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Electrolytes AND Hypokalemia [keywords]
- 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.
- Abiraterone Acetate to Lower Androgens in Women With Classic 21-Hydroxylase Deficiency. [JOURNAL ARTICLE]
- J Clin Endocrinol Metab 2014 Apr 29.:jc20141258.
Context: Chronic supraphysiologic glucocorticoid therapy controls the androgen excess of 21-hydroxylase deficiency (21OHD) but contributes to the high prevalence of obesity, glucose intolerance, and reduced bone mass in these patients. Abiraterone acetate (AA) is a prodrug for abiraterone, a potent CYP17A1 inhibitor used to suppress androgens in the treatment of prostate cancer. Objective: To test the hypothesis that AA added to physiologic hydrocortisone and 9α-fludrocortisone acetate corrects androgen excess in women with 21OHD without causing hypertension or hypokalemia. Design: Phase 1 dose-escalation study. Setting: University Clinical Research Centers. Participants: We screened 14 women with classic 21OHD taking hydrocortisone 12.5-20 mg/d to enroll six participants with serum androstenedione > 345 ng/dl (> 12 nmol/liter). Intervention: AA was administered for 6 days at 100 or 250 mg every morning with 20 mg/d hydrocortisone and 9α-fludrocortisone acetate. Main Outcome Measure: Normalization of mean predose androstenedione on days 6 and 7 (< 230 ng/dl [< 8 nmol/liter]) in > 80% of participants. Secondary endpoints included serum 17-hydroxyprogesterone and testosterone, electrolytes, plasma renin activity, and urine androsterone and etiocholanolone glucuronides. Results: With 100 mg/d AA, mean predose androstenedione fell from 764 to 254 ng/dl (26.7 to 8.9 nmol/liter). At 250 mg/d AA, mean androstenedione normalized in five participants (83%) and decreased from 664 to 126 ng/dl (23.2 to 4.4 nmol/liter), meeting the primary endpoint. Mean androstenedione declined further during day 6 to 66 and 38 ng/dl (2.3 and 1.3 nmol/liter) at 100 and 250 mg/d, respectively. Serum testosterone and urinary metabolites declined similarly. Abiraterone exposure was strongly negatively correlated with mean androstenedione. Hypertension and hypokalemia were not observed. Conclusion: AA 100-250 mg/d added to replacement hydrocortisone normalized several measures of androgen excess in women with classic 21OHD and elevated serum androstenedione.
- Central pontine myelinolysis: electrolytes and beyond. [Journal Article]
- BMJ Case Rep 2014.
Central pontine myelinolysis (CPM), which is a component of the osmotic demyelination syndrome (ODS), is a frequent neurological complication that follows rapid correction of hyponatraemia. However, there are other predisposing risk factors (chronic alcoholism, hypokalaemia) that perpetuate the development of ODS. We report a case of a 39-year-old woman with a history of chronic alcoholism who presented to us with progressive neurological deficits (paraparesis, paresthesias). She was initially detected to have coexisting hypokalaemia which was eventually rectified with potassium supplementation. However, she continued to experience progressive worsening of her neurological symptoms despite adequate potassium supplementation. Therefore, a neurological opinion was sought for and she was diagnosed with CPM based on a background of chronic alcoholism and malnutrition; an MRI of the brain showed a hyperintense signal in the central pontine region. Following the diagnosis of CPM, she was rehabilitated with occupational and physiotherapy.
- Brugada phenocopy: A new electrocardiogram phenomenon. [Journal Article]
- World J Cardiol 2014 Mar 26; 6(3):81-6.
Brugada phenocopies (BrP) are clinical entities that are etiologically distinct from true congenital Brugada syndrome. BrP are characterized by type 1 or type 2 Brugada electrocardiogram (ECG) patterns in precordial leads V1-V3. However, BrP are elicited by various underlying clinical conditions such as myocardial ischemia, pulmonary embolism, electrolyte abnormalities, or poor ECG filters. Upon resolution of the inciting underlying pathological condition, the BrP ECG subsequently normalizes. To date, reports have documented BrP in the context of singular clinical events. More recently, recurrent BrP has been demonstrated in the context of recurrent hypokalemia. This demonstrates clinical reproducibility, thereby advancing the concept of this new ECG phenomenon. The key to further understanding the pathophysiological mechanisms behind BrP requires experimental model validation in which these phenomena are reproduced under strictly controlled environmental conditions. The development of these validation models will help us determine whether BrP are transient alterations of sodium channels that are not reproducible with a sodium channel provocative test or alternatively, a malfunction of other ion channels. In this editorial, we discuss the conceptual emergence of BrP as a new ECG phenomenon, review the progress made to date and identify opportunities for further investigation. In addition, we also encourage investigators that are currently reporting on these cases to use the term BrP in order to facilitate literature searches and to help establish this emerging concept.