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How Does Ketoacidosis Cause Hyperventilation

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetes mellitus is the name given to a group of conditions whose common hallmark is a raised blood glucose concentration (hyperglycemia) due to an absolute or relative deficiency of the pancreatic hormone insulin. In the UK there are 1.4 million registered diabetic patients, approximately 3 % of the population. In addition, an estimated 1 million remain undiagnosed. It is a growing health problem: In 1998, the World Health Organization (WHO) predicted a doubling of the worldwide prevalence of diabetes from 150 million to 300 million by 2025. For a very tiny minority, diabetes is a secondary feature of primary endocrine disease such as acromegaly (growth hormone excess) or Cushing’s syndrome (excess corticosteroid), and for these patients successful treatment of the primary disease cures diabetes. Most diabetic patients, however, are classified as suffering either type 1 or type 2 diabetes. Type 1 diabetes Type 1 diabetes, which accounts for around 15 % of the total diabetic population, is an autoimmune disease of the pancreas in which the insulin-producing β-cells of the pancreas are selectively destroyed, resulting in an absolute insulin deficiency. The condition arises in genetically susceptible individuals exposed to undefined environmental insult(s) (possibly viral infection) early in life. It usually becomes clinically evident and therefore diagnosed during late childhood, with peak incidence between 11 and 13 years of age, although the autoimmune-mediated β-cell destruction begins many years earlier. There is currently no cure and type 1 diabetics have an absolute life-long requirement for daily insulin injections to survive. Type 2 diabetes This is the most common form of diabetes: around 85 % of the diabetic population has type 2 diabetes. The primary prob Continue reading >>

Severe Diabetic Ketoacidosis Complicated By Hypocapnic Seizure

Severe Diabetic Ketoacidosis Complicated By Hypocapnic Seizure

Summary In clinical practice, seizures independent of hypoglycemia are observed in patients with type 1 diabetes mellitus (T1DM) more frequently than expected by chance, suggesting a link. However, seizures during management of diabetic ketoacidosis (DKA) have generally been considered a bad prognostic factor, and usually associated with well-known biochemical or neurological complications. We present the case of a 17-year-old girl with known T1DM managed for severe DKA complicated by hypocapnic seizure. We review the literature on this rare occurrence as well as outline other possible differentials to consider when faced with the alarming combination of DKA and seizure. Learning points: Seizures during DKA treatment require immediate management as well as evaluation to determine their underlying cause. Their etiology is varied, but a lowered seizure threshold, electrolyte disturbances and serious neurological complications of DKA such as cerebral edema must all be considered. Sudden severe hypocapnia may represent a rare contributor to seizure during the treatment of DKA. Background Diabetic ketoacidosis (DKA) is an endocrine emergency occurring in patients with both new-onset and established type 1 diabetes (T1DM). In brief, the diagnosis is based on clinical suspicion followed by fulfillment of biochemical criteria: Hyperglycemia (blood glucose level (BGL) >11 mmol/L); ketonuria and/or ketonemia and metabolic acidosis (pH <7.3, bicarbonate <15 mmol/L). It is a leading acute cause of diabetes-related morbidity and mortality, particularly in children (1), often due to well-described complications of treatment. The most common of these include cerebral edema, and electrolyte disturbances such as hypoglycemia and hypokalemia. Seizure activity occurring during treatment o Continue reading >>

Hyperventilation

Hyperventilation

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 Dealing with Breathing Problems article more useful, or one of our other health articles. The term hyperventilation describes excessive ventilation of the lungs, beyond what is required to achieve normal arterial blood gases. Where hyperventilation occurs chronically or in recurrent episodes and is associated with somatic (respiratory, neurological, intestinal) or psychological (anxiety) symptoms, it is known as hyperventilation syndrome.[1] About 5-10% of general medical outpatients are thought to have this syndrome and, because of the range of somatic symptoms, the risk of misdiagnosis is high. Pathogenesis Hyperventilation has little effect on arterial pO2 and almost no effect on oxygen saturation which is nearly 100% under normal circumstances. Its main effect is to lower pCO2 and produce a respiratory alkalosis. A secondary hypocalcaemia also occurs as calcium dissociation is shifted towards the unionised, bound form. There are many factors that influence the respiratory drive, including the elasticity of the lungs and the resistance in the airways but the most important factors are arterial pH, pCO2 and pO2. Of these, pCO2 is most important, although some people with chronic obstructive pulmonary disease (COPD) can depend on the hypoxic drive. Epidemiology It is quite common but precise prevalence is unknown. A postal survey indicated that 8% of adults without asthma have functional breathing problems (of which symptomatic hyperventilation is the most common).[2] Hyperventilation syndrome is more common in people with asthma and also more common i Continue reading >>

Diabetic Ketoacidosis: A Serious Complication

Diabetic Ketoacidosis: A Serious Complication

A balanced body chemistry is crucial for a healthy human body. A sudden drop in pH can cause significant damage to organ systems and even death. This lesson takes a closer look at a condition in which the pH of the body is severely compromised called diabetic ketoacidosis. Definition Diabetic ketoacidosis, sometimes abbreviated as DKA, is a condition in which a high amount of acid in the body is caused by a high concentration of ketone bodies. That definition might sound complicated, but it's really not. Acidosis itself is the state of too many hydrogen ions, and therefore too much acid, in the blood. A pH in the blood leaving the heart of 7.35 or less indicates acidosis. Ketones are the biochemicals produced when fat is broken down and used for energy. While a healthy body makes a very low level of ketones and is able to use them for energy, when ketone levels become too high, they make the body's fluids very acidic. Let's talk about the three Ws of ketoacidosis: who, when, and why. Type one diabetics are the group at the greatest risk for ketoacidosis, although the condition can occur in other groups of people, such as alcoholics. Ketoacidosis usually occurs in type one diabetics either before diagnosis or when they are subjected to a metabolic stress, such as a severe infection. Although it is possible for type two diabetics to develop ketoacidosis, it doesn't happen as frequently. To understand why diabetic ketoacidosis occurs, let's quickly review what causes diabetes. Diabetics suffer from a lack of insulin, the protein hormone responsible for enabling glucose to get into cells. This inability to get glucose into cells means that the body is forced to turn elsewhere to get energy, and that source is fat. As anyone who exercises or eats a low-calorie diet knows, fa Continue reading >>

Does Chronic Hyperventilation Cause Brain Damage?

Does Chronic Hyperventilation Cause Brain Damage?

“Does chronic hyperventilation cause brain damage?” “…since it causes cerebral hypoxia due to low CO2 level, can we deduce that it cause brain damage?” Voluntarily hyperventilating is unlikely to cause any problems. Your brain and body is generally too intelligent to allow you to damage yourself in such a manner. Low CO2 levels from Hyperventilation can cause cerebral vasoconstriction and ischemia. This usually is only a seen in settings of artificial respiration. Well it does not directly cause brain damage. However, you are correct that it can cause brain damage indirectly. When you hyper ventilate, your brain becomes depleted of oxygen. This is not good. Extened periods of lack of oxygen can cause cells (and neurons) to become damaged, or even die. This should not really be a problem unless it is a regular occurance. Hyperventilating for a few seconds every day wont do much, but if you are hyperventilating for very long periods of time multiple times daily, this could be a problem. I strongly suggest you speak to a doctor about this if you are concerned. If I can help, I suggest practising breathing excersises regularly. This will allow you over time to become more in control of your breathing, and thus be able to control your hyperventilating. It is as simple as breathing in slowly, holding your breath for a few seconds, and then exhaling slowly. Do this for a few minutes each day, it should help. Continue reading >>

Dka And Cerebral Oedema Do We Really Know The Cause?

Dka And Cerebral Oedema Do We Really Know The Cause?

Cerebral oedema is the most feared complication in children presenting with Diabetic Ketoacidosis (DKA). It occurs in about 1% of cases but has a mortality rate of up to 90% (Waldorf J et al Diabetes Care 2006; 29:1150-9). Patients will have a decreased conscious state and may also have cranial nerve palsies, headache and/or bradycardia and hypertension. Its incidence has remained the same since it was described in 1936 and although we have clues as to what may contribute to it, and we know that some patients have subclinical cerebral oedema at presentation(Krane et al NEJM 1985;312:1147-51), we still cant predict who will get it, nor greatly affect its high rate of mortality. There are theories of causative factors, most of which are vasogenic or osmotically based, but there is really no great evidence out there. The studies are small or retrospective, or both. One theory relates to osmolytes accumulating in brain cells. These are the compounds that maintain normal cell volumes. As extracellular osmolality decreases rapidly with treatment, water flows rapidly onto these cells causing the brain to swell. Another theory relates to Na+ / H+ exchanger, such that a correction of acidosis results in Na and water passing onto the brain cells, resulting in oedema. How much has been proven to be the actual mechanism? By my reading, not much. We believe that the following increase the chance of developing cerebral oedema: Rapid change in Osmolality (2xNa + U + Glc): ie rapid decrease in Glucose and a decrease in Sodium Initial pH < 7.1. and in more recent studies (Glaser N et al NEJM 2001;344:264-269) WHAT DOES THIS MEAN IN TERMS OF TREATMENT? FLUIDS:If the patient is hypotensive and crashing then fluid resuscitation is necessary. No question about it. However, how much we give Continue reading >>

Ketoacidosis Versus Ketosis

Ketoacidosis Versus Ketosis

Some medical professionals confuse ketoacidosis, an extremely abnormal form of ketosis, with the normal benign ketosis associated with ketogenic diets and fasting states in the body. They will then tell you that ketosis is dangerous. Testing Laboratory Microbiology - Air Quality - Mold Asbestos - Environmental - Lead emsl.com Ketosis is NOT Ketoacidosis The difference between the two conditions is a matter of volume and flow rate*: Benign nutritional ketosis is a controlled, insulin regulated process which results in a mild release of fatty acids and ketone body production in response to either a fast from food, or a reduction in carbohydrate intake. Ketoacidosis is driven by a lack of insulin in the body. Without insulin, blood sugar rises to high levels and stored fat streams from fat cells. This excess amount of fat metabolism results in the production of abnormal quantities of ketones. The combination of high blood sugar and high ketone levels can upset the normal acid/base balance in the blood and become dangerous. In order to reach a state of ketoacidosis, insulin levels must be so low that the regulation of blood sugar and fatty acid flow is impaired. *See this reference paper. Here's a table of the actual numbers to show the differences in magnitude: Body Condition Quantity of Ketones Being Produced After a meal: 0.1 mmol/L Overnight Fast: 0.3 mmol/L Ketogenic Diet (Nutritional ketosis): 1-8 mmol/L >20 Days Fasting: 10 mmol/L Uncontrolled Diabetes (Ketoacidosis): >20 mmol/L Here's a more detailed explanation: Fact 1: Every human body maintains the blood and cellular fluids within a very narrow range between being too acidic (low pH) and too basic (high pH). If the blood pH gets out of the normal range, either too low or too high, big problems happen. Fact 2: The Continue reading >>

Hyperventilation

Hyperventilation

You breathe in oxygen and breathe out carbon dioxide. Excessive breathing creates a low level of carbon dioxide in your blood. This causes many of the symptoms of hyperventilation. You may hyperventilate from an emotional cause such as during a panic attack. Or, it can be due to a medical problem, such as bleeding or infection. Your health care provider will determine the cause of your hyperventilation. Rapid breathing may be a medical emergency and you need to get treated, unless you have had this before and your provider has told you that you can treat it on your own. If you frequently overbreathe, you may have a medical problem called hyperventilation syndrome. When you're overbreathing, you might not be aware you're breathing fast and deep. But you'll likely be aware of the other symptoms, including: Feeling lightheaded, dizzy, weak, or not able to think straight Feeling as if you can't catch your breath Chest pain or fast and pounding heartbeat Belching or bloating Dry mouth Muscle spasms in the hands and feet Numbness and tingling in the arms or around the mouth Problems sleeping Continue reading >>

What Can Cause Kussmaul Breathing & How Is It Treated?

What Can Cause Kussmaul Breathing & How Is It Treated?

Kussmaul Breathing is the name given to a condition in which the patient develops an extremely deep and labored breathing pattern. This is seen mostly in people who are diabetic and have severe forms of metabolic acidosis, especially diabetic ketoacidosis with kidney dysfunction. Kussmaul Breathing can also be explained as a form of hyperventilation which is a condition in which an individual breathes in such a deep pattern that the level of carbon dioxide decreases in the blood, which is seen mostly in metabolic acidosis where the breathing becomes extremely fast and shallow and as the condition worsens the breathing becomes shallow and deep and it looks as if the individual is virtually gasping for breath. This type of breathing in which the individual is virtually gasping for air is what is termed as Kussmaul Breathing. Kussmaul Breathing is a condition which results due to low levels of carbon dioxide in the blood. It is normally seen in people who have uncontrolled diabetes to level where they develop diabetic ketoacidosis resulting in the patient to have a very shallow and deep breathing. The carbon dioxide level decreases due to the desire of the individual to take a deep breath and exhale more amount of carbon dioxide than the norm resulting in a marked decrease in the level of carbon dioxide in the blood causing hyperventilation or Kussmaul Breathing. The conditions which can cause Kussmaul Breathing are: Diabetic Ketoacidosis: Diabetic ketoacidosis is a condition in which the glucose present in the blood is not able to be used by the body to produce energy because of severe need for insulin which is not there. This results in the inability of the body to get rid of the glucose to produce energy for the body. Metabolic Acidosis: This is a medical condition in w Continue reading >>

Diagnosis And Treatment Of Diabetic Ketoacidosis And The Hyperglycemic Hyperosmolar State

Diagnosis And Treatment Of Diabetic Ketoacidosis And The Hyperglycemic Hyperosmolar State

Go to: Pathogenesis In both DKA and HHS, the underlying metabolic abnormality results from the combination of absolute or relative insulin deficiency and increased amounts of counterregulatory hormones. Glucose and lipid metabolism When insulin is deficient, the elevated levels of glucagon, catecholamines and cortisol will stimulate hepatic glucose production through increased glycogenolysis and enhanced gluconeogenesis4 (Fig. 1). Hypercortisolemia will result in increased proteolysis, thus providing amino acid precursors for gluconeogenesis. Low insulin and high catecholamine concentrations will reduce glucose uptake by peripheral tissues. The combination of elevated hepatic glucose production and decreased peripheral glucose use is the main pathogenic disturbance responsible for hyperglycemia in DKA and HHS. The hyperglycemia will lead to glycosuria, osmotic diuresis and dehydration. This will be associated with decreased kidney perfusion, particularly in HHS, that will result in decreased glucose clearance by the kidney and thus further exacerbation of the hyperglycemia. In DKA, the low insulin levels combined with increased levels of catecholamines, cortisol and growth hormone will activate hormone-sensitive lipase, which will cause the breakdown of triglycerides and release of free fatty acids. The free fatty acids are taken up by the liver and converted to ketone bodies that are released into the circulation. The process of ketogenesis is stimulated by the increase in glucagon levels.5 This hormone will activate carnitine palmitoyltransferase I, an enzyme that allows free fatty acids in the form of coenzyme A to cross mitochondrial membranes after their esterification into carnitine. On the other side, esterification is reversed by carnitine palmitoyltransferase I Continue reading >>

Emergency Management Of Diabetic Ketoacidosis In Adults

Emergency Management Of Diabetic Ketoacidosis In Adults

Diabetic ketoacidosis (DKA) is a potentially fatal metabolic disorder presenting most weeks in most accident and emergency (A&E) departments.1 The disorder can have significant mortality if misdiagnosed or mistreated. Numerous management strategies have been described. Our aim is to describe a regimen that is based, as far as possible, on available evidence but also on our experience in managing patients with DKA in the A&E department and on inpatient wards. A literature search was carried out on Medline and the Cochrane Databases using “diabetic ketoacidosis” as a MeSH heading and as textword. High yield journals were hand searched. Papers identified were appraised in the ways described in the Users’ guide series published in JAMA. We will not be discussing the derangements in intermediary metabolism involved, nor would we suggest extrapolating the proposed regimen to children. Although some of the issues discussed may be considered by some to be outwith the remit of A&E medicine it would seem prudent to ensure that A&E staff were aware of the probable management of such patients in the hours after they leave the A&E department. AETIOLOGY AND DEFINITION DKA may be the first presentation of diabetes. Insulin error (with or without intercurrent illness) is the most common precipitating factor, accounting for nearly two thirds of cases (excluding those where DKA was the first presentation of diabetes mellitus).2 The main features of DKA are hyperglycaemia, metabolic acidosis with a high anion gap and heavy ketonuria (box 1). This contrasts with the other hyperglycaemic diabetic emergency of hyperosmolar non-ketotic hyperglycaemia where there is no acidosis, absent or minimal ketonuria but often very high glucose levels (>33 mM) and very high serum sodium levels (>15 Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Tweet Diabetic ketoacidosis (DKA) is a dangerous complication faced by people with diabetes which happens when the body starts running out of insulin. DKA is most commonly associated with type 1 diabetes, however, people with type 2 diabetes that produce very little of their own insulin may also be affected. Ketoacidosis is a serious short term complication which can result in coma or even death if it is not treated quickly. Read about Diabetes and Ketones What is diabetic ketoacidosis? DKA occurs when the body has insufficient insulin to allow enough glucose to enter cells, and so the body switches to burning fatty acids and producing acidic ketone bodies. A high level of ketone bodies in the blood can cause particularly severe illness. Symptoms of DKA Diabetic ketoacidosis may itself be the symptom of undiagnosed type 1 diabetes. Typical symptoms of diabetic ketoacidosis include: Vomiting Dehydration An unusual smell on the breath –sometimes compared to the smell of pear drops Deep laboured breathing (called kussmaul breathing) or hyperventilation Rapid heartbeat Confusion and disorientation Symptoms of diabetic ketoacidosis usually evolve over a 24 hour period if blood glucose levels become and remain too high (hyperglycemia). Causes and risk factors for diabetic ketoacidosis As noted above, DKA is caused by the body having too little insulin to allow cells to take in glucose for energy. This may happen for a number of reasons including: Having blood glucose levels consistently over 15 mmol/l Missing insulin injections If a fault has developed in your insulin pen or insulin pump As a result of illness or infections High or prolonged levels of stress Excessive alcohol consumption DKA may also occur prior to a diagnosis of type 1 diabetes. Ketoacidosis can occasional Continue reading >>

Pediatric Diabetic Ketoacidosis

Pediatric Diabetic Ketoacidosis

Practice Essentials Diabetic ketoacidosis, in pediatric and adult cases, is a metabolic derangement caused by the absolute or relative deficiency of the anabolic hormone insulin. Together with the major complication of cerebral edema, it is the most important cause of mortality and severe morbidity in children with diabetes. Signs and symptoms Symptoms of acidosis and dehydration include the following: Symptoms of hyperglycemia, a consequence of insulin deficiency, include the following: Patients with diabetic ketoacidosis may also have the following signs and symptoms: Cerebral edema Most cases of cerebral edema occur 4-12 hours after initiation of treatment. Diagnostic criteria of cerebral edema include the following: Major criteria include the following: Minor criteria include the following: See Clinical Presentation for more detail. Laboratory studies The following lab studies are indicated in patients with diabetic ketoacidosis: Imaging studies Head computed tomography (CT) scanning - If coma is present or develops Chest radiography - If clinically indicated Electrocardiography Electrocardiography (ECG) is a useful adjunct to monitor potassium status. Characteristic changes appear with extremes of potassium status. See the images below. Consciousness Check the patient’s consciousness level hourly for up to 12 hours, especially in a young child with a first presentation of diabetes. The Glasgow coma scale is recommended for this purpose. See Workup for more detail. Management Replacement of the following is essential in the treatment of diabetic ketoacidosis: Insulin - Continuous, low-dose, intravenous (IV) insulin infusion is generally considered the safest and most effective insulin delivery method for diabetic ketoacidosis Potassium - After initial resuscitatio Continue reading >>

Hyperventilation Causes

Hyperventilation Causes

Causes of hyperventilation are seriously misunderstood by the mainstream medicine. Internet (Wikipedia, etc.) and professional medical sources grossly misrepresent the prevalence of hyperventilation primarily limiting it to such cases as lung injuries, extreme stress, diabetic ketoacidosis, head injuries and stroke. In reality research provides a different view on presence and prevalence of hyperventilation (breathing more air than the medical norm).  Minute ventilation rates (chronic diseases) Condition Minute ventilation Number of people All references or click below for abstracts Normal breathing 6 l/min - Medical textbooks Healthy Subjects 6-7 l/min >400 Results of 14 studies COPD 14 (+-2) l/min 12 Palange et al, 2001 COPD 12 (+-2) l/min 10 Sinderby et al, 2001 COPD 14 l/min 3 Stulbarg et al, 2001 Cancer 12 (+-2) l/min 40 Travers et al, 2008 Heart disease 15 (+-4) l/min 22 Dimopoulou et al, 2001 var ezzns22 = {3.00:504664,0.80:504559,0.30:504551,2.00:504657,5.00:504669,0.25:504548,1.40:504651,1.50:504652,1.70:504654,1.80:504655,2.20:504658,2.80:504661,0.20:504145,1.90:504656,2.40:504659,4.00:504666,1.30:504650,0.50:504556,0.90:504560,0.10:504141,0.35:504552,0.40:504554,0.70:504558,1.10:504648,3.50:504665,4.50:504667,0.05:504099,0.45:504555,0.60:504557,1.00:504647,0.15:504144,1.60:504653,2.60:504660,1.20:504649,}; var ezoflbf_2_22 = function() { __ez.queue.addFunc('ReloadFromP_1022', 'IL11ILILIIlLLLILILLLLIILLLIIL11111LLILiiLIliLlILlLiiLLIiILL.ReloadFromP', 1022, false, ['banger.js'], false, false, false, true); }; var ezoflbf_22 = function() { eval(ez_write_tag([[300,250],'normalbreathing_com-medrectangle-4','ezslot_4'])); };ezoflbf_22(); var __ezfl_sss_1022 = function() { setTimeout(function(){ var ezflaun = IL11ILILIIlLLLILILLLLIILLLIIL11111LLILiiLIliLlILlLi Continue reading >>

Hyperventilation In Severe Diabetic Ketoacidosis*

Hyperventilation In Severe Diabetic Ketoacidosis*

Abstract To explore whether the carbon dioxide-bicarbonate (P(CO(2))-HCO(3)) buffering system in blood and cerebrospinal fluid (CSF) in diabetic ketoacidosis should influence the approach to ventilation in patients at risk of cerebral edema. Medline search, manual search of references in articles found in Medline search, and use of historical literature from 1933 to 1967. A clinical vignette is used--a child with severe diabetic ketoacidosis who presented with profound hypocapnia and then deteriorated--as a basis for discussion of integrative metabolic and vascular physiology. Studies included reports in diabetic ketoacidosis where arterial and CSF acid-base data have been presented. Studies where simultaneous acid-base, ventilation, respiratory quotient, and cerebral blood flow data are available. We revisit a hypothesis and, by reassessing data, put forward an argument based on the significance of low [HCO(3)](CSF) and rising Pa(CO(2))- hyperventilation in diabetic ketoacidosis and the limit in biology of survival; repair of severe diabetic ketoacidosis and Pa(CO(2))-and mechanical ventilation. The review highlights a potential problem with mechanical ventilation in severe diabetic ketoacidosis and suggests that the P(CO(2))--HCO(3) hypothesis is consistent with data on cerebral edema in diabetic ketoacidosis. It also indicates that the recommendation to avoid induced hyperventilation early in the course of intensive care may be counter to the logic of adaptive physiology. ) “iso-acidity” lines. A, changes in the index case: point 1, at presentation; point 2, 15 mins ABG 7.09 ⫾0.04 14.0 ⫾1.0 5.0 ⫾1.0 Ohman et al. (9) CSF 7.35 ⫾0.03 23.0 ⫾2.0 12.0 ⫾2.0 ABG 7.15 ⫾0.06 19.9 ⫾2.5 7.6 ⫾1.6 Marks et al. (10) CSF 7.22 ⫾0.03 25.0 ⫾2.7 10.2 ⫾1.7 ABG Continue reading >>

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