Low-dose versus high-dose insulin therapy for diabetic ketoacidosis.

The effects of low-dose continuous insulin therapy were compared to those of high-dose subcutaneous and intravenous insulin therapy in six episodes of diabetic ketoacidosis. Time for correction of acidosis, ketosis, and hyperglycemia were similar for both regimens. The high-dose method required more exogenous glucose and supplemental potassium to avoid hypoglycemia and/or hypokalemia during treatment. Levels of cortisol, human growth hormone, and glucagon, initially elevated in most patients, showed a progressive decline with both modes of therapy. Plasma insulin remained remarkably stable during both treatment regimens, but remained within the physiologic range only in patients receiving low-dose therapy. Our study suggest that either modality is effective in the treatment of diabetic ketoacidosis.     

Does bicarbonate therapy improve the management of severe diabetic ketoacidosis?

OBJECTIVE: The use of bicarbonates in the treatment of severe diabetic ketoacidosis remains controversial, especially regarding the benefit/risk ratio. The aim of this study was to assess the efficacy of bicarbonate therapy during severe diabetic ketoacidosis (pH <7.10). DESIGN: Retrospective study. SETTING: The emergency unit of a teaching hospital. PATIENTS: The records of 39 patients consecutively admitted for severe diabetic ketoacidosis were analyzed (pH <7.10).The patients were divided into two groups: group 1 (n = 24; patients with bicarbonate treatment) and group 2 (n = 15; patients without bicarbonate treatment). INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: We compared two groups of patients presenting with severe diabetic ketoacidosis (pH values between 6.83 and 7.08) treated with or without bicarbonate. A group of 24 patients received 120+/-40 mmol sodium bicarbonate. The two groups were similar at admission with regard to clinical and biological parameters. No difference could be demonstrated between the two groups concerning the clinical parameters or the normalization time of biochemical parameters. If the number of patients with hypokalemia was comparable between the two groups, the potassium supply was significantly more important in group 1 compared with group 2 (366+/-74 mmol/L vs. 188+/-109 mmol/L, respectively; p < .001). CONCLUSIONS: Data from the literature and this study are not in favor of the use of bicarbonate in the treatment of diabetic ketoacidosis with pH values between 6.90 and 7.10.     

Diabetic ketoacidosis

A diagnosis of diabetic ketoacidosis requires the patient's plasma glucose concentration to be above 250 mg per dL (although it usually is much higher), the pH level to be less than 7.30, and the bicarbonate level to be 18 mEq per L or less. Beta-hydroxybutyrate is a better measurement of the degree of ketosis than serum ketones. Intravenous insulin and fluid replacement are the mainstays of therapy, with careful monitoring of potassium levels. Phosphorous and magnesium also may need to be replaced. Bicarbonate therapy rarely is needed. Infection, insulin omission, and other problems that may have precipitated ketoacidosis should be treated. Myocardial infarction is a precipitating cause of diabetic ketoacidosis that is especially important to look for in older patients with diabetes. Cerebral edema is a major complication that occurs primarily in children. Education to prevent recurrence should be offered to all patients, including how to manage sick days and when to call a physician.     

糖尿病合并低钾血症279例分析

目的：了解糖尿病所引起的低钾血症的病因及发生率，以便更好地进行预防。方法：回顾性分析20a来明确有低钾血症的糖尿病患279例，分析其低钾的病因构成、因年代不同而出现的病因差异以及与年龄的关系。结果：糖尿病伴低钾血症的原因为服用利尿剂、酮症酸中毒、胃肠道疾病、肾脏疾患等。结论：低钾血症在糖尿病患中较为常见，过去报道其主要原因为酮症酸中毒，但现在发现其主要原因为高血压患服利尿剂所致，可能是因为现在对降糖的重视而使酮症酸中毒减少，但对利尿剂对血钾的影响重视不够。     

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 with severe hypokalemia and persistent hypernatremia in an adolescent girl with COVID‐19 infection

We report a case of new‐onset type 1 diabetes in a girl presenting with severe diabetic ketoacidosis, complicated by profound hypokalemia and hypernatremia. We describe the clinical course, management challenges, and the potential role of the concomitant COVID‐19 infection in the complexity of this case.     

Pseudomyocardial infarction and hyperkalemia: A case report and subject review

A case of diabetic ketoacidosis with hyperkalemia and ECG evidence of pseudomyocardial infarction is presented. Electrocardiogram abnormalities resolved shortly after treatment of the elevated potassium. The electrophysiology of hyperkalemia and theories to explain observed ECG changes are discussed. Pseudoinfarction changes that may be peculiar to patients with diabetic ketoncidosis and hyperkalemia are examined.     

酮症酸中毒起病的糖尿病患者的实验室指标比较

目的 提高临床医师对糖尿病酮症酸中毒(DKA)起病的暴发性1型糖尿病(FT1DM)的认识。方法 93例DKA起病的糖尿病患者根据糖尿病分型分为3组: 2型糖尿病（A）组、非暴发性1型糖尿病（B）组、FT1DM（C）组,对3组年龄、血糖、血钠、血钾、糖化血红蛋白、血pH值进行比较。结果 与2型糖尿病组相比,FT1DM组的血糖、血钾更高,HbA1c、血钠、血pH值更低,随着病程缩短,血pH值的比较无统计学意义。与非暴发性1型糖尿病组相比,FT1DM组的血糖、血钾更高,HbA1c更低,在血钠和血pH值的比较差异无统计学意义。结论 DKA起病的FT1DM患者具有更高的血糖和血钾,注意重视。除糖尿病类型外,糖尿病病程也影响酸中毒的实验室指标。     

Persistent hyperkalemia in a patient with diabetes mellitus: a reversible defect in kaliuresis during bicarbonaturia.

The purpose of this report is to apply recent advances in the understanding of the physiology of the excretion of potassium to a patient who had hyperkalemia due to a low rate of excretion of potassium. The defect was first suspected during therapy for diabetic ketoacidosis, when the concentration of potassium in plasma was unusually high (7.3 mmol/l) on admission and the deficit of potassium, as judged from the quantity of potassium infused to maintain normokalemia (40 mmol/24 h), was much less than expected. After recovery from diabetic ketoacidosis, hyperkalemia persisted despite near-normal values for creatinine and glucose in plasma. Excretion of potassium was low, considering the stimulus of hyperkalemia, and did not rise appreciably after the acute or chronic administration of a mineralocorticoid. The transtubular potassium concentration gradient (TTKG) did not exceed 6 after a large dose of fludrocortisone (200 micrograms) was administered. Notwithstanding, the TTKG rose to 14.4 following the intake of acetazolamide. We speculate that the basis for the hyperkalemia was type II hypoaldosteronism.     

Excessive hypokalemia and hyperkalemia following head injury

A sudden decrease of serum potassium below 2.5 mmol/l carries the risk of dangerous arrhythmias and requires immediate replacement therapy [6]. We refer to a patient with a brain stem compression after head injury, who developed a profound hypokalemia (K⁺=1.2 mmol/l) with life-threatening arrhythmias, probably due to a catecholamine induced intracellular potassium shift (beta-2-stimulation). Only by aggressive potassium replacement up to 80 mmol/h (610 mmol/16h) could potassium levels be increased and cardiac arrhythmias terminated. Although replacement therapy was stopped when the serum K⁺-level increased to 2.4 mmol/l, 3.5 h later the patient became hyperkalemic (8.1 mmol/l). This was probably due to a secondary shift of potassium from intra-to extracellular space. In patients with severe head trauma and the potential risk of excessive catecholamine release special attention must be paid to changes in potassium balance.     

Potassium protocols: in search of evidence

PURPOSE: The purpose of this triangulated study was to evaluate potassium protocols used in clinical practice. RATIONALE: Hypokalemia occurs frequently in the clinical setting and can have serious consequences. It is further complicated by the fact that it has multiple causes and patient symptoms can range from asymptomatic to death. considering the complexity and potential seriousness of hypokalemia, it is important that treatment be appropriate. DESCRIPTION OF THE PROCESS: The triangulated approach included an examination of the empirical evidence, a comparison of potassium protocols currently in use, and an evaluation of the potential benefits and risks of using a potassium protocol in a sample of patients. OUTCOME: There is wide variation in potassium protocols and no empirical evidence in support of or opposition to these protocols. An evaluation of the use of a potassium protocol in a sample of patients indicates that patients not on protocols are not being routinely treated according to general protocol potassium replacement recommendations. CONCLUSIONS: The use of narrowly defined potassium protocols may lead to overtreatment or incorrect treatment in the complex setting of hypokalemia. IMPLICATIONS FOR NURSING PRACTICE: Findings suggest the need for validation of clinically significant hypokalemia, the addition of other electrolyte measures when evaluating and treating hypokalemia, and the use of routine serum potassium levels and maintenance of serum potassium levels equal to or more than 4.0 mmol/L in certain patient populations. Most important, the etiology of hypokalemia, not used in qualifying criteria on any of the potassium protocols examined, should form the basis for treatment.     

Liquorice-induced severe hypokalemic rhabdomyolysis with Gitelman syndrome and diabetes: A case report

BACKGROUND Licorice-induced severe hypokalemic rhabdomyolysis is clinically rare. Gitelman syndrome(GS) is the most common inherited renal tubular disease, while diabetes is one of the most prevalent diseases in the world. Recently, some studies have found that GS patients had higher diabetic morbidity. However, the coexistence of these three diseases has yet to be reported.CASE SUMMARY We report the case of a 62-year-old Chinese man who was admitted with weakness in the extremities, muscle pain, and dark-colored urine. He had consumed liquorice water daily for seven days prior to admission. The laboratory tests revealed a serum potassium level of 1.84 mmol/L, magnesium 0.68 mmol/L, creatinine phosphokinase(CK) 10117 IU/L, and marked hemoglobinuria. Fractional chloride excretion and fractional magnesium excretion were increased. Plasma renin activity and aldosterone concentration were within the normal ranges. Sequence analysis of the SLC12 A3 gene revealed that he had compound heterozygous mutations. The diagnosis of liquoriceinduced severe hypokalemic rhabdomyolysis with GS and diabetes was thus genetically confirmed. Serum potassium and CK quickly improved with potassium replacement therapy, hydration, and discontinuation of liquorice ingestion. Upon follow-up at 3 mo, the levels of CK, myoglobin, and potassium remained normal, and magnesium was above 0.6 mmol/L.CONCLUSION This case emphasizes that liquorice consumption and GS should be considered causes of hypokalemia and that the diabetic status of GS patients should be noted in the clinic.     

Extracorporeal Membrane Oxygenation for Hypokalemia and Refractory Ventricular Fibrillation Associated with Caffeine Intoxication

BackgroundCaffeine has been reported as a cause of cardiac arrest after massive overdose. Here, we report the case of a patient with caffeine intoxication, which can cause fatal dysrhythmias and severe hypokalemia. They were successfully treated with extracorporeal membrane oxygenation (ECMO).Case ReportA 43-year-old woman with a history of bipolar disorder presented to the emergency department after suicidal drug ingestion (caffeine and amitriptyline). Immediately after arrival, she experienced multiple episodes of ventricular fibrillation with severe hypokalemia requiring cardiopulmonary resuscitation and medical therapy. However, conventional treatment was not successful. We instituted ECMO early during resuscitation because prolonged hypokalemia refractory to aggressive potassium replacement precluded the use of antidysrhythmic medications for refractory circulatory compromise with ventricular fibrillation. The use of ECMO provided time to correct hypokalemia (19.3 g potassium) and reduce the caffeine level with hemodialysis. Although she had sustained cardiac arrest, she recovered fully and was discharged home.Why Should an Emergency Physician be Aware of This?Our case indicates the potential effectiveness of ECMO in severely poisoned patients with fatal dysrhythmias. ECMO could provide time for removal of toxic drugs and correction of electrolyte abnormalities.     

Hypokalemic Muscular Paralysis Causing Acute Respiratory Failure Due to Rhabdomyolysis with Renal Tubular Acidosis in a Chronic Glue Sniffer

Case Report: A 34-year-old male was admitted to the emergency department with the development of quadriparesis and respiratory failure due to hypokalemia after prolonged glue sniffing. The patient was subsequently given mechanical ventilatory support for respiratory failure. He was weaned from the ventilator 4 days later after potassium replacement. Toluene is an aromatic hydrocarbon found in glues, cements, and solvents. It is known to be toxic to the nervous system, hematopoietic system, and causes acid-base and electrolyte disorders. Acute respiratory failure with hypokalemia and rhabdomyolysis with acute renal failure should be considered as potential events in a protracted glue sniffing.     

Profound muscle weakness and hypokalemia due to clay ingestion

We have presented the case of a 43-year-old woman with severe myositis due to clay ingestion and hypokalemia. EMG studies revealed a pattern consistent with myositis, and muscle biopsy showed a nonspecific diffuse myositis. The clay was shown to act as a potassium binder. With potassium replacement and discontinuance of clay ingestion, the symptoms and signs abated and laboratory values returned to normal.     

The diabetic child in the emergency room

The WHO announced diabetes mellitus as one of the main threats to human health in the 21st century. In children and adolescents the prevalence of both the autoimmune type 1 and the obesity-related type 2 diabetes is increasing. Common to all types of diabetes is an absolute or relative lack of insulin to keep glucose homeostasis under control. Thus children and adolescents with newly diagnosed diabetes present with hyperglycemia which is often accompanied by ketoacidosis bearing the risk of cerebral edema. Children and adolescents with known diabetes treated with insulin or orale antidiabetic agents may also suffer from hyperglycemia or even ketoacidosis during times of non-compliance with diet and drugs or during concomitant illnesses. Hyperglycemia with ketoacidosis is an emergency situation for which patients need to be admitted to the next hospital for administration of insulin, fluids and potassium. In contrast, insulin treatment in diabetic patients may also lead to a hypoglycemia, the sudden drop in blood glucose, at any moment. Thus recognition and correction of mild hypoglycemia should be familiar to every diabetic child and their caretaker. Severe hypoglycemia with or without seizures may bring the diabetic child in a sudden emergency situation for which the administration of glucagon intramuscularly or glucose intravenously is mandatory. After every severe hypoglycemia the insulin and diet regimen of the diabetic child or adolescent must be reviewed with the diabetes specialist. For unexplained hypoglycemia or major treatment adjustments the diabetic child or adolescent may need to be readmitted to the diabetic ward of a hospital to avoid repeat, potentially life-threatening hypoglycemia.     

Diabetic ketoacidosis in a community-based population

Ninety-two cases of diabetic ketoacidosis were identified in residents of Rochester, Minnesota, over a 52-year period; 42% occurred in patients with juvenile-onset diabetes. The most common cause of diabetic ketoacidosis was infection. In 23% of the patients, diabetic ketoacidosis was the initial manifestation of diabetes mellitus. The frequency of retinopathy, neuropathy, and glomerulosclerosis was significantly increased in the surviving diabetic patients with ketoacidosis in comparison with diabetic patients matched for age and sex who did not experience ketoacidosis. Seven deaths occurred in the first 24 hours of diagnosis of ketoacidosis, but only one could be attributed to ketoacidosis alone. An additional six patients died within 48 hours of the recognition of ketoacidosis. The major cause of all deaths occurring within 48 hours of hospitalization for ketoacidosis was myocardial infarction.     

Fluid management in children with diabetic ketoacidosis

QuestionPrevious research has indicated that rapid rehydration in children with type 1 diabetes who present with diabetic ketoacidosis could result in cerebral edema. I have been treating patients with diabetic ketoacidosis with gradual fluid replacement. With the risk of cerebral injury in these patients, should I continue management with slow fluid rehydration?AnswerRecent research has shown that neither fluid infusion rate nor sodium chloride concentration increases risk of cerebral injury. However, it is possible for subtle brain injury to occur during treatment, regardless of the fluid administration strategy. The 2018 International Society for Pediatric and Adolescent Diabetes guidelines have been updated in light of this research.     

Hypokalemic paralyses: a review of the etiologies, pathophysiology, presentation, and therapy.

Acute hypokalemic paralysis is an uncommon cause of acute weakness. Morbidity and mortality associated with unrecognized disease include respiratory failure and death. Hence, it is imperative for physicians to be knowledgeable about the causes of hypokalemic paralysis, and consider them diagnostically. The hypokalemic paralyses represent a heterogeneous group of disorders with a final common pathway presenting as acute weakness and hypokalemia. Most cases are due to familial hypokalemic paralysis; however, sporadic cases are associated with diverse underlying etiologies including thyrotoxic periodic paralysis, barium poisoning, renal tubular acidosis, primary hyperaldosteronism, licorice ingestion, and gastrointestinal potassium losses. The approach to the patient with hypokalemic paralysis includes a vigorous search for the underlying etiology and potassium replacement therapy. Further therapy depends on the etiology of the hypokalemia. Disposition depends on severity of symptoms, degree of hypokalemia, and chronicity of disease.