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      HIPERKALEMIA Y BRADICARDIA EN UN RECIEN NACIDO PREMATURO PEQUEÑO PARA LA EDAD GESTACIONAL Y DE MUY BAJO PESO

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          Abstract

          El potasio es el principal catión intracelular. La homeostasis del potasio es imprescindible en el balance hidroelectrolítico. La homeostasis del potasio esta regulada por factores renales y no renales (hormonas, estado ácido base, osmolaridad de los líquidos extracelulares y agentes farmacológicos). El estado ácido base tiene particular importancia en los prematuros, en ellos, la acidosis metabólica, acidosis respiratoria o mixta, son fenómenos comunes. El principal regulador del potasio es el riñón. El potasio tiene dos funciones importantes dentro del organismo: rol en el metabolismo celular y principal determinante del potencial de reposo de membrana plasmática. Como consecuencia, las alteraciones de la homeostasis del potasio afectan a los procesos bioeléctricos del organismo, al despolarizar las células excitables, entre ellos: la contracción muscular, conducción nerviosa y marcación eléctrica del ritmo del miocardio. En la presentación de este caso clínico, se describe el caso de un recién nacido de bajo peso para la edad gestacional y de muy bajo peso al nacimiento, este desarrolla bradicardia severa y apnea, todo esto secundario a un proceso de hiperkalemia.

          Translated abstract

          The potassium is the main intracellular catión. The homeostasis of potassium is essential in the hidroelectrolític balance. The homeostasis of potassium this regulated by renal and nonrenal factors (hormones, acid state base, osmolaridad of the extracellular liquid and pharmacological agents). The acid state base has individual importance in the premature ones, in them, the metabolic acidosis. respiratory acidosis or mixed, are common phenomena. The main regulator of potassium is the kidney. The potassium has two important functions within the organism: roll in the cellular metabolism and main determinant of the potential of plasmátic membrane rest. Like consequence, the alterations of the homeostasis of potassium affect the bioeléctric processes of the organism, when depolarizing the excitable cells, among them: the muscular contraction, nervous conduction and electrical bearing of the rate of the myocardium. In the presentation of this clinical case, case of new born of low weight for the gestacional age is described and of very low weight to the birth, this it develops bradicardia severe and apnea, all this secondary one to a process of hiperkalemia.

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          Decreased erythrocyte Na+,K(+)-ATPase activity associated with cellular potassium loss in extremely low birth weight infants with nonoliguric hyperkalemia.

          To determine whether a shift of potassium ions from the intracellular space to the extracellular space accounts, in part, for the hyperkalemia seen in extremely low birth weight infants, we examined potassium concentration in serum and erythrocytes from extremely low birth weight infants with hyperkalemia (n = 12) or with normokalemia (n = 27). In addition, to determine whether the shift of potassium was associated with low sodium-potassium-adenosinetriphosphatase (Na+,K(+)-ATPase) activity, we studied the activity of ATPase in the last 16 infants enrolled in the study. Fluid intake and output were measured during the first 3 days of life. Infants were considered to have hyperkalemia if the serum potassium concentration was 6.8 mmol/L or greater. Blood was obtained daily for intracellular sodium and potassium levels by means of lysis of erythrocytes. The remaining erythrocyte membranes were frozen and analyzed for Na+,K(+)-ATPase activity. There were significantly lower intracellular potassium/serum potassium ratios in the infants with hyperkalemia for each day of the 3-day study (p < 0.001). In the hyperkalemic group, there was lower Na+,K(+)-ATPase activity than in the infants with normokalemia (p = 0.006). Low Na+,K(+)-ATPase activity was associated with lower intracellular potassium/serum potassium ratios (p = 0.006), higher serum potassium values (p = 0.02), and lower intracellular potassium concentration (p = 0.009). The urinary data demonstrated that there was no difference in glomerulotubular balance between the two groups. We conclude that nonoliguric hyperkalemia in extremely low birth weight infants may be due, in part, to a shift of potassium from the intracellular space to the extracellular space associated with a decrease in Na+,K(+)-ATPase activity.
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            Nonoliguric hyperkalemia in the premature infant weighing less than 1000 grams.

            Eighteen very low birth weight premature infants born before 28 weeks gestation and weighing less than 1000 gm were evaluated prospectively for disturbances in serum electrolyte concentrations and for renal glomerular and tubular functions. Clinically symptomatic hyperkalemia resulting in significant electrocardiographic dysrhythmias developed in eight of these infants; 10 babies remained normokalemic. Peak serum potassium concentration ranged from 6.9 to 9.2 mEq/L in the hyperkalemic group; all potassium values in the normokalemic group were less than 6.6 mEq/L. Indices of renal glomerular function and urine output were similar in both groups; no infant had oliguria. Serum creatinine concentrations were the same in both groups (1.04 +/- 0.16 SD mg/dl in normokalemic vs 1.19 +/- 0.24 mg/dl in hyperkalemic infants, beta less than 0.2 at alpha = 0.05), and glomerular filtration rates did not differ significantly (6.29 +/- 1.78 ml/min/1.73 m2 in normokalemic vs 5.70 +/- 1.94 ml/min/1.73 m2 in hyperkalemic infants, beta less than 0.2 at alpha = 0.05). In contrast, indicators of tubular function revealed a significantly larger fractional excretion of sodium in hyperkalemic infants: 13.9 +/- 5.4% versus 5.6 +/- 0.9% in normokalemic control subjects (p less than 0.001). Hyperkalemic infants also had a tendency toward lower urine concentrations of potassium, although there was no significant difference in their net potassium excretion in comparison with that in the normokalemic group. We speculate that hyperkalemia in the tiny baby is in part the result of immature distal tubule function with a compromise in ability to regulate potassium balance.
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              Manual de Neonatología

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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Journal
                gmb
                Gaceta Médica Boliviana
                Gac Med Bol
                Facultad de Medicina de la Universidad Mayor de San Simón (Cochabamba, , Bolivia )
                1012-2966
                2005
                : 28
                : 2
                : 67-71
                Affiliations
                [01] orgnameHospital Materno Infantil ‘Germán Urquidi' orgdiv1Servicio de Neonatología
                [02] orgnameHospital Materno Infantil ‘Germán Urquidi’ orgdiv1Pediatría
                Article
                S1012-29662005000200012
                9fbd141b-8988-461a-9ec8-7dd77fedb099

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

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                Figures: 0, Tables: 0, Equations: 0, References: 9, Pages: 5
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                SciELO Bolivia


                hiperkalemia,bradicardia,recien nacido prematuro,premature new born

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