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Why Does Ketoacidosis Cause Hypokalemia

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 >>

Why Is There Hyperkalemia In Diabetic Ketoacidosis?

Why Is There Hyperkalemia In Diabetic Ketoacidosis?

Lack of insulin, thus no proper metabolism of glucose, ketones form, pH goes down, H+ concentration rises, our body tries to compensate by exchanging K+ from inside the cells for H+ outside the cells, hoping to lower H+ concentration, but at the same time elevating serum potassium. Most people are seriously dehydrated, so are in acute kidney failure, thus the kidneys aren’t able to excrete the excess of potassium from the blood, compounding the problem. On the other hand, many in reality are severely potassium depleted, so once lots of fluid so rehydration and a little insulin is administered serum potassium will plummet, so needs to be monitored 2 hourly - along with glucose, sodium and kidney function - to prevent severe hypokalemia causing fatal arrhythmias, like we experienced decades ago when this wasn’t so well understood yet. In practice, once the patient started peeing again, we started adding potassium chloride to our infusion fluids, the surplus potassium would be peed out by our kidneys so no risk for hyperkalemia. Continue reading >>

What Causes Potassium And Sodium Loss In Diabetic Ketoacidosis (dka)?

What Causes Potassium And Sodium Loss In Diabetic Ketoacidosis (dka)?

What causes potassium and sodium loss in diabetic ketoacidosis (DKA)? Glucosuria leads to osmotic diuresis, dehydration and hyperosmolarity. Severe dehydration, if not properly compensated, may lead to impaired renal function. Hyperglycemia, osmotic diuresis, serum hyperosmolarity, and metabolic acidosis result in severe electrolyte disturbances. The most characteristic disturbance is total body potassium loss. This loss is not mirrored in serum potassium levels, which may be low, within the reference range, or even high. Potassium loss is caused by a shift of potassium from the intracellular to the extracellular space in an exchange with hydrogen ions that accumulate extracellularly in acidosis. Much of the shifted extracellular potassium is lost in urine because of osmotic diuresis. Patients with initial hypokalemia are considered to have severe and serious total body potassium depletion. High serum osmolarity also drives water from intracellular to extracellular space, causing dilutional hyponatremia. Sodium also is lost in the urine during the osmotic diuresis. Glaser NS, Marcin JP, Wootton-Gorges SL, et al. Correlation of clinical and biochemical findings with diabetic ketoacidosis-related cerebral edema in children using magnetic resonance diffusion-weighted imaging. J Pediatr. 2008 Jun 25. [Medline] . Umpierrez GE, Jones S, Smiley D, et al. Insulin analogs versus human insulin in the treatment of patients with diabetic ketoacidosis: a randomized controlled trial. Diabetes Care. 2009 Jul. 32(7):1164-9. [Medline] . [Full Text] . Herrington WG, Nye HJ, Hammersley MS, Watkinson PJ. Are arterial and venous samples clinically equivalent for the estimation of pH, serum bicarbonate and potassium concentration in critically ill patients?. Diabet Med. 2012 Jan. 29(1):32-5 Continue reading >>

What Is Hypokalemia?

What Is Hypokalemia?

If you have hypokalemia, that means you have low levels of potassium in your blood. Potassium is a mineral your body needs to work normally. It helps muscles to move, cells to get the nutrients they need, and nerves to send their signals. It’s especially important for cells in your heart. It also helps keep your blood pressure from getting too high. Causes There are many different reasons you could have low potassium levels. It may be because too much potassium is leaving through your digestive tract. It’s usually a symptom of another problem. Most commonly, you get hypokalemia when: You vomit a lot Your kidneys or adrenal glands don’t work well You take medication that makes you pee (water pills or diuretics) It’s possible, but rare, to get hypokalemia from having too little potassium in your diet. Other things sometimes cause it, too, like: Drinking too much alcohol Diabetic ketoacidosis (high levels of acids called ketones in your blood) Laxatives taken over a long period of time Certain types of tobacco Low magnesium Several syndromes can be associated with low potassium, such as: Gitelman syndrome Liddle syndrome Bartter syndrome Fanconi syndrome Women tend to get hypokalemia more often than men. Symptoms If your problem is temporary, or you’re only slightly hypokalemic, you might not feel any symptoms. Once your potassium levels fall below a certain level, you might experience: Hypokalemia can affect your kidneys. You may have to go to the bathroom more often. You may also feel thirsty. You may notice muscle problems during exercise. In severe cases, muscle weakness can lead to paralysis and possibly respiratory failure. Continue reading >>

[full Text] Correlation Of Acidosis-adjusted Potassium Level And Cardiovascular Ou | Dmso

[full Text] Correlation Of Acidosis-adjusted Potassium Level And Cardiovascular Ou | Dmso

The protocol was registered with PROSPERO (Registration Number: CRD42018098772). An article was included if it met the following criteria: 1) the study reported the prevalence of DKA in adult diabetic patients and assessed admission potassium level and pH; 2) the study qualitatively observed cardiovascular outcomes in DKA patients; 3) the design of the study was a cross-sectional or cohort, or randomized controlled trial. Studies were excluded if 1) it was a case-control, case report, conference proceeding, systematic review, letter to editor, an opinion, or research brief; 2) published in languages other than English; 3) reported DKA secondary to pregnancy or among pediatrics, or 4) studies evaluating therapeutic intervention which includes DKA secondary to sodium-glucose co-transporter 2 inhibitor. Level of serum potassium, and pH-adjusted corrected level of potassium at the time of admission. Cardiovascular outcomes in relation to potassium in DKA episode Specifically, the CV outcomes were noted in relation to the level of potassium at the time of occurrence of CV event and included ECG, report of fibrillation, tachycardia or bradycardia, central venous pressure, cardiac arrest, myocardial infarction, and troponin. Moreover, reports of CV outcomes or signs and symptoms were recorded if the CV outcome was reported as the reason for fatality. It was further noted if any relationship was given by the authors between hypokalemia and the reason for such CV outcome. All references retrieved were initially grouped under the respective search engine. Duplicates were removed, and titles were screened for eligibility. After removal of irrelevant studies, regrouping was done according to the nature of the study, ie, case series, clinical trial, guideline, etc. Relevant demogra Continue reading >>

Management Of Hypokalemia And Hyperkaemia (proceedings)

Management Of Hypokalemia And Hyperkaemia (proceedings)

12Next Over 90% of the potassium in the body is located within cells. External balance for potassium is maintained by matching output to input. Internal balance is maintained by translocation of potassium between intracellular and extracellular fluid. Any change in plasma potassium concentration must arise from a change in intake, distribution, or excretion. HYPOKALEMIA Causes Decreased intake of potassium alone is unlikely to cause hypokalemia but, in chronically ill animals, prolonged anorexia, loss of muscle mass, and ongoing urinary potassium losses may combine to cause hypokalemia. Alkalemia contributes to hypokalemia as potassium ions enter cells in exchange for hydrogen ions. Insulin promotes uptake of glucose and potassium by hepatic and skeletal muscle cells. A syndrome characterized by recurrent episodes of limb muscle weakness and neck ventroflexion, increased creatine kinase concentrations, and hypokalemia has been reported in related young Burmese cats. Gastrointestinal loss of potassium (especially vomiting of stomach contents) is an important cause of hypokalemia in small animals. Chloride depletion and sodium avidity due to volume depletion contribute to perpetuation of potassium depletion and metabolic alkalosis by enhancing urinary losses of potassium and hydrogen ions. Urinary loss of potassium is another important cause of hypokalemia and hypokalemia is common in cats with chronic renal failure. Hypokalemia also may occur in distal renal tubular acidosis in cats. Finally, hypokalemic nephropathy characterized by tubulointerstitial nephritis may develop in cats fed diets marginally replete in potassium and containing urinary acidifiers. Hypokalemia commonly occurs during the postobstructive diuresis that follows relief of urethral obstruction in cats. Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Introduction Diabetic ketoacidosis (DKA) is a dangerous complication of diabetes caused by a lack of insulin in the body. Diabetic ketoacidosis occurs when the body is unable to use blood sugar (glucose) because there isn't enough insulin. Instead, it breaks down fat as an alternative source of fuel. This causes a build-up of a by-product called ketones. Most cases of diabetic ketoacidosis occur in people with type 1 diabetes, although it can also be a complication of type 2 diabetes. Symptoms of diabetic ketoacidosis include: passing large amounts of urine feeling very thirsty vomiting abdominal pain Seek immediate medical assistance if you have any of these symptoms and your blood sugar levels are high. Read more about the symptoms of diabetic ketoacidosis. Who is affected by diabetic ketoacidosis? Diabetic ketoacidosis is a relatively common complication in people with diabetes, particularly children and younger adults who have type 1 diabetes. Younger children under four years of age are thought to be most at risk. In about 1 in 4 cases, diabetic ketoacidosis develops in people who were previously unaware they had type 1 diabetes. Diabetic ketoacidosis accounts for around half of all diabetes-related hospital admissions in people with type 1 diabetes. Diabetic ketoacidosis triggers These include: infections and other illnesses not keeping up with recommended insulin injections Read more about potential causes of diabetic ketoacidosis. Diagnosing diabetic ketoacidosis This is a relatively straightforward process. Blood tests can be used to check your glucose levels and any chemical imbalances, such as low levels of potassium. Urine tests can be used to estimate the number of ketones in your body. Blood and urine tests can also be used to check for an underlying infec Continue reading >>

Potassium Balance In Acid-base Disorders

Potassium Balance In Acid-base Disorders

INTRODUCTION There are important interactions between potassium and acid-base balance that involve both transcellular cation exchanges and alterations in renal function [1]. These changes are most pronounced with metabolic acidosis but can also occur with metabolic alkalosis and, to a lesser degree, respiratory acid-base disorders. INTERNAL POTASSIUM BALANCE Acid-base disturbances cause potassium to shift into and out of cells, a phenomenon called "internal potassium balance" [2]. An often-quoted study found that the plasma potassium concentration will rise by 0.6 mEq/L for every 0.1 unit reduction of the extracellular pH [3]. However, this estimate was based upon only five patients with a variety of disturbances, and the range was very broad (0.2 to 1.7 mEq/L). This variability in the rise or fall of the plasma potassium in response to changes in extracellular pH was confirmed in subsequent studies [2,4]. Metabolic acidosis — In metabolic acidosis, more than one-half of the excess hydrogen ions are buffered in the cells. In this setting, electroneutrality is maintained in part by the movement of intracellular potassium into the extracellular fluid (figure 1). Thus, metabolic acidosis results in a plasma potassium concentration that is elevated in relation to total body stores. The net effect in some cases is overt hyperkalemia; in other patients who are potassium depleted due to urinary or gastrointestinal losses, the plasma potassium concentration is normal or even reduced [5,6]. There is still a relative increase in the plasma potassium concentration, however, as evidenced by a further fall in the plasma potassium concentration if the acidemia is corrected. A fall in pH is much less likely to raise the plasma potassium concentration in patients with lactic acidosis Continue reading >>

Cardiovascular Complications Of Ketoacidosis

Cardiovascular Complications Of Ketoacidosis

US Pharm. 2016;41(2):39-42. ABSTRACT: Ketoacidosis is a serious medical emergency requiring hospitalization. It is most commonly associated with diabetes and alcoholism, but each type is treated differently. Some treatments for ketoacidosis, such as insulin and potassium, are considered high-alert medications, and others could result in electrolyte imbalances. Several cardiovascular complications are associated with ketoacidosis as a result of electrolyte imbalances, including arrhythmias, ECG changes, ventricular tachycardia, and cardiac arrest, which can be prevented with appropriate initial treatment. Acute myocardial infarction can predispose patients with diabetes to ketoacidosis and worsen their cardiovascular outcomes. Cardiopulmonary complications such as pulmonary edema and respiratory failure have also been seen with ketoacidosis. Overall, the mortality rate of ketoacidosis is low with proper and urgent medical treatment. Hospital pharmacists can help ensure standardization and improve the safety of pharmacotherapy for ketoacidosis. In the outpatient setting, pharmacists can educate patients on prevention of ketoacidosis and when to seek medical attention. Metabolic acidosis occurs as a result of increased endogenous acid production, a decrease in bicarbonate, or a buildup of endogenous acids.1 Ketoacidosis is a metabolic disorder in which regulation of ketones is disrupted, leading to excess secretion, accumulation, and ultimately a decrease in the blood pH.2 Acidosis is defined by a serum pH <7.35, while a pH <6.8 is considered incompatible with life.1,3 Ketone formation occurs by breakdown of fatty acids. Insulin inhibits beta-oxidation of fatty acids; thus, low levels of insulin accelerate ketone formation, which can be seen in patients with diabetes. Extr Continue reading >>

Hypokalemia And The Heart

Hypokalemia And The Heart

An article from the E-Journal of the ESC Council for Cardiology Practice Practicing cardiologists must keep potassium levels within normal limits in all their cardiac patients. Unrecognised hypokalemia is a leading cause of iatrogenic mortality among cardiac patients who have an inherent risk for arrhythmias and who frequently use medications that increase the risks of hypokalemia and/or arrhythmia. Symptomatic or severe hypokalemia should be corrected with a solution of intravenous potassium: 10-40 mEq infused over 2-3 h (infusion rate should not to exceed 40 mEq/h). In less urgent situations, oral supplementation is preferred and safer: 50-100 mEq/d divided two-four times per day. Long-term treatment should be based on the recognition of the hypokalemia cause. Hypokalemia and the heart Potassium is the most abundant intracellular cation and is necessary for maintaining a normal charge difference between intracellular and extracellular space. Potassium homeostasis is important for normal cellular function and is regulated by ion-exchange pumps (primarily cellular, membrane-bound, sodium-potassium ATPase pumps). Derangements of potassium regulation often lead to neuromuscular, gastrointestinal and cardiac rhythm abnormalities. The normal level of plasma potassium is 3,8 – 5,1 mmol/l. The deviations to both extremes (hypo- and hyperkalemia) are related to the risk of cardiac arrhythmias. Potassium levels below 3,0 mmol/l cause significant Q-T interval prolongation with subsequent risk of torsade des pointes, ventricular fibrillation and sudden cardiac death. Potassium levels above 6,0 mmol/l cause peaked T waves, wider QRS komplexes and may result in bradycardia, asystole and sudden death. Hyperkalemia is most frequently caused by renal failure (frequently a trigger is Continue reading >>

Profound Hypokalemia Associated With Severe Diabetic Ketoacidosis

Profound Hypokalemia Associated With Severe Diabetic Ketoacidosis

Go to: Abstract Hypokalemia is common during the treatment of diabetic ketoacidosis (DKA); however, severe hypokalemia at presentation prior to insulin treatment is exceedingly uncommon. A previously healthy 8-yr-old female presented with new onset type 1 diabetes mellitus, severe DKA (pH = 6.98), and profound hypokalemia (serum K = 1.3 mmol/L) accompanied by cardiac dysrhythmia. Insulin therapy was delayed for 9 h to allow replenishment of potassium to safe serum levels. Meticulous intensive care management resulted in complete recovery. This case highlights the importance of measuring serum potassium levels prior to initiating insulin therapy in DKA, judicious fluid and electrolyte management, as well as delaying and/or reducing insulin infusion rates in the setting of severe hypokalemia. Keywords: diabetic ketoacidosis, hypokalemia, insulin, low-dose insulin drip, pediatric Nearly one third of children with newly diagnosed type 1 diabetes present in diabetic ketoacidosis (DKA). Higher proportions of young children and those from disadvantaged socioeconomic groups present with DKA (1). DKA is the leading cause of mortality among children with diabetes, and electrolyte abnormalities are a recognized complication of DKA contributing to morbidity and mortality (2, 3). Total body potassium deficiency of 3-6 mEq/kg is expected at presentation of DKA due to osmotic diuresis, emesis, and secondary hyperaldosteronism; however, pretreatment serum potassium levels are usually not low due to the extracellular shift of potassium that occurs with acidosis and insulin deficiency (3, 4). After insulin treatment is initiated, potassium shifts intracellularly and serum levels decline. Replacement of potassium in intravenous fluids is the standard of care in treatment of DKA to prevent Continue reading >>

Hyperglycemic Crisis: Regaining Control

Hyperglycemic Crisis: Regaining Control

CE credit is no longer available for this article. Expired July 2005 Originally posted April 2004 VERONICA CRUMP, RN, BSN VERONICA CRUMP is a nurse on the surgical unit of Morristown Memorial Hospital in Morristown, N.J. She's also a subacute care nurse in the hospital's rehabilitation division. KEY WORDS: hyperosmolar hyperglycemic syndrome (HHS), diabetic ketoacidosis (DKA), hepatic glucose production, proteolysis, hepatic gluconeogenesis, ketone bodies, metabolic acidosis, hyperkalemia, hypokalemia When a patient presents with markedly high blood glucose levels, the consequences can be fatal. Here's how to get your patient through the crisis. Edith Schafer, age 71, has just been admitted to your ICU with pneumonia, which she developed at home. She has a history of Type 2 diabetes. In addition to a temperature of 102° F (38.9° C), she has rapid, shallow breathing and dry, flushed skin. Her blood pressure is 96/70 mm Hg, and she's so lethargic that she's unable to keep her eyes open. Her lab results show a serum glucose level of 900 mg/dL. In addition to the pneumonia, Mrs. Schafer is suffering from hyperosmolar hyperglycemic syndrome (HHS). Severe hyperglycemia is a complication of both Type 1 and Type 2 diabetes. It can indicate HHS or diabetic ketoacidosis (DKA), another life-threatening condition. HHS tends to occur in patients with Type 2 diabetes, like Mrs. Schafer, while Type 1 diabetics are more likely to develop DKA. However, DKA can occur in Type 2 diabetes as well.1 HHS and DKA can be set off by infection, stress, missed medication, and other causes. In Mrs. Schafer's case, the trigger was pneumonia, a common cause of hyperglycemia in patients with diabetes. No matter what the cause, though, a case of HHS or DKA can turn deadly if not caught in time. The m Continue reading >>

Hypokalemia

Hypokalemia

Hypokalemia is when blood’s potassium levels are too low. Potassium is an important electrolyte for nerve and muscle cell functioning, especially for muscle cells in the heart. Your kidneys control your body’s potassium levels, allowing for excess potassium to leave the body through urine or sweat. Hypokalemia is also called: hypokalemic syndrome low potassium syndrome hypopotassemia syndrome Mild hypokalemia doesn’t cause symptoms. In some cases, low potassium levels can lead to arrhythmia, or abnormal heart rhythms, as well as severe muscle weakness. But these symptoms typically reverse after treatment. Learn what it means to have hypokalemia and how to treat this condition. Mild hypokalemia usually shows no signs or symptoms. In fact, symptoms generally don’t appear until your potassium levels are extremely low. A normal level of potassium is 3.6–5.2 millimoles per liter (mmol/L). Being aware of hypokalemia symptoms can help. Call your doctor if you are experiencing these symptoms: weakness fatigue constipation muscle cramping palpitations Levels below 3.6 are considered low, and anything below 2.5 mmol/L is life-threateningly low, according to the Mayo Clinic. At these levels, there may be signs and symptoms of: paralysis respiratory failure breakdown of muscle tissue ileus (lazy bowels) In more severe cases, abnormal rhythms may occur. This is most common in people who take digitalis medications (digoxin) or have irregular heart rhythm conditions such as: tachycardia (heartbeat too fast) bradycardia (heartbeat too slow) premature heartbeats Other symptoms include loss of appetite, nausea, and vomiting. You can lose too much potassium through urine, sweat, or bowel movements. Inadequate potassium intake and low magnesium levels can result in hypokalemia. M Continue reading >>

Successful Use Of Renal Replacement Therapy For Refractory Hypokalemia In A Diabetic Ketoacidosis Patient

Successful Use Of Renal Replacement Therapy For Refractory Hypokalemia In A Diabetic Ketoacidosis Patient

Volume 2019 |Article ID 6130694 | 3 pages | Successful Use of Renal Replacement Therapy for Refractory Hypokalemia in a Diabetic Ketoacidosis Patient 1Department of Medicine, Saint Josephs University Medical Center, 703 Main St, Paterson, NJ, USA 2New York Medical College, Valhalla, NY, USA A 39-year-old African-American female presented to the emergency department with a seven-day history of right upper quadrant abdominal pain accompanied by nausea, vomiting, and diarrhea. She was noted to be alert and following commands, but tachypneic with Kussmaul respirations; and initial laboratory testing supported a diagnosis of diabetic ketoacidosis (DKA) and hypokalemia. To avoid hypokalemia-induced arrhythmias, insulin administration was withheld until a serum potassium (K) level of 3.3 mEq/L could be achieved. Efforts to increase the patients potassium level via intravenous repletion were ineffectual; hence, an attempt was made at more aggressive potassium repletion via hemodialysis using a 4 mEq/L K dialysate bath. The patient was started on Aldactone and continuous veno-venous hemodialysis (CVVH) with ongoing low-dose insulin infusion. This regimen was continued over 24 h resulting in normalization of the patients potassium levels, resolution of acidosis, and improvement in mental status. Upon resolution of her acidemia, the patient was transitioned from insulin infusion to treatment with a subcutaneous insulin aspart and insulin detemir, and did not experience further hypokalemia. Considering our success, we propose CVVH as a tool for potassium repletion when aggressive intravenous (IV) repletion has failed. Hospitalizations for diabetic ketoacidosis (DKA) have soared in incidence over the recent years, increasing 54.9% from 19.5 to 30.2 hospitalizations per 1,000 people 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 >>

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