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Why Are Dka Patients Hypokalemic

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 >>

What Causes Potassium And Sodium Loss In Diabetic Ketoacidosis (dka)?

What Causes Potassium And Sodium Loss In Diabetic Ketoacidosis (dka)?

What causes potassium and sodium loss in diabetic ketoacidosis (DKA)? Glucosuria leads to osmotic diuresis, dehydration and hyperosmolarity. Severe dehydration, if not properly compensated, may lead to impaired renal function. Hyperglycemia, osmotic diuresis, serum hyperosmolarity, and metabolic acidosis result in severe electrolyte disturbances. The most characteristic disturbance is total body potassium loss. This loss is not mirrored in serum potassium levels, which may be low, within the reference range, or even high. Potassium loss is caused by a shift of potassium from the intracellular to the extracellular space in an exchange with hydrogen ions that accumulate extracellularly in acidosis. Much of the shifted extracellular potassium is lost in urine because of osmotic diuresis. Patients with initial hypokalemia are considered to have severe and serious total body potassium depletion. High serum osmolarity also drives water from intracellular to extracellular space, causing dilutional hyponatremia. Sodium also is lost in the urine during the osmotic diuresis. Glaser NS, Marcin JP, Wootton-Gorges SL, et al. Correlation of clinical and biochemical findings with diabetic ketoacidosis-related cerebral edema in children using magnetic resonance diffusion-weighted imaging. J Pediatr. 2008 Jun 25. [Medline] . Umpierrez GE, Jones S, Smiley D, et al. Insulin analogs versus human insulin in the treatment of patients with diabetic ketoacidosis: a randomized controlled trial. Diabetes Care. 2009 Jul. 32(7):1164-9. [Medline] . [Full Text] . Herrington WG, Nye HJ, Hammersley MS, Watkinson PJ. Are arterial and venous samples clinically equivalent for the estimation of pH, serum bicarbonate and potassium concentration in critically ill patients?. Diabet Med. 2012 Jan. 29(1):32-5 Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Abbas E. Kitabchi, PhD., MD., FACP, FACE Professor of Medicine & Molecular Sciences and Maston K. Callison Professor in the Division of Endocrinology, Diabetes & Metabolism UT Health Science Center, 920 Madison Ave., 300A, Memphis, TN 38163 Aidar R. Gosmanov, M.D., Ph.D., D.M.Sc. Assistant Professor of Medicine, Division of Endocrinology, Diabetes & Metabolism, The University of Tennessee Health Science Center, 920 Madison Avenue, Suite 300A, Memphis, TN 38163 Clinical Recognition Omission of insulin and infection are the two most common precipitants of DKA. Non-compliance may account for up to 44% of DKA presentations; while infection is less frequently observed in DKA patients. Acute medical illnesses involving the cardiovascular system (myocardial infarction, stroke, acute thrombosis) and gastrointestinal tract (bleeding, pancreatitis), diseases of endocrine axis (acromegaly, Cushing`s syndrome, hyperthyroidism) and impaired thermo-regulation or recent surgical procedures can contribute to the development of DKA by causing dehydration, increase in insulin counter-regulatory hormones, and worsening of peripheral insulin resistance. Medications such as diuretics, beta-blockers, corticosteroids, second-generation anti-psychotics, and/or anti-convulsants may affect carbohydrate metabolism and volume status and, therefore, could precipitateDKA. Other factors: psychological problems, eating disorders, insulin pump malfunction, and drug abuse. It is now recognized that new onset T2DM can manifest with DKA. These patients are obese, mostly African Americans or Hispanics and have undiagnosed hyperglycemia, impaired insulin secretion, and insulin action. A recent report suggests that cocaine abuse is an independent risk factor associated with DKA recurrence. Pathophysiology In Continue reading >>

How Is Hypokalemia Treated In Diabetic Ketoacidosis (dka) Treated?

How Is Hypokalemia Treated In Diabetic Ketoacidosis (dka) Treated?

How is hypokalemia treated in diabetic ketoacidosis (DKA) treated? Hypokalemia is a complication that is precipitated by failing to rapidly address the total body potassium deficit brought out by rehydration and insulin treatment, which not only reduces acidosis but directly facilitates potassium reentry into the cell. Glaser NS, Marcin JP, Wootton-Gorges SL, et al. Correlation of clinical and biochemical findings with diabetic ketoacidosis-related cerebral edema in children using magnetic resonance diffusion-weighted imaging. J Pediatr. 2008 Jun 25. [Medline] . Umpierrez GE, Jones S, Smiley D, et al. Insulin analogs versus human insulin in the treatment of patients with diabetic ketoacidosis: a randomized controlled trial. Diabetes Care. 2009 Jul. 32(7):1164-9. [Medline] . [Full Text] . Herrington WG, Nye HJ, Hammersley MS, Watkinson PJ. Are arterial and venous samples clinically equivalent for the estimation of pH, serum bicarbonate and potassium concentration in critically ill patients?. Diabet Med. 2012 Jan. 29(1):32-5. [Medline] . Mrozik LT, Yung M. Hyperchloraemic metabolic acidosis slows recovery in children with diabetic ketoacidosis: a retrospective audit. Aust Crit Care. 2009 Jun 26. [Medline] . Bowden SA, Duck MM, Hoffman RP. Young children (12 yr) with type 1 diabetes mellitus have low rate of partial remission: diabetic ketoacidosis is an important risk factor. Pediatr Diabetes. 2008 Jun. 9(3 Pt 1):197-201. [Medline] . Potenza M, Via MA, Yanagisawa RT. Excess thyroid hormone and carbohydrate metabolism. Endocr Pract. 2009 May-Jun. 15(3):254-62. [Medline] . Taylor SI, Blau JE, Rother KI. SGLT2 Inhibitors May Predispose to Ketoacidosis. J Clin Endocrinol Metab. 2015 Aug. 100 (8):2849-52. [Medline] . Zargar AH, Wani AI, Masoodi SR, et al. Causes of mortality Continue reading >>

Hyperkalemia (high Blood Potassium)

Hyperkalemia (high Blood Potassium)

How does hyperkalemia affect the body? Potassium is critical for the normal functioning of the muscles, heart, and nerves. It plays an important role in controlling activity of smooth muscle (such as the muscle found in the digestive tract) and skeletal muscle (muscles of the extremities and torso), as well as the muscles of the heart. It is also important for normal transmission of electrical signals throughout the nervous system within the body. Normal blood levels of potassium are critical for maintaining normal heart electrical rhythm. Both low blood potassium levels (hypokalemia) and high blood potassium levels (hyperkalemia) can lead to abnormal heart rhythms. The most important clinical effect of hyperkalemia is related to electrical rhythm of the heart. While mild hyperkalemia probably has a limited effect on the heart, moderate hyperkalemia can produce EKG changes (EKG is a reading of theelectrical activity of the heart muscles), and severe hyperkalemia can cause suppression of electrical activity of the heart and can cause the heart to stop beating. Another important effect of hyperkalemia is interference with functioning of the skeletal muscles. Hyperkalemic periodic paralysis is a rare inherited disorder in which patients can develop sudden onset of hyperkalemia which in turn causes muscle paralysis. The reason for the muscle paralysis is not clearly understood, but it is probably due to hyperkalemia suppressing the electrical activity of the muscle. Common electrolytes that are measured by doctors with blood testing include sodium, potassium, chloride, and bicarbonate. The functions and normal range values for these electrolytes are described below. Hypokalemia, or decreased potassium, can arise due to kidney diseases; excessive losses due to heavy sweating Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Practice Essentials Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria. Signs and symptoms The most common early symptoms of DKA are the insidious increase in polydipsia and polyuria. The following are other signs and symptoms of DKA: Nausea and vomiting; may be associated with diffuse abdominal pain, decreased appetite, and anorexia History of failure to comply with insulin therapy or missed insulin injections due to vomiting or psychological reasons or history of mechanical failure of insulin infusion pump Altered consciousness (eg, mild disorientation, confusion); frank coma is uncommon but may occur when the condition is neglected or with severe dehydration/acidosis Signs and symptoms of DKA associated with possible intercurrent infection are as follows: See Clinical Presentation for more detail. Diagnosis On examination, general findings of DKA may include the following: Characteristic acetone (ketotic) breath odor In addition, evaluate patients for signs of possible intercurrent illnesses such as MI, UTI, pneumonia, and perinephric abscess. Search for signs of infection is mandatory in all cases. Testing Initial and repeat laboratory studies for patients with DKA include the following: Serum electrolyte levels (eg, potassium, sodium, chloride, magnesium, calcium, phosphorus) Note that high serum glucose levels may lead to dilutional hyponatremia; high triglyceride levels may lead to factitious low glucose levels; and high levels of ketone bodies may lead to factitious elevation of creatinine levels. Continue reading >>

162: Incidence Of Hypokalemia In Patients Presenting To The Emergency Department With Diabetic Ketoacidosis

162: Incidence Of Hypokalemia In Patients Presenting To The Emergency Department With Diabetic Ketoacidosis

Hypokalemia is reported to occur in approximately 3 to 4 percent of patients with diabetic ketoacidosis (DKA). To prevent complications of severe hypokalemia, the American Diabetes Association (ADA) treatment guidelines recommend ensuring that serum potassium levels are > 3.3 mEq/L prior to initiation of insulin in the treatment of DKA. To access this article, please choose from the options below Society Members, full access to the journal is a member benefit. Use your society credentials to access all journal content and features Continue reading >>

Review Of Diabetic Ketoacidosis Management

Review Of Diabetic Ketoacidosis Management

Review of Diabetic Ketoacidosis Management Department of Clinical Health Professions Department of Clinical Health Professions ABSTRACT: Diabetic ketoacidosis (DKA) is a medical emergency caused by insulin deficiency. It is characterized by hyperglycemia, metabolic acidosis, and ketoacidosis. DKA arises from lack of insulin, with or without a precipitating event that leads to a cascade of pathophysiological changes. The goals of DKA treatment are to normalize volume status, hyperglycemia, electrolytes, and ketoacidosis. Pharmacists in community or ambulatory-care settings can assist in preventing DKA, while inpatient pharmacists play a role in management of DKA. Diabetic ketoacidosis (DKA) is a serious medical emergency caused by insulin deficiency that takes a significant toll on the U.S. healthcare system.1,2 There are over 500,000 hospital days per year and $2.4 billion in medical costs attributed to DKA alone. DKA has high rates of morbidity and mortality, especially in younger type 1 diabetic patients. It is the most common cause of death for those under the age of 24 years with type 1 diabetes.3 It is estimated that 27% to 37% of patients with DKA are newly diagnosed with diabetes, usually type 1.1 Trauma, infection, or surgery may increase the risk of DKA in patients with type 2 diabetes.3 Mortality with DKA is generally associated with the underlying illness or comorbidity.1,3,4 Generally, DKA may be characterized by significant hyperglycemia, metabolic acidosis, and ketoacidosis. However, DKA may present in various ways, from euglycemia to severe hyperglycemia with or without dehydration and coma.3-5 The treatment approach for each patient is highly individualized based on a patients clinical factors.5 Simply put, DKA is caused by too little insulin and a resp 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 >>

Hyperglycemic Crisis: Regaining Control

Hyperglycemic Crisis: Regaining Control

CE credit is no longer available for this article. Expired July 2005 Originally posted April 2004 VERONICA CRUMP, RN, BSN VERONICA CRUMP is a nurse on the surgical unit of Morristown Memorial Hospital in Morristown, N.J. She's also a subacute care nurse in the hospital's rehabilitation division. KEY WORDS: hyperosmolar hyperglycemic syndrome (HHS), diabetic ketoacidosis (DKA), hepatic glucose production, proteolysis, hepatic gluconeogenesis, ketone bodies, metabolic acidosis, hyperkalemia, hypokalemia When a patient presents with markedly high blood glucose levels, the consequences can be fatal. Here's how to get your patient through the crisis. Edith Schafer, age 71, has just been admitted to your ICU with pneumonia, which she developed at home. She has a history of Type 2 diabetes. In addition to a temperature of 102° F (38.9° C), she has rapid, shallow breathing and dry, flushed skin. Her blood pressure is 96/70 mm Hg, and she's so lethargic that she's unable to keep her eyes open. Her lab results show a serum glucose level of 900 mg/dL. In addition to the pneumonia, Mrs. Schafer is suffering from hyperosmolar hyperglycemic syndrome (HHS). Severe hyperglycemia is a complication of both Type 1 and Type 2 diabetes. It can indicate HHS or diabetic ketoacidosis (DKA), another life-threatening condition. HHS tends to occur in patients with Type 2 diabetes, like Mrs. Schafer, while Type 1 diabetics are more likely to develop DKA. However, DKA can occur in Type 2 diabetes as well.1 HHS and DKA can be set off by infection, stress, missed medication, and other causes. In Mrs. Schafer's case, the trigger was pneumonia, a common cause of hyperglycemia in patients with diabetes. No matter what the cause, though, a case of HHS or DKA can turn deadly if not caught in time. The m Continue reading >>

Prime Pubmed | Profound Hypokalemia Associated With Severe Diabetic Ketoacidosi

Prime Pubmed | Profound Hypokalemia Associated With Severe Diabetic Ketoacidosi

Hypokalemia is common during the treatment of diabetic ketoacidosis (DKA); however, severe hypokalemia at presentation prior to insulin treatment is exceedingly uncommon. A previously healthy 8-yr-old female presented with new onset type 1 diabetes mellitus, severe DKA (pH = 6.98), and profound hypokalemia (serum K = 1.3 mmol/L) accompanied by cardiac dysrhythmia. Insulin therapy was delayed for 9 h to allow replenishment of potassium to safe serum levels. Meticulous intensive care management resulted in complete recovery. This case highlights the importance of measuring serum potassium levels prior to initiating insulin therapy in DKA, judicious fluid and electrolyte management, as well as delaying and/or reducing insulin infusion rates in the setting of severe hypokalemia. Davis, Shanlee M., et al. "Profound Hypokalemia Associated With Severe Diabetic Ketoacidosis." Pediatric Diabetes, vol. 17, no. 1, 2016, pp. 61-5. Davis SM, Maddux AB, Alonso GT, et al. Profound hypokalemia associated with severe diabetic ketoacidosis. Pediatr Diabetes. 2016;17(1):61-5. Davis, S. M., Maddux, A. B., Alonso, G. T., Okada, C. R., Mourani, P. M., & Maahs, D. M. (2016). Profound hypokalemia associated with severe diabetic ketoacidosis. Pediatric Diabetes, 17(1), pp. 61-5. doi:10.1111/pedi.12246. Davis SM, et al. Profound Hypokalemia Associated With Severe Diabetic Ketoacidosis. Pediatr Diabetes. 2016;17(1):61-5. PubMed PMID: 25430801. * Article titles in AMA citation format should be in sentence-case TY - JOURT1 - Profound hypokalemia associated with severe diabetic ketoacidosis.AU - Davis,Shanlee M,AU - Maddux,Aline B,AU - Alonso,Guy T,AU - Okada,Carol R,AU - Mourani,Peter M,AU - Maahs,David M,Y1 - 2014/11/27/PY - 2014/07/09/receivedPY - 2014/10/29/revisedPY - 2014/10/30/acceptedPY - 2 Continue reading >>

Why Is There Hyperkalemia In Diabetic Ketoacidosis?

Why Is There Hyperkalemia In Diabetic Ketoacidosis?

Lack of insulin, thus no proper metabolism of glucose, ketones form, pH goes down, H+ concentration rises, our body tries to compensate by exchanging K+ from inside the cells for H+ outside the cells, hoping to lower H+ concentration, but at the same time elevating serum potassium. Most people are seriously dehydrated, so are in acute kidney failure, thus the kidneys aren’t able to excrete the excess of potassium from the blood, compounding the problem. On the other hand, many in reality are severely potassium depleted, so once lots of fluid so rehydration and a little insulin is administered serum potassium will plummet, so needs to be monitored 2 hourly - along with glucose, sodium and kidney function - to prevent severe hypokalemia causing fatal arrhythmias, like we experienced decades ago when this wasn’t so well understood yet. In practice, once the patient started peeing again, we started adding potassium chloride to our infusion fluids, the surplus potassium would be peed out by our kidneys so no risk for hyperkalemia. Continue reading >>

Initial Potassium Replacement In Diabetic Ketoacidosis: The Unnoticed Area Of Gap

Initial Potassium Replacement In Diabetic Ketoacidosis: The Unnoticed Area Of Gap

Initial Potassium Replacement in Diabetic Ketoacidosis: The Unnoticed Area of Gap We are experimenting with display styles that make it easier to read articles in PMC. The ePub format uses eBook readers, which have several "ease of reading" features already built in. The ePub format is best viewed in the iBooks reader. You may notice problems with the display of certain parts of an article in other eReaders. Generating an ePub file may take a long time, please be patient. Initial Potassium Replacement in Diabetic Ketoacidosis: The Unnoticed Area of Gap Diabetic ketoacidosis is an acute complication of diabetes mellitus (DM). It affects all the types of DM and hence is a continuous threat for all the diabetes patients ( 1 ). DKA is a well-studied disease. Among the precipitating causes, mostly reported factors are non-compliance of patients with the antidiabetic treatment, and infection; others, however, may not have any precipitating cause ( 1 , 2 ). The progress of disease is very simple; lack of insulin causes hyperglycemia and inability of glucose to enter the cell. In-turn, triglycerides are broken down to free fatty acids which are used as a source of energy ( 1 , 3 , 4 ). In due process, the end-product of this metabolic derangement, i.e., ketones, cause acidification of blood causing major disruption in homeostasis. Similar to pathophysiology, the treatment of DKA is also simple and encompasses administration of insulin to achieve euglycaemia, and administration of crystalloid or colloidal solution to attain euvolaemia and euelectrolytaemia ( 1 3 ). Nevertheless, by the time patient reports for medical attention, these simple derangements and the rectification pathway have had gone significant derailment with potassium being the most affected ion throughout the Continue reading >>

Correction Of Critical Hypokalemia

Correction Of Critical Hypokalemia

I recently assisted in the management of a patient who presented in DKA with critical acidosis and hypokalemia. This presents a variety of therapeutic challenges: what to do about insulin, which treats the acidemia but worsens the hypokalemia? How can I safely supplement potassium as aggressively as possible? In contrast to the previously-posted recommendations from Micromedex, a protocol from the Bon Secours system in Richmond, VA presents the most clinically useful summary we have come across. ___ *If potassium < 3 meq/liter and the patient is symptomatic 40 meq/hour may be administered to intensive care patients. Hourly serum potassium determinations should be drawn to avoid severe hyperkalemia and/or cardiac arrest. Symptoms of hypokalemia include: fatigue, malaise, generalized muscle weakness, respiratory failure, paralysis; EKG changes include T wave flattening or inversion, U waves, or ST segment depression, and arrhythmia’s. Recommended maximum dose should not usually exceed 10 meq/hour or 200 meq for a 24 hour period if the serum potassium level is greater than 2.5 meq/liter per product package insert ___ Additionally, there is literature† to support providing a baseline rate of 40 mEq/hr (through a central line) with hourly supplementation using “runs” of up to 40 mEq (through a central line). Patients having their potassium replaced this aggressively should be on a monitor and have hourly electrolyte checks. Regarding the benefit/drawback of using insulin in DKA patients, the ADA strongly recommends withholding insulin when K < 3.3. If you want to disregard this recommendation, which I do (seems overly cautious), remember you can slow the insulin infusion rather than stop it. The key is to keep a very close eye on your blood gas/chemistry. †Murthy, Continue reading >>

Myths In Dka Management

Myths In Dka Management

Anand Swaminathan, MD, MPH (@EMSwami) is an assistant professor and assistant program director at the NYU/Bellevue Department of Emergency Medicine in New York City. Review questions are available at the end of this post. Background Each year, roughly 10,000 patients present to the Emergency Department in diabetic ketoacidosis (DKA). Prior to the advent of insulin, the mortality rate of DKA was 100% although in recent years, that rate has dropped to approximately 2-5%.1 Despite clinical advances, the mortality rate has remained constant over the last 10 years. With aggressive resuscitative measures and appropriate continued management this trend may change. DKA is defined as: Hyperglycemia (glucose > 250 mg/dl) Acidosis (pH < 7.3) Ketosis In the absence of insulin, serum glucose rises leading to osmotic diuresis. This diuresis leads to loss of electrolytes including sodium, magnesium, calcium and phosphorous. The resultant volume depletion leads to impaired glomerular filtration rate (GFR) and acute renal failure. In patients with DKA, fatty acid breakdown produces 2 different ketone bodies, first acetoacetate, which then further converts to beta-hydroxybutyrate, the latter being the ketone body largely produced in DKA patients. With this background in mind, let’s take a look at four urban legends in the management of DKA and the evidence that dispels these legends. Here’s our case: Although this presentation likely represents DKA, a blood gas is typically obtained to confirm the diagnosis. Often, the question arises as to whether an arterial or venous blood gas is adequate. Urban Legend #1 – An ABG is necessary for the diagnosis and treatment of DKA ABG gets you pH, PaO2, PaCO2, HCO3, Lactate, electrolytes and O2Sat VBG gets all this except for PaO2 (but we have Continue reading >>

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