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How To Counteract Ketoacidosis

What Causes High Ketones In A Canine?

What Causes High Ketones In A Canine?

A dog with a high level of ketones in his urine suffers from a condition known as ketonuria, usually resulting from a buildup of these substances in the dog's blood. A ketone is a type of acid, which, if allowed to accumulate in the blood, can lead to ketoacidosis, a potentially fatal condition. The main health conditions that can cause high ketone levels in a canine are starvation and diabetes. A dog's body breaks down the food that he eats into sugars, also called glucose, that the cells of the body use for energy. The dog's pancreas then produces the hormone insulin to regulate the amount of glucose that the body will absorb. If the insulin to regulate the glucose is insufficient, typically due to chronic diabetes mellitus, the body breaks down alternate sources of fuel for its cells; a dog's body that is starved of nutrition will do the same. One of these sources is the fat stored in the dog's body. When the body breaks down this fat, it produces as a by-product toxic acids known as a ketones. These ketones then build up in the dog's blood and also his urine, leading to ketoacidosis. Always consult an experienced veterinarian regarding the health and treatment of your pet. A dog suffering from high ketone levels in his blood and urine exhibits symptoms of weight loss, vomiting, increased thirst, decreased appetite, increased urination, lethargy, low body temperature and yellowing of the skin and gums, according to PetMD. The dog's breath may also have a sweet, fruity smell due to the presence of acetone caused by ketoacidosis, says VetInfo. To properly diagnose high ketone levels and ketoacidosis in your dog, a veterinarian will take blood tests and a urinalysis, which will also check your dog's blood glucose levels. Depending on the dog's physical condition, hospit 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 >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

A Preventable Crisis People who have had diabetic ketoacidosis, or DKA, will tell you it’s worse than any flu they’ve ever had, describing an overwhelming feeling of lethargy, unquenchable thirst, and unrelenting vomiting. “It’s sort of like having molasses for blood,” says George. “Everything moves so slow, the mouth can feel so dry, and there is a cloud over your head. Just before diagnosis, when I was in high school, I would get out of a class and go to the bathroom to pee for about 10–12 minutes. Then I would head to the water fountain and begin drinking water for minutes at a time, usually until well after the next class had begun.” George, generally an upbeat person, said that while he has experienced varying degrees of DKA in his 40 years or so of having diabetes, “…at its worst, there is one reprieve from its ill feeling: Unfortunately, that is a coma.” But DKA can be more than a feeling of extreme discomfort, and it can result in more than a coma. “It has the potential to kill,” says Richard Hellman, MD, past president of the American Association of Clinical Endocrinologists. “DKA is a medical emergency. It’s the biggest medical emergency related to diabetes. It’s also the most likely time for a child with diabetes to die.” DKA occurs when there is not enough insulin in the body, resulting in high blood glucose; the person is dehydrated; and too many ketones are present in the bloodstream, making it acidic. The initial insulin deficit is most often caused by the onset of diabetes, by an illness or infection, or by not taking insulin when it is needed. Ketones are your brain’s “second-best fuel,” Hellman says, with glucose being number one. If you don’t have enough glucose in your cells to supply energy to your brain, yo Continue reading >>

How To Treat Ketoacidosis

How To Treat Ketoacidosis

Immediately drink a large amount of non-caloric or low caloric fluid. Continue to drink 8 to 12 oz. every 30 minutes. Diluted Gatorade, water with Nu-Salt™ and similar fluids are good because they help restore potassium lost because of high blood sugars. Take larger-than-normal correction boluses every 3 hours until the blood sugar is below 200 mg/dl (11 mmol) and ketones are negative. It will take much more rapid insulin than normal to bring blood sugars down when ketones are present in the urine or blood. Often, one and a half to two times the normal insulin dose for a high blood sugar will be necessary. Higher insulin doses than these will be needed if there is an infection or other major stress. If nausea becomes severe or last 4 hours or more, call your physician. If vomiting starts or you can no longer drink fluids, have a friend or family member call your physician immediately, then go directly to an emergency room for treatment. Never omit your insulin, even if you cannot eat. A reduced insulin dose might be needed, but only if your blood sugar is currently low. When high blood sugars or ketoacidosis happen, it is critical that you drink lots of fluid to prevent dehydration. Take extra amounts of Humalog, Novolog or Regular insulin to bring the blood sugars down. Children with severe ketoacidosis lose 10-15 % of their previous body weight (i.e., a 60 lb. child can lose 6 to 9 lbs. of weight) due to severe dehydration. Replacement of fluids should be monitored carefully. The dehydration is caused by excess urination due to high blood sugars and is quickly worsened when vomiting starts due to the ketoacidosis. The start of vomiting requires immediate attention at an ER or hospital where IV fluid replacement can begin. If only nausea is present and it is possible Continue reading >>

What Is Diabetic Ketoacidosis?

What Is Diabetic Ketoacidosis?

Diabetic ketoacidosis is a serious condition characterized by high blood sugar (hyperglycemia), low insulin, and the presence of moderate to large amounts of ketones in the blood. It's a medical emergency that requires treatment in a hospital. If not treated in a timely fashion, ketoacidosis can lead to coma and death. While diabetic ketoacidosis (or DKA) is much more common among people with type 1 diabetes, it can also occur in people with type 2 diabetes, so ketone monitoring is something everyone with diabetes should understand. Diabetic Ketoacidosis Symptoms Signs and symptoms of ketoacidosis include: Thirst or a very dry mouth Frequent urination Fatigue and weakness Nausea Vomiting Dry or flushed skin Abdominal pain Deep breathing A fruity breath odor What Are Ketones? Ketones, or ketone bodies, are acidic byproducts of fat metabolism. It's normal for everyone to have a small amount of ketones in the bloodstream, and after a fast of 12 to16 hours, there may be detectable amounts in the urine. As is the case with glucose, if blood levels of ketones get too high, they spill over into the urine. An elevated level of ketones in the blood is known as ketosis. People who follow low-carbohydrate diets often speak of ketosis as a desirable state — it's evidence that their bodies are burning fat, not carbohydrate. But the level of ketosis that results from low carbohydrate consumption isn't harmful and is much lower than the level seen in diabetic ketoacidosis. When Should Ketones Be Monitored? Ketone monitoring is less of a concern for people with type 2 diabetes than for those with type 1 diabetes. This is because most people with type 2 diabetes still make some of their own insulin, making diabetic ketoacidosis less likely to develop. Nonetheless, people with type 2 d 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 >>

Ketoacidosis - Put Me In The Hospital

Ketoacidosis - Put Me In The Hospital

First off, I should apologize to my mom, I don't think she previously knew about this and read about it in my last post and expressed her worry. Moms are made to worry, but I should have told her if I hadn't already :) sorry Mom... During our Canadian Thanksgiving in October, we decided to surprise Michelle's mom in Montana for our long weekend. During our visit, I became really ill with what I thought was food poisoning, but could have been a 24 hour bug. Doesn't sound too bad to the normal person, but when you add diabetes to the situation it can be complicated. Managing blood sugars without the ability to eat or drink anything becomes almost impossible. Adding to the mix, I was lacking my Dexcom continuous blood glucose monitor because to my dissatisfaction my insurance does not currently cover my supplies in Canada (I am working on it). Without Dexcom, my ability to know what was happening in my body was extremely tough. After hours of vomiting, my wife searched the internet and came across another blog that cautioned diabetics about ketoacidosis. I had heard of the condition, but honestly had never even checked for this before. I will hopefully add to the knowledge out there to help others understand the condition. How does Ketoacidosis happen? It is typical for diagnosed diabetics with elevated blood sugars for extended amounts of time. I have been diabetic for years and am pretty aware of it, so that wasn't the case. Since I started vomiting at around 9pm and didn't stop until 3am, there was a lot of stress on my body. Added complication, I started vomiting shortly after dinner, so the carbs I had already taken insulin to control were no longer in my body. So my blood sugar dropped because I did not have the expected sugars in my body and too much insulin. To cou Continue reading >>

Advanced Diabetic Ketoacidosis

Advanced Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a dangerous condition characterized by a severe rise in blood sugar or hyperglycemia, depleted bodily fluids, shock, and in some cases unconsciousness. Coma and even death may occur if DKA is left untreated or if it becomes more severe due to excessive vomiting. Symptoms of DKA In the early stages of DKA, the affected individual appears flushed and breathes rapidly and deeply. This is called hyperventilation. As the condition progresses, the skin may turn pale, cool and clammy, dehydration may begin to set in and the heart rate may become rapid and breathing shallow. Nausea, vomiting and severe abdominal cramps. Blurred vision Fruity or pungent smelling breath due to the presence of acetone and ketones in the breath. Pathophysiology Although DKA can occur in patients with type 2 diabetes, it mainly develops in people with type 1 diabetes who need to take insulin for their condition. If individuals do not receive insulin, they will develop DKA. If there is a shortage of insulin, the body fails to use glucose in the blood for energy and instead fats are broken down in the liver. When these fats are broken down, acidic compounds called ketones are produced as a by-product. These ketones build up in the body and eventually cause ketoacidosis. Aside from missed or inadequate doses of insulin, another common cause of DKA is infection or illness as this can raise the level of hormones that counteract the effects of insulin. In addition, the dehydration caused by major injury or surgery can raise levels of these hormones. Diagnosis and treatment Blood tests are performed to check the sugar levels and blood pH, which is classified as acidic if it is below the usual 7.3. Unlike non-ketotic hyperosmolar coma, in DKA the blood and urine levels of keto Continue reading >>

Www.smj.org.sa Saudi Med J 2002; Vol. 23 (2) 247

Www.smj.org.sa Saudi Med J 2002; Vol. 23 (2) 247

www.smj.org.sa Saudi Med J 2002; Vol. 23 (2) 247 High occurence of diabetic ketoacidosis among type 2 African patients. Sir, Eighty years after the discovery of insulin, diabetic ketoacidosis (DKA) still remains the common medical emergency in African countries. Poor compliance with diabetes therapy, diet, infections and lack of health education are the major precipitating factors. Type 2 diabetes is not a mild disease as is sometimes thought, but carries considerable morbidity and mortality. The prevalence of this disease continues to rise in African countries probably due to wide-spreading urbanization and changes of life style.1 Although DKA is classically associated with Type 1 diabetes, the majority of the African patients have Type 2 diabetes.1 In Sudan, in recent years, figures as high as 58% and 37.7% were reported.2 The occurrence of DKA among adult diabetic patients is not as rare as once thought. Of course, there are possibilities that some of the patients labeled as Type 2 may actually have adult- onset insulin-requiring diabetes. Moreover, DKA can be the first presentation for Type 2 patients and may indicate a rapid development of the disease. Some patients who appear to have Type 2 diabetes may actually have a slow progressive form of Type 1 diabetes as evidenced by the presence of islet-cell antibodies and eventually they become dependent on insulin. They show a progressive worsening of diabetic control if treated with diet or oral hypoglycemic agents (OHAS). The OHAS may give only temporary relief and fail to protect the beta-cell from the gradual destruction. The American Diabetes Association has defined this type of diabetes as LADA (Late Autoimmune Diabetes of Adults).3 It is a worldwide decision that the type of diabetes should be made largely on cl Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic Ketoacidosis This is a life threatening, medical emergency. This is the most common way for new type 1 diabetics to present. Ketogenesis Ketogenesis occurs when there is insufficient glucose supply and glycogen stores are exhausted (such as prolonged fasting): The liver takes fatty acids and converts them to ketones. Ketones are water soluble fatty acids that can be used as fuel. They can cross the blood brain barrier and be used by the brain as fuel. Producing ketones is normal and not harmful in healthy patients when under fasting conditions or low carbohydrate, high fat diets. Ketones levels can be measured in the urine (dip stick) and blood (by ketone meter). People in ketosis (producing ketones) have a characteristic acetone smell to their breath. Ketone acids (ketones) are buffered in normal patients, so the blood does not become acidotic. When underlying pathology (i.e. Type 1 Diabetes) causes extreme hyperglycaemic ketosis, this results in a metabolic acidosis that is life threatening (see below). Diabetic Ketoacidosis Pathophysiology When there is no insulin, the cells of the body cannot take glucose from the blood and use it for fuel Therefore, the cells think the body is being fasted and has no glucose supply Meanwhile, the level of glucose in the blood keeps rising (hyperglycaemia) Ketoacidosis Because the cells in the body have no fuel and think they are starving, they initiate the process of ketogenesis, so that they have a usable fuel Over time, the patient gets higher and higher glucose and ketones levels Initially, the kidney produces bicarbonate to counteract the acidic blood and maintain a normal pH Over time, the ketone acids uses up the bicarbonate and the blood starts to become acidic (ketoacidosis) Dehydration The hyperglycaemia overwhelm Continue reading >>

Compensatory Hypochloraemic Alkalosis In Diabetic Ketoacidosis

Compensatory Hypochloraemic Alkalosis In Diabetic Ketoacidosis

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

Severe Diabetic Ketoacidosis In Combination With Starvation And Anorexia Nervosa At Onset Of Type 1 Diabetes: A Case Report

Severe Diabetic Ketoacidosis In Combination With Starvation And Anorexia Nervosa At Onset Of Type 1 Diabetes: A Case Report

Go to: A 53-year-old woman with a history of AN since adolescence was admitted to the psychiatric clinic at the Uppsala University Hospital due to psychotic behaviour and inability to take care of herself. There were reports of paranoid schizophrenia and personality disorders, but her contacts with the psychiatric clinic were sparse, and she used no medications. According to her relatives she had isolated herself the last two weeks, and over the last two months she had barely been eating at all. Twenty-four hours after admission to the psychiatric clinic she was admitted to the clinic of internal medicine and presented at the emergency room (ER) in a cachectic state with hypothermia (32.6°C). Her mental status was altered (reaction level scale 2), and she barely responded to questions, being close to stupor. There were clinical signs of severe dehydration and muscle atrophy. Her breathing was shallow with 30 bpm, whereas blood pressure and pulse rate were normal, 110/60 mmHg and 77 bpm (see Table I for a summary of the initial physical examination). She denied alcohol and any substance abuse. An initial arterial blood gas analysis displayed pH 6.895, pCO2 0.93 kPa, pO2 22 kPa, and P-glucose 40.6 mmol/L. There were no signs of infection, and electrolytes were normal (see Table II for a summary of laboratory screening). She was immediately admitted to the intensive care unit (ICU), where rehydration was initiated with warm fluid combined with re-warming with heated blankets. Bicarbonate (100 mL) was administered i.v. in order to reverse acidosis; pH increased to 7.1, and blood glucose decreased to 35 mmol/L. Six hours after ICU admission insulin infusion was started with initially 0.5 IU/h (0.0128 IU/kg) combined with 5 mmol potassium/h. The patient's pH was normalized 1 Continue reading >>

Euglycemic Dka From Sglt2 Inhibitors: Don't Worry, I Can't Pronounce Them Either

Euglycemic Dka From Sglt2 Inhibitors: Don't Worry, I Can't Pronounce Them Either

Diabetic ketoacidosis in patients with presenting serum blood glucose less than 200 is not common. Particularly when practicing in the Bible/Diabetes belt of the United States. This euglycemic DKA (euDKA) is more often associated in patients with type 1 diabetes in conjunction with starvation and acute illness.[1] It's difficult to determine an incidence of euglycemic serum glucose among all DKA cases in the literature given the migration of the serum glucose cutoff from 300 or less to 200 or less. The best estimation based on an analysis of case reports suggests an incidence anywhere from 0.8% to 7.5%.[1] However, the newest class of unpronounceable medications, the sodium-glucose co-transporter 2 inhibitors (SGLT2inh) (canagliflozin, dapagliflozin, empagliflozin) are making their presence known by inducing this once rare form of DKA.[2-3] SGLT2inhs are a class of oral hypoglycemic drugs indicated only for type 2 diabetes. Their novel mechanism of action prevents glucose reabsorption from the proximal renal tubules resulting in increased glucosuria and decreasing plasma glucose. The resulting effects include lower serum glucose levels, lower HBA1C, and even weight loss. But that's not all. The increased glucose concentration in the bladder is a terrific incubation environment for fungi and bacteria. So much so that the FDA has slapped a post-marketing warning on the drug class for the increased risk of UTI and urosepsis. In other patients, euglycemic DKA may occur. This too has led to the FDA issuing a similar warning of this possible life threat. The proposed mechanism suggests that SGLT2inhs while lowering serum glucose, also reduces insulin secretion from pancreatic beta cells in a negative feedback fashion. The lower serum insulin coupled with lower serum glucose c Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic Ketoacidosis: As Dangerous as it Sounds: Knowing What Diabetic Ketoacidosis is and How to Prevent it Can Save You a Trip to the Hospital When you have diabetes, it’s crucial to make sure there’s enough insulin in your body. One reason is that insulin controls your blood glucose and helps you avoid the complications of diabetes. But there’s another reason: If you don’t have enough insulin, you run the risk of developing a dangerous condition called diabetic ketoacidosis. Keto-what? It sounds like something out of a science fiction movie, but diabetic ketoacidosis, or DKA for short, is serious business. Left untreated, it can be fatal. DKA can occur when you don’t have enough insulin to meet your body’s needs. As your blood glucose goes up, you lose glucose in your urine. When glucose is lost in urine it pulls fluid out with it. If you don’t replace the fluids you lose, you can become dehydrated. Meanwhile, your body begins burning fat and protein from muscle tissue just to maintain health and energy. Normally your body uses carbohydrate (glucose) for maintenance, but because there isn’t enough insulin in your body, your cells can’t access the glucose in your blood. Your body then resorts to burning fat in an unhealthy way. Your liver becomes involved in fat-burning, and the by-product is ketones. The ketones build up and your blood becomes acidic. That’s bad news. As DKA progresses and you become more dehydrated, your body tries to defend itself by rearranging its own chemistry. “It’s a buffer system,” says Carle Hurst, diabetes nurse educator and center manager at Inova Alexandria Hospital in Alexandria, Va. “As your blood becomes acidic from the ketones, your system starts shifting electrolytes around to counter the acid. You retain Continue reading >>

A Physicochemical Acid-base Approach For Managing Diabetic Ketoacidosis

A Physicochemical Acid-base Approach For Managing Diabetic Ketoacidosis

Go to: CASE HISTORY A 21-year-old female presented to the emergency department with a history of weight loss, polyuria and polydipsia over the past 20 days and nausea, dizziness, prostration on the day of admission. Upon arrival to the hospital (10:00 a.m.), she was conscious, alert and dehydrated. Her blood glucose level was 320 mg/dl on admission, with massive glycosuria and ketonuria. Venous blood gas analysis showed a high AG (AG = Na+ - Cl− - HCO3−) metabolic acidosis (Tables 1 and 2). No significant hyperlactemia was present. A diagnosis of DKA was made. Fluid challenge was initiated with 1 liter of normal saline. Five units of regular insulin were given intravenously as a bolus, and a continuous infusion of 5 units/hour was started. The patient’s hyperglycemia was rapidly corrected, and a solution with 5% glucose plus potassium was introduced. Around 3:00 p.m., a new venous blood gas assessment revealed no significant improvements in the severity of her metabolic acidosis (Table 1). The patient was transferred to the ICU around 6:00 p.m. already receiving 2.5 units/hour of IV regular insulin and had a blood glucose level of 222 mg/dl. New exams revealed that there was still no significant improvement in her metabolic acidosis (Table 1) However, a significant increase in chloremia and decrease in the AG was appreciated. By 11:00 p.m., her clinical condition was stable, with only small alterations in the infusion of IV insulin. In addition, she was able to eat and had no abdominal complaints. A new set of exams revealed a small improvement in the degree of metabolic acidosis (Table 1). However, there was still significant hyperchloremia, though her AG had decreased even more. At 7:00 a.m., although there was an increase in lactatemia, her metabolic acidosis c Continue reading >>

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