Lactic Acidosis Ncbi

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Bala Venkatesh (University of Queensland, Australia) busting lactate myths at #SGANZICS on 22 April 2017. Mark your calendar for SGANZICS 17-21 May 2018!

Lactate Versus Non-lactate Metabolic Acidosis: A Retrospective Outcome Evaluation Of Critically Ill Patients

Lactate versus non-lactate metabolic acidosis: a retrospective outcome evaluation of critically ill patients 1Assistant Professor, VCURES (Virginia Commonwealth University Reanimation Engineering Shock Center) Laboratory, Departments of Anesthesiology/Critical Care and Emergency Medicine, Medical College of Virginia/Virginia Commonwealth University, 1200 East Broad Street, Richmond, VA, 23298, USA 2Director, Clinical Research Informatics Service, University of Pittsburgh, 450 Scaife Hall, 200 Lothrop St. Pittsburgh, PA, 15213, USA 3Research Assistant, Department of Biostatistics, University of Pittsburgh, Graduate School of Public Health, Crabtree Hall, Pittsburgh, PA, 15213, USA 4Professor, CRISMA (Clinical Research, Investigation, and Systems Modeling of Acute illness) Laboratory, Department of Critical Care Medicine, University of Pittsburgh, 608, Scaife Hall, 3550 Terrace Street, Pittsburgh, PA 15261, USA 1Assistant Professor, VCURES (Virginia Commonwealth University Reanimation Engineering Shock Center) Laboratory, Departments of Anesthesiology/Critical Care and Emergency Medicine, Medical College of Virginia/Virginia Commonwealth University, 1200 East Broad Street, Richmond, Continue reading >>

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  1. * DKA explanation

    * DKA explanation

    Below you will find a terrific explanation of DKA from one of the instructors at Med School Tutors. If you like what you see and may be interested in learning more about one-on-one instruction from MST, then please visit their website at www.medschooltutors.com
    In order to understand how to treat DKA, it is useful to first understand what is going on in the body when DKA develops. First of all, DKA (diabetic ketoacidosis) typically develops when a Type I diabetic does not take his or her insulin for a prolonged period of time. It may also be the presentation for new onset diabetes. Because these patients are insulin deficient, they are not able to take up glucose into their cells. This results in two important consequences: 1)glucose builds up in the blood and causes hyperglycemia and 2)the body's cells are forced to breakdown fat for energy, instead of glucose.
    These are very significant consequences... The hyperglycemia results in an osmotic diuresis, because the proximal tubule of the kidney can't reabsorb all the glucose filtered into the nephron. What is osmotic diuresis? Simply that the hyperglycemia (usually >300) causes the body to excrete lots and lots of water, because the osmotic pull of all the glucose particles prevents the reabsorbtion of water in the collecting duct. This means that patients with DKA are peeing their brains out!! They pee out sodium, potassium, and water.. And are therefore, very very very DEHYDRATED, sodium depleted, and potassium depleted.
    Now for the metabolism end of things... The body cells are forced to metabolize fat for energy rather than glucose. How do they accomplish this? - beta-oxidation of fatty acids. This results in excess production of ketone bodies which deplete available acid buffers. This causes a significant metabolic acidosis, with a high anion gap due to the presence of ketoacids. The acidosis causes potassium to shift from the intracellular space to the extracellular space. This may result in a normal or high serum potassium level. This normal or high potassium level masks what is typically significant potassium depletion because the person was peeing all their potassium out as a result of the uncontrolled hyperglycemia.
    So what are we going to do now? I will give a very brief answer for now, expect people to ask questions in the meantime, and then provide a more thorough approach to treatment in the coming days.
    1)Give the patient tons of normal saline. Why? - because your patient is dehydrated as all hell. They have been peeing out every last drop of water because of their severe uncontrolled hyperglycemia. These patients require liters of fluid to replenish all the fluid they've lost as a result of the osmotic diuresis.
    2)Give them insulin. Why? - NOT because it will lower the blood glucose level, but because it will cause a shift away from fat metabolism and toward glucose metabolism. This will slow the production of ketone bodies which are precipitating the metabolic acidosis. Thus, I will repeat, we give insulin to shift away from fat metabolism and stop the production of ketone bodies.
    3)Give the patient potassium. Why? - As we discussed earlier, the person has been peeing out all of their potassium stores and are overall very potassium depleted, despite having normal or high serum potassium levels to begin with. In addition to being potassium depleted, the insulin you are giving will cause a shift of potassium from the extracellular space to the intracellular space, which will drop the serum potassium. Thus, we give DKA patients potassium way before they become hypokalemic.
    4)Give the patient dextrose. Why? - They insulin you are giving the patient is obviously going to cause the serum glucose to decrease. We give glucose to prevent hypoglycemia as we continue to give insulin.
    How do we know when we are finished treating these patients? - When the anion gap returns to normal.
    That's all for now. Please ask any questions you have. I will be giving more specifics about DKA management in the near future.
    PS: Does anyone know the dangerous consequence of giving DKA patients fluid too rapidly? What are the symptoms this may cause, and what is the pathophysiology behind these symptoms?

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Hemodialysis For Lactic Acidosis

Department of Critical Care Medicine, Apollo First Med Hospital, Chennai, Tamil Nadu, India 1Department of Critical Care Medicine, Apollo Hospitals, Chennai, Tamil Nadu, India Address for correspondence: Dr. Ashwin K. Mani, Department of Critical Care Medicine, Apollo First Med Hospital, 154, PH Road, Chennai - 600 010, Tamil Nadu, India. E-mail: [email protected] Author information Copyright and License information Disclaimer Copyright : 2017 Indian Journal of Critical Care Medicine This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms. Lactic acidosis (Type A) is common in critically ill patients and usually treated by correcting the underlying etiology. We present the case of a young female who presented with life-threatening lactic acidosis secondary to hematological malignancy. Timely initiation of hemodialysis was lifesaving. The case highlights the importance of considering Type B lactic acidosis (in this case secondary t Continue reading >>

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  1. heatherny2

    My yorkipoo, Rusty, was just diagnosed today and not given a good prognosis. His glucose level was over 400 and ketones were present in his urine. The vet wanted to send him to a specialist to be watched over the weekend, but I can't afford that. We will administer insulin over the weekend, testing him every few hours, and see how he does. He has already developed the cataracts, but is eating and acting fine, so i just didn't have the heart to euthanize him today without giving him a chance over the weekend. My sons will just be devastated if he doesn't pull through.
    Anyone had any experience with this and if so, what was the outcome? Oh, and maybe some jingles will help.

  2. McVillesMom

    I worked with a number of DKA dogs when I was a tech in an emergency/referral hospital. Most of them were in the CCU, unfortunately, and some of them did survive, but it's usually very touch and go for a while. It sounds as though your guy is in better shape than most of my patients were - a lot of them were flat out, essentially comatose, so the fact that he is still eating and acting fine is a good sign. Hopefully, since you just found out, you will be able to get his glucose regulated and he'll do well - just keep a VERY close eye on him and do NOT hesitate to call or take him somewhere if you think he isn't right - they can crash very, very fast.

  3. heatherny2

    Thank you. Yeah, he is acting as normal as he always was, and eating really well (in fact he really likes the special food they gave us). He is also getting used to his glucose testing (with help from DH and a friend). We are, however, all watching him for any changes, so we can immediately get it addressed.

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Anion gap usmle - anion gap metabolic acidosis normal anion gap metabolic acidosis

Metabolic Acidosis.

Abstract Acute metabolic acidosis is frequently encountered in critically ill patients. Metabolic acidosis can occur as a result of either the accumulation of endogenous acids that consumes bicarbonate (high anion gap metabolic acidosis) or loss of bicarbonate from the gastrointestinal tract or the kidney (hyperchloremic or normal anion gap metabolic acidosis). The cause of high anion gap metabolic acidosis includes lactic acidosis, ketoacidosis, renal failure and intoxication with ethylene glycol, methanol, salicylate and less commonly with pyroglutamic acid (5-oxoproline), propylene glycole or djenkol bean (gjenkolism). The most common causes of hyperchloremic metabolic acidosis are gastrointestinal bicarbonate loss, renal tubular acidosis, drugs-induced hyperkalemia, early renal failure and administration of acids. The appropriate treatment of acute metabolic acidosis, in particular organic form of acidosis such as lactic acidosis, has been very controversial. The only effective treatment for organic acidosis is cessation of acid production via improvement of tissue oxygenation. Treatment of acute organic acidosis with sodium bicarbonate failed to reduce the morbidity and mortal Continue reading >>

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  1. CharleneRed

    Sick child with normal blood sugar but ketones in urine?

    My 5yr old has type 1, and has the flu. Her blood sugar is pretty normal to sometimes low as she does not want to eat but is drinking fluids. I tested her urine for ketones and they are 2+. I was told to increase her bg and give insulin every hour. does this make any sense?

  2. foxl

    2+ seems high. Ketones can simply indicate that you are burning fat as fuel -- either your own or dietary.
    My non-D daughter, now 10, used to get horrible ketone breath because when ill, she would NOT EAT!
    But GIVE INSULIN every HOUR??? No.

  3. furball64801

    I would not think insulin every hour could be regulated and you would have the stacking affect, make sure she has plenty of fluid.

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