerg Med 2003 Aug This article requires a subscription for full access. NEJM Journal Watch articles published within the last six months are available to subscribers only. Articles published more than 6 months ago are available to registered users. Continue reading >>

Episode 63 – Pediatric Dka

Episode 63 – Pediatric Dka

Pediatric DKA was identified as one of key diagnoses that we need to get better at managing in a massive national needs assessment conducted by the fine folks at TREKK – Translating Emergency Knowledge for Kids – one of EM Cases’ partners who’s mission is to improve the care of children in non-pediatric emergency departments across the country. You might be wondering – why was DKA singled out in this needs assessment? It turns out that kids who present to the ED in DKA without a known history of diabetes, can sometimes be tricky to diagnose, as they often present with vague symptoms. When a child does have a known history of diabetes, and the diagnosis of DKA is obvious, the challenge turns to managing severe, life-threatening DKA, so that we avoid the many potential complications of the DKA itself as well as the complications of treatment – cerebral edema being the big bad one. The approach to these patients has evolved over the years, even since I started practicing, from bolusing insulin and super aggressive fluid resuscitation to more gentle fluid management and delayed insulin drips, as examples. There are subtleties and controversies in the management of DKA when it comes to fluid management, correcting serum potassium and acidosis, preventing cerebral edema, as well as airway management for the really sick kids. In this episode we‘ll be asking our guest pediatric emergency medicine experts Dr. Sarah Reid, who you may remember from her powerhouse performance on our recent episodes on pediatric fever and sepsis, and Dr. Sarah Curtis, not only a pediatric emergency physician, but a prominent pediatric emergency researcher in Canada, about the key historical and examination pearls to help pick up this sometimes elusive diagnosis, what the value of serum Continue reading >>

Review Easy Blood Gas Analysis: Implications For Nursing

Review Easy Blood Gas Analysis: Implications For Nursing

Introduction Arterial blood gas analysis is a common investigation in emergency departments and intensive care units for monitoring patients with acute respiratory failure. It also has some applications in general practice, such as assessing the need for domiciliary oxygen therapy in patients with chronic obstructive pulmonary disease. An arterial blood gas result can help in the assessment of a patient’s gas exchange, ventilatory control and acid–base balance [1]. However, the investigation does not give a diagnosis and should not be used as a screening test. It is imperative that the results are considered in the context of the patient’s symptoms. While non-invasive monitoring of pulmonary function, such as pulse oximetry, is simple, effective and increasingly widely used, pulse oximetry is no substitute for arterial blood gas analysis [2,3]. Pulse oximetry is solely a measure of oxygen saturation and gives no indication about blood pH, carbon dioxide or bicarbonate concentrations [4]. The arterial blood gas (ABG) is frequently used for monitoring the patient’s respiratory status and ABGs can be sampled as an arterial stab or by drawing blood from an arterial line. Knowledge about interpretation of ABGs is consequently essential for nurses who are working in ICU, to be able to analyze each component of the ABGs to avoid overlooking a change that could result in an inaccurate interpretation and lead to inappropriate treatment. All over the world nurses in ICU use considerable time in drawing, documenting, reporting and interpreting blood gases. Blood gases can be obtained from the arteries, veins or capillaries [1,3]. Arterial blood gases are analyzed with a great frequency. Nurses are usually involved in taking and analyzing the ABGs and normally they report t Continue reading >>

Case Study: Diabetic Ketoacidosis Complications In Type 2 Diabetes

Case Study: Diabetic Ketoacidosis Complications In Type 2 Diabetes

CLINICAL DIABETES VOL. 18 NO. 2 Spring 2000 CASE STUDIES Case Study: Diabetic Ketoacidosis Complications in Type 2 Diabetes Craig D. Wittlesey, MD Presentation A 48-year-old Hispanic woman with a long history of obesity, diabetes, dyslipidemia, and reactive airway disease presented to the hospital emergency department with a 5-day history of weakness, tactile fever, productive cough, nausea, and vomiting. Patient report and chart review confirmed that 2 years before this presentation, her diabetes had been managed with diet alone. In the past year, glipizide (Glucotrol), metformin (Glucophage), and ultralente insulin were added because of poor glycemic control. On examination, her temperature was 99.1° F, blood pressure was 98/64 mmHg, pulse was 136, and respirations were 36. There was a strong smell of ketones in the exam room. The patient was drowsy but cogent. Her head and neck exam revealed poor dentition and periodontal disease. Her lung sounds were clear without wheezes or rhonchi. Her heart sounds were normal. The abdominal exam revealed mild epigastric tenderness to deep palpation but no rebound tenderness or guarding. Extremities were well perfused with symmetric pulses. Laboratory results were remarkable for a room air arterial blood gas with pH of 7.12, pCO2 of 17 mmHg, and bicarbonate of 5.6 mEq/l. Urinalysis revealed 4+ glucose and 3+ ketones. Chemistry panel revealed a glucose of 420 mg/dl, BUN of 16 mg/dl, creatinine of 1.3 mg/dl, sodium of 139 mEq/l, chloride of 112 mEq/l, CO2 of 11.2 mmol/l, and potassium of 5.0 mEq/l. Chest X-ray revealed no infiltrate. Questions Is this patient experiencing diabetic ketoacidosis (DKA)? What type of diabetes does this patient have? What is the etiology of DKA in this patient? What is the rationale for inpatient treatm Continue reading >>

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