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 >>
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 >>
Topics By Science.gov
Bellazzini, Marc A; Meyer, Tom Hyperkalemia-induced electrocardiogram changes such as dysrhythmias and altered T wave morphology are well described in the medical literature. Pseudo-infarction hyperkalemia-induced changes are less well known, but present a unique danger for the clinician treating these critically ill patients. This article describes a case of pseudo anteroseptal myocardial infarction in a type 1 diabetic with hyperkalemia. The most common patterns of pseudo-infarct and their associated potassium concentrations are then summarized from a literature review of 24 cases. ... urine test is positive, contact your child's diabetes health care team. Tests done by a lab or hospital can confirm whether a child has diabetic ketoacidosis , if necessary. Some ... blood for ketones. Ask the diabetes health care team if such a meter is a good ... Katz, J. R.; Edwards, R.; Khan, M.; Conway, G. S. 1996-01-01 Diabetes in acromegaly is usually non-insulin dependent and is secondary to insulin resistance caused by growth hormone excess. Diabetic ketoacidosis is a result of relative insulin deficiency and is a rare feature of acromegaly. We describe a case of acromegaly presenting with diabetic ketoacidosis. We demonstrate that growth hormone excess can cause diabetic ketoacidosis in the presence of relative, but not absolute insulin deficiency. PMID:8944212 Gupta, Arvin; Rohrscheib, Mark; Tzamaloukas, Antonios H 2008-10-01 A patient on hemodialysis for end-stage renal disease secondary to diabetic nephropathy was admitted in a coma with Kussmaul breathing and hypertension (232/124 mmHg). She had extreme hyperglycemia (1884 mg/dL), acidosis (total CO(2) 4 mmol/L), hyperkalemia (7.2 mmol/L) with electrocardiographic abnormalities, and hypertonicity (330.7 mOsm/kg). Initial t Continue reading >>
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 >>
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 >>
Hyperkalemia In Diabetic Ketoacidosis.
Abstract Patients with diabetic ketoacidosis tend to have somewhat elevated serum K+ concentrations despite decreased body K+ content. The hyperkalemia was previously attributed mainly to acidemia. However, recent studies have suggested that "organic acidemias" (such as that produced by infusing beta-hydroxybutyric acid) may not cause hyperkalemia. To learn which, if any, routinely measured biochemical indices might correlate with the finding of hyperkalemia in diabetic ketoacidosis, we analyzed the initial pre-treatment values in 131 episodes in 91 patients. Serum K+ correlated independently and significantly (p less than 0.001) with blood pH (r = -0.39), serum urea N (r = 0.38) and the anion gap (r = 0.41). The mean serum K+ among the men was 5.55 mmol/l, significantly higher than among the women, 5.09 mmol/l (p less than 0.005). Twelve of the 16 patients with serum K+ greater than or equal to 6.5 mmol/l were men, as were all eight patients with serum K+ greater than or equal to 7.0 mmol/l. Those differences paralleled a significantly higher mean serum urea N concentration among the men (15.1 mmol/l) than the women (11.2 mmol/l, p less than 0.01). The greater tendency to hyperkalemia among the men in this series may have been due partly to their greater renal dysfunction during the acute illness. However, other factors that were not assessed, such as cell K+ release associated with protein catabolism, and insulin deficiency per se, may also have affected serum K+ in these patients. Continue reading >>
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 >>
Causes And Evaluation Of Hyperkalemia In Adults
INTRODUCTION Hyperkalemia is a common clinical problem. Potassium enters the body via oral intake or intravenous infusion, is largely stored in the cells, and is then excreted in the urine. The major causes of hyperkalemia are increased potassium release from the cells and, most often, reduced urinary potassium excretion (table 1). This topic will review the causes and evaluation of hyperkalemia. The clinical manifestations, treatment, and prevention of hyperkalemia, as well as a detailed discussion of hypoaldosteronism (an important cause of hyperkalemia), are presented elsewhere. (See "Clinical manifestations of hyperkalemia in adults" and "Treatment and prevention of hyperkalemia in adults" and "Etiology, diagnosis, and treatment of hypoaldosteronism (type 4 RTA)".) BRIEF REVIEW OF POTASSIUM PHYSIOLOGY An understanding of potassium physiology is helpful when approaching patients with hyperkalemia. Total body potassium stores are approximately 3000 meq or more (50 to 75 meq/kg body weight) [1]. In contrast to sodium, which is the major cation in the extracellular fluid and has a much lower concentration in the cells, potassium is primarily an intracellular cation, with the cells containing approximately 98 percent of body potassium. The intracellular potassium concentration is approximately 140 meq/L compared with 4 to 5 meq/L in the extracellular fluid. The difference in distribution of the two cations is maintained by the Na-K-ATPase pump in the cell membrane, which pumps sodium out of and potassium into the cell in a 3:2 ratio. The ratio of the potassium concentrations in the cells and the extracellular fluid is the major determinant of the resting membrane potential across the cell membrane, which sets the stage for the generation of the action potential that is e Continue reading >>
Chapter 250. Potassium And Magnesium Disorders
Chapter 250. Potassium and Magnesium Disorders Steven M. Gorbatkin, MD, PhD; Lynn Schlanger, MD; James L. Bailey, MD Gorbatkin SM, Schlanger L, Bailey JL. Gorbatkin S.M., Schlanger L, Bailey J.L. Gorbatkin, Steven M., et al.Chapter 250. Potassium and Magnesium Disorders. In: McKean SC, Ross JJ, Dressler DD, Brotman DJ, Ginsberg JS. McKean S.C., Ross J.J., Dressler D.D., Brotman D.J., Ginsberg J.S. Eds. Sylvia C. McKean, et al.eds. Principles and Practice of Hospital Medicine New York, NY: McGraw-Hill; 2012. Accessed April 14, 2018. Gorbatkin SM, Schlanger L, Bailey JL. Gorbatkin S.M., Schlanger L, Bailey J.L. Gorbatkin, Steven M., et al.. "Chapter 250. Potassium and Magnesium Disorders." Principles and Practice of Hospital Medicine McKean SC, Ross JJ, Dressler DD, Brotman DJ, Ginsberg JS. McKean S.C., Ross J.J., Dressler D.D., Brotman D.J., Ginsberg J.S. Eds. Sylvia C. McKean, et al. New York, NY: McGraw-Hill, 2012, What are the causes of potassium and magnesium disorders? What are the potential consequences of potassium and magnesium disorders? How are potassium and magnesium disorders treated? How are potassium disorders treated in clinical situations with rapid potassium shifts, such as diabetic ketoacidosis, hyperglycemic hyperosmolar state, and periodic paralysis? Potassium and magnesium disorders are common in the hospital setting. About 12% of hospitalized patients have hypokalemia, 3% have hyperkalemia, and 11% have hypomagnesemia. Potassium disorders are a particular challenge for hospitalists, as the first clinical manifestation of a severe potassium abnormality may be a cardiac arrhythmia. Potassium (K+) is the most abundant intracellular cation. In a 70 kg adult, the total body K+ is approximately 3500 mmol (50 mmol/kg). About 98% is located in the intracel Continue reading >>
Diabetic Ketoacidosis
Professor of Pediatric Endocrinology University of Khartoum, Sudan Introduction DKA is a serious acute complications of Diabetes Mellitus. It carries significant risk of death and/or morbidity especially with delayed treatment. The prognosis of DKA is worse in the extremes of age, with a mortality rates of 5-10%. With the new advances of therapy, DKA mortality decreases to > 2%. Before discovery and use of Insulin (1922) the mortality was 100%. Epidemiology DKA is reported in 2-5% of known type 1 diabetic patients in industrialized countries, while it occurs in 35-40% of such patients in Africa. DKA at the time of first diagnosis of diabetes mellitus is reported in only 2-3% in western Europe, but is seen in 95% of diabetic children in Sudan. Similar results were reported from other African countries . Consequences The latter observation is annoying because it implies the following: The late diagnosis of type 1 diabetes in many developing countries particularly in Africa. The late presentation of DKA, which is associated with risk of morbidity & mortality Death of young children with DKA undiagnosed or wrongly diagnosed as malaria or meningitis. Pathophysiology Secondary to insulin deficiency, and the action of counter-regulatory hormones, blood glucose increases leading to hyperglycemia and glucosuria. Glucosuria causes an osmotic diuresis, leading to water & Na loss. In the absence of insulin activity the body fails to utilize glucose as fuel and uses fats instead. This leads to ketosis. Pathophysiology/2 The excess of ketone bodies will cause metabolic acidosis, the later is also aggravated by Lactic acidosis caused by dehydration & poor tissue perfusion. Vomiting due to an ileus, plus increased insensible water losses due to tachypnea will worsen the state of dehydr Continue reading >>
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 >>
Diabetic Ketoacidosis
Author: Osama Hamdy, MD, PhD; Chief Editor: Romesh Khardori, MD, PhD, FACP more... Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria. The most common early symptoms of DKA are the insidious increase in polydipsia and polyuria. The following are other signs and symptoms of DKA: Malaise, generalized weakness, and fatigability Nausea and vomiting; may be associated with diffuse abdominal pain, decreased appetite, and anorexia Rapid weight loss in patients newly diagnosed with type 1 diabetes History of failure to comply with insulin therapy or missed insulin injections due to vomiting or psychological reasons or history of mechanical failure of insulin infusion pump Altered consciousness (eg, mild disorientation, confusion); frank coma is uncommon but may occur when the condition is neglected or with severe dehydration/acidosis Signs and symptoms of DKA associated with possible intercurrent infection are as follows: 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 Continue reading >>
(pdf) Diabetic Ketoacidosis Producing Extreme Hyperkalemia In A Patient With Type 1 Diabetes On Hemodialysis
hyperkalemia in a patient with type 1 diabetes HodakaYamada1, ShunsukeFunazaki1, MasafumiKakei1, KazuoHara1 and 1Division of Endocrinology and Metabolism, Jichi Medical University Saitama Medical Center, Saitama, Japan and 2Division of Endocrinology and Metabolism, International University of Health and Welfare Hospital, 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 decit. 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 Patients on hemodialysis who develop ketoacidosis may have hyperkalemia because of anuria. Absolute insulin decit 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 uid infusions may worsen heart failure in patients with ketoacidosis who routinely require hemodialysis. Diabetic ketoacidosis (DKA) is a very common endocrinology emergency. It is usually associated with severe circulatory volume depletion. Management Continue reading >>
Hypokalemia And Hyperkalemia
Sort Adrenal causes of hyperkalemia? Adrenal gland is important in secreting hormones such as cortisol and aldosterone. Aldosterone causes the kidneys to retain sodium and fluid while excreting potassium in the urine. Therefore diseases of the adrenal gland, such as Addison's disease, that lead to decreased aldosterone secretion can decrease kidney excretion of potassium, resulting in body retention of potassium, and hence hyperkalemia. How trauma leads to hyperkalemia Another cause of hyperkalemia is tissue destruction, dying cells release potassium into the blood circulation. Examples of tissue destruction causing hyperkalemia include: trauma, burns, surgery, hemolysis (disintegration of red blood cells), massive lysis of tumor cells, and rhabdomyolysis (a condition involving destruction of muscle cells that is sometimes associated with muscle injury, alcoholism, or drug abuse). What is role of potassium binders (Sodium polystyrene suffocate: SPS) SPS exchanges sodium for potassium and binds it in the gut, primarily in the large intestine, decreasing the total body potassium level by approximately 0.5-1 mEq/L. Multiple doses are usually necessary. Onset of action ranges from 2 to 24 hours after oral administration and is even longer after rectal administration. The duration of action is 4-6 hours. Do not use SPS as a first-line therapy for severe life-threatening hyperkalemia; use it in the second stage of therapy. Continue reading >>
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Pseudomyocardial Infarction In A Patient With Severe Diabetic Ketoacidosis And Mild Hyperkalemia
Volume 2019 |Article ID 4063670 | 4 pages | Pseudomyocardial Infarction in a Patient with Severe Diabetic Ketoacidosis and Mild Hyperkalemia ,1 ngel No del Cueto-Aguilera,1 Ral Alberto Jimnez-Castillo,1 Olga Norali de la Cruz-Mata,1 Mariana Fikir-Ordoez,1 Raymundo Vera-Pineda,1 Dal Alejandro Hernndez-Guajardo,1 Alejandro Ordaz-Faras 1Internal Medicine Department, Hospital Universitario, Universidad Autnoma de Nuevo Len, Monterrey, Nuevo Len, Mexico 2Echocardiography Laboratory, Cardiology Service, Hospital Universitario, Universidad Autnoma de Nuevo Len, Monterrey, Nuevo Len, Mexico A 48-year-old male with a prior diagnosis of diabetes mellitus presented to the emergency department with malaise and nausea. On work-up, he was found with hyperglycemia and high anion gap metabolic acidosis, with a blood . A diagnosis of severe diabetic ketoacidosis was established; serum electrolyte analysis showed mild hyperkalemia. On work-up, a 12-lead electrocardiogram was obtained, and it showed an ST-segment elevation on anterior leads that completely resolved with diabetic ketoacidosis treatment. ST-segment elevation myocardial infarction can be a precipitant factor for diabetic ketoacidosis, and evaluation of diabetic patients with suspected myocardial infarction can be challenging since they can present with atypical or little symptoms. Hyperkalemia, which usually accompanies diabetic ketoacidosis, can cause electrocardiographic alterations that are well described, but ST-segment elevation is uncommon. A pseudomyocardial infarction pattern has been described in patients with diabetic ketoacidosis; of note, most of these patients presented severe hyperkalemia. We believe this is of great importance for clinicians because they must be able to recognize those patients that present w Continue reading >>
