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Is Ketoacidosis Metabolic Or Respiratory

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 >>

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 >>

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 Balance

Acid Base Balance

Concept- ACID BASE BALANCE Concept Definition The process of regulating the pH, bicarbonate concentration and partial pressure of carbon dioxide of body fluids. Key definitions: Acid – a substance that releases hydrogen ions (H+) Base – a substance that takes up hydrogen ions (H+) Bicarbonate (HCO3) - is the most important “base†in the body pH – is the measurement of acidity, alkalinity in a solution, the negative logarithm of hydrogen ion concentration, inverse relationship exists between hydrogen ion concentration and pH) Exemplars Diabetic Ketoacidosis (DKA) – Metabolic Acidosis Hyperventilation-(birthing mother, panic attack) – Respiratory Alkalosis Gastro-intestinal Losses – (pediatric) – Metabolic Alkalosis Drug Overdose with Hypoventilation – Respiratory Acidosis Objectives 1. Explain the correlation between Diabetic Ketoacidosis (DKA) – Metabolic Acidosis, Hyperventilation-(birthing mother, panic attack) – Respiratory Alkalosis, Gastro-intestinal Losses – (pediatric) – Metabolic Alkalosis, and/or Drug Overdose with Hypoventilation – Respiratory Acidosis to the concept of Acid Base Balance (including compromised antecedents, deficit measurement in attributes, a list of negative consequences, and the interrelated concepts which may be involved). 2. Identify conditions that place an individual at risk for imbalance leading to a compromised concept(s) resulting in Diabetic Ketoacidosis (DKA) – Metabolic Acidosis, Hyperventilation-(birthing mother, panic attack) – Respiratory Alkalosis, Gastro-intestinal Losses – (pediatric) – Metabolic Alkalosis, and/or Drug Overdose with Hypoventilation – Respiratory Acidosis. 3. Apply the nursing 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 >>

Understanding The Presentation Of Diabetic Ketoacidosis

Understanding The Presentation Of Diabetic Ketoacidosis

Hypoglycemia, diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar nonketotic syndrome (HHNS) must be considered while forming a differential diagnosis when assessing and managing a patient with an altered mental status. This is especially true if the patient has a history of diabetes mellitus (DM). However, be aware that the onset of DKA or HHNS may be the first sign of DM in a patient with no known history. Thus, it is imperative to obtain a blood glucose reading on any patient with an altered mental status, especially if the patient appears to be dehydrated, regardless of a positive or negative history of DM. In addition to the blood glucose reading, the history — particularly onset — and physical assessment findings will contribute to the formulation of a differential diagnosis and the appropriate emergency management of the patient. Pathophysiology of DKA The patient experiencing DKA presents significantly different from one who is hypoglycemic. This is due to the variation in the pathology of the condition. Like hypoglycemia, by understanding the basic pathophysiology of DKA, there is no need to memorize signs and symptoms in order to recognize and differentiate between hypoglycemia and DKA. Unlike hypoglycemia, where the insulin level is in excess and the blood glucose level is extremely low, DKA is associated with a relative or absolute insulin deficiency and a severely elevated blood glucose level, typically greater than 300 mg/dL. Due to the lack of insulin, tissue such as muscle, fat and the liver are unable to take up glucose. Even though the blood has an extremely elevated amount of circulating glucose, the cells are basically starving. Because the blood brain barrier does not require insulin for glucose to diffuse across, the brain cells are rece 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 >>

Acidosis

Acidosis

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: Chest deformities, such as kyphosis Chest injuries Chest muscle weakness Chronic lung disease Overuse of sedative drugs 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) Prolonged lack of oxygen from shock, heart failure, or seve Continue reading >>

Cm-acid/base

Cm-acid/base

Sort Respiratory disorders Related to change in PCO2: Partial pressure of carbon dioxide in the blood The "acid" portion of the ABG Has an INDIRECT relationship with pH Normal range 35-45 mm Hg > 45 mm Hg is acidosis < 35 mm Hg is alkalosis Meteabolic disorders HCO3- represents metabolic change: "Base" or "alkaline" component of blood Normal range 20-28 mEq/L There is a DIRECT relationship between HCO3- and pH HCO3 > 28 is alkalosis HCO3 < 20 is acidosis Not as easy to break down as Respiratory Disorders because of number of causes and potential Anion Gap ALWAYS do anion gap for metabolic Metabolic alkalosis High HCO3- with alkalemia (pH > 7.45) Causes divided into 2 groups based on "saline responsiveness" using urine chloride (Cl-) levels as a marker of volume status Saline responsive: sign of extracellular volume contraction (more common) Saline un-responsive: excessive body total bicarb (HCO3-)-may be tumor or iatrogenic Treatment: mild alkalosis -none. pH>7.60 needs treatment (based on type) Causes of metabolic acidosis Another way to view the causes: Lactic acidosis Ketoacidosis (alcoholic or diabetic) Ingested Toxins Methanol Uremia DKA Paraldehyde Iron/INH/inborn metabolic error Lactic acidosis Ethylene glycol Salicylates Hyporeninemic hypoaldosteronemic RTA Type of renal tubular acidosis Hyporeninemic hypoaldosteronemic RTA (Type IV) Most common RTA in practice Deficiency or antagonism of aldosterone Impairs distal nephron Na, K and H excretion Common causes: diabetic nephropathy, tubulointersitial disease, hypertensive nephrosclerosis, AIDS Continue reading >>

Disorders Of Acid-base Balance

Disorders Of Acid-base Balance

Learning Objectives By the end of this section, you will be able to: Identify the three blood variables considered when making a diagnosis of acidosis or alkalosis Identify the source of compensation for blood pH problems of a respiratory origin Identify the source of compensation for blood pH problems of a metabolic/renal origin Normal arterial blood pH is restricted to a very narrow range of 7.35 to 7.45. A person who has a blood pH below 7.35 is considered to be in acidosis (actually, “physiological acidosis,” because blood is not truly acidic until its pH drops below 7), and a continuous blood pH below 7.0 can be fatal. Acidosis has several symptoms, including headache and confusion, and the individual can become lethargic and easily fatigued. A person who has a blood pH above 7.45 is considered to be in alkalosis, and a pH above 7.8 is fatal. Some symptoms of alkalosis include cognitive impairment (which can progress to unconsciousness), tingling or numbness in the extremities, muscle twitching and spasm, and nausea and vomiting. Both acidosis and alkalosis can be caused by either metabolic or respiratory disorders. As discussed earlier in this chapter, the concentration of carbonic acid in the blood is dependent on the level of CO2 in the body and the amount of CO2 gas exhaled through the lungs. Thus, the respiratory contribution to acid-base balance is usually discussed in terms of CO2 (rather than of carbonic acid). Remember that a molecule of carbonic acid is lost for every molecule of CO2 exhaled, and a molecule of carbonic acid is formed for every molecule of CO2 retained. Metabolic Acidosis: Primary Bicarbonate Deficiency Metabolic acidosis occurs when the blood is too acidic (pH below 7.35) due to too little bicarbonate, a condition called primary bicar Continue reading >>

Compensatory Hypochloraemic Alkalosis In Diabetic Ketoacidosis

Compensatory Hypochloraemic Alkalosis In Diabetic Ketoacidosis

Diabetic ketoacidosis acid-base imbalance hypochloraemia DKA Diabetic ketoacidosis [HCO3−] concentration of bicarbonate in arterial plasma [Na+] concentration of sodium in arterial plasma [Cl−] concentration of chloride in arterial plasma [Na+]/[Cl−] ratio sodium/chloride ratio in arterial plasma [XA−] concentration of unmeasured anions in arterial plasma [A−] sum of negative charged albumin and phosphate in arterial plasma [K+] concentration of potassium in arterial plasma Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes mellitus. Metabolic acidosis caused by ketoacids is an essential component of DKA and can have detrimental effects on cardiac, respiratory and metabolic function [1]. The only known compensatory response to metabolic acidosis in DKA is hyperventilation with consecutive respiratory alkalosis [1]. The effect of chloride on acid-base state has been known for many years. Hyperchloraemia and hypochloraemia cause metabolic acidosis and metabolic alkalosis, respectively [2, 3]. Recent research indicates that changes in chloride play an important role in the compensation of lactic acidosis [4]. Although chloride concentrations are frequently decreased in DKA, it is not known, whether these changes play a role in the acid-base state in this entity. The aim of this study was to investigate the effect of hypochloraemic alkalosis on acid-base state of patients with DKA. A total of 21 patients with DKA (11 women, 10 men, 44±16 years) admitted to the emergency department of a primary care hospital were studied. Fluid, insulin or bicarbonate had not been administered before the investigation. Of these patients, four had new onset diabetes and 17 patients had known insulin-dependent diabetes. DKA was triggered by inadequate insulin 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 >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus.[1] Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness.[1] A person's breath may develop a specific smell.[1] Onset of symptoms is usually rapid.[1] In some cases people may not realize they previously had diabetes.[1] DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances.[1] Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids.[1] DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies.[3] DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine.[1] The primary treatment of DKA is with intravenous fluids and insulin.[1] Depending on the severity, insulin may be given intravenously or by injection under the skin.[3] Usually potassium is also needed to prevent the development of low blood potassium.[1] Throughout treatment blood sugar and potassium levels should be regularly checked.[1] Antibiotics may be required in those with an underlying infection.[6] In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended.[1][6] Rates of DKA vary around the world.[5] 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.[1][5] DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost univ Continue reading >>

Diabetic Ketoacidosis (dka) - Topic Overview

Diabetic Ketoacidosis (dka) - Topic Overview

Diabetic ketoacidosis (DKA) is a life-threatening condition that develops when cells in the body are unable to get the sugar (glucose) they need for energy because there is not enough insulin. When the sugar cannot get into the cells, it stays in the blood. The kidneys filter some of the sugar from the blood and remove it from the body through urine. Because the cells cannot receive sugar for energy, the body begins to break down fat and muscle for energy. When this happens, ketones, or fatty acids, are produced and enter the bloodstream, causing the chemical imbalance (metabolic acidosis) called diabetic ketoacidosis. Ketoacidosis can be caused by not getting enough insulin, having a severe infection or other illness, becoming severely dehydrated, or some combination of these things. It can occur in people who have little or no insulin in their bodies (mostly people with type 1 diabetes but it can happen with type 2 diabetes, especially children) when their blood sugar levels are high. Your blood sugar may be quite high before you notice symptoms, which include: Flushed, hot, dry skin. Feeling thirsty and urinating a lot. Drowsiness or difficulty waking up. Young children may lack interest in their normal activities. Rapid, deep breathing. A strong, fruity breath odor. Loss of appetite, belly pain, and vomiting. Confusion. Laboratory tests, including blood and urine tests, are used to confirm a diagnosis of diabetic ketoacidosis. Tests for ketones are available for home use. Keep some test strips nearby in case your blood sugar level becomes high. When ketoacidosis is severe, it must be treated in the hospital, often in an intensive care unit. Treatment involves giving insulin and fluids through your vein and closely watching certain chemicals in your blood (electrolyt Continue reading >>

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 >>

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