Water, electrolyte, acid-base, and trace elements alterations in cirrhotic patients.

Chronic hepatic patients, and particularly those suffering from cirrhosis, are predisposed to different sort of water, electrolyte, acid-base, and trace elements disorders due to their altered liver function, and also to their exposition to infectious, inflammatory, oncologic, and pharmacologic variables whose combination undermines their homeostatic capability. Hyponatremia, hypokalemia, hyperkalemia, hypocalcemia, metabolic acidosis, respiratory, and metabolic alkalosis are the main internal milieu alterations in this group.

Involvement of sinoaortic afferents in renal sympathoinhibition and vasodilation induced by acute hypernatremia.

Despite the abundance of evidence that supports the important role of aortic and carotid afferents to short-term regulation of blood pressure and detection of variation in the arterial PO2 , PCO2 and pH, relatively little is known regarding the role of these afferents during changes in the volume and composition of extracellular compartments. The present study sought to determine the involvement of these afferents in the renal vasodilation and sympathoinhibition induced by hypertonic saline (HS) infusion. Sinoaortic-denervated and sham male Wistar rats were anaesthetised with intravenous (i.v.) urethane (1.2 g/kg body weight (bw)) prior to the measurement of the mean arterial pressure (MAP), renal vascular conductance (RVC) and renal sympathetic nerve activity (RSNA). In the sham group, the HS infusion (3 mol/L NaCl, 1.8 mL/kg bw, i.v.) induced transient hypertension (12 ± 4 mmHg from baseline, peak at 10 min; P < 0.05), an increase in RVC (127 ± 9% and 150 ± 13% from baseline, at 20 and 60 min respectively; P < 0.05) and a decrease in RSNA (-34 ± 10% and -29 ± 5% from baseline, at 10 and 60 min respectively; P < 0.05). In sinoaortic-denervated rats, HS infusion promoted a sustained pressor response (30 ± 5 and 17 ± 6 mmHg of baseline values, at 10 and 30 min respectively; P < 0.05) and abolished the increase in RVC (85 ± 8% from baseline, at 10 min) and decrease in RSNA (-4 ± 3% from baseline, at 10 min). These results suggest that aortic and carotid afferents are involved in cardiovascular and renal sympathoinhibition responses induced by acute hypernatremia.

Predialysis hypernatremia is a prognostic marker in acute kidney injury in need of renal replacement therapy.

BACKGROUND AND OBJECTIVES: The present study aimed to evaluate the prognostic impact of predialysis dysnatremia in patients with acute kidney injury requiring renal replacement therapy (RRT). DESIGN, SETTING, PARTICIPANTS, AND MEASUREMENTS: A secondary analysis of a prospective multicenter cohort study was performed. Serum sodium (Na) concentrations were categorized immediately before the first RRT as normonatremia (135≤Na ≤145mEq/L), hyponatremia (mild [130≤Na ≤134mEq/L] or severe [Na ≤129mEq/L]), and hypernatremia (mild [146≤Na ≤155mEq/L] or severe [Na ≥156mEq/L]). Multivariable logistic regression was used to estimate the impact of sodium levels categories on hospital mortality. RESULTS: Dysnatremia occurred in 47.3% of 772 included patients. Hypernatremia was more frequent than hyponatremia (33.7% vs 13.6%, P=.001). Intensive care unit (ICU) and hospital mortality rates were 64.6% and 69%, respectively. Hospital mortality was higher in severe hypernatremia (89.1% [95% confidence interval {CI}, 78.7%-95.8%] vs 64.6% [CI, 59.8%-69.2%], P<.001, in normonatremia). Older patients, clinical admission, number of comorbidities, length of ICU stay before the beginning of RRT, and the number of organ dysfunctions were associated with higher hospital mortality. In multivariate analysis, severe hypernatremia (odds ratio, 2.87; 95% CI, 1.2-6.9), poor chronic heath status, severity of illness, sepsis, and lactate were independently associated with outcome. CONCLUSION: Almost 50% of patients with acute kidney injury in need of RRT in the ICU had mild or severe dysnatremia before dialysis initiation. Hypernatremia was the main sodium disturbance and independently associated with poor outcome in the study population.

Central diabetes insipidus: alert for dehydration in very low birth weight infants during the neonatal period. A case report / Diabete insípido central: alerta para desidratação no período neonatal em recém-nascidos de muito baixo peso. Um relato de caso

CONTEXT: Central diabetes insipidus (CDI) is a rare cause of hypernatremia during the neonatal period. The diagnosis is particularly difficult in very low birth weight (VLBW) newborns. CASE REPORT: We report on a preterm newborn who presented CDI soon after birth. On the third day of life, signs of dehydration were present despite normal fluid supply. The diuresis rate was 4.4 ml/kg/h. Although the fluid supply was then increased, the dehydration continued, with hypernatremia, normal glycemia, diuresis of 7.4 ml/kg/h and urine density of 1005 mOsmol/l. Thus, a diagnostic hypothesis of diabetes insipidus was raised. A test with a nasal vasopressin analogue (dDAVP) was performed and CDI was confirmed. Reduction of the fluid supply became possible through appropriate treatment. CONCLUSION: The diagnosis of CDI is rarely made during the neonatal period, especially in VLBW newborns, because of the difficulty in detecting elevated diuresis. Persistent hypernatremia, usually accompanied by hyperthermia despite abundant fluid supply, weight loss and low urine osmolality are important signs of alert. .

CONTEXTO: Diabete insípido central (DIC) é uma rara causa de hipernatremia durante o período neonatal. O diagnóstico é difícil, particularmente em recém-nascidos (RN) de muito baixo peso (RNMBP). RELATO DE CASO: Relatamos um RN que apresentou DIC logo após o nascimento. No terceiro dia de vida, apresentava sinais de desidratação, embora estivesse recebendo aporte adequado de líquidos. A diurese aferida era de 4,4 ml/kg/h. Apesar do aumento do aporte hídrico, manteve-se desidratado, com hipernatremia, valores normais de glicemia e diurese de 7,4 ml/kg/h com densidade urinária de 1005 mOsmol/l. Desta forma, a hipótese diagnóstica de diabete insípido foi considerada. O teste com análogo da vasopressina (dDAVP) foi realizado e DIC foi confirmado. A redução do aporte de líquidos foi possível com o tratamento adequado. CONCLUSÃO: O diagnóstico de DIC raramente é realizado durante o período neonatal, particularmente em RNMBP, devido à dificuldade em detectar diurese aumentada. Hipernatremia persistente, geralmente acompanhada de hipertermia, apesar do abundante aporte de água, perda de peso e osmolaridade urinaria baixa, são importantes sinais de alerta. .

Central diabetes insipidus: alert for dehydration in very low birth weight infants during the neonatal period. A case report.

CONTEXT: Central diabetes insipidus (CDI) is a rare cause of hypernatremia during the neonatal period. The diagnosis is particularly difficult in very low birth weight (VLBW) newborns. CASE REPORT: We report on a preterm newborn who presented CDI soon after birth. On the third day of life, signs of dehydration were present despite normal fluid supply. The diuresis rate was 4.4 ml/kg/h. Although the fluid supply was then increased, the dehydration continued, with hypernatremia, normal glycemia, diuresis of 7.4 ml/kg/h and urine density of 1005 mOsmol/l. Thus, a diagnostic hypothesis of diabetes insipidus was raised. A test with a nasal vasopressin analogue (dDAVP) was performed and CDI was confirmed. Reduction of the fluid supply became possible through appropriate treatment. CONCLUSION: The diagnosis of CDI is rarely made during the neonatal period, especially in VLBW newborns, because of the difficulty in detecting elevated diuresis. Persistent hypernatremia, usually accompanied by hyperthermia despite abundant fluid supply, weight loss and low urine osmolality are important signs of alert.

Pediatric liver transplant outcome using severe hypernatremic donors.

INTRODUCTION: Pediatric liver transplantation is limited by donation. In the last 5 years, urgent conditions have forced transplant teams to accept donors with minor suboptimal conditions, termed "extended donor criteria." Among those, the risk of using severe hypernatremic donors (SHD) for liver transplant is not yet well established. The aim of this study is to report the outcome of pediatric patients receiving grafts from SHD. METHODS: Clinical records of patients transplanted in the last 3 years at Hospital Luis Calvo Mackenna, Santiago, Chile, were reviewed. Outcome was evaluated in terms of patient and graft survival and complications potentially associated to the donor condition. RESULTS: Five of 33 deceased donor transplants presented with SHD. All recipients were waiting transplant in an acute condition, one of them in acute liver failure (ALF). No living related donor was available. Donors' serum sodium was 169 to 193 mEq/L before medical management and between 157 and 172 mEq/L at procurement. One patient died from sepsis related to biliary complications, and the patient suffering ALF developed primary graft nonfunction, received a second transplant 2 weeks later, and recovered to stable medical condition. No other complication was registered in these patients. DISCUSSION: Our findings allow us to postulate that hypernatremic deceased donors may be used for pediatric liver transplant under special circumstances.

Encefalopatía crónica no progresiva secundaria a enfermedad vascular cerebral hemorrágica por deshidratación hipernatrémica: a propósito de un caso / Non progressive chronic encephalopathy secondary to cerebral vascular hemorrhage due to hipernatremic dehydration: a purpose of a case

El estudio en los últimos años de las enfermedades vasculares cerebrales en la infancia ha permitido el reconocimiento de los factores de riesgo para este grupo etario. La hiperosmolaridad (policitemia, trombocitosis, hiperglicemia, hipernatremia), que a nivel del sistema nervioso central provoca trombosis de vasos arteriales y venosos con ruptura de los mismos y sangramientos intracerebrales, subdurales, subaracnoides, puede ser causa de fenómenos isquémicos y/o hemorrágicos cerebrales, conllevando a largo plazo a lesiones estructurales. El presente trabajo se basa en la descripción clínica y procedimientos diagnósticos de un niño con encefalopatía crónica no progresiva, secundaria a enfermedad vascular cerebral hemorrágica por deshidratación hipernatrémica, tomando los datos de la historia clínica y la evaluación directa del mismo. El paciente se evaluó en Barquisimeto, estado Lara en el año 2007.

Studies in the last years on cerebral vascular illnesses in childhood has allowed the recognition of risk factors for this age group. Increase in osmolarity (increase in the viscosity of the blood, polycitemia thrombocitocys, hyperglycemia, hypernatrenia) can cause ischemic phenomena and/or cerebral hemorrhage, causing long term structural lesions. The present work is based on the clinical description and aboy's diagnostic procedures with chronic non progressive encephalopaty secondary to cerebral vascular hemorrhagic illness due to hypernatrenic dehydration. The patient was evaluated in the city of Barquisimeto, Lara state in the year 2007.

Hypernatremic diarrheal dehydration treated with oral glucose-electrolyte solution containing 90 or 75 mEq/L of sodium.

Of 33 infants with hypernatremic dehydration (serum Na+ of greater than or equal to 150 mEq/L) 7 were excluded, 6 because severe alteration of the level of consciousness or shock precluded oral rehydration and 1 because he was given glucose-electrolyte solution plus water. We studied the remaining 27 infants. Twenty (group A) were treated with the World Health Organization-recommended oral rehydration solution (90 mEq/L Na+) and seven (group B) were treated with Pedialyte-RS (Abbott Laboratories Ltd.; 75 mEq/L Na+). The rehydrating solutions were administered in a volume equivalent to twice the clinically estimated fluid deficit. Initial serum sodium was 156.7 +/- 0.9 mEq/L for group A and 155.8 +/- 1.8 mEq/L for group B (mean +/- SEM). The mean time to achieve rehydration was 14.3 and 16.6 h for groups A and B, respectively. Twenty-four hours after commencing oral rehydration, serum Na+ had decreased to 144.8 +/- 1.8 mEq/L for group A and 144.5 +/- 0.9 mEq/L for group B. In two patients in group A, the serum Na+, which, had not decreased to less than 150 mEq/L at 24 h, did so at 48 h. Only in one case (group A) did the serum Na+ increase. This patient had high stool output and failed to become rehydrated after 24 h of unsuccessful oral rehydration. None of the patients had seizures or persistent CNS dysfunction. We conclude that the slow administration of oral rehydration solutions containing either 90 or 75 mEq/L Na+ is a safe and effective treatment of hypernatremic dehydration.

Intracranial hemorrhages in kittens: hypernatremia versus hypoxia.

Although CNS hemorrhages have long been observed in infants with hyaline membrane disease, the etiology of these hemorrhages is still unknown. Two proposed etiologies are hypoxia with acidosis and iatrogenic hypernatremia secondary to sodium bicarbonate therapy. An experiment on kittens comparing these two hypotheses suggested that intracranial hemorrhages were related only to elevated serum sodium concentrations. The CNS hemorrhages were independent of experimentally induced hypoxemia and its consequent acidosis.