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Does Ketoacidosis Cause Hyperkalemia

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Diabetic ketoacidosis is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. Hyperglycemia causes an osmotic diuresis with significant fluid and electrolyte loss. DKA occurs mostly in type 1 diabetes mellitus (DM). It causes nausea, vomiting, and abdominal pain and can progress to cerebral edema, coma, and death. DKA is diagnosed by detection of hyperketonemia and anion gap metabolic acidosis in the presence of hyperglycemia. Treatment involves volume expansion, insulin replacement, and prevention of hypokalemia. Diabetic ketoacidosis (DKA) is most common among patients with type 1 diabetes mellitus and develops when insulin levels are insufficient to meet the body’s basic metabolic requirements. DKA is the first manifestation of type 1 DM in a minority of patients. Insulin deficiency can be absolute (eg, during lapses in the administration of exogenous insulin) or relative (eg, when usual insulin doses do not meet metabolic needs during physiologic stress). Common physiologic stresses that can trigger DKA include Some drugs implicated in causing DKA include DKA is less common in type 2 diabetes mellitus, but it may occur in situations of unusual physiologic stress. Ketosis-prone type 2 diabetes is a variant of type 2 diabetes, which is sometimes seen in obese individuals, often of African (including African-American or Afro-Caribbean) origin. People with ketosis-prone diabetes (also referred to as Flatbush diabetes) can have significant impairment of beta cell function with hyperglycemia, and are therefore more likely to develop DKA in the setting of significant hyperglycemia. SGLT-2 inhibitors have been implicated in causing DKA in both type 1 and type 2 DM. Continue reading >>

St-segment Elevation Resulting From Hyperkalemia

St-segment Elevation Resulting From Hyperkalemia

A 20-year-old man with a history of type 1 diabetes mellitus presented to the emergency department with nausea, vomiting, and abdominal pain of 8 hours’ duration. Diabetic ketoacidosis was diagnosed based on a glucose of 68.8 mmol/L (1240 mg/dL), bicarbonate of 5 mmol/L, pH of 6.92, and a positive urine dipstick for ketones. Serum potassium measured 9.4 mmol/L. An ECG (Figure 1) revealed ST-segment elevation (asterisks); a wide QRS complex tachycardia; absent P waves; and tall, peaked, and tented T waves (arrows). One hour after the patient received intravenous fluid, calcium gluconate, bicarbonate, and insulin, the electrocardiographic abnormalities had resolved (Figure 2), leaving only sinus tachycardia secondary to volume depletion and minimal peaking of the T waves (arrows). Serum potassium now measured 5.7 mmol/L. Creatine kinase, creatine kinase-MB, and troponin I values were normal. At the time of discharge, the patient was in good condition, with a normal ECG. Figure 1. ECG obtained on presentation to the emergency department demonstrating a wide complex tachycardia, absent P waves, peaked T waves (arrows), and ST-segment elevation (asterisks) in leads V1, V2, and aVR. Serum potassium measured 9.4 mmol/L. Hyperkalemia can cause several characteristic ECG abnormalities that are often progressive. Initially, the T wave becomes tall, symmetrically peaked, and tented. Widening of the QRS complex with an intraventricular conduction delay then occurs. Additional elevation of serum potassium leads to a decrease in the amplitude of the P wave and its eventual disappearance from the ECG. Rarely, ST-segment elevation mimicking myocardial infarction, described as a “pseudoinfarction” pattern, is present. Further progression of hyperkalemia leads to a sine wave appear Continue reading >>

Diabetic Ketoacidosis Producing Extreme Hyperkalemia In A Patient With Type 1 Diabetes On Hemodialysis

Diabetic Ketoacidosis Producing Extreme Hyperkalemia In A Patient With Type 1 Diabetes On Hemodialysis

Diabetic ketoacidosis producing extreme hyperkalemia in a patient with type 1 diabetes on hemodialysis. 1. Division of Endocrinology and Metabolism, Jichi Medical University Saitama Medical Center, Saitama, Japan. 2. Division of Endocrinology and Metabolism, International University of Health and Welfare Hospital, Nasushiobara, Japan. Endocrinology, Diabetes & Metabolism Case Reports, 04 Sep 2017, 2017 DOI: 10.1530/EDM-17-0068 PMID: 28924484PMCID: PMC5592707 Share this article Share with emailShare with twitterShare with linkedinShare with facebook Diabetic ketoacidosis (DKA) is a critical complication of type 1 diabetes associated with water and electrolyte disorders. Here, we report a case of DKA with extreme hyperkalemia (9.0 mEq/L) in a patient with type 1 diabetes on hemodialysis. He had a left frontal cerebral infarction resulting in inability to manage his continuous subcutaneous insulin infusion pump. Electrocardiography showed typical changes of hyperkalemia, including absent P waves, prolonged QRS interval and tented T waves. There was no evidence of total body water deficit. After starting insulin and rapid hemodialysis, the serum potassium level was normalized. Although DKA may present with hypokalemia, rapid hemodialysis may be necessary to resolve severe hyperkalemia in a patient with renal failure.Patients with type 1 diabetes on hemodialysis may develop ketoacidosis because of discontinuation of insulin treatment.Patients on hemodialysis who develop ketoacidosis may have hyperkalemia because of anuria.Absolute insulin deficit alters potassium distribution between the intracellular and extracellular space, and anuria abolishes urinary excretion of potassium.Rapid hemodialysis along with intensive insulin therapy can improve hyperkalemia, while fluid infu Continue reading >>

On The Relationship Between Potassium And Acid-base Balance

On The Relationship Between Potassium And Acid-base Balance

The notion that acid-base and potassium homeostasis are linked is well known. Students of laboratory medicine will learn that in general acidemia (reduced blood pH) is associated with increased plasma potassium concentration (hyperkalemia), whilst alkalemia (increased blood pH) is associated with reduced plasma potassium concentration (hypokalemia). A frequently cited mechanism for these findings is that acidosis causes potassium to move from cells to extracellular fluid (plasma) in exchange for hydrogen ions, and alkalosis causes the reverse movement of potassium and hydrogen ions. As a recently published review makes clear, all the above may well be true, but it represents a gross oversimplification of the complex ways in which disorders of acid-base affect potassium metabolism and disorders of potassium affect acid-base balance. The review begins with an account of potassium homeostasis with particular detailed attention to the renal handling of potassium and regulation of potassium excretion in urine. This discussion includes detail of the many cellular mechanisms of potassium reabsorption and secretion throughout the renal tubule and collecting duct that ensure, despite significant variation in dietary intake, that plasma potassium remains within narrow, normal limits. There follows discussion of the ways in which acid-base disturbances affect these renal cellular mechanisms of potassium handling. For example, it is revealed that acidosis decreases potassium secretion in the distal renal tubule directly by effect on potassium secretory channels and indirectly by increasing ammonia production. The clinical consequences of the physiological relation between acid-base and potassium homeostasis are addressed under three headings: Hyperkalemia in Acidosis; Hypokalemia w Continue reading >>

How Does Diabetes Cause Hyperkalemia?

How Does Diabetes Cause Hyperkalemia?

Potassium and Hyperkalemia Potassium is a mineral in your body cells that performs several important body functions. Hyperkalemia is the condition when your blood has too much potassium in it. Adrenal glands are tiny structures that sit on the top parts of your kidneys. They secrete (hide and release) a chemical called “aldosterone”. Aldosterone signals the kidneys to release potassium along with urine. By doing so, the body is able to keep up a constant level of potassium in the blood. However, if your adrenals are not working properly, the levels of aldosterone start to fall and your kidneys are no longer able to release the potassium in your urine. When aldosterone starts to fall and the kidneys are no longer able to release potassium in the urine, the potassium starts to accumulate in the blood causing hyperkalemia- high blood potassium. Why Diabetes Causes Hyperkalemia? If you have diabetes, your body is unable to produce insulin- the chemical that regulates sugar levels in your blood. This triggers the fat cells to break down and release ketones. Ketones are chemicals that increase the acidity of your blood. High blood acidity, combined with high blood sugar, acts to force the potassium in your body cells to move out into your blood. Therefore, the potassium content of your blood increases. Further, high blood glucose in diabetes is capable of destroying the blood vessels in the kidneys and the adrenal glands. This reduces their capacity to release potassium with urine and eventually you develop hyperkalemia. This is how your diabetes may lead to hyperkalemia. Symptoms of hyperkalemia are: Muscle Fatigue Weakness Paralysis Heart beating in an irregular way Nausea If you have any of these symptoms, talk to your doctor. Your doctor may order blood tests to diagn Continue reading >>

205 Severe Hyperkalemia And Metabolic Acidosis In Diabetes: Beyond Ketoacidosis | Journal Of Investigative Medicine

205 Severe Hyperkalemia And Metabolic Acidosis In Diabetes: Beyond Ketoacidosis | Journal Of Investigative Medicine

205 SEVERE HYPERKALEMIA AND METABOLIC ACIDOSIS IN DIABETES: BEYOND KETOACIDOSIS SOUTHERN ABSTRACTS: Renal, Electrolyte and Hypertension Joint Poster Session 5:00 PM: Thursday, February 24, 2005 205 SEVERE HYPERKALEMIA AND METABOLIC ACIDOSIS IN DIABETES: BEYOND KETOACIDOSIS 1Louisiana State University Health Sciences Center 2Overton Brooks VA Medical Center, Shreveport, LA. Persistent hyperkalemia results from impaired urinary potassium excretion, which is mainly controlled by aldosterone. Metabolic acidosis further worsens hyperkalemia with transcellular shifts. We report a 62 yr/M, diabetic, who presented for elective cholecystectomy. His baseline serum creatinine was 1.7 mg/dL with normal acid base and electrolyte status until 5 months prior to presentation when he was started on angiotensin-converting enzyme inhibitor (ACEi) and a potassium-sparing diuretic, triamterene. Four months after ACEi initiation his renal functions were serum creatinine 1.9 mg/dL, serum K 5.1 meq/L, Na 136 meq/L, Cl 109 meq/L, and CO2 15 mmol/L. The reasons for poor follow-up or lack of interventions are unknown. Preoperatively, on this admission, his serum K 8.2 meq/L, Na 130 meq/L, Cl 107 meq/L, CO2 10 mmol/L, anion gap 13, glucose 383 mg/dL, creatinine 2.6 mg/dL, lactate 1.4 and negative serum ketones. Urinalysis: pH 5.0, no WBC/RBC, proteins and ketones negative. Random urinary potassium was 10.6 mmol/L. Arterial blood gas: pH 7.23, pCO2 32 mm Hg, pO2 99 mm Hg, HCO3 12.8 mmol/L. Hyperkalemia was treated with calcium gluconate, insulin/glucose, and bicarbonate infusions. ACEi and potassium-sparing diuretic were discontinued; loop diuretics, oral bicarbonate, and potassium binding resins were administered, which resulted in lowering of serum K and correction of his metabolic acidosis. Thi Continue reading >>

Hyperkalemia

Hyperkalemia

Objectives The objectives of this module will be to: Describe the classic presentation of a patient with hyperkalemia. Name the electrocardiographic manifestations of hyperkalemia. List the principles of managing a patient with hyperkalemia. Introduction Hyperkalemia is a metabolic abnormality seen frequently in the Emergency Department. The most common condition leading to hyperkalemia is missed dialysis in a patient with end stage renal disease (ESRD), but many other conditions can predispose an individual to hyperkalemia, such as acute renal failure, extensive burns, trauma, or severe rhabdomyolysis or severe acidosis. Other conditions that can be associated with hyperkalemia are acute digoxin toxicity and adrenal insufficiency. In rare circumstances, hyperkalemia can become so significant that cardiac dysrhythmias and subsequent death can occur; therefore, rapid identification and appropriate treatment are paramount to properly treating this condition. Initial Actions and Primary Survey The primary survey should focus on assessing airway, breathing and circulation. Since many patients with severe hyperkalemia will have renal dysfunction, some may be fluid overloaded and may present with pulmonary edema and respiratory distress. Traditionally, the electrocardiogram (ECG) has been used as a surrogate marker for clinically significant hyperkalemia. Patients suspected of having hyperkalemia (chronic renal failure, severe diabetic ketoacidosis, etc.) should be placed on a cardiac monitor and a 12-lead electrocardiogram should be performed immediately. Concurrently, intravenous access should be obtained and a blood sample should be sent to the laboratory for a basic metabolic profile. Differential Diagnosis Hyperkalemia Pseudohyperkalemia Thrombocytosis Erythrocytosis Leu Continue reading >>

Serum Potassium In Lactic Acidosis And Ketoacidosis

Serum Potassium In Lactic Acidosis And Ketoacidosis

Abstract METABOLIC acidosis has been thought to elevate serum potassium concentration.1 , 2 However, hyperkalemia was not found in recent studies in patients with postictal lactic acidosis3 or in dogs infused with lactic acid4 , 5 or 3-hydroxybutyric acid5 — observations that raise questions about the association between metabolic acidosis and hyperkalemia: Does metabolic acidosis cause hyperkalemia or is the latter an epiphenomenon? Does metabolic acidosis (or acidemia) cause hyperkalemia only when acidosis is due to excess "mineral acids," and not to excess organic acids? With the hope of providing some clarification of these questions, I have reviewed initial laboratory data and clinical findings in . . . Continue reading >>

Hyperkalaemia In Adults

Hyperkalaemia In Adults

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find the Dietary Potassium article more useful, or one of our other health articles. Description Hyperkalaemia is defined as plasma potassium in excess of 5.5 mmol/L[1]. The European Resuscitation Guidelines further classify hyperkalaemia as: Mild - 5.5-5.9 mmol/L. Moderate - 6.0-6.4 mmol/L. Severe - >6.5 mmol/L. Potassium is the most abundant intracellular cation - 98% of it being located intracellularly. Hyperkalaemia has four broad causes: Renal causes - eg, due to decreased excretion or drugs. Increased circulation of potassium - can be exogenous or endogenous. A shift from the intracellular to the extracellular space. Pseudohyperkalaemia. Epidemiology The time of greatest risk is at the extremes of life. Reported incidence in hospitals is 1-10%, with reduced renal function causing a five-fold increase in risk in patients on potassium-influencing drugs[2]. Men are more likely than women to develop hyperkalaemia, whilst women are more likely to experience hypokalaemia. Renal causes Acute kidney injury (AKI). Chronic kidney disease (CKD): Normally all potassium that is ingested is absorbed and excretion is 90% renal and 10% alimentary. Most excretion by the gut is via the colon and in CKD this can maintain a fairly normal blood level of potassium. It seems likely that the elevated potassium levels in CKD trigger the excretion of potassium via the colon[3]. Patients with CKD must be careful of foods rich in potassium. Hyperkalaemic renal tubular acidosis. Mineralocorticoid deficiency. Medicines that interfere with potassium excretion - eg, amiloride, spironolac Continue reading >>

) And Reflects A Severe Shift From Glycolysis To Lipolysis For Energy Needs.

) And Reflects A Severe Shift From Glycolysis To Lipolysis For Energy Needs.

Acidosis Hyperkalemia Ketosis Lead Beta Blocker s Prostaglandin Inhibitor Methyldopa Carbonic anhydrase inhibitor Acetazolamide Mefenamic acid Post-hypocapnia Excessive Normal Saline infused (liters) Hyperkalemia[fpnotebook.com] It is due to the accumulation of ketoacids (via excessive ketosis) and reflects a severe shift from glycolysis to lipolysis for energy needs.[en.wikipedia.org] Causes: Metabolic Acidosis and Elevated Anion Gap (Mnemonic: "MUD PILERS") Methanol , Metformin Uremia Diabetic Ketoacidosis (DKA), Alcohol ic ketoacidosis or starvation ketosis[fpnotebook.com] Metabolic Acidosis Hyperkalemia Correction of hyperkalemia leads to correction of metabolic acidosis in many patients, pointing to the central role of hyperkalemia in the pathogenesis of this acidosis.[emedicine.medscape.com] Ketosis-prone type 2 diabetes is a variant of type 2 diabetes, which is sometimes seen in obese individuals, often of African (including African-American or Afro-Caribbean[merckmanuals.com] The acidosis and hyperkalemia, however, are out of proportion to the degree of renal failure.[emedicine.medscape.com] List represents a sample of symptoms, diseases, and other queries. Updated weekly. Hungry Bones Syndrome Altitude Sickness Cavernous Sinus Thrombosis Posterior Subcapsular Cataract Cellulitis Splenic Infarction Megaloblastic Anemia Islet Cell Tumor Chronic Phase of Chronic Myeloid Leukemia Penile Fracture Tuberous Sclerosis Primary Sclerosing Cholangitis Odynophagia, unilateral throat pain Costovertebral Angle Tenderness Dyspepsia Tenesmus Oliguria Scrotal Ulcer Choledochal Cyst Anal Fistula Essential Hypertension Enthesitis-Related Arthritis Glioblastoma Multiforme Leiomyosarcoma Brain Neoplasm Hyperventilation Wolff-Parkinson-White Syndrome Ethmoid Sinusitis Dementia with Continue reading >>

Diabetic Ketoacidosis Producing Extreme Hyperkalemia In A Patient With Type 1 Diabetes On Hemodialysis

Diabetic Ketoacidosis Producing Extreme Hyperkalemia In A Patient With Type 1 Diabetes On Hemodialysis

Go to: Abstract Diabetic ketoacidosis (DKA) is a critical complication of type 1 diabetes associated with water and electrolyte disorders. Here, we report a case of DKA with extreme hyperkalemia (9.0 mEq/L) in a patient with type 1 diabetes on hemodialysis. He had a left frontal cerebral infarction resulting in inability to manage his continuous subcutaneous insulin infusion pump. Electrocardiography showed typical changes of hyperkalemia, including absent P waves, prolonged QRS interval and tented T waves. There was no evidence of total body water deficit. After starting insulin and rapid hemodialysis, the serum potassium level was normalized. Although DKA may present with hypokalemia, rapid hemodialysis may be necessary to resolve severe hyperkalemia in a patient with renal failure. Learning points: Patients with type 1 diabetes on hemodialysis may develop ketoacidosis because of discontinuation of insulin treatment. Patients on hemodialysis who develop ketoacidosis may have hyperkalemia because of anuria. Absolute insulin deficit alters potassium distribution between the intracellular and extracellular space, and anuria abolishes urinary excretion of potassium. Rapid hemodialysis along with intensive insulin therapy can improve hyperkalemia, while fluid infusions may worsen heart failure in patients with ketoacidosis who routinely require hemodialysis. Go to: Background Diabetic ketoacidosis (DKA) is a very common endocrinology emergency. It is usually associated with severe circulatory volume depletion. Management of fluids, metabolic acidosis and electrolyte disorders is mandatory. In DKA, mild-to-moderate elevation of serum potassium is usually seen despite total body potassium wasting (1). After intravenous insulin infusion to treat DKA, even if the initial serum Continue reading >>

Diabetic Ketoacidosis-induced Hyperkalemia

Diabetic Ketoacidosis-induced Hyperkalemia

Abstract We report the biochemical data of 22 hospital admissions because of untreated diabetic ketoacidosis. Fifty percent of admitted patients showed an initial serum potassium between 4.6 and 6.0 mEq/1 whereas severe hyperkalemia (value>6.1 mEq/l) occurred in 32%. Initial potassium levels show a slight negative correlation with pH but a stronger correlation (p<0.001) was found between the initial serum potassium and glucose values. We suggest that hyperglycemia due to insulinopenia must be one of the factors in the pathogenesis of this hyperkalemia. Preview Unable to display preview. Download preview PDF. Continue reading >>

Starvation Ketoacidosis

Starvation Ketoacidosis

Etiology xxx Physiology Accumulation of Ketones Generated by Metabolism of Free Fatty Acids Diagnosis Anion Gap: usually >20 Osmolal Gap: increased Serum Ketones: positive Serum Potassium: normal (ketoacidosis does not cause hyperkalemia) Clinical Manifestations Neurologic Manifestations xxxx Renal Manifestations Anion Gap Metabolic Acidosis (AGMA) (see Metabolic Acidosis-Elevated Anion Gap, [[Metabolic Acidosis-Elevated Anion Gap]]) Diagnosis Delta Gap/Delta Bicarbonate Ratio: usually 1.1 Ketoacidosis xxx Elevated Osmolal Gap (see Serum Osmolality, [[Serum Osmolality]]) Physiology: increased (due to presence of osmotically-active, acetone) Other Manifestations xxx xxx Treatment Nutritional Support References xxx Continue reading >>

Management Of Diabetic Ketoacidosis

Management Of Diabetic Ketoacidosis

Diabetic ketoacidosis is an emergency medical condition that can be life-threatening if not treated properly. The incidence of this condition may be increasing, and a 1 to 2 percent mortality rate has stubbornly persisted since the 1970s. Diabetic ketoacidosis occurs most often in patients with type 1 diabetes (formerly called insulin-dependent diabetes mellitus); however, its occurrence in patients with type 2 diabetes (formerly called non–insulin-dependent diabetes mellitus), particularly obese black patients, is not as rare as was once thought. The management of patients with diabetic ketoacidosis includes obtaining a thorough but rapid history and performing a physical examination in an attempt to identify possible precipitating factors. The major treatment of this condition is initial rehydration (using isotonic saline) with subsequent potassium replacement and low-dose insulin therapy. The use of bicarbonate is not recommended in most patients. Cerebral edema, one of the most dire complications of diabetic ketoacidosis, occurs more commonly in children and adolescents than in adults. Continuous follow-up of patients using treatment algorithms and flow sheets can help to minimize adverse outcomes. Preventive measures include patient education and instructions for the patient to contact the physician early during an illness. Diabetic ketoacidosis is a triad of hyperglycemia, ketonemia and acidemia, each of which may be caused by other conditions (Figure 1).1 Although diabetic ketoacidosis most often occurs in patients with type 1 diabetes (formerly called insulin-dependent diabetes mellitus), more recent studies suggest that it can sometimes be the presenting condition in obese black patients with newly diagnosed type 2 diabetes (formerly called non–insulin-depe Continue reading >>

Hyperkalemia In A Young Woman With Type 1 Diabetes Mellitus

Hyperkalemia In A Young Woman With Type 1 Diabetes Mellitus

A 32-year-old woman with multiple medical problems was brought to the emergency department with lethargy and weakness. The family noted progressive confusion and fatigue over 2 days, coupled with extreme weakness. The patient and family denied all other complaints as well as any traumatic or toxicologic events. The medical history included juvenile-onset diabetes mellitus, hypertension, renal insufficiency, and diabetic retinopathy with visual impairment; the patient used insulin and lisinopril as well as several other unknown medications. On examination, she was confused and lethargic but was aroused by stimuli and spoke coherently. Vital signs were: blood pressure, 188/106 mmHg; pulse, approximately 70 beats/min; respiratory rate, 24 breaths/min; temperature, 36.1°C (97°F); and oxygen saturation, 94% on room air; the ECG monitor demonstrated the rhythm strip in Figure 1. A bedside glucose test was 256 mg/dL. The remainder of the examination was unremarkable. Results of a 12-lead ECG are seen in Figure 2. Based upon the ECG findings noted in Figures 1 and 2, which of the following best describe the patient’s risk of an adverse event and the most appropriate management: A. Low risk; atropine IV and glucagon IV B. Intermediate risk; transcutaneous pacing and IV epinephrine infusion C. High risk; synchronized electrical cardioversion with amiodarone IV D. Extremely high risk; calcium IV, sodium bicarbonate IV, and dextrose/insulin IV Correct Answer: D. Extremely high risk; calcium IV, sodium bicarbonate IV, and dextrose/insulin IV Discussion Hyperkalemia presents across a spectrum of severity, ranging from asymptomatic discovery to cardiorespiratory arrest. Of the various electrolyte disorders, it is perhaps the most serious with the potential for severe adverse outco Continue reading >>

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