Poliuria en el adulto. Una aproximación diagnóstica basada en la fisiopatología / Polyuria in adults. A diagnostic approach based on pathophysiology

La poliuria es una condición clínica frecuente caracterizada por un volumen de orina inapropiadamente alto para los niveles de presión arterial y sodio plasmático del paciente (volumen de orina >3L/24h). Desde el punto de vista fisiopatológico se clasifica en 2 tipos: debido a una mayor excreción de solutos (osmolaridad urinaria >300mOsm/L) o debido a una incapacidad de aumentar la concentración de solutos (osmolaridad urinaria <150mOsm/L). En ocasiones pueden coexistir ambos mecanismos (osmolaridad urinaria 150-300mOsm/L). La poliuria supone un reto diagnóstico y su tratamiento correcto exige una evaluación de la historia clínica, la determinación de la osmolaridad urinaria, la estimación del aclaramiento de agua libre, el uso de pruebas de deprivación hídrica en la poliuria acuosa y la medición de electrólitos en sangre y orina en el caso de la poliuria osmótica (AU)

Polyuria is a common clinical condition characterized by a urine output that is inappropriately high (more than 3 liters in 24 hours) for the patient's blood pressure and plasma sodium levels. From a pathophysiological point of view, it is classified into two types: polyuria due to a greater excretion of solutes (urine osmolality >300 mOsm/L) or due to an inability to increase solute concentration (urine osmolality <150 mOsm/L). Sometimes both mechanisms can coexist (urine osmolality 150-300 mOsm/L). Polyuria is a diagnostic challenge and its proper treatment requires an evaluation of the medical record, determination of urine osmolality, estimation of free water clearance, use of water deprivation tests in aqueous polyuria, and measurement of electrolytes in blood and urine in the case of osmotic polyuria (AU)

Polyuria in adults. A diagnostic approach based on pathophysiology.

Polyuria is a common clinical condition characterized by a urine output that is inappropriately high (more than 3 L in 24 h) for the patient's blood pressure and plasma sodium levels. From a pathophysiological point of view, it is classified into two types: polyuria due to a greater excretion of solutes (urine osmolality >300 mOsm/L) or due to an inability to increase solute concentration (urine osmolality <150 mOsm/L). Sometimes both mechanisms can coexist (urine osmolality 150-300 mOsm/L). Polyuria is a diagnostic challenge and its proper treatment requires an evaluation of the medical record, determination of urine osmolality, estimation of free water clearance, use of water deprivation tests in aqueous polyuria, and measurement of electrolytes in blood and urine in the case of osmotic polyuria.

Fatal case of hospital-acquired hypernatraemia in a neonate: lessons learned from a tragic error.

A 3-week-old boy with viral gastroenteritis was by error given 200 mL 1 mmol/mL hypertonic saline intravenously instead of isotonic saline. His plasma sodium concentration (PNa) increased from 136 to 206 mmol/L. Extreme brain shrinkage and universal hypoperfusion despite arterial hypertension resulted. Treatment with glucose infusion induced severe hyperglycaemia. Acute haemodialysis decreased the PNa to 160 mmol/L with an episode of hypoperfusion. The infant developed intractable seizures, severe brain injury on magnetic resonance imaging and died. The most important lesson is to avoid recurrence of this tragic error. The case is unique because a known amount of sodium was given intravenously to a well-monitored infant. Therefore the findings give us valuable data on the effect of fluid shifts on the PNa, the circulation and the brain's response to salt intoxication and the role of dialysis in managing it. The acute salt intoxication increased PNa to a level predicted by the Edelman equation with no evidence of osmotic inactivation of sodium. Treatment with glucose in water caused severe hypervolaemia and hyperglycaemia; the resulting increase in urine volume exacerbated hypernatraemia despite the high urine sodium concentration, because electrolyte-free water clearance was positive. When applying dialysis, caution regarding circulatory instability is imperative and a treatment algorithm is proposed.

The Link between Hypermetabolism and Hypernatremia in Severely Burned Patients.

Hypernatremia is common in critical care, especially in severely burned patients. Its occurrence has been linked to increased mortality. Causes of hypernatremia involve a net gain of sodium or a loss of free water. Renal loss of electrolyte-free water due to urea-induced osmotic diuresis has been described as causative in up to 10% of hypernatremic critical ill patients. In this context, excessive urea production due to protein catabolism acts as major contributor. In severe burn injury, muscle wasting occurs as result of hypermetabolism triggered by ongoing systemic inflammation. In this retrospective study, severely burned patients were analysed for the occurrence of hypernatremia and subsequent signs of hypermetabolism. The urea: creatinine ratio-as a surrogate for hypermetabolism-sufficiently discriminated between two groups. Four of nine hypernatremic burn patients (44%) had a highly elevated urea: creatinine ratio, which was clearly associated with an increased urea production and catabolic index. This hypermetabolism was linked to hypernatremia via an elevated urea- and reduced electrolyte-fraction in renal osmole excretion, which resulted in an increased renal loss of electrolyte-free water. In hypermetabolic severely burned patients, the electrolyte-free water clearance is a major contributor to hypernatremia. A positive correlation to serum sodium concentration was shown.

Hypernatremia due to Urea-Induced Osmotic Diuresis: Physiology at the Bedside.

Hypernatremia secondary to urea-induced solute diuresis is due to the renal excretion of electrolyte-free water. This concept is explained here step-wise physiologically with the help of a clinical vignette.

Hypervolemic hypernatremia is the most common type of hypernatremia in the intensive care unit.

BACKGROUND: A high incidence of hypervolemic hypernatremia has been described in patients recovering from acute kidney injury (AKI) in intensive care units. However, this has been limited to only a few cases. METHODS: One hundred fifty adult patients recovering from AKI in the intensive care unit of a single institution during a 6-year period, who developed hypernatremia during the course of their illness, were investigated. Serum and urine electrolytes, osmolality, urea nitrogen and creatinine were measured. The weights of these patients at the time of hypernatremia development and at presentation to the hospital were also measured. RESULTS: Even though the hypernatremia was mild in most patients (146-160 mEq/L), the average rise in serum sodium concentration was 14.5 ± 7.1 mEq/L. Of the 34 patients who had all urinary studies available, the average urine osmolality was 436 ± 128 mmol/kg of which 172 ± 54 mmol/L was contributed by sodium, potassium and their accompanying anion. Another 204 ± 96 mmol/L was accounted for by urea and creatinine (mainly urea). Almost all the patients had hypervolemia as evidenced by the presence of edema and an average weight gain of more than 9 ± 11 kg between the time of presentation and the onset of hypernatremia despite likely having lost muscle mass from being in the intensive care unit for several days. The weight data were available in 54 patients, and only eight of these patients had lost weight at the time of the development of hypernatremia. CONCLUSION: Hypervolemic hypernatremia is by far the most common cause of hypernatremia in patients in the intensive care unit. Even though the patients are in negative fluid balance at the time of the development of the hypernatremia, earlier saline administration has caused massive volume overload despite the ongoing losses. Post-AKI diuresis in the face of inability to maximally concentrate the urine because of renal failure often leads to mainly mild elevations in serum sodium concentration. The urine solute is mainly urea because of the often high serum urea concentrations with little electrolytes being present in the urine.

Body salt and water balances in cardiothoracic surgery patients with intensive care unit-acquired hyponatremia.

PURPOSE: Hyponatremia is frequently observed in intensive care unit (ICU) patients, but there is still lack information on the physiological mechanisms of development. MATERIALS AND METHODS: In this retrospective analysis we performed tonicity balances in 54 patients with ICU acquired hyponatremia. We calculated fluid and solute in and outputs during 24 hours in 106 patient days with decreasing serum-sodium levels. RESULTS: We could observe a positive fluid balance as a single reason for hyponatremia in 25% of patients and a negative solute balance in 57%. In 18% both factors contributed to the decrease in serum-sodium. Hyponatremic patients had renal water retention, measured by electrolyte free water clearance calculation in 79% and positive input of free water in 67% as reasons for decline of serum-sodium. The theoretical change of serum sodium during 24 hours according to the calculations of measured balances correlated well with the real change of serum sodium (r = 0.78, P < .01). CONCLUSIONS: Balance studies showed that renal water retention together with renal sodium loss and high electrolyte free water input are the major contributors to the development of hyponatremia. Control of renal water and sodium handling by urine analysis may contribute to a better fluid management in the ICU population.