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Electrolytes AND Hypokalemia [keywords]
- Low-Dose vs Standard-Dose Insulin in Pediatric Diabetic Ketoacidosis: A Randomized Clinical Trial. [JOURNAL ARTICLE]
- JAMA Pediatr 2014 Sep 29.
The standard recommended dose (0.1 U/kg per hour) of insulin in diabetic ketoacidosis (DKA) guidelines is not backed by strong clinical evidence. Physiologic dose-effect studies have found that even lower doses could adequately normalize ketonemia and acidosis. Lowering the insulin dose may be advantageous in the initial hours of therapy when a gradual decrease in glucose, electrolytes, and resultant osmolality is desired.To compare the efficacy and safety of low-dose insulin against the standard dose in children with DKA.This was a prospective, open-label randomized clinical trial conducted in the pediatric emergency department and intensive care unit of a tertiary care teaching hospital in northern India from November 1, 2011, through December 31, 2012. A total of 50 consecutive children 12 years or younger with a diagnosis of DKA were randomized to low-dose (n = 25) and standard-dose (n = 25) groups.Low-dose (0.05 U/kg per hour) vs standard-dose (0.1 U/kg per hour) insulin infusion.The primary outcome was the rate of decrease in blood glucose until a level of 250 mg/dL or less is reached (to convert to millimoles per liter, multiply by 0.0555). The secondary outcomes included time to resolution of acidosis, episodes of treatment failures, and incidences of hypokalemia and hypoglycemia.The mean (SD) rate of blood glucose decrease until a level of 250 mg/dL or less is reached (45.1 [17.6] vs 52.2 [23.4] mg/dL/h) and the mean (SD) time taken to achieve this target (6.0 [3.3] vs 6.2 [2.2] hours) were similar in the low- and standard-dose groups, respectively. Mean (SD) length of time to achieve resolution of acidosis (low vs standard dose: 16.5 [7.2] vs 17.2 [7.7] hours; P = .73) and rate of resolution of acidosis were also similar in the groups. Hypokalemia was seen in 12 children (48%) receiving the standard dose vs 5 (20%) of those receiving the low dose (P = .07); the tendency was more pronounced in malnourished children (7 [88%] vs 2 [28%]). Five children (20%) and 1 child (4%) receiving standard- and low-dose infusion (P = .17), respectively, developed hypoglycemia. Treatment failure was rare and comparable. One child in the standard-dose group developed cerebral edema, and no deaths occurred during the study period.Low dose is noninferior to standard dose with respect to rate of blood glucose decrease and resolution of acidosis. We advocate a superiority trial with a larger sample size before 0.05 U/kg per hour replaces 0.1 U/kg per hour in the practice recommendations.ctri.nic.in Identifier: CTRI/2012/04/002548.
- Severe hypokalemia and hypophosphatemia presenting with carpopedal spasm associated with rhabdomyolysis. [Journal Article]
- Acta Biomed 2014; 85(2):167-70.
Background Severe hypokalemia, defined as serum potassium < 2.5 mEq/L, may lead to neuromuscular, gastrointestinal, and ECG abnormalities. Neuromuscular consequences of hypokalemia include weakness, cramps, rarely paralysis, eventually progressing to rhabdomyolysis. Case presentation We report a case of a 4-year-old girl presenting carpopedal spasm and rhabdomyolysis due to severe hypokalemia associated to hypophosphatemia and hypovolemia. At one month of age she underwent an ileal resection because of a neonatal necrotizing enterocolitis, and a bowel resection at two years of age, because of sub-occlusive episodes. The child had frequent episodes of diarrhoea and was treated with oral white clay (kaolin) and a restrictive diet. Three days prior the admission to the hospital she had numerous episodes of watery diarrhoea. Laboratory tests revealed severe hypokalemia, hypophosphatemia, normal calcium levels associated with marked dehydration. An ECG demonstrated sinus bradycardia, ST-segment depression, T-wave flattening, U-wave, and long-QTc. Symmetric carpal and pedal spasms were observed. A marked rise of creatinine phosphokinase and myoglobin associated to cola colored urine was observed. Intravenous supplementation of potassium phosphate as well as adequate volume repletion led to an improvement of the clinical condition, to the disappearance of carpal and pedal spasms, to normalisation of ECG. Conclusions Careful electrolytes and volume supplementation led to the correction of potential life-threatening arrhythmias and obtained a complete recovery from carpopedal spasm and rhabdomyolysis. Dietary restriction and pharmacological preparations as kaolin have to be administered with caution to treat diarrhea in children and particularly in those who may present other pre-existing risk factors.
- "Fixing a heart": the game of electrolytes in anorexia nervosa. [JOURNAL ARTICLE]
- Nutr J 2014 Sep 5; 13(1):90.
Case: A 25-year-old woman with chronic anorexia nervosa and depression presented with sudden weakness and fatigue. Psychosocial history was notable for binge-starve cycles over the past year and a decline in overall well-being. Vitals on presentation were notable for hypothermia, hypotension, and bradycardia. Initial exam was significant for emaciation, lethargy, and lower extremity edema. Laboratory work-up revealed markedly elevated LFTs, hypoglycemia, thrombocytopenia and elevated INR and lipase. ECG showed sinus bradycardia with prolonged QTc. Ultrasound revealed normal liver and biliary tree. Serum acetaminophen, alcohol level, and urinary toxicology were unremarkable. Work up for infectious, autoimmune, and genetic causes of hepatitis was negative. Echocardiogram revealed left ventricular hypokinesis and EF 10-15%. Nutritional support was begun slowly, however electrolyte derangements began to manifest on hospital day 2, with hypophosphatemia, hypokalemia, hypocalcemia, and hypomagnesemia. Multiple medical and psychiatric disciplines were consulted, and aggressive electrolyte monitoring and repletion were done. The patient's overall clinical status improved slowly during her hospital course. Her liver enzymes trended down, and her QTc interval eventually returned toward the normal range. Repeat echocardiogram following treatment revealed improvement of her EF to 40%.Anorexia nervosa is an eating disorder characterized by extremely low body weight, fear of gaining weight or distorted perception of body image, and amenorrhea. Anorexia can lead to life threatening medical complications, and thus constitutes a major challenge to manage. Central to the pathogenesis of the refeeding syndrome is a weakened cardiopulmonary system, electrolytes abnormalities, hepatic dysfunction, liver hypoperfusion and failure.Given the clinical presentation, this patient likely presented on the brink of developing frank refeeding syndrome, with cardiac dysfunction and hypovolemia, leading to hepatic hypoperfusion and ischemic hepatitis. Subsequently, she developed electrolyte disturbances characteristic of refeeding syndrome, which were managed without major complication. Her hospital course is encouraging not only for her recovery, but for the collaboration of the different teams involved in her care, and it highlights the importance of a multidisciplinary approach to caring for patients with the potential dire complications of a complex psychiatric illness.
- Correction of hyponatremia and osmotic demyelinating syndrome: have we neglected to think intracellularly? [JOURNAL ARTICLE]
- Clin Exp Nephrol 2014 Aug 24.
Osmotic demyelination syndrome (ODS) is a complication generally associated with overly rapid correction of hyponatremia. Traditionally, nephrologists have been trained to focus solely on limiting the correction rate. However, there is accumulating evidence to suggest that the prevention of ODS is beyond achieving slow correction rates.We (1) reviewed the literature for glial intracellular protective alterations during hyperosmolar stress, a state presumed equivalent to the rapid correction of hyponatremia, and (2) analyzed all available hyponatremia-associated ODS cases from PubMed for possible contributing factors including correction rates and concurrent metabolic disturbances involving hypokalemia, hypophosphatemia, hypomagnesemia, and/or hypoglycemia.In response to acute hyperosmolar stress, glial cells undergo immediate extracellular free water shift, followed by active intracellular Na(+), K(+) and amino acid uptake, and eventual idiogenic osmoles synthesis. At minimum, protective mechanisms require K(+), Mg(2+), phosphate, amino acids, and glucose. There were 158 cases of hyponatremia-associated ODS where both correction rates and other metabolic factors were documented. Compared with the rapid correction group (>0.5 mmol/L/h), the slow correction group (≤0.5 mmol/L/h) had a greater number of cases with concurrent hypokalemia (49.4 vs. 33.3 %, p = 0.04), and a greater number of cases with any concurrent metabolic derangements (55.8 vs. 38.3 %, p = 0.03).Glial cell minimizes volume changes and injury in response to hyperosmolar stress via mobilization and/or utilization of various electrolytes and metabolic factors. The prevention of ODS likely requires both minimization of correction rate and optimization of intracellular response during the correction phase when a sufficient supply of various factors is necessary.
- Fanconi syndrome and severe polyuria: an uncommon clinicobiological presentation of a Gitelman syndrome. [JOURNAL ARTICLE]
- BMC Pediatr 2014 Aug 11; 14(1):201.
Gitelman syndrome is an autosomal recessive tubulopathy characterized by hypokalemia, hypomagnesemia, metabolic alkalosis and hypocalciuria. The majority of patients do not present with symptoms until late childhood or adulthood, and the symptoms are generally mild. We report here the first case of Gitelman syndrome presenting with the biological features of Fanconi syndrome and an early polyuria since the neonatal period. We discuss in this article the atypical electrolytes losses found in our patient, as well as the possible mechanisms of severe polyuria.A 6-year-old Caucasian girl was admitted via the Emergency department for vomiting, and initial laboratory investigations found hyponatremia, hypokalemia, metabolic acidosis with normal anion gap, hypophosphatemia, and hypouricemia. Urinalysis revealed Na, K, Ph and uric acid losses. Thus, the initial biological profile was in favor of a proximal tubular defect. However, etiological investigations were inconclusive and the patient was discharged with potassium chloride and phosphorus supplementation. Three weeks later, further laboratory analysis indicated persistent hypokalemia, a metabolic alkalosis, hypomagnesemia, and hypocalciuria. We therefore sequenced the SLC12A3 gene and found a compound heterozygosity for 2 known missense mutations.Gitelman syndrome can have varying and sometimes atypical presentations, and should be suspected in case of hypokalemic tubular disorders that do not belong to any obvious syndromic entity. In this case, the proximal tubular dysfunction could be secondary to the severe hypokalemia. This report emphasizes the need for clinicians to repeat laboratory tests in undiagnosed tubular disorders, especially not during decompensation episodes.
- Hypokalemia in acute medical patients: risk factors and prognosis. [JOURNAL ARTICLE]
- Am J Med 2014 Aug 5.
Hypokalemia is one of the most common electrolyte disorders in hospitalized patients. It is associated with a high mortality rate among patients with cardiovascular disease. Whether hypokalemia confers a similar risk in an unselected hospitalized population is not well established.We conducted a prospective cohort study involving all first time admissions (n=11988) to the Acute Medical Department at Odense University Hospital linking potassium level at admission with registry data on patient characteristics, laboratory data, redeemed prescriptions and time of death for the period from August 2009 to August 2011. We estimated hazard ratios for all cause mortality within 0-7 days and 8-30 days after admission, comparing patients with hypokalemia at admission (plasma [K(+)] level < 3.4 mmol/L) with patients with eukalemia at admission ([K(+)] level of 3.4-3.8 mmol/l).Hypokalemia occurred in 16.8% of first time admissions (n=2011). It was associated with an adjusted hazard ratio [HR] of 1.34 (95% confidence interval [CI], 0.98-1.85) for 7-day mortality and 1.56 (CI, 1.18-3.06) for 8-30 day mortality. Among patients with more severe hypokalemia (plasma [K(+)]<2.9 mmol/l) the adjusted HR was 2.17 (CI, 1.34-3.49) for 7-day mortality and 1.90 (CI,1.18-3.06) for 8-30 day mortality. Prognostic factors for both 7-day and 8-30 day mortality among hypokalemic patients were increasing age and Charlson comobidity index whereas there was no prognostic effect of current diuretic or betagonist use.In a mixed population of hospitalized medical patients, hypokalemia is common and plasma [K(+)]<2.9 mmol/l is associated with increased 7-day and 8-30 day mortality.
- A rare case of watery diarrhea, hypokalemia and achlorhydria syndrome caused by pheochromocytoma. [JOURNAL ARTICLE]
- BMC Cancer 2014 Jul 31; 14(1):553.
A rare syndrome of watery diarrhea, hypokalemia and achlorhydria (WDHA) is usually caused by pancreatic endocrine tumors that secrete excessive vasoactive intestinal polypeptide (VIP). Here we report a rare case of WDHA caused by a pheochromocytoma.A 45-year old male presented with persistent and progressive watery diarrhea for half a year, and was treated with dialysis due to azotemia, hypokalemia, hypercalcemia and metabolic acidosis. A right adrenal mass was found by ultrasonography, and Positron Emission Tomography-Computed Tomography (PET-CT) showed the tumor was hyper-metabolic. Levels of plasma normetanephrine (NMN) and serum chromogranin A (CgA) were significantly elevated. Immunohistochemistry analysis of the adrenal tumor was strongly positive for CgA, synaptophysin and VIP. The patient fully recovered from WDHA syndrome soon after surgery, as reflected in that diarrhea stopped, levels of plasma NMN, serum CgA, and electrolytes returned to normal thus no dialysis was needed. The patient remained disease free in a 12-months follow-up period.We report an extremely rare case of pheochromocytoma causing WDHA syndrome and uremia, which the patient completely recovered from after tumor resection.
- Fluid Therapy in Mature Cattle. [REVIEW]
- Vet Clin North Am Food Anim Pract 2014 Jul; 30(2):429-439.
Fluid therapy for mature cattle differs from that for calves because the common conditions that result in dehydration and the metabolic derangements that accompany these conditions are different. The veterinarian needs to know which problem exists, what to administer to correct the problem, in what quantity, by what route, and at what rate. Mature cattle more frequently suffer from alkalosis; therefore, acidifying solutions containing K(+) and Cl(-) in concentrations greater than that of plasma are frequently indicated. The rumen provides a large-capacity reservoir into which oral rehydration solutions may be administered, which can save time and money.
- Hypokalemia Syndrome in Cattle. [REVIEW]
- Vet Clin North Am Food Anim Pract 2014 Jul; 30(2):351-357.
This article describes hypokalemia syndrome. Lactating dairy cows seem to be at the highest risk, but younger animals may also develop the disease. At present, except for animals treated with repeated isoflupredone acetate administration, the exact determinants causing hypokalemia syndrome remain uncertain. Affected animals are anorexic, weak to recumbent, and most often show signs of gastrointestinal stasis. Treatment is directed toward supportive care and oral potassium supplementation.
- Intentional insulin overdose associated with minimal hypoglycemic symptoms in a non-diabetic patient. [Journal Article]
- Maedica (Buchar) 2013 Sep; 8(4):365-9.
Non-accidental suicidal insulin overdose is a rare presentation among non-diabetic patients. It seems to be more common among working medical professionals.Objectives: To present the case of a young patient, who despite injecting a large dose of rapid-acting insulin presented with only mild symptoms, and to familiarize the medical professionals involved in managing this condition with the recognition, pathophysiology and appropriate therapeutic interventions.Materials and methods: We report the case of a previously healthy non-diabetic young medical professional who presented with a rapid-acting insulin overdose. On initial assessment the patient was alert and oriented, and glucose measurement was 1.4 mmol/L. The oral glucose gel and intramuscular glucagon failed to raise the glucose. Hypokalaemia, hypomagnesaemia, hypophosphataemia, lactic acidosis and ECG changes completed the presentation.Outcomes: The treatment consisted of dextrose infusion and appropriate electrolytes replacement. An uneventful recovery was made, so 36 hours later the patient was discharged with psychiatric follow-up.Conclusions: Insulin overdose should be considered as a differential diagnosis in hypoglycaemic patients when blood glucose fails to correct as expected. Improper management carries a significant risk of hypoglycaemic encephalopathy, which can cause lifelong cerebral changes.