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Why Is There Acidosis In Dka?

Haemofiltration As A Treatment Option In Refractory Life-threatening Diabetic Ketoacidosis

Haemofiltration As A Treatment Option In Refractory Life-threatening Diabetic Ketoacidosis

Background: Treating life-threatening diabetic ketoacidosis (DKA) with a pH of <6.9 is extremely challenging and often refractory to treatment using standard fixed dose insulin DKA management protocols which may not work effectively at this low pH because of increased insulin resistance. I.v. bicarbonate (HCO3) use in this situation can be considered but remains controversial due to the risk of significant side effects as well as limited evidence in literature. Here we attempt to describe a case of fulminant DKA without renal failure, where treatment with haemofiltration (HF) for severe metabolic acidosis was successful. Case history: A 23-year-old female with history of recurrent episodes of DKA and poor diabetes control secondary to non-compliance, presented to the emergency department via ambulance after being found collapsed and had successful cardiopulmonary resuscitation for pulseless electrical activity and was subsequently treated with standard DKA protocol. Investigations on admission: pH 6.752, HCO3 1.3, lactate 3.1, base excess −30, blood glucose 45 mmol/l, blood ketones 6 mmol/l, creatinine 133 mmol, urea 10.8 mmol, and eGFR 43. Treatment: Despite maximal DKA treatment over three hours, including 5 l of i.v. fluid, and maximum fixed rate i.v. insulin at 15 units/h, she continued to be in severe metabolic acidosis with pH 6.772, HCO3 1.7, ketones 5, and blood glucose 40.1, without any improvement in her Glasgow coma scale of 8. Options were discussed at length with critical care and endocrine teams regarding use of i.v. bicarbonate therapy vs HF. She was then put on HF which resolved the metabolic acidosis completely within 12 h. Discussion: Our patient responded to HF with resolution of severe metabolic acidosis. There are no guidelines at present that com 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 >>

Management Of A Dka Patient With Severe Metabolic And Ketoacidosis With Chronic Renal Insufficiency Brian Albany Otterbein University, Boomer.albany@otterbein.edu

Management Of A Dka Patient With Severe Metabolic And Ketoacidosis With Chronic Renal Insufficiency Brian Albany Otterbein University, [email protected]

Otterbein University Digital Commons @ Otterbein MSN Student Scholarship Student Research & Creative Work Fall 2014 Follow this and additional works at: Part of the Endocrine System Diseases Commons, Medical Pathology Commons, and the Nursing Commons This Project is brought to you for free and open access by the Student Research & Creative Work at Digital Commons @ Otterbein. It has been accepted for inclusion in MSN Student Scholarship by an authorized administrator of Digital Commons @ Otterbein. For more information, please contact [email protected] Recommended Citation Albany, Brian, "Management of a DKA patient with severe metabolic and ketoacidosis with chronic renal insufficiency" (2014). MSN Student Scholarship. Paper 6. Implications for nursing care Management of a DKA patient with severe metabolic and ketoacidosis with chronic renal insufficiency Brian Albany BSN, CCRN Introduction Case Study References Underlying Pathophysiology Diabetic ketoacidosis (DKA) serves as one the leading causes of mortality in diabetic patients [14]. The mortality has decreased over the past several decades due to the rapid recognition of the disease state and the improvement of management of DKA [14]. Despite a decline in mortality rates over the past twenty years from 7.96% to 0.67%, errors in management of the disease state are associated with significant morbidity and mortality [2]. Utilization of DKA protocols in the acute care setting have allowed congruency in care and delivery of effective lifesaving treatment. Despite advances in standardized DKA protocols, there still remains a gap in how to manage specific patient populations with end stage renal disease. Understanding the pathophysiology behind these patient populations will yield better outcomes with the ultimate Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

4 Evaluation 5 Management Defining features include hyperglycemia (glucose > 250mg/dl), acidosis (pH < 7.3), and ketonemia/ketonuria Leads to osmotic diuresis and depletion of electrolytes including sodium, magnesium, calcium and phosphorous. Further dehydration impairs glomerular filtration rate (GFR) and contributes to acute renal failure Due to lipolysis / accumulation of of ketoacids (represented by increased anion gap) Compensatory respiratory alkalosis (i.e. tachypnea and hyperpnea - Kussmaul breathing) Breakdown of adipose creates first acetoacetate leading to conversion to beta-hydroxybutyrate Causes activation of RAAS in addition to the osmotic diuresis Cation loss (in exchange for chloride) worsens metabolic acidosis May be the initial presenting of an unrecognized T1DM patient Presenting signs/symptoms include altered mental status, tachypnea, abdominal pain, hypotension, decreased urine output. Perform a thorough neurologic exam (cerebral edema increases mortality significantly, especially in children) Assess for possible inciting cause (especially for ongoing infection; see Differential Diagnosis section) Ill appearance. Acetone breath. Drowsiness with decreased reflexes Tachypnea (Kussmaul's breathing) Signs of dehydration with dry mouth and dry mucosa. Perform a thorough neurologic exam as cerebral edema increases mortality significantly, especially in children There may be signs from underlying cause (eg pneumonia) Differential Diagnosis Insulin or oral hypoglycemic medication non-compliance Infection Intra-abdominal infections Steroid use Drug abuse Pregnancy Diabetic ketoacidosis (DKA) Diagnosis is made based on the presence of acidosis and ketonemia in the setting of diabetes. Bicarb may be normal due to compensatory and contraction alcoholosis so the 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 >>

Understanding And Treating Diabetic Ketoacidosis

Understanding And Treating Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a serious metabolic disorder that can occur in animals with diabetes mellitus (DM).1,2 Veterinary technicians play an integral role in managing and treating patients with this life-threatening condition. In addition to recognizing the clinical signs of this disorder and evaluating the patient's response to therapy, technicians should understand how this disorder occurs. DM is caused by a relative or absolute lack of insulin production by the pancreatic b-cells or by inactivity or loss of insulin receptors, which are usually found on membranes of skeletal muscle, fat, and liver cells.1,3 In dogs and cats, DM is classified as either insulin-dependent (the body is unable to produce sufficient insulin) or non-insulin-dependent (the body produces insulin, but the tissues in the body are resistant to the insulin).4 Most dogs and cats that develop DKA have an insulin deficiency. Insulin has many functions, including the enhancement of glucose uptake by the cells for energy.1 Without insulin, the cells cannot access glucose, thereby causing them to undergo starvation.2 The unused glucose remains in the circulation, resulting in hyperglycemia. To provide cells with an alternative energy source, the body breaks down adipocytes, releasing free fatty acids (FFAs) into the bloodstream. The liver subsequently converts FFAs to triglycerides and ketone bodies. These ketone bodies (i.e., acetone, acetoacetic acid, b-hydroxybutyric acid) can be used as energy by the tissues when there is a lack of glucose or nutritional intake.1,2 The breakdown of fat, combined with the body's inability to use glucose, causes many pets with diabetes to present with weight loss, despite having a ravenous appetite. If diabetes is undiagnosed or uncontrolled, a series of metab Continue reading >>

Pulmcrit- Dominating The Acidosis In Dka

Pulmcrit- Dominating The Acidosis In Dka

Management of acidosis in DKA is an ongoing source of confusion. There isn’t much high-quality evidence, nor will there ever be (1). However, a clear understanding of the physiology of DKA may help us treat this rationally and effectively. Physiology of ketoacidosis in DKA Ketoacidosis occurs due to an imbalance between insulin dose and insulin requirement: Many factors affect the insulin requirement: Individuals differ in their baseline insulin resistance and insulin requirements. Physiologic stress (e.g. hypovolemia, inflammation) increases the level of catecholamines and cortisol, which increases insulin resistance. Hyperglycemia and metabolic acidosis themselves increase insulin resistance (Souto 2011, Gosmanov 2014). DKA treatment generally consists of two phases: first, we must manage the ketoacidosis. Later, we must prepare the patient to transition back to their home insulin regimen. During both phases, success depends on balancing insulin dose and insulin requirement. Phase I (Take-off): Initial management of the DKA patient with worrisome acidosis Let’s start by considering a patient who presents in severe DKA with worrisome acidosis. This is uncommon. Features that might provoke worry include the following: bicarbonate < 7 mEq/L pH < 7 (if measured; there is generally little benefit from measuring pH) clinically ill-appearing (e.g., dyspnea, marked Kussmaul respirations) These patients generally have severe metabolic acidosis with respiratory compensation. This creates two concerns: If the metabolic acidosis worsens, they may decompensate. The patient is depending on respiratory compensation to maintain their pH. If they should fatigue and lose the ability to hyperventilate, their pH would drop. It is important to reverse the acidosis before the patient m Continue reading >>

Pathophysiology Of Diabetic Ketoacidosis

Pathophysiology Of Diabetic Ketoacidosis

Diabetic ketoacidosis is one of the potentially life-threatening acute complications of diabetes mellitus. In the past, diabetic ketoacidosis was considered as the hallmark of Type I diabetes, but current data show that it can be also diagnosed in patients with type II diabetes mellitus. It is often seen among patients who are poorly compliant to insulin administration during an acute illness. It is commonly precipitated by an acute stressful event such as the development of infection leading to overt sepsis, organ infarction such as stroke and heart attack, burns, pregnancy or intake of drugs that affect carbohydrate metabolism such as corticosteroids, anti-hypertensives, loop diuretics, alcohol, cocaine, and ecstasy. The presence of these stressful conditions incite the release of counter-regulatory hormones such as glucagon, catecholamines and growth hormone. These hormones induce the mobilization of energy stores of fat, glycogen and protein. The net effect of which is the production of glucose. As a result of absent or deficient insulin release, diabetic ketoacidosis present with the following metabolic derangements: profound hyperglycemia, hyperketonemiaand metabolic acidosis. The production of ketones outweighs its excretion by the kidneys. This results in further reduction of systemic insulin, elevated concentrations of glucagon, cortisol, growth hormone and catecholamine. In peripheral tissues, such as the liver, lipolysis occurs to free fatty acids, resulting in further production of excess ketones. Thereby, causing ketosis and metabolic acidosis. Symptoms of diabetic ketoacidosis usually develop within 24 hours. Gastrointestinal symptoms such as nausea and vomiting are very prominent. If these symptoms are present in diabetics, investigation for diabetic keto Continue reading >>

Lactic Acidosis Associated With Ketoacidosis

Lactic Acidosis Associated With Ketoacidosis

Surely there are enough reasons to have a nice acidosis when you are full of ketones. But on top of all that, you can also get a lactic acidosis. There is an association of diabetic ketoacidosis and lactic acidosis that goes beyond the tendency of diabetics to be on metformin. Indeed, in one case series there was “significant” lactate levels (i.e. over 4.0 mmol/L) in 40% of the patients. Glucose levels tended to correlated with lactate levels, suggesting that the lactate here is being produced as a result of some sort of abnormal cellular carbohydrate handing. The authors of this recent paper have admitted that this association is poorly researched. There does not seem to be a good mechanism worked out at this stage. Again, endogenous catecholamine excess is implicated. It is known that adrenaline levels correlate with DKA severity. D-lactate production may also play a role. A 2011 study has correlated D-lactate levels to the size of the anion gap in diabetic ketoacidosis; the article also ventures a hypothetical mechanism as to how this comes about. In any case, a much earlier study has demonstrated that whereas the ketone body levels correlated well with pH, the lactate did not, which suggests that lactate plays a fairly minor role in the actual acidosis. Additionally, Kerry Brandis reports on the interaction of lactate and ketoacids (specifically, on how lactate production tends to reduce the concentration of acetoacetate, thus fooling the most common ketone tests Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic acidosis is a life-threatening condition that can occur in people with type 1 diabetes. Less commonly, it can also occur with type 2 diabetes. Term watch Ketones: breakdown products from the use of fat stores for energy. Ketoacidosis: another name for diabetic acidosis. It happens when a lack of insulin leads to: Diabetic acidosis requires immediate hospitalisation for urgent treatment with fluids and intravenous insulin. It can usually be avoided through proper treatment of Type 1 diabetes. However, ketoacidosis can also occur with well-controlled diabetes if you get a severe infection or other serious illness, such as a heart attack or stroke, which can cause vomiting and resistance to the normal dose of injected insulin. What causes diabetic acidosis? The condition is caused by a lack of insulin, most commonly when doses are missed. While insulin's main function is to lower the blood sugar level, it also reduces the burning of body fat. If the insulin level drops significantly, the body will start burning fat uncontrollably while blood sugar levels rise. Glucose will then begin to show up in your urine, along with ketone bodies from fat breakdown that turn the body acidic. The body attempts to reduce the level of acid by increasing the rate and depth of breathing. This blows off carbon dioxide in the breath, which tends to correct the acidosis temporarily (known as acidotic breathing). At the same time, the high secretion of glucose into the urine causes large quantities of water and salts to be lost, putting the body at serious risk of dehydration. Eventually, over-breathing becomes inadequate to control the acidosis. What are the symptoms? Since diabetic acidosis is most often linked with high blood sugar levels, symptoms are the same as those for diabetes Continue reading >>

Lactic Acidosis In Diabetic Ketoacidosis

Lactic Acidosis In Diabetic Ketoacidosis

Go to: Discussion Lactate acidosis is a common finding in DKA. Several pathophysiological mechanisms are responsible for the extremely high lactate values sometimes found in patients with ketoacidotic. Originally, elevated lactate values in patients with DKA were thought to be the result of inadequate tissue perfusion and oxygenation (due to a contracted intravascular volume, aggravated by the presence of macrovascular disease and microangiopathies, an increased amount of glycosylated Hb, and an abnormal platelet function).1–3 The resulting relative hypoxaemia stimulates the process of anaerobic glycolysis, where pyruvic acid is converted to l-lactate, yielding two ATP molecules. More recently, however, it was demonstrated that the metabolic derangements itself present in DKA might contribute as well to the elevated lactate levels.4 Various studies have reported the presence of a positive correlation between glucose levels and ketone (β-hydroxybutyrate) levels on the one hand, and lactate levels on the other hand.4 5 This could be explained by various intracellular and extracellular mechanisms. First, an increased amount of d-lactate is formed in erythrocytes. Since erythrocytes do not require insulin for glucose uptake, intracellular glucose concentrations approach ambient extracellular levels during ketoacidosis. A substantial portion of the glucose in the erythrocyte is converted to pyruvate and finally l-lactate by aerobic glycolysis to produce ATP. The remainder is metabolised by the sorbitol pathway and the pentose-phosphate shunt to produce methylglyoxal, which is a toxic endogenous glucose metabolite, that is degraded by the glyoxalase system to produce d-lactate. Methylglyoxal (and thereby d-lactate) is also formed directly in the plasma via an interaction b Continue reading >>

Diabetes With Ketone Bodies In Dogs

Diabetes With Ketone Bodies In Dogs

Studies show that female dogs (particularly non-spayed) are more prone to DKA, as are older canines. Diabetic ketoacidosis is best classified through the presence of ketones that exist in the liver, which are directly correlated to the lack of insulin being produced in the body. This is a very serious complication, requiring immediate veterinary intervention. Although a number of dogs can be affected mildly, the majority are very ill. Some dogs will not recover despite treatment, and concurrent disease has been documented in 70% of canines diagnosed with DKA. Diabetes with ketone bodies is also described in veterinary terms as diabetic ketoacidosis or DKA. It is a severe complication of diabetes mellitus. Excess ketone bodies result in acidosis and electrolyte abnormalities, which can lead to a crisis situation for your dog. If left in an untreated state, this condition can and will be fatal. Some dogs who are suffering from diabetic ketoacidosis may present as systemically well. Others will show severe illness. Symptoms may be seen as listed below: Change in appetite (either increase or decrease) Increased thirst Frequent urination Vomiting Abdominal pain Mental dullness Coughing Fatigue or weakness Weight loss Sometimes sweet smelling breath is evident Slow, deep respiration. There may also be other symptoms present that accompany diseases that can trigger DKA, such as hypothyroidism or Cushing’s disease. While some dogs may live fairly normal lives with this condition before it is diagnosed, most canines who become sick will do so within a week of the start of the illness. There are four influences that can bring on DKA: Fasting Insulin deficiency as a result of unknown and untreated diabetes, or insulin deficiency due to an underlying disease that in turn exacerba 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 >>

Hypothermia: A Complication Of Diabetic Ketoacidosis

Hypothermia: A Complication Of Diabetic Ketoacidosis

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Any Benefit To Sodium Bicarbonate In Dka?

Any Benefit To Sodium Bicarbonate In Dka?

In a prior post, we discussed the use of an initial insulin bolus in the management of diabetic ketoacidosis (DKA). Today we will address another facet of DKA management, for which there is less than optimal evidence and that is: Any benefit to sodium bicarbonate in DKA? Consensus guidelines for the management of DKA recommended administering sodium bicarbonate to DKA patients who present with an initial blood gas pH of < 7.0. That recommendation was updated and changed in 2009 to limit sodium bicarbonate use to DKA patients with blood gas pH of < 6.9. More recently, Chua et al. published a systematic review of 44 articles discussing bicarbonate administration and Duhon et al. published the largest retrospective review of DKA patient with presenting pH of < 7.0. What are the most recent studies evaluating: Any benefit to sodium bicarbonate in DKA? Chua et al (21906367) Duhon et al (23737516) Objective Efficacy and risk of bicarb administration in severe acidemia in DKA Determine whether bicarb therapy is associated with reduced time to resolution of acidemia Methods Systematic review of pubmed database Retrospective cohort of DKA pts with initial pH < 7.0 who did vs did not receive bicarb Results 44 articles included -Heterogeneity in pH threshold, concentration, amount, & timing of bicarb administration -Transient improvement in metabolic acidosis -No improved glycemic control -Associated risk of cerebral edema in pediatric pts No study involved patients with a pH < 6.85 86 patients -No difference found in: 1. Time to resolution of acidemia 2. Time to hospital discharge 3. Time on IV insulin 4. Potassium requirement in 1st 24 hrs -Subgroup analysis of pH <6.9 (n=20) showed no statistical diff in time to resolution of acidemia Conclusion Evidence does not justify the ad Continue reading >>

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