Association between hypokalemia and small bowel capsule endoscopy completion rates in patients in South China: A prospective single-center study.

BACKGROUND/AIMS: Approximately 20-30% of small bowel capsule endoscopies (SBCEs) do not reach the cecum at the completion of the examination. We aimed to determine whether hypokalemia influences the completion rate and small bowel transit time (SBTT) of SBCE. PATIENTS AND METHODS: From January to December 2017, 112 patients (18-75 years old) who underwent SBCE were assessed consecutively for enrolment in our study. On the day of the procedure, a blood test was performed prior to capsule ingestion. The completion rate, gastric transit time (GTT), SBTT, and diagnostic yield were recorded for each SBCE. RESULTS: The SBCE completion rate was lower in the hypokalemia group than that in the normal potassium group (55.6% (15/27) vs. 76.5% (65/85), P = 0.036). The median GTT was 55.5 ± 47.1 min in the hypokalemia group and 46.7 ± 44.5 min in the normal potassium group (P > 0.05). The median SBTT was 412.8 ± 123.3 min in the hypokalemia group and 367.3 ± 172.5 min in the normal potassium group (P > 0.05). The diagnostic yields of the hypokalemia and normal potassium groups were 74.1% and 78.8%, respectively (P = 1.00). CONCLUSION: Hypokalemia may decrease the SBCE completion rate. Physicians should consider the possibility of hypokalemia after bowel preparation because this condition is not rare. Potassium deficiencies should be rectified prior to performing SBCE procedures to increase the SBCE completion rate.

A paper which changed clinical practice (slowly). Jacob Holler on potassium deficiency in diabetic acidosis (1946).

It is often said that the introduction of insulin into clinical medicine made a 'dramatic' difference to the mortality resulting from diabetic coma. This is true in the sense that before 1922 it was almost uniformly fatal, but until the 1950s the mortality in many large hospitals was as high as 30-50%. Often autopsy did not establish a cause of death. Many may have been a result of hypokalaemia, a complication which was not recognized until 1946; in that year in the Journal of the American Medical Association, Jacob Holler described a patient who developed respiratory paralysis 12h into treatment that, after several hours in an iron lung, was cured by potassium infusion. In the 5 years after Holler's paper there were many reports of deaths resulting from hypokalaemia, as well as several 'near misses', but clinicians were extremely cautious about early replacement probably, as an editorialist in The Lancet suggested, because 'the frightening effects of intravenous injections of potassium made clinicians reluctant to believe in a lack of potassium as a cause of trouble, except in very rare conditions such as familial periodic paralysis'. It had been known since 1923 that insulin lowered serum potassium, but this was not of great interest because the symptoms of hypokalaemia were not known. Also, potassium was not an electrolyte with which clinicians were familiar. Until the introduction of flame photometry in 1950, it was only measured in research studies as chemical methods took several hours to complete.

Nefropatía tubular por carencia prolongada de potasio / Tubular nephropathy from chronic potassium deficiency

Fueron estudiados 2 casos con desnutrición crónica avanzada e hipokalemia acentuada en los cuales se encontraron disminución de la filtración glomerular y del flujo renal plasmático, presencia de poliuria con hiposmolaridad sérica e hipotonía urinaria, las cuales no se modificaron durante la administración de hormona antidiurética. Uno de dichos casos tuvo una evolución fatal, a pesar de la administración de suplemento de potasio por vía oral, y el estudio histopatológico de sus riñones demostró la conservación de los glomérulos y la presencia de degeneración vacuolar hidrópica en el epitelio de los túbulos proximales. El otro caso evolucionó favorablemente hacia la recuperación y un nuevo estudio practicado al mes de su ingreso demostró la normalización de sus alteraciones fisiopatológicas. Tanto las alteraciones anatómicas, como las funcionales se han descrito en diversas condiciones patológicas que tienen en común la pérdida crónica de potasio por diferentes vías. Se ha observado la reversibilidad de estas lesiones pero igualmente existe la posibilidad de una falta de respuesta a la administración de potasio y la evolución hacia la insuficiencia renal y a la muerte. El curso del trastorno puede estar condicionado por la intensidad y la duración de la depleción de potasio. Los estudios experimentales en que se ha impedido la aparición de estas lesiones en ratas deplecionadas de potasio que recibían rubidio y cesio, así como la desaparición de las lesiones ya presentadas con la administración de estos elementos, han sugerido que no sea propiamente la deficiencia de potasio la responsable directa de esta neforpatía, sino

Magnesium and potassium deficiency. Its diagnosis, occurrence and treatment in diuretic therapy and its consequences for growth, protein synthesis and growth factors.

Thiazides and loop diuretics facilitate the loss of K and Mg through the kidneys leading to deficiencies that may require treatment with supplements. These losses may be overlooked, however, because serum concentrations may remain normal even when the muscle concentrations are appreciably reduced. In 76 patients who had received diuretics for 1-17 years, the mean concentrations of K, Mg and Na,K-pumps in skeletal muscle biopsies were significantly lower than in those from an age- and sexmatched control group, and muscle Mg and K concentrations were significantly correlated. The serum concentrations, however, were only below the control range in a few patients. The fact that Mg,K deficiencies may often be overlooked emphasises the need for data on the contents of skeletal muscle. A recently developed simple biopsy needle procedure permitted the detection of disorders of electrolytes during long-term diuretic treatment despite normal serum concentrations. With the same technique it was possible to detect repletion of the muscle electrolytes after a Mg supplementation period. Oral Mg supplementation could reestablish normal Mg as well as K status in patients in long-term diuretic therapy, provided that the supplementation was maintained for 6 months. Moreover, the normalization of muscle Mg and K was accompanied by a restoration of the concentration of Na,K-pumps measured as the [3H]ouabain binding site capacity in skeletal muscle. Mg and K contents were closely correlated in human muscle biopsies from patients on diuretic treatment, but also in rat muscle which had been moderately Mg depleted in vivo or in vitro. In isolated soleus muscle, which had been moderately Mg-depleted in vitro, reduction in cellular K could not be ascribed to reduced Na,K-pump mediated K-influx. The reduced K content might rather be related to increased K efflux from the muscles. In rats, insufficient dietary supplies of K, Mg and Zn were characterized by inhibition of growth and protein synthesis. These effects could not readily be related to the loss of these elements from muscle tissue, but rather should be seen as a response to a general deficiency. The most marked evidence of deficiency was seen in the serum levels, which pointed to the serum concentration as a possible mediator for the regulation of tissue growth. IGF-I is a low molecular weight peptide possessing growth promoting properties in many tissues probably as an interplay of both autocrine/paracrine and endocrine actions. In both animals and man insufficient supplies of energy and protein are accompanied by growth retardation and a decrease in serum IGF-I.(ABSTRACT TRUNCATED AT 400 WORDS)

[Rapid intravenous rehydration in acute diarrhea]. / Rehidratación endovenosa rápida en diarrea aguda.

With the use of oral rehydration, the need for the use of endovenous rehydration has decreased considerably. Albeit, the use is still necessary in severely dehydrated patients or when oral rehydration fails. Textbooks produced in developed countries recommend slow administration of fluids to correct dehydration in 12 to 24 hours. In developing countries, due to the great number of severely dehydrated patients, this approach is not useful. We developed, during the last 20 years, an approach to intravenous rehydration that permits rehydration of the severely ill patient in a much shorter time (2 to 3 hours) and permits an early refeeding. It can be used in all patients, even newborns or malnourished. No laboratory tests are necessary. Only a small number of simple and readily available solutions are used to prepare the electrolyte mixtures.

PIP: This work argues that rapid intravenous rehydration is desirable in cases of acute diarrhea. It provides detailed instructions for preparing and administering the correct solutions and for recognizing patients who are hyponatremia or suffering from acute acidosis. With widespread use of oral rehydration therapy, i.v. rehydration is limited to patients with acute dehydration or contraindications to oral rehydration. For purposes of prognosis, dehydration is usually classified according to the concentration of serum sodium or the degree of fluid loss. The objectives of i.v., rehydration are to eliminate the deficits of water and electrolytes, replace losses so that the patient will not become dehydrated again, and permit early feeding. The water deficit is variable and may amount to 100-150 ml/kg in the severely dehydrated. The sodium deficit is 9-17 mmol/kg and the potassium deficit is 3-15 mmol/kg. Early feeding after no more than 8 hours of fasting is currently considered more effective in preventing malnutrition in children with diarrhea and dehydration. Since the presence of deficits prevents feeding, the initial period of dehydration should not be prolonged beyond 4 hours. In developed countries, i.v. rehydration takes place over 12-24 hours with periods of fasting of 24-48 hours, but the mortality associated with this method of treatment in dehydrated children with diarrhea is higher. To meet its objectives, i.v., rehydration should take place in 3 phases, a rapid initial phase followed by simultaneously occurring phases of maintenance and of replacement in which normal and abnormal losses are replaced. The initial rapid phase should restore the normal perfusion of vital organs by eliminating deficits of sodium and water in no more than 2 hours. All sings of dehydration should disappear. The weight of the child before dehydration and thus the weight loss is seldom known, but experience with the method allows adequate approximations to be made. The solution used in almost all patients is a mixture of physiological solution of NaCl .9% and 5% dextrose solution (PS:DS5% 1:1). The only exceptions are patients with very low sodium levels or severe acidosis, who can be recognized by the experienced practitioner based on their characteristic clinical symptoms. The final concentration of sodium in the solution is .45% of NaCl and that of dextrose 2.5%. The patient is always reevaluated after 1 hour of treatment to detect possible complications. Treatment of hyponatremia and acidosis requires adjusting levels in the 1st hour of treatment with special formulas so that the standard formula may be administered. Instructions are provided for calculating the quantity and content of fluids for the maintenance and replacement stages, which are customarily administered in segments of 6-8 hours.

[Progressive complications associated with the use of a bovine heterograft for vascular access]. / Complications évolutives associées à l'utilisation d'une hétérogreffe bovine comme abord vasculaire.

Three bovine carotid heterografts, used for vascular access, were analysed after removal following the development of aneurysms in two cases and thrombosis in one. The first prosthesis was implanted in a 17-year-old man who suffered from myasthenia gravis and was undergoing plasmapheresis. It became notably dilated several months after implantation, and resection was necessary 14 months after insertion. The second graft was placed in a 31-year-old woman being treated for a severe chronic potassium insufficiency. It was removed 16 months after insertion because of thrombosis. The third bovine carotid heterograft was inserted in a 48-year-old patient on long-term hemodialysis and was removed 3.5 months later because of aneurysmal dilatation adjacent to the arterial anastomosis. These evolutionary and degenerative changes associated with the bovine carotid heterograft illustrate the limitations of this material as an interpositional limb for arteriovenous fistulas in angioaccess therapy. Small weaknesses have sometimes been noted in the microstructure of the graft material studied before implantation.

Total body potassium depletion and the need for preoperative nutritional support in Chrohn's disease.

Significant intracellular potassium depletion was documented in 57 patients with Crohn's disease by measurements of total body potassium, body water compartments, and red cell Na,K-ATPase units. Total body potassium deficits paralleled the activity of illness, but were not correlated to serum potassium levels. Treatment before surgery to improve individual body potassium content resulted in a reduced surgical mortality and complication rate compared with a retrospective series of 56 patients in whom pretreatment had simply been aimed at normalizing serum albumin and other standard serum parameters. In conclusion, preoperative nutritional support in Crohn's disease is recommended for patients with a total body potassium level less than 70% of normal. If whole body counting for direct measurement of total body potassium is not available, a Crohn's Disease Activity Index above 225 is proposed as the deciding level, and the parenteral administration of a standardized regimen consisting of 150 to 200 mval potassium plus 2500 to 3000 kcal daily for a two-week period is recommended.