Insensible Water Loss Research Articles

Differences in Temperature Changes in Premature Infants During Invasive Procedures in Incubators and Radiant Warmers

ABSTRACTPremature infants tend to lose heat quickly. This loss can be aggravated when they have received an invasive procedure involving a venous puncture. This research uses crossover design by conducting 2 intervention tests to compare 2 different treatments on the same sample. This research involved 2 groups with 18 premature infants in each. The process of data analysis used a statistical independent t test. Interventions conducted in an open incubator showed a p value of .001 which statistically related to heat loss in premature infants. In contrast, the radiant warmer p value of .001 statistically referred to a different range of heat gain before and after the venous puncture was given. The radiant warmer saved the premature infant from hypothermia during the invasive procedure. However, it is inadvisable for routine care of newborn infants since it can increase insensible water loss.

Can birds do it too? Evidence for convergence in evaporative water loss regulation for birds and mammals.

Birds have many physiological characteristics that are convergent with mammals. In the light of recent evidence that mammals can maintain a constant insensible evaporative water loss (EWL) over a range of perturbing environmental conditions, we hypothesized that birds might also regulate insensible EWL, reflecting this convergence. We found that budgerigars (Melopsittacus undulatus) maintain EWL constant over a range of relative humidities at three ambient temperatures. EWL, expressed as a function of water vapour pressure deficit, differed from a physical model where the water vapour pressure deficit between the animal and the ambient air is the driver of evaporation, indicating physiological control of EWL. Regulating EWL avoids thermoregulatory impacts of varied evaporative heat loss; changes in relative humidity had no effect on body temperature, metabolic rate or thermal conductance. Our findings that a small bird can regulate EWL are evidence that this is a common feature of convergently endothermic birds and mammals, and may therefore be a fundamental characteristic of endothermy.

Thermoregulatory role of insensible evaporative water loss constancy in a heterothermic marsupial.

'Insensible' evaporative water loss of mammals has been traditionally viewed as a passive process, but recent studies suggest that insensible water loss is under regulatory control, although the physiological role of this control is unclear. We test the hypothesis that regulation of insensible water loss has a thermoregulatory function by quantifying for the first time evaporative water loss control, along with metabolic rate and body temperature, of a heterothermic mammal during normothermia and torpor. Evaporative water loss was independent of ambient relative humidity at ambient temperatures of 20 and 30°C, but not at 25°C or during torpor at 20°C. Evaporative water loss per water vapour pressure deficit had a positive linear relationship with relative humidity at ambient temperatures of 20 and 30°C, but not at 25°C or during torpor at 20 or 25°C. These findings suggest that insensible water loss deviates from a physical model only during thermoregulation, providing support for the hypothesis that regulation of insensible evaporative water loss has a thermoregulatory role.

Cumulative changes in weight but not fluid volume balances reflect fluid accumulation in ICU patients.

The cumulative fluid balance of critically ill patients seems to be an outcome-relevant variable. However, there are no validated data for their reliability calculated for longer (> 5 days) periods of time. All ICU patients ≥ 18 years, with an ICU stay ≥ 5 days and a body weight ≤ 195 kg were evaluated from 1 January 2013 to 31 December 2013. Daily standardized weighing was performed using bed-integrated scales simultaneously with the daily 24-h fluid balance. Simultaneously, a fluid balance without and with insensible perspiration (10 ml/kg/day) was calculated for each 24 h. Primary endpoint: difference between cumulative fluid balance and body weight changes at the day of transfer to the normal ward or the day of death in the ICU, respectively, in each patient. All data are presented as medians with interquartile ranges (IQR) with 25 and 75 percentiles (IQR/25/75) unless otherwise noted. One hundred and six critically ill patients were evaluated; 82 survivors and 24 nonsurvivors. Cumulative 24-h fluid balances rose continuously while body weight decreased over time. Correction of cumulative fluid balances for insensible perspiration (10 ml/kg/day) also did not match with body weight changes. Only survivors had a significant loss in body weight -1.8 (27.5/-6.1/1.0) kg. Assuming that changes in body weight reflect changes in whole body water content cumulative daily fluid volume balances without or with correction for insensible water loss are not useful for estimating cumulative fluid balance of ICU patients. Survivors but not nonsurvivors had a significant loss of weight over time.

Case 1: Newborn with Skin and Other Abnormalities

A female infant is born precipitously via vaginal delivery after spontaneous rupture of membranes. The mother is a 24-year-old African American woman whose history includes 2 cesearean deliveries with no other medical concerns. The current pregnancy is complicated by limited prenatal care. The gestational age is unknown. The infant’s birthweight is 1,870 g, and her Ballard score is consistent with an estimated 32 weeks of gestation. In the delivery room, the neonate has a spontaneous cry but with frothy oral secretions and a low heart rate requiring positive pressure ventilation, intubation, and brief cardiopulmonary resuscitation. Apgar scores are 5 and 7 at 1 and 5 minutes, respectively. Physical examination is significant for extensive blistering of her face, neck, chest, and extremities. She is placed in a plastic bag for skin protection, thermoregulation, and reduction of insensible water losses. The patient is then transferred to the NICU, where mechanical ventilation is ordered and umbilical line placement is attempted. Admission examination reveals sloughing of oral mucosa as well as diffuse sloughing of perioral skin, right eyelid contraction, auricle skin denudation with hypoplastic and posteriorly rotated bilateral ears, and depressed nasal bridge (Fig 1). The extremities show congenital localized absence of skin (Fig 2), nail dystrophy, and muscle wasting (Fig 3). The skin is dressed with moisturizer and sterile dressing. Figure 1. Denudation of eyelid, ears, and perioral and oral mucosa with depressed nasal bridge. …

Dysautonomia Complicated by DDAVP Use for Diabetes Insipidus

This is the case of a normal, healthy 42-year old woman who sustained injuries in a spinning motor vehicle accident, leaving her with a series of diagnoses including Dysautonomia, that stumped all doctors. Because she was a Stanfordtrained anesthesiologist and intensivist, she was able to self-diagnose several major illnesses, including traumatic brain injury (TBI), diabetes insipidus (DI), vertebral artery dissection (VAD) with aneurysm, oculo-vestibular dysfunction, and hypothyroidism. The DI required prescription DDAVP therapy to prevent dehydration and death. Here, we focus on the entities of the “see-saw” effect that DDAVP has on Total Body Water (TBW), hyponatremia, hypernatremia, and the complications arising from the chronic, underlying hypovolemic state of dysautonomia. Dysautonomia, an “Invisible Illness” causing dysfunction of the autonomic nervous system, is a frequently undiagnosed, hypovolemic state that can lead to syncope. The best-case scenario is to titrate the DDAVP clinically with a tendency to under rather than to over-dose, preventing hypervolemia and hyponatremia. One can also provide ambient temperature and avoid overheating, consider insensible water loss, allow the pituitary gland healing, prevent further falls or head injuries, and recognize when it is time to go off the DDAVP. There are a paucity of scientific data on DI, and its incidence is rare with coincidental dysautonomia. These entities need to be appreciated and diagnosed, especially when they occur simultaneously. The patient is in a precarious position of dying from either too much TBW (i.e., hyponatremia, brain swelling, orbital swelling) or from too little TBW (i.e., decreased glomerular filtration rate, need for dialysis, death, and the need for fluid resuscitation that can also lead to death). Let us learn in a step-by-step fashion.

Alterations in Body Fluid Balance During Fin Swimming in 29 °C Water in a Population of Special Forces Divers.

Highly trained "combat swimmers" encounter physiological difficulties when performing missions in warm water. The aim of this study was to assess the respective roles of immersion and physical activity in perturbing fluid balance of military divers on duty in warm water. 12 trained divers performed 2 dives each (2 h, 3 m depth) in fresh water at 29 °C. Divers either remained Static or swam continuously (Fin) during the dive. In the Fin condition, oxygen consumption and heart rate were 2-fold greater than during the Static dive. Core and skin temperatures were also higher (Fin: 38.5±0.4 °C and 36.2±0.3 °C and Static: 37.2±0.3 °C and 34.3±0.3 °C; respectively p=0.0002 and p=0.0003). During the Fin dive, the average mass loss was 989 g (39% urine loss, 41% sweating and 20% insensible water loss and blood sampling); Static divers lost 720 g (84% urine loss, 2% sweating and 14% insensible water loss and blood sampling) (p=0.003). In the Fin condition, a greater decrease in total body mass and greater sweating occurred, without effects on circulating renin and aldosterone concentrations; diuresis was reduced, and plasma volume decreased more than in the Static condition.

Insensible water loss through adult extracorporeal membrane oxygenation circuit: an in vitro study.

Patients on extracorporeal membrane oxygenation (ECMO) are critically ill, and fluid balance need to be managed as accurately as possible. Previous studies have focused on insensible water loss through neonatal ECMO circuit and showed that water loss through the ECMO circuit was correlated with the sweep-gas flow rates. Current study is the first study focusing on insensible water loss through adult ECMO circuit. An in vitro extracorporeal circuit consisting of Jostra Quadrox D membrane oxygenator and centrifugal pump was primed with normal saline. The amount of water loss through the ECMO circuit was found to be linearly correlated with the sweep-gas flow rate and fluid temperature. For every liter per minute of sweep-gas flow at 37°C, 0.046 ml/min of water will be lost, and for every change of fluid temperature by 1°C, water content loss will be changed by 0.0026 ml/min by multiple linear regression (R = 0.996). The average daily water loss for every liter per minute of sweep-gas flow at 33, 34, 35, 36, 37, 38, and 39°C were 51.3, 55, 58.8, 62.5, 66.2, 70.0, and 73.7 ml/day, respectively.

Fever: Measuring and Managing

1. Henry M. Adam, MD 1. Editor, In Brief, Bronx, NY 1. 1. Sullivan JE, 2. Farrar HC Clinical Report—Fever & Antipyretic Use in Children. Sullivan JE, Farrar HC Section on Clinical Pharmacology & Therapeutics and Committee on Drugs. Pediatrics. 2011;127:580–587 [OpenUrl][1][Abstract/FREE Full Text][2] 2. 1. Schmitt BD Fever Phobia: Misconceptions of Parents about Fevers. Schmitt BD. Am J Dis Child. 1980;134:176–181 [OpenUrl][3][CrossRef][4][PubMed][5] 3. 1. May A, 2. Bauchner H Fever Phobia: The Pediatrician’s Contribution. May A, Bauchner H. Pediatrics. 1992;90:851–854 [OpenUrl][6][Abstract/FREE Full Text][7] 4. 1. Simon HB Hyperthermia. Simon HB. N Engl J Med. 1993;329:483–487 [OpenUrl][8][CrossRef][9][PubMed][10][Web of Science][11] 5. 1. Adam HM 1. McInerny TK, 2. Adam HM, 3. Campbell DE, 4. Kamat DM, 5. Kelleher KJ Physiology & Management of Fever. Adam HM. In: McInerny TK, Adam HM, Campbell DE, Kamat DM, Kelleher KJ, eds. American Academy of Pediatrics Textbook of Pediatric Care. Elk Grove Village, IL: American Academy of Pediatrics; 2009:418–422 At least in Western cultures we have a strong tradition of viewing fever not only as a response to illness but also as a disease itself. Although our science teaches us that fever, as part of the inflammatory response, is only a sign or symptom of the real pathologic process, our nomenclature (blackwater, cat scratch, dengue, hay, jungle, puerperal, rat bite, relapsing, rheumatic, Rocky Mountain spotted, scarlet, typhoid, and yellow fever) reinforces the temptation to treat fever as if it were the noxious culprit itself. Fever, as opposed to hyperthermia, rarely poses a threat to a child’s well-being; in fact, as an energy-expensive phenomenon, fever is not likely to have weathered evolution without conferring some survival benefit. Considering that fever is the most common signal of illness in children, serving as the cause of as many as a third of all pediatric office visits, we would do well to clarify our approach to its management that is distinct from the illnesses that cause it. Fever is a regulated elevation of body temperature, mediated by the anterior hypothalamus, which occurs in response to any insult that stimulates the body’s inflammatory defenses. Similar to a thermostat, the hypothalamic set point controls the temperature the body tries to maintain. Some provocation, in children most commonly a viral infection, induces macrophages to release cytokines that function as endogenous pyrogens. They circulate to the anterior hypothalamus, where they increase local levels of prostaglandin E2 and induce an increase in the set point. Several mechanisms then come into play to bring the core temperature (the temperature of blood within the pulmonary artery) up to the new set point. Because … [1]: {openurl}?query=rft.jtitle%253DPediatrics%26rft_id%253Dinfo%253Adoi%252F10.1542%252Fpeds.2010-3852%26rft_id%253Dinfo%253Apmid%252F21357332%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [2]: /lookup/ijlink?linkType=ABST&journalCode=pediatrics&resid=127/3/580&atom=%2Fpedsinreview%2F34%2F8%2F368.atom [3]: {openurl}?query=rft.jtitle%253DArchives%2Bof%2BPediatrics%2Band%2BAdolescent%2BMedicine%26rft.stitle%253DArch%2BPediatr%2BAdolesc%2BMed%26rft.issn%253D0002-922X%26rft.aulast%253DSchmitt%26rft.auinit1%253DB.%2BD.%26rft.volume%253D134%26rft.issue%253D2%26rft.spage%253D176%26rft.epage%253D181%26rft.atitle%253DFever%2BPhobia%253A%2BMisconceptions%2Bof%2BParents%2BAbout%2BFevers%26rft_id%253Dinfo%253Adoi%252F10.1001%252Farchpedi.1980.02130140050015%26rft_id%253Dinfo%253Apmid%252F7352443%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [4]: /lookup/external-ref?access_num=10.1001/archpedi.1980.02130140050015&link_type=DOI [5]: /lookup/external-ref?access_num=7352443&link_type=MED&atom=%2Fpedsinreview%2F34%2F8%2F368.atom [6]: {openurl}?query=rft.jtitle%253DPediatrics%26rft.stitle%253DPediatrics%26rft.issn%253D0031-4005%26rft.aulast%253DMay%26rft.auinit1%253DA.%26rft.volume%253D90%26rft.issue%253D6%26rft.spage%253D851%26rft.epage%253D854%26rft.atitle%253DFever%2BPhobia%253A%2BThe%2BPediatrician%2527s%2BContribution%26rft_id%253Dinfo%253Apmid%252F1437424%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [7]: /lookup/ijlink?linkType=ABST&journalCode=pediatrics&resid=90/6/851&atom=%2Fpedsinreview%2F34%2F8%2F368.atom [8]: {openurl}?query=rft.jtitle%253DNew%2BEngland%2BJournal%2Bof%2BMedicine%26rft.stitle%253DNEJM%26rft.issn%253D0028-4793%26rft.aulast%253DSimon%26rft.auinit1%253DH.%2BB.%26rft.volume%253D329%26rft.issue%253D7%26rft.spage%253D483%26rft.epage%253D487%26rft.atitle%253DHyperthermia%26rft_id%253Dinfo%253Adoi%252F10.1056%252FNEJM199308123290708%26rft_id%253Dinfo%253Apmid%252F8332154%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [9]: /lookup/external-ref?access_num=10.1056/NEJM199308123290708&link_type=DOI [10]: /lookup/external-ref?access_num=8332154&link_type=MED&atom=%2Fpedsinreview%2F34%2F8%2F368.atom [11]: /lookup/external-ref?access_num=A1993LR44300008&link_type=ISI

Effects of 6-h exposure to low relative humidity and low air pressure on body fluid loss and blood viscosity

The purpose of this study was to investigate the effects of 6-h exposure to low relative humidity (RH) and low air pressure in a simulated air cabin environment on body fluid loss (BFL) and blood viscosity. Fourteen young healthy male subjects were exposed to four conditions, which combined RH (10% RH or 60% RH) and air pressure (NP: sea level or LP: equivalent to an altitude of 2000m). Subjects remained seated on a chair in the chamber for 6h. Their diet and water intake were restricted before and during the experiment. Insensible water loss (IWL) in LP10% condition was significantly greater than in NP60% condition; thus, combined 10%RH and LP conditions promoted a greater amount of IWL. The BFL under the LP condition was significantly greater than that under the NP condition. Blood viscosity significantly increased under LP conditions. Increases in red blood cell counts (RBCs) and BFL likely contributed to the increased blood viscosity. These findings suggest that hypobaric-induced hypoxia, similar to the conditions in the air cabin environment, may cause increased blood viscosity and that the combined low humidity and hypobaric hypoxia conditions increase IWL.

Regional variations in transepidermal water loss, eccrine sweat gland density, sweat secretion rates and electrolyte composition in resting and exercising humans

Literature from the past 168 years has been filtered to provide a unified summary of the regional distribution of cutaneous water and electrolyte losses. The former occurs via transepidermal water vapour diffusion and secretion from the eccrine sweat glands. Daily insensible water losses for a standardised individual (surface area 1.8 m2) will be 0.6–2.3 L, with the hands (80–160 g.h−1) and feet (50–150 g.h−1) losing the most, the head and neck losing intermediate amounts (40–75 g.h−1) and all remaining sites losing 15–60 g.h−1. Whilst sweat gland densities vary widely across the skin surface, this same individual would possess some 2.03 million functional glands, with the highest density on the volar surfaces of the fingers (530 glands.cm−2) and the lowest on the upper lip (16 glands.cm−2). During passive heating that results in a resting whole-body sweat rate of approximately 0.4 L.min−1, the forehead (0.99 mg.cm−2.min−1), dorsal fingers (0.62 mg.cm−2.min−1) and upper back (0.59 mg.cm−2.min−1) would display the highest sweat flows, whilst the medial thighs and anterior legs will secrete the least (both 0.12 mg.cm−2.min−1). Since sweat glands selectively reabsorb electrolytes, the sodium and chloride composition of discharged sweat varies with secretion rate. Across whole-body sweat rates from 0.72 to 3.65 mg.cm−2.min−1, sodium losses of 26.5–49.7 mmol.L−1 could be expected, with the corresponding chloride loss being 26.8–36.7 mmol.L−1. Nevertheless, there can be threefold differences in electrolyte losses across skin regions. When exercising in the heat, local sweat rates increase dramatically, with regional glandular flows becoming more homogeneous. However, intra-regional evaporative potential remains proportional to each local surface area. Thus, there is little evidence that regional sudomotor variations reflect an hierarchical distribution of sweating either at rest or during exercise.

Insensible Water Loss during the First Week of Life of Extremely Low Birth Weight Infants Less than 25 Gestational Weeks under High Humidification

Insensible Water Loss during the First Week of Life of Extremely Low Birth Weight Infants Less than 25 Gestational Weeks under High Humidification

Hypertension in Severe Pediatric Diabetic Ketoacidosis

Dehydration from fluid loss secondary to glycosuria is the central pathogenesis of diabetic ketoacidosis (DKA). Decreased oral intake and increased insensible water loss are also common in DKA. Severe dehydration should lead to hypovolemia and hypotension. We present a case of DKA with severe dehydration and hypertension in contrast to expected hypotension. The aim of this article was to increase awareness that pediatric DKA could present with hypertension, and this should be looked at and included in DKA management protocols.

Insensible water loss from the Hilite 2400LT oxygenator: an in vitro study

Neonatal extracorporeal membrane oxygenation (ECMO) patients are particularly vulnerable to the effects of uncompensated insensible water loss resulting in hypernatraemia. There exists a long-standing relationship between hypernatraemia and varying degrees of cerebral dysfunction. The aim of this study is to explore the degree to which free water loss occurs across a commonly used ECMO oxygenator, the polymethylpentene (PMP) membrane Hilite 2400LT (Medos, Medizintechnik AG, Stolberg, Germany). The secondary aim is to assess to what extent the addition of heat and/or humidity ameliorates this water loss. An ECMO circuit consisting of a centrifugal pump and a Hilite 2400LT oxygenator was primed with crystalloid and albumin. Each experimental trial was carried out in triplicate, with gas flow rates of 1, 3 and 4.8 L/min being investigated. Fluid loss was assessed at six time points over a 24-hour period. Water loss increased significantly from 1 to 3 L/min gas flow (p=0.05) and from 3 to 4.8 L/min gas flow (p=0.025). The mean water loss differences between the differing gas flow trials per L/min gas flow were non-significant (72.4 ±3.9 ml/24 hrs). The effect of heating the gas to 37 °C did not significantly alter water loss, whereas heat and humidity reduced water loss significantly (p=0.009). Insensible water loss from a Hilite 2400LT oxygenator is approximately 72 ml/day per L/min gas flow over 24 hrs. Heating and humidifying the gas reduces the fluid loss significantly to approximately 8 ml/L/min gas flow over 24 hrs (p=0.009).

A Clinical Approach to the Treatment of Chronic Hypernatremia

Hypernatremia is a commonly encountered electrolyte disorder occurring in both the inpatient and outpatient settings. Community-acquired hypernatremia typically occurs at the extremes of age, whereas hospital-acquired hypernatremia affects patients of all age groups. Serum sodium concentration is linked to water homeostasis, which is dependent on the thirst mechanism, arginine vasopressin, and kidney function. Because both hypernatremia and the rate of correction of hypernatremia are associated with significant morbidity and mortality, prompt effective treatment is crucial. Chronic hypernatremia can be classified into 3 broad categories, hypovolemic, euvolemic, and hypervolemic forms, with each form having unique treatment considerations. In this teaching case, we provide a clinically based quantitative approach to the treatment of both hypervolemic and hypovolemic hypernatremia, which occurred in the same patient during the course of a prolonged illness.

Early Skin-to-Skin Care in Extremely Preterm Infants: Thermal Balance and Care Environment

To evaluate infant thermal balance and the physical environment in extremely preterm infants during skin-to-skin care (SSC). Measurements were performed in 26 extremely preterm infants (gestational age 22-26 weeks; postnatal age, 2-9 days) during pretest (in incubator), test (during SSC), and posttest (in incubator) periods. Infants' skin temperature and body temperature, ambient temperature, and relative humidity were measured. Evaporimetry was used to determine transepidermal water loss, and insensible water loss through the skin was calculated. The infants maintained a normal body temperature during SSC. Transfer to and from SSC was associated with a drop in skin temperature, which increased during SSC. Ambient humidity and temperature were lower during SSC than during incubator care. Insensible water loss through the skin was higher during SSC. SSC can be safely used in extremely preterm infants. SSC can be initiated during the first week of life and is feasible in infants requiring neonatal intensive care, including ventilator treatment. During SSC, the conduction of heat from parent to infant is sufficiently high to compensate for the increase in evaporative and convective heat loss. The increased water loss through the skin during SSC is small and should not affect the infant's fluid balance.

Monitoring fluid balance in the neonate

In this issue of Acta Paediatrica, Bekhof et al. report on the reliability of fluid balance charts for newborn infants (1), demonstrating that charts relate poorly to serial determinations of body weight. Of further concern, their results reveal no systematic deviation, that is, the charts seem both to overand underestimate the balance in a non-predictable manner. From their data, one cannot conclude whether the deviations are due mainly to errors in the recording of inor output of fluid, or both. The results are in accordance with studies in adults (2). The authors should be commended for their effort to elucidate the performance of one of the most common monitoring methods used in the neonatal intensive care unit. Perturbations of fluid and electrolyte homeostasis are commonly encountered in the ill and ⁄or preterm neonate. Most disturbances are primarily related to imbalances in the amount of water ⁄fluid provided relative to the losses, with deviations in electrolyte concentrations occurring concomitantly. Didactic examples are the rapid weight loss and hypernatraemia often observed in extremely preterm infants during the first days because of their high insensible water losses, and the overhydration and hyponatraemia commonly encountered in asphyxiated infants with transient oliguric renal failure. Needless to say, recording urinary output and keeping track of the fluid volumes provided has an important role in the monitoring of the intensive care patient, but the data do not provide reliable information on net fluid balance and might indeed be misleading. The maintenance of an adequate fluid balance has a tremendous potential impact on the shortand long-term outcome in babies receiving neonatal intensive care. In many cases, fluid balance disturbances complicate the management of and delay recovery from the primary illness. Moreover, the fluid balance disturbance per se (e.g. hyperor hyponatraemia) has repeatedly been shown to impact on the infants’ future health. It is encouraging to note that, in the high-tech setting of modern neonatology, a low-tech and low-cost care routine receives attention, and most importantly, merits publication. In several studies in the field of fluid management, conclusions have been drawn by retrospectively relating important neonatal outcomes such as the prevalence of BPD and PDA to the amount of fluid (derived from charts) provided during the first postnatal days (3,4). These studies suggest that a careful fluid restriction might reduce the risk of BPD and ⁄or PDA. In perspective of the conclusions from the Bekhof’s study, such analyses may have been greatly influenced by (the lack of) fluid chart performance. So – if fluid charts are of limited value – what methodology should we pursue for further evaluation and development? Weighing is considered the gold standard and is invaluable, being simple, reasonably low-cost and in most situations reliable (5,6). However, monitoring weight alone does not provide information on fluid input vs. output or on the relative changes in hydration and body solids. In addition, several studies support the notion that an early postnatal reduction in body water (commonly referred to as the physiological contraction of the extracellular fluid space) may take place in spite of an early increase in body weight (7,8). Thus, by judging fluid balance solely from a gain in weight, the Invited Commentary for Asperen et al., Reliability of the fluid balance in neonates, pages 479–483. Acta Paediatrica ISSN 0803–5253

The effect of agility exercise on eicosanoid excretion, oxidant status, and plasma lactate in dogs

BackgroundThe objective was to determine the effects of agility exercise on dogs of different skill levels with respect to urinary eicosanoids, urinary 15F2t-isoprostane (lipid peroxidation marker) and hematological/biochemical changes in plasma. Fifteen adult dogs had blood and urine samples obtained prior to, immediately and 4-hours following an agility exercise.ResultsHematocrit, red blood cells (RBC), albumin, and hemoglobin increased following exercise, with greatest increases correlating to increased skill group (novice, intermediate, masters); at 4-hours post-exercise, hematocrit, RBC, and hemoglobin were decreased. Phosphorus increased following exercise with the greatest increase in novice and intermediates. Plasma lactate increased 3.6-fold in masters, 3.2-fold in intermediates, and 1.2-fold in novice dogs. Urine thromboxane B2 (TXB2) more than tripled 4-hours post-exercise while 6-keto prostaglandin F1α (PGF1α, prostacyclin metabolite), prostaglandin E2 metabolites (13,14-dihydro-15-keto-prostaglandin A2 and 13,14-dihydro-15-keto-prostaglandin E2), and 13,14-dihydro-15-keto prostaglandin F2α were unaffected as determined by a competitive enzyme immunoassay and standardized by division with urine creatinine. Urine 15F2t-isoprostane increased insignificantly.ConclusionsAlterations in the plasma post-exercise were likely due to hemoconcentration from insensible water loss, splenic contraction and sympathetic stimulation while 4-hours later autohemodilution reduced RBC parameters. Elevations in plasma lactate and urinary TXB2 correlated with advanced skill level/speed of the dogs.

Increased Insensible Water Loss Contributes to Aging Related Dehydration

Dehydration with aging is attributed to decreased urine concentrating ability and thirst. We further investigated by comparing urine concentration and water balance in 3, 18 and 27 month old mice, consuming equal amounts of water. During water restriction, 3 month old mice concentrate their urine sufficiently to maintain water balance (stable weight). 18 month old mice concentrate their urine as well, but still lose weight (negative water balance). 27 month old mice do not concentrate their urine as well and lose even more weight than the 18 month old mice, indicating a larger negative water balance. Negative water balance in older mice is accompanied by increased vasopressin excretion, providing further evidence of dehydration. All 3 groups maintain water balance while consuming only the water in gel food containing 56% water. However, both older groups excrete a smaller volume of urine of higher osmolality, indicating greater extra urinary water loss. Since their feces also contain less water, the excess water lost by the older mice apparently is through other routes, presumably insensible loss through the respiratory tract and skin. The greater insensible water loss occurs at an earlier age (18 months) than decreased urine concentrating ability (27 months). We propose that insensible water loss through skin and respiration increases with age, making a major contribution to aging related dehydration.

Increased insensible water loss contributes to the aging related disturbance of water balance

Disturbed water balance that occurs with aging was previously attributed to reduced urinary concentrating ability and thirst. We investigated the phenomenon by measuring urinary concentrating ability and water balance in 3, 18 and 27 month old mice, consuming constant amounts of food and water. During water restriction, 3 month mice concentrated their urine sufficiently to maintain water balance (stable weight). 18 month mice concentrated their urine as well as the younger mice, but still lost weight, indicating negative water balance. 27 month mice did not concentrate their urine as well as younger mice and lost even more weight than the 18 month mice, indicating a larger negative water balance. All 3 groups maintained water balance while consuming only the water in gel food containing 56% water. However, both older groups excreted a smaller volume of urine of higher osmolality, indicating greater extra urinary water loss. Since their feces contained less water, the excess water lost by the older mice apparently was through other routes, namely insensible loss through the respiratory tract and skin. The greater insensible water loss occurred at an earlier age (18 months) than decreased urinary concentrating ability (27 months). We propose that water loss through those routes increases with age, making a major contribution to aging related deficit of water balance. Supported by the Intramural Program of NHLBI