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Vasopressin gene transcription increases in response to decreases in plasma volume, but not to increases in plasma osmolality, in chronically dehydrated rats.

The synthesis of arginine vasopressin (AVP) in the magnocellular neurons of the supraoptic (SON) and paraventricular nuclei (PVN) is physiologically regulated by plasma osmolality and volume. To clarify how the regulation of AVP gene transcription is affected by chronic dehydration, we examined changes in the transcriptional activities of AVP gene by plasma osmolality and volume in both euhydrated and dehydrated conditions. Euhydrated rats had free access to water, whereas dehydrated rats had been deprived of water for 3 days before experiments. Rats in both conditions were subjected to acute hypertonic stimuli or hypovolemia, and changes in AVP heteronuclear (hn)RNA levels, an indicator of gene transcription, in the SON and PVN were examined with in situ hybridization. The intraperitoneal (i.p.) injection (2% body wt) of hypertonic (1.5 M) saline increased plasma Na levels by approximately 40 meq/l in both euhydrated and dehydrated conditions. However, expression levels of AVP hnRNA in the SON and PVN were increased only in euhydrated, not dehydrated, rats. On the other hand, i.p. injection of polyethylene glycol decreased the plasma volume by approximately 16-20%, and AVP hnRNA levels in the SON and PVN were significantly increased in both conditions. Thus it is demonstrated that signaling pathways regulating AVP gene transcription in the magnocellular neurons were completely refractory to acute osmotic stimuli under the chronic dehydration and that AVP gene transcription could probably respond to acute hypovolemia through different intracellular signal transduction pathways from those for osmoregulation.

Animals↗

Modulation of jejunal ion and water absorption by endogenous angiotensin after dehydration.

In the pentobarbital sodium-anesthetized rat, dehydration for 24 h increased ion and water absorption from the jejunum. Dehydration also elevated plasma concentrations of angiotensin peptides and plasma renin activity but did not significantly alter plasma aldosterone concentrations. Infusion of tyramine, norepinephrine, and angiotensin II (AII) also stimulated jejunal absorption in a manner similar to dehydration. The elevation of jejunal absorption in response to dehydration is totally inhibited by the converting enzyme inhibitor captopril and the angiotensin receptor antagonist [lle7]AIII. Thus, increased jejunal absorption following dehydration is mediated by the renin-angiotensin system and is not secondary to either aldosterone or to antidiuretic hormone release. Further experiments demonstrated that the increase in jejunal absorption in response to dehydration was unaffected by propranolol but was totally abolished by phentolamine, prazosin, and peripheral sympathectomy. It is proposed that AII stimulates jejunal absorption by enhancing transepithelial transport processes and/or by altering the balance of Starling forces governing fluid absorption across enteric capillaries. Angiotensin thus appears to be a physiologically important mediator of jejunal absorption in states characterized by extracellular volume depletion.

Absorption↗

Angiotensin II antagonists in dehydrated rabbits without baroreceptor reflexes.

Blood pressure effects of angiotensin II antagonists were studied in sham-operated and baroreceptor-denervated rabbits in the normal water-replete state or after 6 days of water deprivation (dehydrated). Experiments were performed in awake rabbits. Dehydrated rabbits had significantly higher plasma sodium concentrations, hematocrits, and plasma renin activities, but lower plasma potassium concentrations and body weights than water-replete rabbits. Administration of angiotensin II antagonists caused a significant decrease in mean arterial pressure in dehydrated rabbits (-16 mmHg in sham-dehydrated and -19 mmHg in denervated-dehydrated) but not in water-replete ones, whether the baroreceptor reflexes were intact or not (-1 mmHg in sham replete and -4 mmHg in denervated replete). The open-loop feedback gain of the renin-angiotensin system in blood pressure control was calculated as -1.6. The results demonstrate an important role of angiotensin II in blood pressure regulation during the high-renin, dehydrated state, but not during the normal renin, water-replete state. Abolishment of baroreceptor reflexes did not unmask an important role of normal levels of angiotensin II in blood pressure regulation.

Angiotensin II↗

Influence of vasoconstrictor systems on leg vasodilation during heating of dehydrated baboons.

This study, carried out in two parts, sought to determine the importance of vasopressin (VP), the renin-angiotensin system (RAS), and the sympathetic nervous system in the dehydration-produced attenuation of hindlimb (cutaneous) vasodilation during environmental heating (EH). Baboons, chronically instrumented for blood sampling and for measurement of mean iliac blood flow (MIBF), arterial pressure, and core temperature (Tc), were subjected to EH while in euhydrated and dehydrated (64-72 h of water deprivation) states. EH consisted of exposure to an elevated ambient temperature (40-42 degrees C) until Tc reached 39.5 degrees C. In part I, indexes of the above vasoconstrictor systems were measured. Base-line plasma renin activity (PRA) and VP and norepinephrine concentrations were all significantly elevated by dehydration. In addition, the increase in PRA during EH was accentuated by dehydration. In part II, the effects of blockades of the RAS, the pressor action of VP, and the innervation of the hindlimb on hindlimb vasodilation during EH were assessed. None of these blockades, singly or together, reversed the dehydration-produced attenuation of the increase in MIBF during EH. Thus we conclude that other mechanisms are responsible for the dehydration-produced attenuation of cutaneous vasodilation in baboons during EH.

Animals↗

Vasopressin contributes to maintenance of arterial blood pressure in dehydrated baboons.

This study primarily sought to determine whether the role of vasopressin (VP) in maintenance of arterial blood pressure is enhanced in awake, chronically instrumented baboons after 68-72 h of dehydration. This question was approached by pharmacologically blocking vasopressin V1-receptors in euhydrated and dehydrated baboons with or without a normally functioning renin-angiotensin system (RAS). VP blockade during dehydration produced a rapidly occurring (within 5 min), statistically significant (P less than 0.05) decrease in mean arterial pressure (MAP) of 5 +/- 1 mmHg in the RAS-intact condition and an identical decline in MAP (5 +/- 1 mmHg) during blockade of the RAS by captopril, an angiotensin I-converting enzyme inhibitor. At 15 min after induction of VP blockade, heart rate was elevated by 9 +/- 2 beats/min in the RAS-intact condition and by 20 +/- 5 beats/min in the RAS-blocked condition. In addition, VP blockade in the dehydrated state produced small and equal increases in hindlimb vascular conductance in RAS-intact and RAS-blocked conditions. None of these cardiovascular changes were produced by VP blockade in the euhydrated state. RAS blockade produced modest declines in MAP in both hydration states, but the fall was larger by 7 +/- 4 mmHg in the dehydrated state. Thus both VP and the RAS contribute to the maintenance of arterial blood pressure during dehydration in the conscious baboon.

Animals↗

Dehydration induces sodium depletion in rats, rabbits, and sheep.

The effect of water deprivation for 1 day on Na balance was measured in rats, rabbits, and sheep. In all three species, dehydration induced a considerable increase in the daily output of Na in urine. This resulted in the water-deprived animals becoming Na depleted as well as water deficient. Experiments were also designed to control for the reduced food intake that results from water deprivation in rats and rabbits. The results showed that decreased food intake was not the cause of the natriuresis and subsequent Na depletion that occurred during dehydration. When water was again made available to the dehydrated animals, a period of urinary Na retention ensued. This Na retention usually continued until the Na deficit that had accrued during the period of dehydration had been ameliorated. It seems likely that natriuresis in response to dehydration is common in mammals. We postulate that such a natriuretic response may serve a homeostatic function in buffering increases in plasma [Na] and osmolality that result from dehydration.

Animals↗

Regional alterations in hexokinase activity within rat brain during dehydration and rehydration.

Histochemical localization and photodensitometric quantification of the metabolic enzyme, hexokinase (HK), were used to study changes in brain metabolic activity that occur during the development of (5 days) and recovery from (7 days) dehydration. In water-deprived (WD) rats, HK activity increased after 2 days in the subfornical organ (SFO, 22%), nucleus circularis (NC, 36%), parvo- and magnocellular divisions of the paraventricular nucleus (pPVH, 17%; mPVH, 46%) and supraoptic nucleus (SON, 46%). Activity in SFO declined to control levels at 3 days but increased again thereafter. In pPVH, mPVH, and SON, activity was elevated until the end of the experiment. In NC, activity returned to control levels within 2 days of drinking by the rats. In salt-loaded (2% NaCl in water) rats, changes were similar to those of WD rats up to 2 days of dehydration (SFO, 25%; NC, 20%; pPVH, 16%; mPVH, 38%; SON, 50%). Activity in SFO and pPVH returned to control levels after 3 days and remained unchanged. In mPVH, SON, and NC, activity remained elevated and declined to control levels when salt-free water was provided. Results confirm that water deprivation is a stronger dehydrating stimulus than salt loading. In addition, metabolic activity, as measured by HK activity, varies daily during periods of dehydration and rehydration. These changes cannot always be predicted from results obtained only at the end of a period of dehydration. It is concluded that it is necessary to study dehydration-induced changes in brain metabolism on a daily basis to more fully understand the roles of discrete brain regions in the regulation of body fluids.

Animals↗

Osmoregulation and body fluid compartmentalization in dehydrated heat-exposed pigeons.

Osmoregulatory and volume-regulatory responses of heat-acclimated pigeons (Columba livia) were studied during normal hydration and dehydration combined with heat exposure. Dehydrated heat-exposed pigeons (exposure to 50 degrees C following 48 h of water deprivation; 16-18% mass loss) could recover 97% of their initial body mass within 30 min of free drinking at the end of heat exposure. At the end of heat exposure, body temperature increased by 3 degrees C and hematocrit increased by 12.5%. Serum electrolyte and protein concentrations increased by 33-53% (P less than 0.001). Serum osmolality reached an outstanding mean value of 436.7 +/- 28.5 mosmol/kg (n = 11), 30.5% higher than the normal mean value. Serum glutamic-pyruvic transaminase and glutamic-oxaloacetic transaminase concentrations did not change during dehydration, suggesting no impairment in circulatory function. Blood urea nitrogen increased sixfold, indicating a total shutdown of the kidney. Relative plasma volume was maintained during dehydration at the expense of extravascular spaces and with a decreased vascular permeability as indicated by the increase in Evans blue-labeled albumin half-life (control, 104 +/- 53 min; dehydration, approaching infinity). Altogether, extracellular fluid volume and intracellular fluid volume contributed 53 and 47% of the evaporative water loss, respectively. It is concluded that plasma volume regulation may play an important role in the effective thermoregulatory responses of heat-exposed dehydrated pigeons. This regulation is achieved by preferential shifts of body water reserves among the various body water compartments coinciding with a remarkable tolerance to high osmotic pressures.

Acclimatization↗

Angiotensin-converting enzyme inhibitor inhibits dehydration-enhanced fever induced by endotoxin in rats.

It has been reported that a host develops a marked fever under dehydrated conditions compared with normally hydrated conditions (11). The present study was carried out to investigate whether ANG II is involved in the enhancement seen in dehydrated rats of the fever induced by bacterial endotoxin. The results showed that intravenous injection of bacterial endotoxin produced a fever in dehydrated rats (rats deprived of water for 24 h) that was significantly greater than that seen in normally hydrated rats. In contrast, dehydration had no effect on the fever induced by intravenous interleukin-1beta (IL-1beta). Under dehydrated conditions, the enhanced endotoxin-induced fever was significantly inhibited by the angiotensin-converting enzyme inhibitor lisinopril, but the IL-1beta fever was not. These results suggest that the dehydration-induced enhancement of endotoxin fever is due, at least in part, to the action of ANG II, which elicits an increased production of pyrogenic cytokines such as IL-1.

Analysis of Variance↗

P2Y2 receptor-mediated release of prostaglandin E2 by IMCD is altered in hydrated and dehydrated rats: relevance to AVP-independent regulation of IMCD function.

Circulating vasopressin levels change in hydrated and dehydrated conditions and thus control osmotic water permeability (P(f)) of the inner medullary collecting duct (IMCD). Prostaglandin E2 (PGE2) antagonizes vasopressin-induced P(f) of IMCD. Previously, we showed that activation of P2Y2 receptor (P2Y2-R) in IMCD results in production and release of PGE2, and P2Y2-R mRNA and protein are significantly elevated in inner medullas of hydrated rats compared with dehydrated rats. Therefore, we examined whether the altered expression of P2Y2-R in hydrated and dehydrated states is associated with corresponding changes in P2Y2-R-mediated PGE2 release by the IMCD. Rats were hydrated by providing sucrose water as the sole drinking fluid or dehydrated by water deprivation for 2 days. This resulted in high output-low osmolality and low output-high osmolality urines in hydrated and dehydrated rats, respectively. In hydrated rats, there was a significant increase in tubular fluid PGE2, measured indirectly by assessing the urinary PGE2 metabolite. Stimulation of freshly isolated IMCD preparations in vitro with P2Y2-R agonist (ATPgammaS) showed a marked increase in the release of PGE2 in hydrated rats compared with normal rats. These responses were blunted in the IMCD prepared from dehydrated rats. The P2Y2-R-mediated PGE2 release in the IMCD of hydrated rats was mediated largely by cyclooxygenase (COX)-1 as COX-1-specific inhibitor valeroyl salicylate completely blocked the release. The COX-2-specific inhibitor N5398 had only a modest and insignificant inhibitory effect. In conclusion, the increased sensitivity of purinergic-prostanoid interaction seen in the IMCD of hydrated rats may represent a novel vasopressin-independent regulatory mechanism of IMCD function.

Adenosine Triphosphate↗

Contribution of vasopressin to the maintenance of blood pressure during dehydration.

Normal Long-Evans rats, when dehydrated for up to 72 h, have a progressive rise in plasma vasopressin that is associated with a fall in body weight and urine volume, a rise in plasma and urine osmolality, and the maintenance of normal systolic blood pressure. In contrast, Brattleboro diabetes insipidus rats, genetically deficient in vasopressin, when dehydrated to achieve an equivalent body weight loss, have a significant 15 mmHg fall in systolic blood pressure. Even when fluid balance is corrected in the Brattleboro rats by the continuous administration of 1-desamino-8-D-arginine vasopressin, a synthetic vasopressin analogue with potent antidiuretic properties but minimal pressor activity, blood pressure still falls when the animals are dehydrated. In contrast, Brattleboro rats infused with exogenous arginine vasopressin to produce a plasma vasopressin level of 18.9 +/- 3.5 pg X ml-1 are able to maintain normal blood pressure during 48 h of dehydration. This level of vasopressin is comparable to the level found endogenously in dehydrated Long-Evans rats and is nonpressor in normal rats. These results suggest that both the antidiuretic and vasoconstrictor properties of vasopressin are important in the cardiovascular response to dehydration.

Angiotensin II↗

Acute dehydration: body water distribution in acclimated and nonacclimated Psammomys obesus.

Body water distribution after "acute dehydration" treatment (37 degrees C) was studied in Psammonys obesus before and after acclimation at 34 +/- 1 degrees C for 16-18 days. Determinations of water compartment volumes were performed on anaesthetized (thiopental sodium) nephrectomized animals. Plasma volume (PV) and extracellular volume (ECV) were measured by T-1824 and [14C]inulin, respectively. Total body water was determined after desiccating the animals. Albumin outflux was calculated from the half-life (T1/2) of T-1824 and total plasma albumin mass. Nonacclimated animals conserved PV as long as dehydration did not exceed 10-11% loss of body wt. This conservation was at the expense of ECV and was associated with diminished albumin outflux (T1/2 T-1824 approached infinity). With increased dehydration PV retention failed and a resumption of albumin outflux occurred. Acclimation resulted in diminished albumin outflux in both control and dehydrated animals (T1/2 T-1824 approached infinity). Most of the water lost during dehydration was of intracellular origin. It was concluded that reduction in permeability of the capillary bed during dehydration and acclimatization plays an important role in PV and ECV regulation.

Acclimatization↗

Dehydration-induced renin secretion: involvement of histaminergic neurons.

Renin secretion is controlled locally in the kidneys as well as via central neuronal mechanisms. The neuronal mechanisms are not fully understood but may involve the neurotransmitter histamine (HA) since centrally infused HA stimulates renin secretion. This, however, does not prove that HA is of any physiological importance for the regulation of renin secretion. Dehydration is a physiological stimulus of renin secretion and, therefore, we studied the possible role of hypothalamic histaminergic neurons in dehydration-induced renin secretion in conscious male rats. In addition, we expanded on our previous investigations of HA-induced renin secretion. Twenty-four hours of dehydration induced a 3-fold increase in plasma renin activity (PRA). Pretreatment with the HA synthesis inhibitor alpha-fluoromethylhistidine inhibited the dehydration-induced PRA secretion by 80% whereas pretreatment with the H1 receptor antagonist mepyramine (MEP) or the H2 receptor antagonist ranitidine (RAN) inhibited the PRA response to dehydration by approximately 40%. In euhydrated control rats, none of the HA-blocking agents had any significant effect on basal PRA secretion. Central administration of HA stimulated PRA almost 2-fold and the maximum concentration of PRA was reached after 15 min. Pretreatment with the H1 receptor antagonist MEP or the H2 receptor antagonist RAN totally inhibited the HA-induced PRA secretion. We conclude that HA activates renin secretion via H1 and H2 receptors and that HA seems to be a physiological mediator of dehydration-induced renin secretion via activation of H1 and H2 receptors. The effect is probably indirect and may among others involve the catecholaminergic and serotonergic systems.

Animals↗

Topographic distribution of aquaporin 2 mRNA in the kidney of dehydrated rats.

BACKGROUND: Stimulation of arginine vasopressin results in an immediate redistribution of water channels (aquaporin 2; AQP2) in the apical membrane of the collecting ducts, leading to water reabsorption. Water restriction for >/=24 h increases AQP2 proteins in the whole collecting duct which is highest in the inner medulla of the kidney, indicating that dehydration enhances synthesis of this protein. Although increased expression of AQP2 mRNA under this condition has been reported, the increased ratio of mRNA expression in the three regions of the kidney, cortex, outer medulla, and inner medulla, during the dehydration is still unclear. METHODS: We investigated the AQP2 transcripts using male Sprague-Dawley rats deprived of water for 24 h. Mimic cDNA for competitive polymerase chain reaction (PCR) was constructed by deleting 180 bp at the middle of a 780-bp partial PCR product for rat AQP2 cDNA. In situ hybridization of the kidney and Northern blotting of inner medulla were performed using a 60-bp oligo-cDNA probe which identified rat AQP2 transcripts in the collecting duct. RESULTS: Dehydration resulted in a significant increase in plasma osmolality and arginine vasopressin concentration and urinary osmolality. Competitive PCR demonstrated that dehydration increased AQP2 transcripts in all parts of the kidney, but was highest in the inner medulla. Northern blotting confirmed the high increased rate of AQP2 transcription in the inner medulla. In situ hybridization showed markedly intensified signals in the inner medulla of dehydrated rats. CONCLUSIONS: Our data indicate that dehydration increases the abundance of AQP2 transcripts which may be closely associated with enhancement in AQP2 protein synthesis reported previously. This topographically variable increase in transcription is considered to be one of the mechanisms involved in long-term regulation of water permeability in the collecting duct.

Animals↗

Distribution of dehydration rates generated by maximal Gardos-channel activation in normal and sickle red blood cells.

The Ca(2+)-activated K+ channels of human red blood cells (RBCs) (Gardos channels, hIK1, hSK4) can mediate rapid cell dehydration, of particular relevance to the pathophysiology of sickle cell disease. Previous investigations gave widely discrepant estimates of the number of Gardos channels per RBC, from as few as 1 to 3 to as many as 300, with large cell-to-cell differences, suggesting that RBCs could differ extensively in their susceptibility to dehydration by elevated Ca2+. Here we investigated the distribution of dehydration rates induced by maximal and uniform Ca2+ loads in normal (AA) and sickle (SS) RBCs by measuring the time-dependent changes in osmotic fragility and RBC volume distributions. We found a remarkable conservation of osmotic lysis and volume distribution profiles during Ca(2+)-induced dehydration, indicating overall uniformity of dehydration rates among AA and SS RBCs. In light of these results, alternative interpretations were suggested for the previously proposed low estimates and heterogeneity of channel numbers per cell. The results support the view that stochastic Ca2+ permeabilization rather than Gardos-channel variation is the main determinant selecting which SS cells dehydrate through Gardos channels in each sickling episode.

Adenosine Triphosphate↗

Dehydration-induced synaptic plasticity in magnocellular neurons of the hypothalamic supraoptic nucleus.

Norepinephrine plays a critical role in the regulation of hypothalamic neuroendocrine function, in large part through modulation of synaptic glutamate and gamma-aminobutyric acid (GABA) release. Hypothalamic magnocellular neuroendocrine cells undergo dramatic changes in synaptic organization under conditions of increased hormone release, including increased numbers of glutamatergic, GABAergic and noradrenergic synapses. We studied the functional plasticity of magnocellular neurons of the rat supraoptic nucleus induced by chronic dehydration using whole-cell recordings in hypothalamic slices. Dehydrated rats showed increases in glutamate and GABA release onto magnocellular neurons, as evidenced by an increase in the frequency of spontaneous excitatory (29%) and inhibitory (33%) postsynaptic currents. The change in glutamate release was likely due to increased numbers of release sites because paired-pulse facilitation analysis did not reveal a change in the probability of transmitter release. In untreated rats, norepinephrine facilitates glutamate release and attenuates GABA release onto magnocellular neurons. Dehydration resulted in a marked enhancement of norepinephrine's actions, doubling both the norepinephrine-induced increase in glutamate release and decrease in GABA release. The norepinephrine dose-response curve was shifted to the left with dehydration, revealing an increase in norepinephrine sensitivity. Thus, dehydration leads to an increase in glutamate and GABA release onto supraoptic magnocellular neurons as well as a marked enhancement of the facilitatory effect of norepinephrine on glutamate release and inhibitory effect on GABA release. This synaptic plasticity would be expected to increase the excitability of the magnocellular neurons and support the enhanced bursting capacity and facilitated hormone secretion observed in vivo with chronic dehydration.

Animals↗

Comparison of nasogastric and intravenous methods of rehydration in pediatric patients with acute dehydration.

OBJECTIVE: To assess the safety, efficacy, and cost-effectiveness of rapid nasogastric hydration (RNG) and rapid intravenous hydration (RIV) administered in the emergency department (ED) to young children suffering with uncomplicated, acute moderate dehydration. METHODS: Ninety-six children aged 3 to 36 months, who presented with signs and symptoms of uncomplicated, acute moderate dehydration caused by vomiting and/or diarrhea, presumed to be caused by viral gastroenteritis, were randomly assigned to receive either RNG with a standard oral rehydration solution or RIV with normal saline. Each solution was administered at a rate of 50 mL/kg of body weight, delivered over a 3-hour period in our urban pediatric ED. All participants were weighed pretreatment and posttreatment and underwent initial and final measurements of their serum electrolytes, blood urea nitrogen, creatinine, and glucose levels, along with urine chemistry and urine specific gravity. Telephone follow-up by completion of a standardized questionnaire was obtained approximately 24 hours after discharge from the ED. RESULTS: Ninety-two of 96 enrolled patients completed the study. Three patients failed treatment (2 RIV and 1 RNG) and were excluded and hospitalized because of severe, intractable vomiting, and 1 patient was withdrawn secondary to an intussusception. Among 92 evaluable patients, 2 were found to be severely dehydrated (>10% change in body weight) and were excluded from analysis, leaving 90 patients (RNG: N = 46 and RIV: N = 44), who completed the study. Both RNG and RIV were found to be a safe and efficacious means of treating uncomplicated, acute moderate dehydration in the ED. Determinations of electrolytes, blood urea nitrogen, creatinine, or glucose were not found to be of value on an intent-to-treat basis in the care of these patients. The urine specific gravity and incidence of ketonuria declined from levels commensurate with moderate dehydration in the RNG group, but not as consistently so in the RIV group. Both RNG and RIV were substantially less expensive to administer than standard care with intravenous fluid deficit therapy in-hospital, and RNG was more cost-effective to administer over RIV in the outpatient setting. CONCLUSION: RNG and RIV administered in the ED are safe, efficacious, and cost-effective alternatives to the standard treatment for uncomplicated, acute moderate dehydration in young children. RNG is as efficacious as RIV, is no more labor intensive than RIV, and is associated with fewer complications. In addition, we found that most routine laboratory testing is of little value in these patients and should be avoided, except when clearly clinically indicated.

Child, Preschool↗

A novel imaging technique to measure capillary-refill time: improving diagnostic accuracy for dehydration in young children with gastroenteritis.

BACKGROUND: Assessment of dehydration in young children currently depends on clinical judgment, which is relatively inaccurate. By using digital videography, we developed a way to assess capillary-refill time more objectively. OBJECTIVE: Our goal was to determine whether digitally measured capillary-refill time assesses the presence of significant dehydration (> or = 5%) in young children with gastroenteritis more accurately than conventional capillary refill and overall clinical assessment. METHODS: We prospectively enrolled children with gastroenteritis, 1 month to 5 years of age, who were evaluated in a tertiary-care pediatric emergency department and judged by a triage nurse to be at least mildly dehydrated. Before any treatment, we measured the weight and digitally measured capillary-refill time of these children. Pediatric emergency physicians determined capillary-refill time by using conventional methods and degree of dehydration by overall clinical assessment by using a 7-point Likert scale. Postillness weight gain was used to estimate fluid deficit; beginning 48 hours after assessment, children were reweighed every 24 hours until 2 sequential weights differed by no more than 2%. We compared the accuracy of digitally measured capillary-refill time with conventional capillary refill and overall clinical assessment by determining sensitivities, specificities, likelihood ratios, and area under the receiver operator characteristic curves. RESULTS: A total of 83 patients were enrolled and had complete follow-up; 13 of these patients had significant dehydration (> or = 5% of body weight). The area under the receiver operator characteristic curves for digitally measured capillary-refill time and overall clinical assessment relative to fluid deficit (< 5% vs > or = 5%) were 0.99 and 0.88, respectively. Positive likelihood ratios were 11.7 for digitally measured capillary-refill time, 4.5 for conventional capillary refill, and 4.1 for overall clinical assessment. CONCLUSIONS: Results of this prospective cohort study suggest that digitally measured capillary-refill time more accurately predicts significant dehydration (> or = 5%) in young children with gastroenteritis than overall clinical assessment.

Blood Flow Velocity↗