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Is Ketoacidosis Metabolic Or Respiratory

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Diabetic ketoacidosis is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. Hyperglycemia causes an osmotic diuresis with significant fluid and electrolyte loss. DKA occurs mostly in type 1 diabetes mellitus (DM). 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. Diabetic ketoacidosis (DKA) is most common among patients with type 1 diabetes mellitus and develops when insulin levels are insufficient to meet the body’s basic metabolic requirements. DKA is the first manifestation of type 1 DM in a minority of patients. Insulin deficiency can be absolute (eg, during lapses in the administration of exogenous insulin) or relative (eg, when usual insulin doses do not meet metabolic needs during physiologic stress). Common physiologic stresses that can trigger DKA include Some drugs implicated in causing DKA include DKA is less common in type 2 diabetes mellitus, but it may occur in situations of unusual physiologic stress. Ketosis-prone type 2 diabetes is a variant of type 2 diabetes, which is sometimes seen in obese individuals, often of African (including African-American or Afro-Caribbean) origin. People with ketosis-prone diabetes (also referred to as Flatbush diabetes) can have significant impairment of beta cell function with hyperglycemia, and are therefore more likely to develop DKA in the setting of significant hyperglycemia. SGLT-2 inhibitors have been implicated in causing DKA in both type 1 and type 2 DM. Continue reading >>

An Exceptional Case Of Diabetic Ketoacidosis

An Exceptional Case Of Diabetic Ketoacidosis

Copyright © 2017 Celine Van de Vyver et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract We present a case of diabetic ketoacidosis, known as one of the most serious metabolic complications of diabetes. We were confronted with rapid neurological deterioration and unseen glycaemic values, which reached almost 110 mmol/L, subsequently resulting in hyperkalaemia and life-threatening dysrhythmias. This is the first reported live case with such high values of blood glucose and a favourable outcome. 1. Introduction Diabetic ketoacidosis (DKA) is known as one of the most serious complications of diabetes, besides hyperosmolar hyperglycaemic syndrome (HHS), and it is associated with significant morbidity and mortality. The symptoms are often nonspecific and there are many diseases that mimic the presentation. The clinical course usually evolves within a short time frame (<24 h). DKA exists of a triad of uncontrolled hyperglycaemia, metabolic acidosis, and increased total body ketone concentration [1]. These three criteria are needed for diagnosis. The most common precipitating factors of DKA are infections and discontinuation of or inadequate insulin therapy. Mainstays of treatment are correction of hypovolemia and hyperglycaemia, rapid administration of insulin, and electrolyte management. Glycaemic values in DKA normally do not exceed 33 mmol/L. In contrast, blood glucose in HHS is often higher [2, 3]. We present a case of severe diabetic ketoacidosis with glycaemic values of almost 110 mmol/L, leading to neurologic sequelae and requiring more aggressive treatment. A similar case report detailing th Continue reading >>

5.5 Metabolic Acidosis - Compensation

5.5 Metabolic Acidosis - Compensation

Acid-Base Physiology 5.5.1 Hyperventilation Compensation for a metabolic acidosis is hyperventilation to decrease the arterial pCO2. This hyperventilation was first described by Kussmaul in patients with diabetic ketoacidosis in 1874. The metabolic acidosis is detected by both the peripheral and central chemoreceptors and the respiratory center is stimulated. The initial stimulation of the central chemoreceptors is due to small increases in brain ISF [H+]. The subsequent increase in ventilation causes a fall in arterial pCO2 which inhibits the ventilatory response. Maximal compensation takes 12 to 24 hours The chemoreceptor inhibition acts to limit and delay the full ventilatory response until bicarbonate shifts have stabilised across the blood brain barrier. The increase in ventilation usually starts within minutes and is usually well advanced at 2 hours of onset but maximal compensation may take 12 to 24 hours to develop. This is �maximal� compensation rather than �full� compensation as it does not return the extracellular pH to normal. In situations where a metabolic acidosis develops rapidly and is short-lived there is usually little time for much compensatory ventilatory response to occur. An example is the acute and sometimes severe lactic acidosis due to a prolonged generalised convulsion: this corrects due to rapid hepatic uptake and metabolism of the lactate following cessation of convulsive muscular activity, and hyperventilation due to the acidosis does not occur. The expected pCO2 at maximal compensation can be calculated from a simple formula The arterial pCO2 at maximal compensation has been measured in many patients with a metabolic acidosis. A consistent relationship between bicarbonate level and pCO2 has been found. It can be estimated from the Continue reading >>

Acid-base And Electrolyte Disturbances In Patients With Diabetic Ketoacidosis

Acid-base And Electrolyte Disturbances In Patients With Diabetic Ketoacidosis

Abstract We undertook the present study to examine the acid-base and electrolyte disturbances in relation to hydration status in patients with diabetic ketoacidosis (DKA). A total of 40 insulin-dependent diabetes mellitus patients (22 male, 18 female), aged 18–61 years with DKA admitted to our hospital during the last 2 years, were studied. The duration of diabetes averaged 9 ± 2 years. In all cases a detailed investigation of the acid-base status and electrolyte parameters was performed. Twenty-one patients had a pure metabolic acidosis with an increased serum anion gap, seven had DKA combined with hyperchloremic metabolic acidosis, nine had DKA coexisting with metabolic alkalosis, while three had DKA with a concurrent respiratory alkalosis. Hydration status as evidenced by the ratio of urea/creatinine seems to play an important role in the development of mixed acid-base disorders (detected by changes in the ratios Δ anion gap/Δ bicarbonate () and sodium/chloride ()). In fact, hyperchloremic acidosis developed in the patients with the better hydration status. However, contradictorily, the severely dehydrated patients who experienced recurrent episodes of vomiting developed DKA with a concurrent metabolic alkalosis. Finally, patients with pneumonia or gram-negative septicemia exhibited DKA combined with a primary respiratory alkalosis. We conclude that patients with DKA commonly develop mixed acid-base disorders, which are partly dependent on patients' hydration status. Continue reading >>

Acid/base (alkalosis Vs Acidosis, Metabolic Vs Respiratory)

Acid/base (alkalosis Vs Acidosis, Metabolic Vs Respiratory)

This is the general way to approach an acid-base disturbance. They’re not really as bad as they seem at first. You just need to remember that CO2 is acidic and HCO3- is basic. So an increase in CO2 makes the body acidotic and an increase in HCO3- makes the body alkalotic. It’s also good to remember to calculate the anion gap when doing these calculations. AG = Na – (Cl- + HCO3-) it’s just the cations minus the anions. If this gap between the cations and anions is large, it means that the anions are stacking their team and have an extra anion helping out. The classic mnemonic is MUDPILES Methanol Uremia Diabetic ketoacidosis Paraldehyde Isopropyl alcohol Lactic acidosis Ethylene glycol Salicylates If the anion gap is big, it’s good to look at the ratio between the change in the gap and the change in the HCO3-. Increase in AG < decrease in HCO3- = coexisting non-anion gap metabolic acidosis Increase in AG > decrease in HCO3- = coexisting metabolic alkalosis Continue reading >>

Acid-base Disturbances In Children, Acidosis, Alkalosis

Acid-base Disturbances In Children, Acidosis, Alkalosis

Acid-base disturbances Poor feeding Failure to thrive Lethargy Altered mental status Seizures Hypotonia Ataxia Developmental delay Optic nerve atrophy Deafness Tachypnea, hyperventilation, Kussmaul breathing Nausea/vomiting - due to increased β-hydroxybutyrate Dehydration Polydipsia Lethargy Polyuria, nocturia Acetone "fruity" breath Weight loss Altered mental status; in severe cases, coma Encephalopathy Vomiting Often present as neonates Elevated urine pH, greater than 5.5 Infantile, recessive form Severe hyperchloremic acidosis, serum bicarbonate may be less than 10 mEq/L Growth retardation Hypokalemia Dehydration Rickets Nephrocalcinosis Hearing loss Adolescent form, dominant Nephrocalcinosis Mild acidosis Mild hypokalemia CNS: disturbances of the respiratory regulation - apneustic respirations (or agonal respirations - deep, gasping breaths with pause at full inspiration), central neurogenic hyperventilation (deep, rapid), Cheyne-Stokes respirations (oscillatory pattern of breathing of deep breathing then apnea followed again by deep breaths) due to tumor, meningitis, encephalitis, psychosis or pain. Hyperammonemia. Anxiety and panic attacks. Fever. Nicotine. Salicylates. Methylxanthines. Progesterone. Hyperthyroidism. Paresthesias. Dizziness. Headache. Slurred speech. Brief loss of consciousness due to the combination of hypocarbia-induced cerebral vascular vasoconstriction and decreased off-loading of oxygen from hemoglobin due to the Bohr effect. Hypokalemia. Hypophosphatemia. Hypocalcemia. Extracorporeal removal of toxic metabolite via hemofiltration or hemodialysis. Avoid catabolism. Specific emergency treatment depends upon the diesease entity. A few are below: Urea cycle defects: Arginine Sodium benzoate Sodium phenylacetate Sodium phenylbutyrate Methylmalon Continue reading >>

Ricardo Duarte1; Denise Maria Nunes Simã•es1; Khadine Kazue Kanayama1; Mã¡rcia Mery Kogika1

Ricardo Duarte1; Denise Maria Nunes Simã•es1; Khadine Kazue Kanayama1; Mã¡rcia Mery Kogika1

325 Braz. J. Vet. Res. Anim. Sci., São Paulo, v. 49, n. 4, p. 325-332, 2012 Acid-base abnormalities in dogs with diabetic ketoacidosis: a prospective study of 60 cases Distúrbios ácido-base em cães com cetoacidose diabética: estudo prospectivo de 60 casos 1School of Veterinary Medicine and Animal Science, University of São Paulo, São Paulo-SP, Brazil Abstract Diabetic ketoacidosis (DKA) is considered a typical high anion gap metabolic acidosis due to the retention of ketoanions. The objective of this study was to describe the acid-base disturbances of dogs with DKA and further characterize them, according to their frequency, adequacy of the secondary physiologic response, and occurrence of mixed disturbances. Sixty dogs with DKA were enrolled in the study. Arterial blood pH and gas tensions, plasma electrolytes, serum b-hydroxybutyrate (b-OHB), glucose, albumin and urea concentrations were determined for all dogs included in the study. All dogs were evaluated individually and systematically by the traditional approach to the diagnosis of acid- base disorders. Most of the dogs had a high anion gap acidosis, with appropriated respiratory response (n = 18; 30%) or concurrent respiratory alkalosis (n = 14; 23%). Hyperchloremic acidosis with moderated to marked increases in b-OHB was observed in 18 dogs (30%) and 7 of these patients had concurrent respiratory alkalosis. Hyperchloremic acidosis with mild increase in b-OHB was observed in 6 dogs (10%). Four dogs (7%) had a high anion gap acidosis with mild increase in b-OHB and respiratory alkalosis. Most of dogs with DKA had a high anion gap acidosis, but mixed acid-base disorders were common, chiefly high anion gap acidosis and concurrent respiratory alkalosis, and hyperchloremic acidosis with mo Continue reading >>

Ketoacidosis

Ketoacidosis

GENERAL ketoacidosis is a high anion gap metabolic acidosis due to an excessive blood concentration of ketone bodies (keto-anions). ketone bodies (acetoacetate, beta-hydroxybutyrate, acetone) are released into the blood from the liver when hepatic lipid metabolism has changed to a state of increased ketogenesis. a relative or absolute insulin deficiency is present in all cases. CAUSES The three major types of ketosis are: (i) Starvation ketosis (ii) Alcoholic ketoacidosis (iii) Diabetic ketoacidosis STARVATION KETOSIS when hepatic glycogen stores are exhausted (eg after 12-24 hours of total fasting), the liver produces ketones to provide an energy substrate for peripheral tissues. ketoacidosis can appear after an overnight fast but it typically requires 3 to 14 days of starvation to reach maximal severity. typical keto-anion levels are only 1 to 2 mmol/l and this will usually not alter the anion gap. the acidosis even with quite prolonged fasting is only ever of mild to moderate severity with keto-anion levels up to a maximum of 3 to 5 mmol/l and plasma pH down to 7.3. ketone bodies also stimulate some insulin release from the islets. patients are usually not diabetic. ALCOHOLIC KETOSIS Presentation a chronic alcoholic who has a binge, then stops drinking and has little or no oral food intake for a few days (ethanol and fasting) volume depletion is common and this can result in increased levels of counter regulatory hormones (eg glucagon) levels of free fatty acids (FFA) can be high (eg up to 3.5mM) providing plenty of substrate for the altered hepatic lipid metabolism to produce plenty of ketoanions GI symptoms are common (eg nausea, vomiting, abdominal pain, haematemesis, melaena) acidaemia may be severe (eg pH down to 7.0) plasma glucose may be depressed or normal or Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

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 one of our health articles more useful. See also separate Lactic Acidosis and Arterial Blood Gases - Indications and Interpretations articles. Description Metabolic acidosis is defined as an arterial blood pH <7.35 with plasma bicarbonate <22 mmol/L. Respiratory compensation occurs normally immediately, unless there is respiratory pathology. Pure metabolic acidosis is a term used to describe when there is not another primary acid-base derangement - ie there is not a mixed acid-base disorder. Compensation may be partial (very early in time course, limited by other acid-base derangements, or the acidosis exceeds the maximum compensation possible) or full. The Winter formula can be helpful here - the formula allows calculation of the expected compensating pCO2: If the measured pCO2 is >expected pCO2 then additional respiratory acidosis may also be present. It is important to remember that metabolic acidosis is not a diagnosis; rather, it is a metabolic derangement that indicates underlying disease(s) as a cause. Determination of the underlying cause is the key to correcting the acidosis and administering appropriate therapy[1]. Epidemiology It is relatively common, particularly among acutely unwell/critical care patients. There are no reliable figures for its overall incidence or prevalence in the population at large. Causes of metabolic acidosis There are many causes. They can be classified according to their pathophysiological origin, as below. The table is not exhaustive but lists those that are most common or clinically important to detect. Increased acid Continue reading >>

Acidosis

Acidosis

Acidosis is a condition in which there is too much acid in the body fluids. It is the opposite of alkalosis (a condition in which there is too much base in the body fluids). Causes The kidneys and lungs maintain the balance (proper pH level) of chemicals called acids and bases in the body. Acidosis occurs when acid builds up or when bicarbonate (a base) is lost. Acidosis is classified as either respiratory or metabolic acidosis. Respiratory acidosis develops when there is too much carbon dioxide (an acid) in the body. This type of acidosis is usually caused when the body is unable to remove enough carbon dioxide through breathing. Other names for respiratory acidosis are hypercapnic acidosis and carbon dioxide acidosis. Causes of respiratory acidosis include: Metabolic acidosis develops when too much acid is produced in the body. It can also occur when the kidneys cannot remove enough acid from the body. There are several types of metabolic acidosis: Diabetic acidosis (also called diabetic ketoacidosis and DKA) develops when substances called ketone bodies (which are acidic) build up during uncontrolled diabetes. Hyperchloremic acidosis is caused by the loss of too much sodium bicarbonate from the body, which can happen with severe diarrhea. Poisoning by aspirin, ethylene glycol (found in antifreeze), or methanol Lactic acidosis is a buildup of lactic acid. Lactic acid is mainly produced in muscle cells and red blood cells. It forms when the body breaks down carbohydrates to use for energy when oxygen levels are low. This can be caused by: Cancer Drinking too much alcohol Exercising vigorously for a very long time Liver failure Low blood sugar (hypoglycemia) Medications, such as salicylates MELAS (a very rare genetic mitochondrial disorder that affects energy production Continue reading >>

Potassium Balance In Acid-base Disorders

Potassium Balance In Acid-base Disorders

INTRODUCTION There are important interactions between potassium and acid-base balance that involve both transcellular cation exchanges and alterations in renal function [1]. These changes are most pronounced with metabolic acidosis but can also occur with metabolic alkalosis and, to a lesser degree, respiratory acid-base disorders. INTERNAL POTASSIUM BALANCE Acid-base disturbances cause potassium to shift into and out of cells, a phenomenon called "internal potassium balance" [2]. An often-quoted study found that the plasma potassium concentration will rise by 0.6 mEq/L for every 0.1 unit reduction of the extracellular pH [3]. However, this estimate was based upon only five patients with a variety of disturbances, and the range was very broad (0.2 to 1.7 mEq/L). This variability in the rise or fall of the plasma potassium in response to changes in extracellular pH was confirmed in subsequent studies [2,4]. Metabolic acidosis — In metabolic acidosis, more than one-half of the excess hydrogen ions are buffered in the cells. In this setting, electroneutrality is maintained in part by the movement of intracellular potassium into the extracellular fluid (figure 1). Thus, metabolic acidosis results in a plasma potassium concentration that is elevated in relation to total body stores. The net effect in some cases is overt hyperkalemia; in other patients who are potassium depleted due to urinary or gastrointestinal losses, the plasma potassium concentration is normal or even reduced [5,6]. There is still a relative increase in the plasma potassium concentration, however, as evidenced by a further fall in the plasma potassium concentration if the acidemia is corrected. A fall in pH is much less likely to raise the plasma potassium concentration in patients with lactic acidosis Continue reading >>

Types Of Disturbances

Types Of Disturbances

The different types of acid-base disturbances are differentiated based on: Origin: Respiratory or metabolic Primary or secondary (compensatory) Uncomplicated or mixed: A simple or uncomplicated disturbance is a single or primary acid-base disturbance with or without compensation. A mixed disturbance is more than one primary disturbance (not a primary with an expected compensatory response). Acid-base disturbances have profound effects on the body. Acidemia results in arrythmias, decreased cardiac output, depression, and bone demineralization. Alkalemia results in tetany and convulsions, weakness, polydipsia and polyuria. Thus, the body will immediately respond to changes in pH or H+, which must be kept within strict defined limits. As soon as there is a metabolic or respiratory acid-base disturbance, body buffers immediately soak up the proton (in acidosis) or release protons (alkalosis) to offset the changes in H+ (i.e. the body compensates for the changes in H+). This is very effective so minimal changes in pH occur if the body is keeping up or the acid-base abnormality is mild. However, once buffers are overwhelmed, the pH will change and kick in stronger responses. Remember that the goal of the body is to keep hydrogen (which dictates pH) within strict defined limits. The kidney and lungs are the main organs responsible for maintaining normal acid-base balance. The lungs compensate for a primary metabolic condition and will correct for a primary respiratory disturbance if the disease or condition causing the disturbance is resolved. The kidney is responsible for compensating for a primary respiratory disturbance or correcting for a primary metabolic disturbance. Thus, normal renal function is essential for the body to be able to adequately neutralize acid-base abnor Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic Acidosis Definition Metabolic acidosis is a pH imbalance in which the body has accumulated too much acid and does not have enough bicarbonate to effectively neutralize the effects of the acid. Description Metabolic acidosis, as a disruption of the body's acid/base balance, can be a mild symptom brought on by a lack of insulin, a starvation diet, or a gastrointestinal disorder like vomiting and diarrhea. Metabolic acidosis can indicate a more serious problem with a major organ like the liver, heart, or kidneys. It can also be one of the first signs of drug overdose or poisoning. Causes and symptoms Metabolic acidosis occurs when the body has more acid than base in it. Chemists use the term "pH" to describe how acidic or basic a substance is. Based on a scale of 14, a pH of 7.0 is neutral. A pH below 7.0 is an acid; the lower the number, the stronger the acid. A pH above 7.0 is a base; the higher the number, the stronger the base. Blood pH is slightly basic (alkaline), with a normal range of 7.36-7.44. Acid is a natural by-product of the breakdown of fats and other processes in the body; however, in some conditions, the body does not have enough bicarbonate, an acid neutralizer, to balance the acids produced. This can occur when the body uses fats for energy instead of carbohydrates. Conditions where metabolic acidosis can occur include chronic alcoholism, malnutrition, and diabetic ketoacidosis. Consuming a diet low in carbohydrates and high in fats can also produce metabolic acidosis. The disorder may also be a symptom of another condition like kidney failure, liver failure, or severe diarrhea. The build up of lactic acid in the blood due to such conditions as heart failure, shock, or cancer, induces metabolic acidosis. Some poisonings and overdoses (aspirin, Continue reading >>

Causes For Acidosis, Metabolic, Lactic, Respiratory, Renal Acidosis And Diabetic Ketoacidosis Symptoms

Causes For Acidosis, Metabolic, Lactic, Respiratory, Renal Acidosis And Diabetic Ketoacidosis Symptoms

Acidosis simply means your body’s fluids have an unhealthy excess of acid. This either occurs from a buildup of acid or a loss of bicarbonate (base). Your lungs and kidneys are the maintenance organs for a healthy “acid to base” ph balance. Primary categories causing symptoms of acidosis: Metabolic acidosis is excessive acidity of your blood. It can be caused by many conditions or situations, notably: Primary symptom for metabolic acidosis is rapid breathing. Confusion or lethargy may also occur. Severe metabolic acidosis can cause death. Lactic acidosis is a build up of lactic acid in your bloodstream, generally produced when oxygen levels drop. It’s most common cause is intensive or prolonged exercise. Yet, it can also be caused by: cancer alcohol hypoglycemia respiratory failure medications ~ salicylates, metformin Symptoms of lactic acidosis are: Diabetic acidosis, also termed diabetic ketoacidosis, is usually a diabetes complication occurring when glucose (sugar) is unavailable due to insufficient insulin. So instead, fat is used as your energy source, producing a ketone build up. This is rarely a complication of type 2 diabetes. Diabetic ketoacidosis might as well be caused by: Symptoms of diabetic acidosis: mental stupor rapid breathing muscle stiffness, aching Left untreated, it can be fatal. Respiratory acidosis happens when your lungs can’t remove all of your body’s carbon dioxide (an acid) production. It is also referred to as hypercapnic acidosis or carbon dioxide acidosis. Causes of respiratory acidosis include: scoliosis ~ makes lungs less efficient nerve & muscle diseases affecting inflation, deflation of lungs Chronic respiratory acidosis leads to a stabilized ph, because your kidneys adjusts to help restore a healthy balance. But, in the cas Continue reading >>

Acid Base Statuses

Acid Base Statuses

A B Metabolic Acidosis (1) results from cold stress Respiratory Alkalosis (1) results from excessive CO2 blown off Body decr carbonic acid (1) results in slow respirations so that CO2 is retained Acidosis (1) symptoms (a) CNS depression (b) errors in judgment (c) disorientation (d) drowsiness (e) stupor (f) coma Hydrogen Ions excess (1) results in acidosis as pH falls below 7.35 (2) hydrogen ions are forced into the cells causing K+ to move into the cells Diabetic Ketoacidosis metabolic acidosis Metabolic Acidosis dehydration after an extended bout of diarrhea COPD respiratory acidosis Diarrhea (1) respirtory acidosis Anxiety (1)results in respiratory alkalosis (2) associated w/hyperventilation (2) during hyperventilation CO2 is blown off which lowers the amount of acid in the system Severe Asthma Respiratory Alkalosis Acute Renal Failure (1) metabolic acidosis (2) hypermagnesemia (3) hyperkalemia (4) hypocalcemia Diarrhea (1) metabolic acidosis (2) leads to meta acid because there is an over-elimination of bicarbonate Alkalosis (1) signs (a) tingling fingers, toes & face (b) estreme nervousness (c) twitching of muscles (d) tetany Severe Asthma respiratory acidosis Vomiting (1) metabolic alkalosis (2) leads to metabolic alkalosis as hydrochloric acid is lost from the stomach Aspirin metabolic acidosis Overdose of Morphine respiratory acisosis Vigorous Diuresis metabolic alkalosis End Stage Muscular Distrophy respiratory acidosis Severe Hypokalemia metabolic alkalosis Renal Failure (1) results in metabolic acisosis as fluid build up turns acidic Shock (1) metabolic acidosis (2) meta acid because acid is added to the system (3) anaerobic metabolic pathways result in lactate and hydrogen irons (forming lactic acid) Hyperventilation (1) respiratory alkalosis (2) leads to re Continue reading >>

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