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When Is Dka Resolved

Management Of Adult Diabetic Ketoacidosis

Management Of Adult Diabetic Ketoacidosis

Go to: Abstract Diabetic ketoacidosis (DKA) is a rare yet potentially fatal hyperglycemic crisis that can occur in patients with both type 1 and 2 diabetes mellitus. Due to its increasing incidence and economic impact related to the treatment and associated morbidity, effective management and prevention is key. Elements of management include making the appropriate diagnosis using current laboratory tools and clinical criteria and coordinating fluid resuscitation, insulin therapy, and electrolyte replacement through feedback obtained from timely patient monitoring and knowledge of resolution criteria. In addition, awareness of special populations such as patients with renal disease presenting with DKA is important. During the DKA therapy, complications may arise and appropriate strategies to prevent these complications are required. DKA prevention strategies including patient and provider education are important. This review aims to provide a brief overview of DKA from its pathophysiology to clinical presentation with in depth focus on up-to-date therapeutic management. Keywords: DKA treatment, insulin, prevention, ESKD Go to: Introduction In 2009, there were 140,000 hospitalizations for diabetic ketoacidosis (DKA) with an average length of stay of 3.4 days.1 The direct and indirect annual cost of DKA hospitalizations is 2.4 billion US dollars. Omission of insulin is the most common precipitant of DKA.2,3 Infections, acute medical illnesses involving the cardiovascular system (myocardial infarction, stroke) and gastrointestinal tract (bleeding, pancreatitis), diseases of the endocrine axis (acromegaly, Cushing’s syndrome), and stress of recent surgical procedures can contribute to the development of DKA by causing dehydration, increase in insulin counter-regulatory hor Continue reading >>

15l. Loriaux (ed.), Endocrine Emergencies: Recognition And Treatment, Contemporary Endocrinology 74, Doi 10.1007/978-1-62703-697-9_2, © Springer Science+business Media New York 2014

15l. Loriaux (ed.), Endocrine Emergencies: Recognition And Treatment, Contemporary Endocrinology 74, Doi 10.1007/978-1-62703-697-9_2, © Springer Science+business Media New York 2014

Précis 1. Clinical setting—Any altered state of well being in the context of signifi cant hyperglycemia in a patient with type 1 (DKA) or advanced type 2 diabetes mel- litus (DKA or HHS), particularly during acute illness, may signify one of these diabetic emergencies. 2. Diagnosis (a) History: Most patients with diabetic ketoacidosis (DKA) or with hyperos- molar hyperglycemic state (HHS) will have a history of diabetes, and a his- tory of altered insulin dose, infection, signifi cant medical “stressâ€. Antecedent symptoms of polyuria and polydipsia, lassitude, blurred vision, and mental status changes may predominate the clinical picture. With DKA, abdominal pain and tachypnea are often present. (b) Physical examination usually reveals an altered sensorium, signs of volume contraction/dehydration (tachycardia, hypotension, dry mucus membranes, “tenting†of the skin); in DKA, the odor of acetone in the breath. (c) Laboratory evaluation. The diagnostic criteria for DKA include blood glu- cose above 250 mg/dL, arterial pH < 7.30, serum bicarbonate < 15 mEq/l Chapter 2 Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic Syndrome Beatrice C. Lupsa and Silvio E. Inzucchi B. C. Lupsa , M.D. (*) • S. E. Inzucchi , M.D. Section of Endocrinology , Yale University School of Medicine , Yale-New Haven Hospital, 333 Cedar Street, FMP 107 , P.O. Box 208020 , New Haven , CT 06520 , USA e-mail: [email protected] 16 and moderate degree of ketonemia and/or ketonuria. Patients with HHS present with extreme hyperglycemia (blood glucose > 600 mg/dL), increased osmolality (> 320 mOsm/kg) and profound dehydration/volume contrac- tion. The laboratory evaluation of a patient with hyperglycemic emergency should include measurement of blood glucose and he 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

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 >>

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 >>

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

Diabetic Ketoacidosis

Initial Evaluation Initial evaluation of patients with DKA includes diagnosis and treatment of precipitating factors (Table 14–18). The most common precipitating factor is infection, followed by noncompliance with insulin therapy.3 While insulin pump therapy has been implicated as a risk factor for DKA in the past, most recent studies show that with proper education and practice using the pump, the frequency of DKA is the same for patients on pump and injection therapy.19 Common causes by frequency Other causes Selected drugs that may contribute to diabetic ketoacidosis Infection, particularly pneumonia, urinary tract infection, and sepsis4 Inadequate insulin treatment or noncompliance4 New-onset diabetes4 Cardiovascular disease, particularly myocardial infarction5 Acanthosis nigricans6 Acromegaly7 Arterial thrombosis, including mesenteric and iliac5 Cerebrovascular accident5 Hemochromatosis8 Hyperthyroidism9 Pancreatitis10 Pregnancy11 Atypical antipsychotic agents12 Corticosteroids13 FK50614 Glucagon15 Interferon16 Sympathomimetic agents including albuterol (Ventolin), dopamine (Intropin), dobutamine (Dobutrex), terbutaline (Bricanyl),17 and ritodrine (Yutopar)18 DIFFERENTIAL DIAGNOSIS Three key features of diabetic acidosis are hyperglycemia, ketosis, and acidosis. The conditions that cause these metabolic abnormalities overlap. The primary differential diagnosis for hyperglycemia is hyperosmolar hyperglycemic state (Table 23,20), which is discussed in the Stoner article21 on page 1723 of this issue. Common problems that produce ketosis include alcoholism and starvation. Metabolic states in which acidosis is predominant include lactic acidosis and ingestion of drugs such as salicylates and methanol. Abdominal pain may be a symptom of ketoacidosis or part of the inci 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 >>

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 >>

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 >>

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 >>

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 >>

Pulmcrit – Four Dka Pearls

Pulmcrit – Four Dka Pearls

Introduction I have a confession to make: I love treating DKA. It’s satisfying to take a patient from severe acidosis, electrolytic disarray, and hypovolemia to normal physiology during an ICU shift. Although it's usually straightforward, there are some pitfalls and a few tricks that may help your patients improve faster.0 Pearl #1: Avoid normal saline A common phenomenon observed when starting a DKA resuscitation with normal saline (NS) is worseningof the patient’s acidosis with decreasing bicarbonate levels (example below). This occurs despite an improvement in the anion gap, and is explained by a hyperchloremic metabolic acidosis caused by bolusing with NS. This could be a real problem for a patient whose initial bicarbonate level is extremely low.1 A while ago I made the switch from NS to lactated ringers (LR) for resuscitation of DKA patients, and have not observed this phenomenon when using LR. Example of the effect of normal saline resuscitation during the initial phase of DKA resuscitation. This patient received approximately 3 liters normal saline between admission labs and the next set of labs as well as an insulin infusion, all textbook management per American Diabetes Association guidelines. The anion gap decreased from 33 mEq/L to 30 mEq/L, indicating improvement of ketoacidosis. However, the bicarbonate decreased from 8 mEq/L to 5 mEq/L due to a hyperchloremic metabolic acidosis caused by the normal saline. Note the increase in chloride over four hours. Failure of the potassium to decrease significantly despite insulin infusion may reflect potassium shifting out of the cells in response to the hyperchloremic metabolic acidosis. There is only one randomized controlled trial comparing NS to LR for resuscitation in DKA (Zyl et al, 2011). These authors fou Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is characterized by a biochemical triad of hyperglycemia, ketonemia, and acidemia, with rapid symptom onset. An acute metabolic complication of diabetes that is potentially fatal if not properly treated. Common symptoms and signs include polyuria, polydipsia, polyphagia, weakness, weight loss, tachycardia, dry mucous membranes, poor skin turgor, hypotension, and, in severe cases, shock. Successful treatment includes correction of volume depletion, hyperglycemia, electrolyte imbalances, and comorbid precipitating events, with frequent monitoring. Complications of treatment include hypoglycemia, hypokalemia, hypoxemia, and rarely pulmonary edema. Cerebral edema, a rare but potentially rapidly fatal complication, occurs mainly in children. It is prevented by avoiding overly rapid fluid and electrolyte replacement. polyuria polyphagia polydipsia weight loss weakness nausea or vomiting abdominal pain dry mucous membranes poor skin turgor sunken eyes tachycardia hypotension Kussmaul respiration acetone breath altered mental status hypothermia plasma glucose ABG capillary or serum ketones U/A serum BUN serum creatinine serum sodium serum potassium serum chloride serum magnesium serum calcium serum phosphate anion gap calculation serum creatine phosphokinase serum lactate LFT serum amylase serum lipase serum osmolality CBC CXR ECG myocardial enzymes blood, urine, or sputum cultures 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 >>

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