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Is Ketoacidosis Reversible

How Can Diabetic Ketoacidosis Cause Cerebral Edema In Infants?

How Can Diabetic Ketoacidosis Cause Cerebral Edema In Infants?

Diabetic Ketoacidosis (DKA) in and of itself does not cause cranial edema. What happens with DKA is the excess glucose in the blood changes the osmolarity of the blood, and causes fluid shift from intracelluar to extracellular. This causes the cells to shrink somewhat. Upon finding the patient in the DKA state, the teatment is insulin and IV fluids. Insulin and the hydration IV fluids reverse the DKA state, and also the osmolarity of the extracellular fluid, causing a fluid shift back into the cell. With the osmolarity reversed, the cells begin swelling—sometimes sometimes larger than before: this is what causes the edema in the cerebrum. This is particularly dangerous because the brain cells have nowhere to go, being encased within the skull. Even though infants have fontanelles and the skull has not fused solid, the extra fluid causes compression within the brain, which in turn can adversely affect the brain function. Continue reading >>

Posterior Reversible Encephalopathy Syndrome Complicating Diabetic Ketoacidosis; An Important Treatable Complication

Posterior Reversible Encephalopathy Syndrome Complicating Diabetic Ketoacidosis; An Important Treatable Complication

Abstract Development of acute neurological symptoms secondary to cerebral oedema is well described in diabetic ketoacidosis (DKA) and often has a poor prognosis. We present the clinical and radiological data of a 17-yr-old girl who developed cortical blindness, progressive encephalopathy, and seizures caused by posterior reversible encephalopathy syndrome (PRES) that developed after her DKA had resolved. Vasogenic oedema in PRES resolves if the underlying trigger is identified and eliminated. In this case, hypertension was identified as the likely precipitating factor and following treatment her vision and neurological symptoms rapidly improved. We suggest how recent DKA may have contributed to the development of PRES in this patient. Continue reading >>

Diabetic Coma

Diabetic Coma

Diabetic coma is a reversible form of coma found in people with diabetes mellitus. It is a medical emergency.[1] Three different types of diabetic coma are identified: Severe low blood sugar in a diabetic person Diabetic ketoacidosis (usually type 1) advanced enough to result in unconsciousness from a combination of a severely increased blood sugar level, dehydration and shock, and exhaustion Hyperosmolar nonketotic coma (usually type 2) in which an extremely high blood sugar level and dehydration alone are sufficient to cause unconsciousness. In most medical contexts, the term diabetic coma refers to the diagnostical dilemma posed when a physician is confronted with an unconscious patient about whom nothing is known except that they have diabetes. An example might be a physician working in an emergency department who receives an unconscious patient wearing a medical identification tag saying DIABETIC. Paramedics may be called to rescue an unconscious person by friends who identify them as diabetic. Brief descriptions of the three major conditions are followed by a discussion of the diagnostic process used to distinguish among them, as well as a few other conditions which must be considered. An estimated 2 to 15 percent of diabetics will suffer from at least one episode of diabetic coma in their lifetimes as a result of severe hypoglycemia. Types[edit] Severe hypoglycemia[edit] People with type 1 diabetes mellitus who must take insulin in full replacement doses are most vulnerable to episodes of hypoglycemia. It is usually mild enough to reverse by eating or drinking carbohydrates, but blood glucose occasionally can fall fast enough and low enough to produce unconsciousness before hypoglycemia can be recognized and reversed. Hypoglycemia can be severe enough to cause un Continue reading >>

Characteristics Of Severe Alcoholic Ketoacidosis With A Reversible Visual Disturbance

Characteristics Of Severe Alcoholic Ketoacidosis With A Reversible Visual Disturbance

No. Age Sex Alcohol intake Alcoho history Conscious Level Pupil diameter Light reflex Systolic BP unit year g/day year mm mmHg 1 66 Male ? 24 Alert 4 none 82 2 53 Male 100 20 Semicoma 6 none 90 3 63 Male ? ? Alert ? ? 90 4 44 Male 200 over 5 Alert 7 none 80 5 59 Male 170 40 Alert 4 sluggish 73 6 48 Male 180 over 8 Semicoma 7 none 87 7 61 Male ? ? Disoriented 5 ? 65 8 49 Male ? ? Alert ? ? 73 9 48 Female over 110 ? Disoriented ? sluggish 134 10 68 Male ? ? Disoriented 3.5 none 150 11 56 Male ? ? Disoriented 5 none 79 12 49 Female ? ? Alert 3 none 130 13 43 Male 180 over 10 Disoriented ? ? 80 14 57 Female ? ? Alert Dilated sluggish 120 No. pH PCO2 PO2 HCO3 Base excess Lactate Glucose Alcohol BHBA AAA Thiamine deficiency Require of_IC Arrest DH Outcome unit mmHg mmHg mmHg mg/dl mg/dl mmol/l mmol/l mg/dl μmol/l μmol/l 1 6.855 13.9 190.5 2.5 -31.4 ? 69 45.8 140 14 no yes no survival 2 6.497 51 ? 3.8 -29 ? ? 8 1190 332 no yes yes survival 3 6.612 14 ? 1.5 -28 ? ? not exam 6360 261 no yes yes survival 4 6.707 13.6 272.8 1.6 -30 ? 91 0 245 11 no yes yes death 5 6.748 13 134 1.7 -33 270 70 not exam 2160 220 no yes no survival 6 6.748 20.3 151 2.6 -33.9 297 85 27.4 ? ? not exam yes no survival 7 6.623 35.0 231 3.5 -34 ? ? ? 2960 460 no yes yes death 8 6.78 15.5 118 2.3 -31 ? ? ? ? ? no no no survival 9 6.64 8.3 159 ? -37.5 109 153 not exam 823 272 no yes yes survival 10 6.79 11.8 137.2 1.8 -33 ? 38 not exam 4825 210 not exam yes no survival 11 6.55 44.4 198 3.7 -29.4 ? 20 not exam not exam not exam not exam yes no survival 12 6.79 8 196 ? ? 90 ? 68 ? 8.82 no ? no survival Arrest No-Arrest p-value n=6 n=8 Age 52.0 + 3.4 56.5 + 2.7 n.s. Sex (Male/Female) 5/1 6/2 n.s. Consciousness (number of alert) 2 5 n.s. Systolic blood pressure (mmHg) 89.8 + 9.5 99.2 + 10.5 n.s. pH 6.637 + 0.0 Continue reading >>

Brief Report Reversible Blindness Associated With Alcoholic Ketoacidosis

Brief Report Reversible Blindness Associated With Alcoholic Ketoacidosis

Abstract To report a case of reversible blindness associated with severe alcoholic ketoacidosis. A 44-year-old male presented with gradual bilateral blindness that developed within a 24-hour period. He suffered from ethanol-induced severe ketoacidosis and shock and was resuscitated with epinephrine and sodium bicarbonate. The treatment of acidosis led to a rapid resolution of the patient's blindness. Conclusions It is important to understand the role of severe acidosis as the sole causative factor of reversible bilateral blindness. 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 In The Pediatric Population With Type 1 Diabetes

Diabetic Ketoacidosis In The Pediatric Population With Type 1 Diabetes

Diabetic Ketoacidosis in the Pediatric Population with Type 1 Diabetes Abstract: Diabetic ketoacidosis (DKA) is a leading cause of morbidity and mortality in patients with type 1 diabetes (T1DM). Individuals familiar with this complication of diabetes should be able to identify the earliest signs and symptoms and act promptly to prevent further deterioration. However, even in patients with established diabetes, the rates of DKA are considerable. This chapter discusses in detail the various aspects of DKA in the pediatric population with T1DM. The prevalence and regional effects on the prevalence of DKA as well as the specific risk factors, whether disease, patient, or physician related, are reviewed. Patients with DKA experience a condition of starvation despite the abundance of metabolic substrate (i.e., glucose); the pathophysiological mechanisms responsible for the development of DKA are outlined. Next, a detailed discussion of the clinical aspects of DKA is provided. This includes the clinical findings at presentation, the approach to treatment, and potential complications. Prevention is the best method for reducing rates of DKA. Somewhat different factors apply in patients with new-onset diabetes when compared with those with established diabetes and these are reviewed. Continue reading >>

Id: 64: Reversible Blindness Associated With Diabetic Ketoacidosis: A Rare Combination

Id: 64: Reversible Blindness Associated With Diabetic Ketoacidosis: A Rare Combination

Introduction A wide spectrum of ocular diseases is associated with diabetes mellitus (DM) and most of them lead to gradual loss of vision that is almost always irreversible. Sudden vision loss in severe diabetic ketoacidosis (DKA) that is reversible with treatment of the metabolic abnormality is a very rare complication that has been reported three times previously. Case Presentation A 59 year-old male with Type 1 DM presented with altered consciousness, epigastric pain, hypothermia and sudden complete bilateral vision loss for three days. He was not complaint with insulin. There was no history or laboratory evidence of ethanol, methanol, ethylene glycol ingestion, head trauma, baseline vision problem, cold or intense bright light exposure. Physical examination revealed rapid shallow breathing at 55/min, blood pressure 90/60 mm Hg, heart rate 102/min and temperature 90.2F. He was oriented only to place,pupils were dilated and non-reactive to light. No light perception in both eyes. Fundoscopy was normal without any evidence of retinal pallor, retinal detachment, retinal hemorrhages, papilledema or cataract. Labs revealed blood glucose 1100 mg/dl, pH 6.95,positive serum and urine ketones, pCO2 11 mm Hg and anion gap 36. He received aggressive warm fluid resuscitation, electrolyte replacements and intravenous insulin infusion with close monitoring. 18 hrs later his blood glucose, pH,anion gap and body temperature normalized and vision spontaneously returned to normal. A repeat fundoscopy exam by ophthalmologist and magnetic resonance image (MRI) brain was completely normal; ruling out posterior ischemic optic neuropathy and occipital stroke. He recovered very well, resumed diet, was ambulatory and had an uneventful rest of hospital course. Discussion Sudden painless visio Continue reading >>

Medline ® Abstracts For References 32-35

Medline ® Abstracts For References 32-35

TI The use of atypical antipsychotic agents is associated with the induction of both an indolent progression to insulin-resistant diabetes and an idiosyncratic beta-cell toxicity presenting as diabetic ketoacidosis, both of which are usually reversible or improved subsequent to cessation of treatment. The underlying mechanisms are unclear at present. Nonetheless, in light of the now numerous reports on the adverse metabolic effects of these drugs, the Consensus Development Conference which met in November 2003 recommends that metabolic risks be considered when starting atypical antipsychotic drugs. Their operative checklist includes baseline screening of candidates for antipsychotic treatment, which includes personal/family history of diabetes, weight, waist circumference, blood pressure, fasting plasma glucose and fasting lipid profile, and then follow-up of these parameters. Furthermore, the health professionals, patients, family and caregivers should be aware of the signs and symptoms of diabetes, especially when acute decompensation occurs which is commensurate with diabetic ketoacidosis. We wish, through this short report, to raise the awareness of physicians treating psychiatric patients to the possibility of new-onset diabetes during therapy with atypical antipsychotic drugs and to emphasize the necessity for increased vigilance and close metabolic follow-up of these patients. Moreover, the choice of the best antipsychotic treatment for each patient should take into consideration the diabetogenic effect of the different treatment options as well the other side effects. AD Department of Medicine and Diabetes Unit, Soroka Medical Center, Faculty of Health Sciences, Beer Sheva, Israel. [email protected] TI OBJECTIVE: The purpose of the study was to determin Continue reading >>

How Do You Cure Type 2 Diabetes Naturally With Diet?

How Do You Cure Type 2 Diabetes Naturally With Diet?

I’m a specialist practitioner in obesity and diabetes. Type 2 diabetes can be reversed through diet. Absolutely. Firstly this is what is a normal insulin reaction looks like: Insulin is manufactured in the pancreas and secreted when your blood sugar levels rise. Blood sugar needs to be not too high and not too low. Insulin’s mechanism to remove sugar from blood is to put it into cells, like your muscles. If there is an excess after blood glucose has gone into cells it is then put in the liver and further excess becomes fat. What happens with type 2 When insulin is secreted the body’s cells have ‘‘receptors’ that accept the insulin’s key that then open the doors to the cell to let the glucose in. Sadly in type 2 the receptors become resistant to the insulin key. Therefore not enough energy gets into the cell. The body has a negative feedback system. Once the cells do not get enough energy a signal is sent back to the pancreas to manufacture even more insulin. This is a vicious cycle. Insulin keeps going up and resistance keeps getting worse. A drug, called metformin works by making cells receptive again but it has limitations and eventually other drugs are needed. This is not ideal; so how can we reverse this? Well quite simply really. The crux of this scenario is that it is the sugar spikes in the blood that are causing the high levels of insulin in the first place. Certain foods cause insulin to enter the system in a fast and high volume way and some foods hardly disturb insulin at all. The insulin index is similar to the GI system and by picking foods that cause little insulin response the type 2 diabetes begins to reverse. This is a snapshot. The lower the number the lower the insulin response Sadly many government guidelines are not beneficial and larg Continue reading >>

Feline Diabetic Ketoacidosis

Feline Diabetic Ketoacidosis

Fall 2008 Ketoacidosis is a metabolic imbalance that is most commonly seen as a sequel to unmanaged or poorly regulated diabetes mellitus. It is caused by the breakdown of fat and protein in a compensatory effort for the need of more metabolic energy. The excessive breakdown of these stored reserves creates a toxic by-product in the form of ketones. As ketones build up in the blood stream, pH and electrolyte imbalances proceed. This condition is a potentially life-threatening emergency that requires immediate medical attention. Diabetes mellitus is a common endocrine disease in geriatric felines. It is caused by a dysfunction in the beta cells of the exocrine pancreas resulting in an absolute or relative deficiency of insulin. Insulin has been called the cells' gatekeeper. It attaches to the surface of cells and permits glucose, the cells' primary energy source, to enter from the blood. A lack of insulin results in a build up of glucose in the blood, physiologically causing a state of cellular starvation. In response to this condition the body begins to increase the mobilization of protein and fat storage. Fatty acids are released from adipose tissue, which are then oxidized by the liver. Normally, these fatty acids are formed into triglycerides. However, without insulin, these fatty acids are converted into ketone bodies, which cannot be utilized by the body. Together with the increased production and decreased utilization an abnormally high concentration of ketone bodies develop. These fixed acids are buffered by bicarbonate; however, the excessive amounts overwhelm and deplete the bicarbonate leading to an increase in arterial hydrogen ion concentration and a decrease in serum bicarbonate. This increase in hydrogen ions lowers the body's pH, leading to a metabolic ac Continue reading >>

Treatment Of Diabetic Ketoacidosis Associated With Antipsychotic Medication: Literature Review

Treatment Of Diabetic Ketoacidosis Associated With Antipsychotic Medication: Literature Review

Background The second-generation antipsychotics (SGAs) are associated with metabolic disturbances. Diabetic ketoacidosis (DKA) is a rare, but potentially fatal sign of acute glucose metabolism dysregulation, which may be associated with the use of SGAs. This study aims to review published reports of patients with schizophrenia and antipsychotic drug–associated DKA, focusing on the effective management of both conditions. Methods Using a predefined search strategy, we searched PubMed and EMBASE from their inception to July 2016. The search terms were related to “diabetic ketoacidosis” and “antipsychotic medication.” Case reports, case series, and reviews of case series written in English language were included in the review. Results Sixty-five reports were analyzed. In most patients who developed antipsychotic-associated DKA, 1 or more suspected antipsychotic medications were discontinued. In 5 cases, a rechallenge test was trialed, and in only 1 case, it resulted in the elevation of blood glucose. The majority was subsequently treated with a different SGA in combination with insulin/oral hypoglycemic agents; although approximately a third of patients had a complete resolution of symptoms or could control diabetes with diet only at the point of discharge. Conclusions Patients taking antipsychotic medications should be regularly screened for insulin resistance and educated about potential complications of antipsychotic medications. This will allow clinicians to individualize treatment decisions and reduce iatrogenic contribution to morbidity and mortality. To achieve best treatment outcomes, antipsychotic-induced DKA should be treated jointly by psychiatry and endocrinology teams. Continue reading >>

Pediatric Diabetic Ketoacidosis

Pediatric Diabetic Ketoacidosis

Practice Essentials Diabetic ketoacidosis, in pediatric and adult cases, is a metabolic derangement caused by the absolute or relative deficiency of the anabolic hormone insulin. Together with the major complication of cerebral edema, it is the most important cause of mortality and severe morbidity in children with diabetes. Signs and symptoms Symptoms of acidosis and dehydration include the following: Symptoms of hyperglycemia, a consequence of insulin deficiency, include the following: Patients with diabetic ketoacidosis may also have the following signs and symptoms: Cerebral edema Most cases of cerebral edema occur 4-12 hours after initiation of treatment. Diagnostic criteria of cerebral edema include the following: Major criteria include the following: Minor criteria include the following: See Clinical Presentation for more detail. Laboratory studies The following lab studies are indicated in patients with diabetic ketoacidosis: Imaging studies Head computed tomography (CT) scanning - If coma is present or develops Chest radiography - If clinically indicated Electrocardiography Electrocardiography (ECG) is a useful adjunct to monitor potassium status. Characteristic changes appear with extremes of potassium status. See the images below. Consciousness Check the patient’s consciousness level hourly for up to 12 hours, especially in a young child with a first presentation of diabetes. The Glasgow coma scale is recommended for this purpose. See Workup for more detail. Management Replacement of the following is essential in the treatment of diabetic ketoacidosis: Insulin - Continuous, low-dose, intravenous (IV) insulin infusion is generally considered the safest and most effective insulin delivery method for diabetic ketoacidosis Potassium - After initial resuscitatio Continue reading >>

Is A Ketogenic Diet Effective?

Is A Ketogenic Diet Effective?

The short answer to your question, is yes, a ketogenic diet is safe and effective for most people. Of course, as with any major change in diet or exercise, you should consult with your doctor so that he or she can help you understand whether this diet is safe for YOU. And especially if you are a Type 1 diabetic, I would be concerned about you starting keto without being under close supervision by a doctor because you could go into ketoacidosis which is a dangerous condition. (Ketoacidosis is different than ketosis, which is a safe metabolic condition that your body enters when you cut carbs and raise your fat levels. It’s important not to confuse the two because while ketoacidosis is very dangerous, ketosis is healthy and is actually the goal for most people on the keto diet. Check out this research for the science behind ketosis vs. ketoacidosis.) Basically, a ketogenic diet is very low carb, moderate protein, and high fat. On keto, you should start out eating less than 20 net carbs per day - which is usually what everyone focuses on. But you also need to focus on your protein and fat levels. Women should eat between 50 and 75 grams of protein per day and men should stay between 100–125 grams of protein per day. And then for the fun part of keto - the FAT - your fat should be between a 1:1 and 1:2 ratio of protein to fat. Which means that if I eat 50 grams of protein a day, I should be eating between 50 and 100 grams of fat per day. And this is the yummy kind of fat - saturated fat is great on keto. So eat that bacon and slather on the butter because eating all that fat will help you lose weight and get healthy - as long as you have cut the carbs. And the fat helps you feel full so you won’t get hungry as often and you won’t feel deprived. And don’t worry tha Continue reading >>

Diabetic Ketoacidosis Due To Fulminant Type 1 Diabetes: A Rare Subtype Of Type 1 Diabetes Leading To Unusual Sequelae

Diabetic Ketoacidosis Due To Fulminant Type 1 Diabetes: A Rare Subtype Of Type 1 Diabetes Leading To Unusual Sequelae

An 18-year-old Filipino male presented to the Emergency Department with a three-day history of lethargy, vomiting, tachypnoea and increasing drowsiness. There was no known past medical history, nor any history of polyuria, polydipsia or weight loss. On initial examination, his vital signs were as follows: heart rate 130 beats/min; blood pressure 105/48 mmHg; respiratory rate 24 breaths/min; oxygen saturation 90% on 6 L oxygen/min; temperature 34.0℃, GCS 8/15 (E1M5V2). He also demonstrated voluntary guarding on abdominal palpation and neck stiffness. He had thin body habitus without central adiposity (BMI 20.6 kg/m2). His arterial blood gas showed pH 7.13; PaO2 7.46 kPa; PaCO2 3.6 kPa; HCO3- 9 mmol/L; BE −20 mmol/L; glucose 50 mmol/L and lactate 5 mmol/L. He was diagnosed with DKA due to new onset T1D and treated with intravenous fluids and a fixed-rate insulin infusion. Subsequent laboratory analysis of the patient’s blood showed urea 32.6 mmol/L; creatinine 379 µmol/L; glucose 107.3 mmol/L; anion gap 45 mmol/L and ketones 7.1 mmol/L. The serum lipase was not elevated. An initial ECG showed sinus tachycardia with no other acute changes. Due to his altered level of consciousness, he received a CT scan of his brain, which was unremarkable, and a lumber puncture which showed a high glucose but no other abnormalities. His conscious level and blood pressure decreased and he was intubated, ventilated, commenced on a noradrenaline infusion and transferred to the ICU for further management. His initial ECG on arrival to the ICU showed ST elevation in leads II, III and aVF with right bundle branch block (Figure 1). Immediate transthoracic echocardiography (TTE) showed global left ventricular (LV) hypokinesis with apical akinesis/dyskinesis (Figures 2(a) to (c) and 3) with Continue reading >>

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