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When Is Dka Resolved

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 >>

Management Of Diabetic Ketoacidosis In Children And Adolescents

Management Of Diabetic Ketoacidosis In Children And Adolescents

Objectives After completing this article, readers should be able to: Describe the typical presentation of diabetic ketoacidosis in children. Discuss the treatment of diabetic ketoacidosis. Explain the potential complications of diabetic ketoacidosis that can occur during treatment. Introduction Diabetic ketoacidosis (DKA) represents a profound insulin-deficient state characterized by hyperglycemia (>200 mg/dL [11.1 mmol/L]) and acidosis (serum pH <7.3, bicarbonate <15 mEq/L [15 mmol/L]), along with evidence of an accumulation of ketoacids in the blood (measurable serum or urine ketones, increased anion gap). Dehydration, electrolyte loss, and hyperosmolarity contribute to the presentation and potential complications. DKA is the most common cause of death in children who have type 1 diabetes. Therefore, the best treatment of DKA is prevention through early recognition and diagnosis of diabetes in a child who has polydipsia and polyuria and through careful attention to the treatment of children who have known diabetes, particularly during illnesses. Presentation Patients who have DKA generally present with nausea and vomiting. In individuals who have no previous diagnosis of diabetes mellitus, a preceding history of polyuria, polydipsia, and weight loss usually can be elicited. With significant ketosis, patients may have a fruity breath. As the DKA becomes more severe, patients develop lethargy due to the acidosis and hyperosmolarity; in severe DKA, they may present with coma. Acidosis and ketosis cause an ileus that can lead to abdominal pain severe enough to raise concern for an acutely inflamed abdomen, and the elevation of the stress hormones epinephrine and cortisol in DKA can lead to an elevation in the white blood cell count, suggesting infection. Thus, leukocytosi Continue reading >>

What Causes You To Wake Up Extremely Thirsty Every Morning?

What Causes You To Wake Up Extremely Thirsty Every Morning?

Don’t forget to visit you doc to rule out diabetes. Extreme thirst is known as polydipsia. When you get dehydrated this can cause a rise in blood sugars that is the leading cause of associated problems with this horrible disorder. Dehydration in diabetes can cause a condition known as Diabetic Ketoacidosis, DKA, this causes acids to build up in the body and can lead to coma, organ failure and death. There is a test known as A1c which requires a small amount of blood. It is used to measure glucose control over the last 2–3 months… results of less than 6–7 % is good. You will do good to visit your physician to rule this out, and hopefully resolve any other concerns, so your mind can rest easier. Take care:) Continue reading >>

Diabetic Ketoacidosis - Symptoms

Diabetic Ketoacidosis - Symptoms

A A A Diabetic Ketoacidosis Diabetic ketoacidosis (DKA) results from dehydration during a state of relative insulin deficiency, associated with high blood levels of sugar level and organic acids called ketones. Diabetic ketoacidosis is associated with significant disturbances of the body's chemistry, which resolve with proper therapy. Diabetic ketoacidosis usually occurs in people with type 1 (juvenile) diabetes mellitus (T1DM), but diabetic ketoacidosis can develop in any person with diabetes. Since type 1 diabetes typically starts before age 25 years, diabetic ketoacidosis is most common in this age group, but it may occur at any age. Males and females are equally affected. Diabetic ketoacidosis occurs when a person with diabetes becomes dehydrated. As the body produces a stress response, hormones (unopposed by insulin due to the insulin deficiency) begin to break down muscle, fat, and liver cells into glucose (sugar) and fatty acids for use as fuel. These hormones include glucagon, growth hormone, and adrenaline. These fatty acids are converted to ketones by a process called oxidation. The body consumes its own muscle, fat, and liver cells for fuel. In diabetic ketoacidosis, the body shifts from its normal fed metabolism (using carbohydrates for fuel) to a fasting state (using fat for fuel). The resulting increase in blood sugar occurs, because insulin is unavailable to transport sugar into cells for future use. As blood sugar levels rise, the kidneys cannot retain the extra sugar, which is dumped into the urine, thereby increasing urination and causing dehydration. Commonly, about 10% of total body fluids are lost as the patient slips into diabetic ketoacidosis. Significant loss of potassium and other salts in the excessive urination is also common. The most common Continue reading >>

Management Of Diabetic Ketoacidosis In The Picu

Management Of Diabetic Ketoacidosis In The Picu

DKA - A common PICU diagnosis Incidence 4.6 – 8 per 1000 person years among people with diabetes Pediatric mortality rate is 1-2% DKA causes profound dehydration Hyperglycemia leads to osmotic diuresis Often 10-15% down from baseline weight Profound urinary free water and electrolyte loss Free water follows glucose into urine Electrolytes follow free water into urine Electrolyte abnormalities Pseudo-hyponatremia with hyperglycemia Sodium should rise with correction of glucose Profound total-body K+ depletion Urinary loss, decreased intake, emesis Initial K+ may be high due to acidosis, low insulin Aggressive K+ replacement necessary to prevent arrhythmias Phosphate, magnesium, calcium require replacement Initial DKA management - ED Resuscitation aimed at shock reversal Begin with 10-20 mL/kg NS bolus, may repeat if signs of shock persist Bolus fluids only necessary if signs of shock present Avoid overly-aggressive fluid resuscitation Concern for inciting cerebral edema, though no clear data Initial DKA management - ED NEVER give bicarbonate Increases risk of cerebral edema Begin insulin infusion at 0.1 units/kg/hr Should be initiated prior to leaving ED SQ or bolus insulin not indicated Pre-PICU arrival Order several bags of dextrose-containing and non-dextrose-containing IVF pre-PICU arrival Often takes pharmacy 1 hour to custom-make IVF No dextrose-containing fluids stocked in PICU Fluid Management - PICU 3 components to replacement fluids Deficit (often 10-15% total body water deficit) Ongoing losses (polyuria, emesis) Maintenance Possible to calculate the above, or give: 1.5X maintenance if moderately dehydrated 2X maintenance if severely dehydrated Isotonic fluid with potassium NS + 20 mEq/L KCl + 20 mEq/L KPhos Start with 40 mEq/L of potassium if K+ < 5 K+ Continue reading >>

Diabetic Ketoacidosis And Hyperglycemic Hyperosmolar Syndrome

Diabetic Ketoacidosis And Hyperglycemic Hyperosmolar Syndrome

In Brief Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic syndrome (HHS) are two acute complications of diabetes that can result in increased morbidity and mortality if not efficiently and effectively treated. Mortality rates are 2–5% for DKA and 15% for HHS, and mortality is usually a consequence of the underlying precipitating cause(s) rather than a result of the metabolic changes of hyperglycemia. Effective standardized treatment protocols, as well as prompt identification and treatment of the precipitating cause, are important factors affecting outcome. The two most common life-threatening complications of diabetes mellitus include diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar syndrome (HHS). Although there are important differences in their pathogenesis, the basic underlying mechanism for both disorders is a reduction in the net effective concentration of circulating insulin coupled with a concomitant elevation of counterregulatory hormones (glucagon, catecholamines, cortisol, and growth hormone). These hyperglycemic emergencies continue to be important causes of morbidity and mortality among patients with diabetes. DKA is reported to be responsible for more than 100,000 hospital admissions per year in the United States1 and accounts for 4–9% of all hospital discharge summaries among patients with diabetes.1 The incidence of HHS is lower than DKA and accounts for <1% of all primary diabetic admissions.1 Most patients with DKA have type 1 diabetes; however, patients with type 2 diabetes are also at risk during the catabolic stress of acute illness.2 Contrary to popular belief, DKA is more common in adults than in children.1 In community-based studies, more than 40% of African-American patients with DKA were >40 years of age and more than 2 Continue reading >>

What Is The Treatments For Ketoacidosis?

What Is The Treatments For Ketoacidosis?

Management of diabetic ketoacidos Time: 0–60 mins 1. Commence 0.9% sodium chloride If systolic BP > 90 mmHg, give 1 L over 60 mins If systolic BP < 90 mmHg, give 500 mL over 10–15 mins, then re-assess. If BP remains < 90 mmHg, seek senior review 2. Commence insulin treatment 50 U human soluble insulin in 50 mL 0.9% sodium chloride infused intravenously at 0.1 U/kg body weight/hr Continue with SC basal insulin analogue if usually taken by patient 3. Perform further investigations: see text 4. Establish monitoring schedule Hourly capillary blood glucose and ketone testing Venous bicarbonate and potassium after 1 and 2 hrs, then every 2 hrs Plasma electrolytes every 4 hrs Clinical monitoring of O2 saturation, pulse, BP, respiratory rate and urine output every hour 5. Treat any precipitating cause Time: 60 mins to 12 hrs • IV infusion of 0.9% sodium chloride with potassium chloride added as indicated below 1 L over 2 hrs 1 L over 2 hrs 1 L over 4 hrs 1 L over 4 hrs 1 L over 6 hrs • Add 10% glucose 125 mL/hr IV when glucose < 14 mmol/L • Be more cautious with fluid replacement in elderly, young people, pregnant patients and those with renal or heart failure. If plasma sodium is > 155 mmol/L, 0.45% sodium chloride may be used. • Adjust potassium chloride infusion Plasma potassium (mmol/L) Potassium replacement (mmol/L of infusion) > 5.5 Nil 3.5–5.5 40 < 3.5 Senior review – additional potassium required Time: 12–24 hrs • Ketonaemia and acidosis should have resolved (blood ketones < 0.3 mmol/L, venous bicarbonate > 18 mmol/L). Request senior review if not improving • If patient is not eating and drinking Continue IV insulin infusion at lower rate of 2–3 U/kg/hr Continue IV fluid replacement and biochemical monitoring • If ketoacidosis has resolved and Continue reading >>

Diabetic Ketoacidosis Treatment & Management

Diabetic Ketoacidosis Treatment & Management

Approach Considerations Managing diabetic ketoacidosis (DKA) in an intensive care unit during the first 24-48 hours always is advisable. When treating patients with DKA, the following points must be considered and closely monitored: It is essential to maintain extreme vigilance for any concomitant process, such as infection, cerebrovascular accident, myocardial infarction, sepsis, or deep venous thrombosis. It is important to pay close attention to the correction of fluid and electrolyte loss during the first hour of treatment. This always should be followed by gradual correction of hyperglycemia and acidosis. Correction of fluid loss makes the clinical picture clearer and may be sufficient to correct acidosis. The presence of even mild signs of dehydration indicates that at least 3 L of fluid has already been lost. Patients usually are not discharged from the hospital unless they have been able to switch back to their daily insulin regimen without a recurrence of ketosis. When the condition is stable, pH exceeds 7.3, and bicarbonate is greater than 18 mEq/L, the patient is allowed to eat a meal preceded by a subcutaneous (SC) dose of regular insulin. Insulin infusion can be discontinued 30 minutes later. If the patient is still nauseated and cannot eat, dextrose infusion should be continued and regular or ultra–short-acting insulin should be administered SC every 4 hours, according to blood glucose level, while trying to maintain blood glucose values at 100-180 mg/dL. The 2011 JBDS guideline recommends the intravenous infusion of insulin at a weight-based fixed rate until ketosis has subsided. Should blood glucose fall below 14 mmol/L (250 mg/dL), 10% glucose should be added to allow for the continuation of fixed-rate insulin infusion. [19, 20] In established patient Continue reading >>

Hyperglycemic Crises In Diabetes

Hyperglycemic Crises In Diabetes

Ketoacidosis and hyperosmolar hyperglycemia are the two most serious acute metabolic complications of diabetes, even if managed properly. These disorders can occur in both type 1 and type 2 diabetes. The mortality rate in patients with diabetic ketoacidosis (DKA) is <5% in experienced centers, whereas the mortality rate of patients with hyperosmolar hyperglycemic state (HHS) still remains high at ∼15%. The prognosis of both conditions is substantially worsened at the extremes of age and in the presence of coma and hypotension (1–10). This position statement will outline precipitating factors and recommendations for the diagnosis, treatment, and prevention of DKA and HHS. It is based on a previous technical review (11), which should be consulted for further information. PATHOGENESIS Although the pathogenesis of DKA is better understood than that of HHS, the basic underlying mechanism for both disorders is a reduction in the net effective action of circulating insulin coupled with a concomitant elevation of counterregulatory hormones, such as glucagon, catecholamines, cortisol, and growth hormone. These hormonal alterations in DKA and HHS lead to increased hepatic and renal glucose production and impaired glucose utilization in peripheral tissues, which result in hyperglycemia and parallel changes in osmolality of the extracellular space (12,13). The combination of insulin deficiency and increased counterregulatory hormones in DKA also leads to the release of free fatty acids into the circulation from adipose tissue (lipolysis) and to unrestrained hepatic fatty acid oxidation to ketone bodies (β-hydroxybutyrate [β-OHB] and acetoacetate), with resulting ketonemia and metabolic acidosis. On the other hand, HHS may be caused by plasma insulin concentrations that are in Continue reading >>

How Does Ketoacidosis Affect The Human Brain?

How Does Ketoacidosis Affect The Human Brain?

Diabetic Ketoacidosis (DKA) is the body’s emergency reaction to glucose starvation in the absence of insulin. It is a disastrous reaction — in general, it makes things worse rather than better, and starts a vicious cycle of blood acidity, rising blood glucose, dehydration, and blood hyperosmolality (high concentration of dissolved stuff) that can be hard to break. One of the hardest-hit organs in DKA is the brain, due to the dehydration and acidic blood entering that sensitive organ. Severe DKA may lead to brain swelling (edema) which is life-threatening. But recent studies have shown that even a short, apparently fully-recovered stint of DKA leads to measurable brain injury. Diabetic Ketoacidosis (DKA) is a life–threatening consequence of diabetes. DKA occurs when there is a lack of insulin in the body causing hyperglycemia. As a result of the inability of glucose to enter the cells, the body must find other means to obtain energy. As such, fat breakdown occurs resulting in the accumulation of fatty acids. The fatty acids are metabolized to ketones that cause the blood to become acidotic (pH less than7.3). Because glucose remains in the blood, there is an increase in thirst and drinking to eliminate the solute load of glucose, which also results in increased urination (polyuria and polydipsia). Thus, the combination of increased serum acidity, weight loss, polyuria, and polydipsia may lead to extreme dehydration, coma, or brain damage. Without a doubt, the most severe acute complication of DKA is cerebral edema. Many cases of new onset type 1 diabetes present DKA (15-70 percent depending on age and geographic region, according to multiple studies), hence the importance of an early diagnosis of diabetes in order to avoid potential consequences. Much research is be Continue reading >>

What Is The Most Hurtful Thing Someone Has Said To You?

What Is The Most Hurtful Thing Someone Has Said To You?

3 words I'll never forget. “Cut it out!” My son had died of a heroin overdose at 29 years old. We were at the funeral that was held 20 minutes from home in a small town in MD. My mother said “Well! If you're holding it there, no one will come.” They did. They came from Baltimore, Delaware, even Atlanta. She sat stoically at the funeral, speaking to no one. When time came for the service, she sat next to me. I was weeping openly when she said the only three words she said to me all day “Cut it out!” to which I replied “I will not!” About a year later, after searching for grief counseling and finding none, I went to NJ to take a course to become a Grief Recovery Specialist. When I returned, she called (rare) to ask me where I'd been. Something told me she already knew. When I told her, she burst out laughing and said “Leave it to you to make money from this!” I said “Or…help somebody.” She said “Yea. Or that.” It didn't take long for me to become a sought after speaker, in my circles, on the subject of Grief and Addiction…how to heal and stay clean. Btw…the answer is to help somebody. My mother was sitting at my kitchen table when she learned that I had been the closing speaker of a large convention that morning. A huge honor. She waited until we were alone and I was distracted by something on my computer. Then, very quietly she said “Randy (my husband) doesn't listen to you, does he?” I said “What? I'm sorry. I didn't get that. What did you say?” She said “Randy…he doesn't listen to you, does he? Because you just drone on and on in a voice that doesn't inspire anyone to listen to you. As a matter of fact, the dog doesn't even look up when you speak.” I stopped doing what I was doing and said “Actually, not 3 hours ago, 10 Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Diabetic ketoacidosis is a condition that results from when the body is deprived of the ability to use glucose as an energy source. Usually this is due to a lack of insulin. Insulin is used to uptake glucose into the cells to be used for energy. If there is no insulin or the cells are resistant to insulin, the blood sugar levels increase to dangerous levels for the patient. It seems counter intuitive that the patient wouldn't have energy with such high levels of glucose, but this glucose is essentially unusable without insulin. Because your body needs energy to survive, it starts turning to alternative fuel sources (fat). Fat cells start breaking down and, as a result, release ketones (which are acidic) into the bloodstream. Hence the name: diabetic ketoacidosis. “High levels of ketones can poison the body. When levels get too high, you can develop DKA. DKA may happen to anyone with diabetes, though it is rare in people with type 2. Treatment for DKA usually takes place in the hospital. But you can help prevent it by learning the warning signs and checking your urine and blood regularly.” Causes The most common causes of DKA are not getting enough insulin, having a severe infection, becoming dehydrated, or a combination of these issues. It seems like it occurs mainly in patients with type one diabetes. Symptoms Some of the symptoms that people experience with DKA include the following: Excessive thirst and urination (more water is pulled into the urine as a result of high ketone loss in the urine) Lethargy Breathing very quickly (patients have a very high level of acids in their bloodstream and they try to "blow" off carbon dioxide by breathing quickly) A fruity odor on their breath (ketones have a fruity smell) Nausea and vomiting (the body tries to get rid of acid Continue reading >>

How Can You Tell If A Person Has Diabetes? I Am Having An Urge To Urinate When I Am In The Bathroom. Also, Is Vertigo A Symptom Of Diabetes? I Am Currently Having Vertigo, For Almost A Week. The Ent Said I Have Labyrinthitis. Can Diabetes Cause This?

How Can You Tell If A Person Has Diabetes? I Am Having An Urge To Urinate When I Am In The Bathroom. Also, Is Vertigo A Symptom Of Diabetes? I Am Currently Having Vertigo, For Almost A Week. The Ent Said I Have Labyrinthitis. Can Diabetes Cause This?

Diabetes (DM) requires fasting blood glucose testing a few times, besides some additional testing sometimes. HgbA1c is a helpful (but not diagnostic) test in that it gives a snapshot of how your blood glucose levels have been over past few months (its almost always elevated in diabetics). Now a story about human CELLS and INSULIN. Glucose (the fuel) circulating in our arteries enters each & every cell in our bodies to provide energy. Insulin facilitates the entry of glucose into the cells. Glucose can’t enter a cell without the help of insulin. But if there is too much insulin circulating in our vessels (and vessels are present wherever cells are present, which means everywhere in any body), then it is damaging to them (ie the vessels). This damage to the vessels by high concentrations of insulin is how diabetes harms every imaginable part of human body, causing diseases like CAD CHF, CVA, PAD leading to lower extremity amputations, blindness, renal failure, peripheral neuropathy etc etc. It also causes HTN (hypertension) which is another disease (2nd WORST disease overall) that harms every part and organ in human body, too. THIS IS WHY DIABETES IS THE WORST OF ALL HUMAN DISEASES. PERIOD. Imagine the artery to be a street outside your room - the room being analogus to a human cell. You aren’t able to open the door yourself. You don’t even have the key to the door. Insulin has the key, and must physically open the door for you every time. Insulin molecules are like guards running around on the streets (ie in the arteries) - and they’ll come immediately to your room door and open it for you to enter. Now what happens if your door deteriorates (due to a disease like rust) and it becomes harder and harder to open over time? You’ll gradually have to increase the nu Continue reading >>

The Management Of Diabetic Ketoacidosis In Adults

The Management Of Diabetic Ketoacidosis In Adults

Action 1: Commence 0.9% sodium chloride solution (use large bore cannula) via infusion pump. See Box 2 for rate of fluid replacement Action 2: Commence a fixed rate intravenous insulin infusion (IVII). (0.1unit/kg/hr based on estimate of weight) 50 units human soluble insulin (Actrapid® or Humulin S®) made up to 50ml with 0.9% sodium chloride solution. If patient normally takes long acting insulin analogue (Lantus®, Levemir®) continue at usual dose and time Action 3: Assess patient o Respiratory rate; temperature; blood pressure; pulse; oxygen saturation o Glasgow Coma Scale o Full clinical examination Action 4: Further investigations • Capillary and laboratory glucose • Venous BG • U & E • FBC • Blood cultures • ECG • CXR • MSU Action 5: Establish monitoring regimen • Hourly capillary blood glucose • Hourly capillary ketone measurement if available • Venous bicarbonate and potassium at 60 minutes, 2 hours and 2 hourly thereafter • 4 hourly plasma electrolytes • Continuous cardiac monitoring if required • Continuous pulse oximetry if required Action 6: Consider and precipitating causes and treat appropriately BOX 1: Immediate management: time 0 to 60 minutes (T=0 at time intravenous fluids are commenced) If intravenous access cannot be obtained request critical care support immediately Systolic BP (SBP) below 90mmHg Likely to be due to low circulating volume, but consider other causes such as heart failure, sepsis, etc. • Give 500ml of 0.9% sodium chloride solution over 10-15 minutes. If SBP remains below 90mmHg repeat whilst requesting senior input. Most patients require between 500 to 1000ml given rapidly. • Consider involving the ITU/critical care team. • 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 >>

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