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Dka Abg Example

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 >>

Diabetic Ketoacidosis Workup

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. [17] 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 >>

Arterial Blood Gas Analysis: Example Set 1

Arterial Blood Gas Analysis: Example Set 1

Case A A patient is brought back to the floor from the operating room on a patient controlled analgesia (PCA) pump with hydromorphone. The patient hits his PCA button several times in the first hour. Shortly thereafter, the nurse walks in the room and finds him somnolent and difficult to arouse. His SpO2 is only 88% so the nurse obtains a blood gas that reveals: Step 1: pH is low (acidemia) Step 2: The PCO2 is high (respiratory acidosis) and the bicarbonate is normal. A low pH with a high PCO2 indicates that the primary process is a respiratory acidosis. Summary In this case, the patient started hypoventilating because he had likely given himself too much narcotic pain medications. Case B A patient presents with a one-day history of productive cough, fevers and increasing dyspnea. In the ER, the chest x-ray shows a right middle lobe opacity. His oxygen saturation is 90% on room air. An arterial blood gas is obtained and it reveals a Step 1: The pH is high (alkalemia) Step 2: The PCO2 is low (respiratory alkalosis) and the bicarbonate is on the low side of normal. A high pH with a low PCO2 indicates that the primary process is a respiratory alkalosis. Summary In this case, the patient is likely hyperventilating because he is hypoxemic. This is a good example of the hypoxemic ventilatory response. Case C A patient with Type I diabetes presents to the ER complaining of feeling poorly two days after running out of his insulin. An arterial blood gas is obtained and shows Step 1: The pH is low (acidemia) Step 2: The PCO2 is low (respiratory alkalosis) and the bicarbonate is low (metabolic acidosis). A low pH and low bicarbonate signifies that the metabolic acidosis is the primary process. Summary In this case, the patient is likely in diabetic ketoacidosis because he was not Continue reading >>

Common Laboratory (lab) Values - Abgs

Common Laboratory (lab) Values - Abgs

A B C D E F G H I J K L M N O P Q R S T U V W X Y Z Laboratory VALUES Home Page Arterial Blood Gases Arterial blood gas analysis provides information on the following: 1] Oxygenation of blood through gas exchange in the lungs. 2] Carbon dioxide (CO2) elimination through respiration. 3] Acid-base balance or imbalance in extra-cellular fluid (ECF). Normal Blood Gases Arterial Venous pH 7.35 - 7.45 7.32 - 7.42 Not a gas, but a measurement of acidity or alkalinity, based on the hydrogen (H+) ions present. The pH of a solution is equal to the negative log of the hydrogen ion concentration in that solution: pH = - log [H+]. PaO2 80 to 100 mm Hg. 28 - 48 mm Hg The partial pressure of oxygen that is dissolved in arterial blood. New Born – Acceptable range 40-70 mm Hg. Elderly: Subtract 1 mm Hg from the minimal 80 mm Hg level for every year over 60 years of age: 80 - (age- 60) (Note: up to age 90) HCO3 22 to 26 mEq/liter (21–28 mEq/L) 19 to 25 mEq/liter The calculated value of the amount of bicarbonate in the bloodstream. Not a blood gas but the anion of carbonic acid. PaCO2 35-45 mm Hg 38-52 mm Hg The amount of carbon dioxide dissolved in arterial blood. Measured. Partial pressure of arterial CO2. (Note: Large A= alveolor CO2). CO2 is called a “volatile acid” because it can combine reversibly with H2O to yield a strongly acidic H+ ion and a weak basic bicarbonate ion (HCO3 -) according to the following equation: CO2 + H2O <--- --> H+ + HCO3 B.E. –2 to +2 mEq/liter Other sources: normal reference range is between -5 to +3. The base excess indicates the amount of excess or insufficient level of bicarbonate in the system. (A negative base excess indicates a base deficit in the blood.) A negative base excess is equivalent to an acid excess. A value outside of the normal r Continue reading >>

Abg Interpretation

Abg Interpretation

Arterial blood gas (ABG) interpretation is something many medical students find difficult to grasp (we’ve been there). We’ve created this guide, which aims to provide a structured approach to ABG interpretation whilst also increasing your understanding of each results relevance. The real value of an ABG comes from its ability to provide a near immediate reflection of the physiology of your patient, allowing you to recognise and treat pathology more rapidly. To see how to perform an arterial blood gas check out our guide here. If you want to put your ABG interpretation skills to the test, check out our ABG quiz here. Normal ranges pH: 7.35 – 7.45 PaCO2: 4.7-6.0 kPa PaO2: 11-13 kPa HCO3-: 22-26 mEg/L Base excess: -2 to +2 mmol/L Patient’s clinical condition Before getting stuck into the details of the analysis, it’s important to look at the patient’s current clinical status, as this provides essential context to the ABG result. Below are a few examples to demonstrate how important context is when interpreting an ABG. A normal PaO2 in a patient on high flow oxygen – this is abnormal as you would expect the patient to have a PaO2 well above the normal range with this level of oxygen therapy A normal PaCO2 in a hypoxic asthmatic patient – a sign they are tiring and need ITU intervention A very low PaO2 in a patient who looks completely well, is not short of breath and has normal O2 saturations – likely a venous sample Oxygenation (PaO2) Your first question when looking at the ABG should be “Is this patient hypoxic?” (because this will kill them long before anything else does). PaO2 should be >10 kPa on air in a healthy patient If the patient is receiving oxygen therapy their PaO2 should be approximately 10kPa less than the % inspired concentration / FiO 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 >>

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 >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Initial Evaluation Initial evaluation of patients with DKA includes diagnosis and treatment of precipitating factors (Table 14–18). The most common precipitating factor is infection, followed by noncompliance with insulin therapy.3 While insulin pump therapy has been implicated as a risk factor for DKA in the past, most recent studies show that with proper education and practice using the pump, the frequency of DKA is the same for patients on pump and injection therapy.19 Common causes by frequency Other causes Selected drugs that may contribute to diabetic ketoacidosis Infection, particularly pneumonia, urinary tract infection, and sepsis4 Inadequate insulin treatment or noncompliance4 New-onset diabetes4 Cardiovascular disease, particularly myocardial infarction5 Acanthosis nigricans6 Acromegaly7 Arterial thrombosis, including mesenteric and iliac5 Cerebrovascular accident5 Hemochromatosis8 Hyperthyroidism9 Pancreatitis10 Pregnancy11 Atypical antipsychotic agents12 Corticosteroids13 FK50614 Glucagon15 Interferon16 Sympathomimetic agents including albuterol (Ventolin), dopamine (Intropin), dobutamine (Dobutrex), terbutaline (Bricanyl),17 and ritodrine (Yutopar)18 DIFFERENTIAL DIAGNOSIS Three key features of diabetic acidosis are hyperglycemia, ketosis, and acidosis. The conditions that cause these metabolic abnormalities overlap. The primary differential diagnosis for hyperglycemia is hyperosmolar hyperglycemic state (Table 23,20), which is discussed in the Stoner article21 on page 1723 of this issue. Common problems that produce ketosis include alcoholism and starvation. Metabolic states in which acidosis is predominant include lactic acidosis and ingestion of drugs such as salicylates and methanol. Abdominal pain may be a symptom of ketoacidosis or part of the inci 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 >>

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 >>

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 >>

Comparison Of Arterial And Venous Ph, Bicarbonate, Pco2 And Po2 In Initial Emergency Department Assessment

Comparison Of Arterial And Venous Ph, Bicarbonate, Pco2 And Po2 In Initial Emergency Department Assessment

Go to: Patients and method A convenience sample of adult patients presenting to the ED of a tertiary care 1000 bed teaching hospital in Northern India, from September to December 2006, were enrolled. Patients were eligible if the on‐duty emergency physician decided to obtain an ABG sample for the initial assessment. After having the study explained, a verbal consent was obtained from the patient or the relative, and patients were sampled for arterial and venous blood with minimum delay (always <2 min) between the samples. For arterial samples (0.5–1 ml), a minimally heparinised plastic syringe with 24 G needle was used to puncture the radial artery. For venous sampling, blood was obtained at the time of intravenous cannula placement or using peripheral venepuncture. The two samples were taken as close as possible in time and before the initiation of any form of treatment. The samples were analysed as quickly as possible using the blood gas analyser located in the ED. Data were analysed using SPSS version 10.0.1.299 and Prism 5 for Windows (Graph pad, version 5). The Bland‐Altman method was used to calculate agreement between arterial and venous measurements. The study was approved by the ethics committee of the All India Institute of Medical Sciences, New Delhi, India. Continue reading >>

Abg’s—it’s All In The Family

Abg’s—it’s All In The Family

By Cyndi Cramer, BA, RN, OCN, PCRN RealNurseEd.com 3.0 Contact Hour Self Learning Module Objectives: Identify the components of the ABG and their normal ranges Interpret ABG values and determine the acid base abnormality given Identify the major causes of acid base abnormalities Describe symptoms associated with acid base abnormalities Describe interventions to correct acid base abnormalities Identify the acceptable O2 level per ABG and Pulse Oximetry Identify four causes of low PaO2 The Respiratory System (Acid); CO2 is a volatile acid If you increase your respiratory rate (hyperventilation) you "blow off" CO2 (acid) therefore decreasing your CO2 acid—giving you ALKLAOSIS If you decrease your respiratory rate (hypoventilation) you retain CO2 (acid) therefore increasing your CO2 (acid)—giving you ACIDOSIS The Renal System (Base); the kidneys rid the body of the nonvolatile acids H+ (hydrogen ions) and maintain a constant bicarb (HCO3). Bicarbonate is the body’s base You have Acidosis when you have excess H+ and decreased HCO3- causing a decrease in pH. The Kidneys try to adjust for this by excreting H+ and retaining HCO3- base. The Respiratory System will try to compensate by increasing ventilation to blow off CO2 (acid) and therefore decrease the Acidosis. You have Alkalosis when H+ decreases and you have excess (or increased) HCO3- base. The kidneys excrete HCO3- (base) and retain H+ to compensate. The respiratory system tries to compensate with hypoventilation to retain CO2 (acid) To decrease the alkalosis Compensation The respiratory system can effect a change in 15-30 minutes The renal system takes several hours to days to have an effect. RESPIRATORY ACIDOSIS: pH < 7.35 (Normal: 7.35 - 7.45) CO2 > 45 (Normal: 35 – 45) 1. Causes: Hypoventilation a. Depressio 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 >>

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