Biomarkers in premature calves with and without respiratory distress syndrome.

BACKGROUND: Approaches to the evaluation of pulmonary arterial hypertension (PAH) in premature calves by using lung-specific epithelial and endothelial biomarkers are needed. OBJECTIVE: To investigate the evaluation of PAH in premature calves with and without respiratory distress syndrome (RDS) by using lung-specific epithelial and endothelial biomarkers and determine the prognostic value of these markers in premature calves. ANIMALS: Fifty premature calves with RDS, 20 non-RDS premature calves, and 10 healthy term calves. METHODS: Hypoxia, hypercapnia, and tachypnea were considered criteria for RDS. Arterial blood gases (PaO2 , PaCO2 , oxygen saturation [SO2 ], base excess [BE], and serum lactate concentration) were measured to assess hypoxia. Serum concentrations of lung-specific growth differentiation factor-15 (GDF-15), asymmetric dimethylarginine (ADMA), endothelin-1 (ET-1), vascular endothelial growth factor (VEGF), and surfactant protein D (SP-D) were measured to assess PAH. RESULTS: Arterial blood pH, PaO2 , SO2 , and BE of premature calves with RDS were significantly lower and PaCO2 and lactate concentrations higher compared to non-RDS premature and healthy calves. The ADMA and SP-D concentrations of premature calves with RDS were lower and serum ET-1 concentrations higher than those of non-RDS premature and healthy calves. No statistical differences for GDF-15 and VEGF were found among groups. CONCLUSIONS AND CLINICAL IMPORTANCE: Significant increases in serum ET-1 concentrations and decreases in ADMA and SP-D concentrations highlight the utility of these markers in the diagnosis of PAH in premature calves with RDS. Also, we found that ET-1 was a reliable diagnostic and prognostic biomarker for PAH and predicting mortality in premature calves.

Profiling of miRNAs in neonatal cloned bovines with collapsed lungs and respiratory distress.

Neonatal respiratory distress is a major mortality factor in cloned animals; however, the pathogenesis of this disease has rarely been investigated. Previous studies have shown that miRNAs regulate critical genes related to lung development, cell differentiation, surfactant synthesis, secretion and lung disease. This study aimed to examine differentially expressed miRNAs in collapsed lungs of cloned bovine neonates and normal lungs in order to identify key pathways and functions that might be related to the pathogenesis of neonatal respiratory distress. In this study, miRNA transcriptomes of collapsed lungs of neonatal cloned bovines and normal lungs were analysed by next-generation sequencing and the results were validated using quantitative real-time PCR (qRT-PCR). A total of 177 differentially expressed miRNAs were identified in the two groups (fold change > 2, RPM ≥ 5), some of which were associated with type II cell differentiation, for example, mmu-miR-29a-5p_L-2R+1, hsa-miR-200c-5p_L-1R+1 and mmu-miR-18a-3p_R+1. The differentially expressed miRNAs were predicted to 6,031 target genes. By Gene Ontology (GO) and Kyoto Encyclopeida of Genes and Genomes (KEGG) DATA base, 133 significant GO terms (p < .05) and 13 significant KEGG pathways (p < .05) were obtained. Many of them were associated with lung development and surfactant homoeostasis, such as lipid biosynthetic processes, protein transport, endocytosis, lysosome, endosome, Golgi apparatus and membrane. Our results of miRNAs express profiles may partially explain the respiratory distress and lung collapse in neonatal bovine clones and could provide novel insights into roles of miRNAs in regulation of lung collapse and neonatal respiratory distress in cloned farm animals.

Neonatal respiratory distress syndrome and underlying mechanisms in cloned cattle.

Neonatal respiratory distress is a major mortality factor in cloned animals, but the pathogenesis of this disease is rarely investigated. In this study, four neonatal cloned cattle, born after full-term gestation, exhibited symptoms of neonatal respiratory distress syndrome (NRDS), which included symptoms of hyaline membrane disease as well as disordered surfactant homeostasis in their collapsed lungs. No differences in DNA methylation or histone modifications correlated with the suppressed SPB and SPC transcription observed in the cloned cattle group (p > 0.05), whereas TTF-1 occupancy at SPB and SPC promoter regions in cloned cattle was significantly reduced to 24% and 20% that of normal lungs, respectively (SPB, p < 0.05; SPC, p < 0.01). Decreased TTF1 expression, dysregulation of SPB and SPC transcription by TTF-1, and disordered proteolytic processing of Surfactant protein B precursor together potentially contribute to the disruption of surfactant homeostasis and NRDS in bovine clones. Elucidation of the associated mechanisms should facilitate the development of novel preventive or therapeutic strategies to reduce the mortality rate of cloned animals and to improve the efficiency of SCNT technology.

Venous lactate, pH and partial pressure of carbon dioxide levels as prognostic indicators in 110 premature calves with respiratory distress syndrome.

Hyperlactatemia, hypercapnia, low pH and low oxygen saturation (SatO2) are commonly observed in premature calves. These clinical indicators are associated with increased mortality in preterm human newborns with respiratory distress syndrome (RDS). The aim of this study was to investigate the prognostic importance of venous pH, partial pressure of carbon dioxide (pCO2) and lactate level and which parameters are related with mortality in premature calves with RDS. All premature calves (52 male/58 female) were admitted to clinic within 12-24 hours after birth and blood samples were also taken into heparinised plastic syringes from the jugular vein within 30 minutes following admission. Diagnosis of RDS was made by both clinical signs and blood gas results. For the evaluation of independent samples, t test was used to compare the venous blood gas indicators of surviving and non-surviving premature calves. Receiver operating characteristics curves were used to determine a cut-off value in terms of lactate and pCO2 measurements among non-surviving and surviving calves. Venous pH, pCO2, SatO2, base deficit, bicarbonate (HCO3) and lactate levels showed a significant variance between surviving and non-surviving calves. Mean venous pH, pCO2, SatO2, lactate levels in non-surviving premature calves was 7.05, 78.9 mm Hg, 16.1 per cent and 9.50 mmol/l, respectively. Mean pH, pCO2, SatO2 and lactate levels in surviving premature calves were 7.29, 56.3 mm Hg, 25.5 per cent and 5.1 mmol/l, respectively. The cut-off values for lactate and pCO2 were 7.5 mmol/l and 63.5 mm Hg, respectively. In conclusion, the results of the study show that venous blood lactate and pCO2 have prognostic importance in premature calves with RDS.

Cardiac biomarkers in premature calves with respiratory distress syndrome.

The aim of this study was to determine the clinical relevance of cardiac biomarkers [troponin I and T, creatine kinase-MB fraction (CK-MB) and lactate dehydrogenase (LDH)] in premature calves with respiratory distress syndrome. Seventy premature calves were admitted to the clinic within 24 h after birth. Respiratory distress syndrome was diagnosed in premature calves by clinical examination and venous blood gas analysis. Ten healthy calves, aged 5 days, were used as control. Cardiac troponin I and T were analysed using ELISA and ELFA, respectively. Serum CK-MB and LDH were also analysed in an automatic analyser. The calves had low venous pH, pO2, O2 saturation and high pCO2 values consistent with dyspnoea, hypoxaemia, and inadequate oxygen delivery. Mean serum troponin I, troponin T, CK-MB and LDH levels were increased in the premature calves compared to the control group. In conclusion, the results in this study demonstrated that serum CK-MB, troponin I and troponin T concentrations could be used for evaluating myocardial injury in premature calves with respiratory distress syndrome.

Cerebral Effect of Intratracheal Aerosolized Surfactant Versus Bolus Therapy in Preterm Lambs.

OBJECTIVE: Aerosolization has been proposed as a useful alternative to rapid intratracheal instillation for the delivery of exogenous surfactant in neonatal respiratory distress syndrome. However, there is a lack of information regarding the likely safety of this new therapeutic approach for the neonatal brain. We aimed to compare the cerebral effects of aerosolized versus bolus surfactant administration in premature lambs with respiratory distress syndrome. DESIGN: Prospective randomized study. SETTING: BioCruces Institute Animal Research Facility. SUBJECTS: Fourteen intensively monitored and mechanically ventilated preterm lambs. INTERVENTIONS: Preterm lambs were randomly assigned to receive intratracheal aerosolized surfactant or bolus surfactant. Brain hemodynamics (cerebral and regional cerebral blood flow) and cerebral oxygen metabolism (cerebral oxygen delivery, cerebral metabolic rate of oxygen, and oxygen extraction fraction) were measured every 30 minutes for 6 hours. We also performed cerebral biochemical and histological analysis. MEASUREMENTS AND MAIN RESULTS: In preterm lambs with respiratory distress syndrome, cerebral blood flow, regional cerebral blood flow, cerebral oxygen delivery, and cerebral metabolic rate of oxygen increased significantly in the bolus surfactant group during the first 5 minutes, without changes in cerebral oxygen extraction fraction. By 60 minutes, all parameters had decreased in both groups, cerebral blood flow and regional cerebral blood flow (in inner and cerebellum brainstem regions) remaining higher in the bolus surfactant than in the aerosolized surfactant group. Overall, the impact of aerosol surfactant was not significantly different to that of bolus surfactant in terms of cerebral necrosis, edema, inflammation, hemorrhage, infarct, apoptosis, or oxidative stress. CONCLUSIONS: In preterm lambs with severe respiratory distress syndrome, aerosol surfactant administration seems to be as safe as bolus administration, showing more stable cerebral hemodynamics and cerebral oxygen metabolism to the same dose of surfactant administered as a standard bolus.

Treatment of premature calves with clinically diagnosed respiratory distress syndrome.

BACKGROUND: Respiratory distress syndrome (RDS) has been reported previously in premature calves. However, there have been no published data on the effect of surfactant replacement therapy in the treatment of premature calves with RDS. HYPOTHESIS: Surfactant replacement therapy added to the standard treatment for premature calves clinically diagnosed with RDS would increase the viability of the calves. ANIMALS: Twenty-seven premature calves with clinically diagnosed RDS. METHODS: Twenty calves were instilled intratracheally with bovine lung surfactant extract and provided with standard treatment for RDS (surfactant group). Seven calves were given only standard care for RDS without surfactant therapy and placed in the control group. Standard treatment for newborn calves with RDS includes warming, administration of intranasal oxygen, fluid replacement, administration of antibiotics, and immunoglobulin solution. Arterial blood samples were collected from the calves at 3 observation points, the first just before treatment (hour 0) and at 2 hours (hour 2) and 24 hours (hour 24) after treatment was started to determine if ventilation was adequate, improving, or deteriorating. Blood gases, pH, bicarbonate, and lactate concentrations were measured. RESULTS: In the surfactant group, mean partial pressure of oxygen significantly increased at hours 2 and 24. Mean partial pressure of carbon dioxide decreased and mean arterial blood pH increased at hour 24 in the surfactant group compared with the control group (P < .05). Of the 20 calves in the surfactant group, 12 survived and 8 died. All 7 calves in the control group died. CONCLUSIONS AND CLINICAL IMPORTANCE: The results of this study suggest that surfactant replacement therapy may reduce neonatal deaths in premature calves with clinically diagnosed RDS.

Asociación molecular y función del agente tensioactivo pulmonar de ternera / Molecular association and function of calf lung surfactant

El agente tensioactivo pulmonar es un material compuesto de fosfolípidos, lípidos neutros y proteínas que se encuentra en la superficie alveolar de los pulmones y facilita la ventilación alveolar. La organización molecular de los componentes del agente tensioactivo aislado de pulmones de ternera fue analizada por calorimetría diferencial de barrido y por dispersión dinámica de luz y posteriormente comparada con los componentes organizados en liposomas uni y multilamelares; además, se probó la actividad de superficie al desarrollar en cobayos el síndrome de dificultad respiratoria. Los estudios de calorimetría mostraron que las interacciones lípido-proteína fueron considerablemente abatidas en el agente tensioactivo nativo, en comparación con las del agente tensioactivo en forma de liposomas uni o multilamelares. Los experimentos de dispersión dinámica de luz indicaron que el agente tensioactivo nativo tiene forma fibrilar con interacciones limitadas entre lípidos y proteínas, lo que sugiere que se encuentra organizado en una estructura en forma de reja formando una película de estructura estable. Los resultados obtenidos resaltan la importancia de la organización molecular del agente tensioactivo. Cuando éste fue usado para tratar a los animales con síndrome de dificultad respiratoria, los valores del pH arterial y de PaCO2 mejoraron casi hasta alcanzar los valores normales; cuando se utilizó el agente tensioactivo reconstituído como liposomas uni o multilamelares, los animales no se recuperaron. Es importante enfatizar que el método seguido en el protocolo de aislamiento del agente tensioactivo pulmonar de ternera permitió obtenerlo en una forma fisiológicamente activa.

Surfactant, a highly surface-active material composed of phospholipids, neutral lipids and proteins, lines the lungs' alveolar surface facilitating alveolar ventilation. The molecular organization of surfactant components isolated from calf-lungs was analyzed by differential-scanning calorimetry and dynamic light-scattering, and subsequently compared to surfactant components organized in uni and multilamellar liposomes. The respiratory distress syndrome developed in adult guinea pigs was used for assessing surfactant activity. Calorimetry studies showed that lipid-protein interactions were considerably abated in native surfactant as compared to those of surfactant in uni or multi-lamellar liposomes. Light-scattering experiments indicated that native surfactant has a fibrillar shape with limited lipid-protein interactions, suggesting that it is organized in a lattice-like structure forming a stable film. These findings underscore the importance of the native molecular organization of surfactant. When surfactant reconstituted as uni- or multilamellar liposomes was administred to animals under respiratory distress, they did not recover. In contrast, when native surfactant was used to treat sick animals, arterial pH and PaCO2 values improved, almost reaching normal values. It is important to emphasize that fewer steps in the protocol for isolation of calf lung surfactant made it possible to obtain it in a physiologically active molecular form.

Respiratory problems of newborn calves.

Cardiopulmonary development of fetus is a timely event that proceeds to the point that birth can take place. Calves may be born premature, and because of surfactant deficiency, develop the respiratory distress syndrome. More research needs to be done on fetal lung development in calves to determine the age when maturity has been reached for compatibility with extrauterine life. Also, more specific therapy regimens need to be developed that will enhance lung development. The birthing process is a major event that must proceed in a timely fashion. Any delay in delivery will compromise further the already hypoxic fetus. Practitioners need to recognize the severely hypoxic/ asphyxiated calf and be prepared to therapeutically support the cardiopulmonary systems.

Prophylaxis of respiratory distress syndrome in premature calves by administration of dexamethasone or a prostaglandin F2 alpha analogue to their dams before parturition.

OBJECTIVE: To investigate effects of preterm induction of calving by administration of flumethasone and dinoprost on the lecithin-to-sphingomyelin ratio in amniotic fluid and on neonatal respiratory distress after birth. ANIMALS: 45 dairy cows and their newborn calves. PROCEDURE: Amniotic fluid from 45 cows was obtained and tested between days 258 and 270 of gestation. Cows were then given flumethasone (10 mg; n = 15), dinoprost (25 mg; n = 15), or saline solution (n = 15). Thirty hours later, left flank cesarean section was performed, amniotic fluid was collected, and the calf was delivered. Blood for determination of progesterone was withdrawn at amniotic fluid sample collections and before induction of calving. Blood for analysis of pH and base deficit was collected from calves during cesarean section and repeatedly after birth. Phospholipids in amniotic fluid were measured by thin-layer chromatography, and progesterone was determined by radioimmunoassay. Base deficit and pH were measured, using a blood gas analyzer. RESULTS: Before treatments, a corpus luteum was present in all cows and the lecithin-to-sphingomyelin ratio in amniotic fluid did not differ between groups. Thirty hours after injections of flumethasone and dinoprost, progesterone concentration had decreased (P < 0.05) and the lecithin-to-sphingomyelin ratio was significantly (P < 0.05) higher than values in controls. In calves delivered after flumethasone or dinoprost treatments, the degree of acidosis was significantly (P < 0.05) less than that in controls. CONCLUSIONS: Flumethasone and dinoprost, given to pregnant cows, accelerate fetal lung maturation and improve respiratory function after birth.

A profile of amino acid and catecholamine levels during endotoxin-induced acute lung injury in sheep: searching for potential markers of the acute respiratory distress syndrome.

The identification of plasma markers of the course of the acute respiratory distress syndrome (ARDS) is needed to improve its treatment and to further advance the development of new therapeutic agents. The status of markers of lung injury in ARDS is reviewed and some new potential markers are proposed. This study focused on plasma amino acids, related amino compounds, and catecholamine levels during the acute phase of endotoxin-induced lung injury in 8 sheep characterized by the onset of pulmonary edema caused by increased microvascular permeability. A number of significant changes from baseline values were found. During the sixth hour of a 12-hour period of endotoxin infusion, norepinephrine, epinephrine, and alanine levels increased whereas the isoleucine level decreased. During the sixth hour of the immediate postendotoxin period, the taurine level increased while the levels of arginine, citrulline, glycine, isoleucine, methionine, ornithine, serine, threonine, and tryptophan decreased. These findings are compared with prior studies in human subjects detailing the amino acid profile characteristic of advanced sepsis. We conclude that the present profile of catecholamine and amino acid changes during endotoxemia in sheep deserves further study in human subjects to determine its significance as a marker of the early stage of ARDS.

[Experiences in diagnosis and therapy of puppy diseases in the fist days of life]. / Erfahrungen in der Diagnostik und Therapie von Welpenerkrankungen in den ersten Lebenstagen.

In a survey covering 145 puppies in 60 litters diseases after parturition and within the first week of life are discussed. Problems in the diagnosis and therapy are correlated with further investigations, i.e. bacteriology, sensitivity tests and in some cases necropsy. Neonatal respiratory distress syndrome and bacterial infections have been found to be the most common diseases in the first days of life in puppies.

Lung injury leading to respiratory distress syndrome in young Dalmatian dogs.

A progressive pulmonary disease resulting in severe respiratory failure and death in an average of 3 weeks was diagnosed in 11 young Dalmatian dogs. The dogs were from 4 litters, all genetically related by a common ancestor. The initial clinical signs were tachypnea and noisy respiration. Respiratory distress developed shortly before death and was characterized by strenuous and rapid respirations, along with cyanosis and vomiting. On blood gas analysis, there were severe arterial hypoxemia, hypercapnia, and marked alveolar-arterial oxygen difference. Radiographically, a diffuse pattern of alveolar, interstitial, and peribronchial densities was observed in the lungs. Most dogs developed pneumomediastinum and gastroesophageal intussusception in the terminal phase of the disease. There was no response to treatment with antibiotics, corticosteroids, diuretics, or oxygen. At necropsy, the lungs were wet, heavy, and relatively airless. Absence of 1 kidney in 2 dogs and severe internal hydrocephalus in 2 dogs were additional necropsy findings. Pulmonary histopathology included metaplasia and atypia of the alveolar and bronchiolar epithelium, a nonpurulent inflammatory reaction characterized mainly by mononuclear cells and macrophages, eosinophilic hyaline membrane formation, and focal pulmonary fibrosis. The histological manifestations were typical of acute lung injury. Clinically, the findings were consistent with adult respiratory distress syndrome (ARDS), except for the relatively long course. No known risk factors for ARDS, such as trauma, toxin exposure, infection, or endotoxemia could be identified. The relationship of the other abnormalities (ie, renal aplasia, hydrocephalus) to the pulmonary disease also remains obscure. An inherited defect is suspected, because segregation analysis of the 4 litters suggests autosomal recessive inheritance.

Ionophore antibiotic (narasin) poisoning in rabbits.

Outbreaks of narasin poisoning in rabbits from several commercial rabbit-raising farms in the state of Parana, Brazil, are reported. Approximately 5,000/35,000 rabbits died after having consumed a pelleted ration to which poultry ration premix had been added. Clinical signs included apathy, anorexia, muscle weakness, impaired walking, diarrhea, respiratory distress, and opistothonus. Gross findings were not remarkable, but varying degrees of degeneration, necrosis and regeneration of skeletal muscles were consistent histopathological features in affected rabbits. Myocardial changes were mild or absent. Thirty ppm of narasin were detected in the ration fed the rabbits. The disease was experimentally reproduced by feeding the suspected ration and by administering narasin po to rabbits.

Role of alveolar type II cells and of surfactant-associated protein C mRNA levels in the pathogenesis of respiratory distress in mink kits infected with Aleutian mink disease parvovirus.

Neonatal mink kits infected with Aleutian mink disease parvovirus (ADV) develop an acute interstitial pneumonia with clinical symptoms and pathological lesions that resemble those seen in preterm human infants with respiratory distress syndrome and in human adults with adult respiratory distress syndrome. We have previously suggested that ADV replicates in the alveolar type II epithelial cells of the lung. By using double in situ hybridization, with the simultaneous use of a probe to detect ADV replication and a probe to demonstrate alveolar type II cells, we now confirm this hypothesis. Furthermore, Northern (RNA) blot hybridization showed that the infection caused a significant decrease of surfactant-associated protein C mRNA produced by the alveolar type II cells. We therefore suggest that the severe clinical symptoms and pathological changes characterized by hyaline membrane formation observed in ADV-infected mink kits are caused by a dysfunction of alveolar surfactant similar to that observed in respiratory distress syndrome in preterm infants. However, in the infected mink kits the dysfunction is due to the replication of ADV in the lungs, whereas the dysfunction of surfactant in preterm infants is due to lung immaturity.

[AST, GLDH, gamma-GT, total bilirubin and CK values during the first week of life in healthy premature calves or calves with a late asphyxia syndrome]. / AST-, GLDH-, gamma-GT-, Gesamtbilirubin- und CK-Werte bei frühgeborenen gesunden oder an einer Spätasphyxie erkrankten Kälbern im Verlauf der ersten Lebenswoche.

The physical condition of 44 calves delivered by caesarean section before term was monitored by clinical and repeated laboratory examinations (analysis of AST, GLDH, gamma-GT, CPK, total bilirubin) during the first seven days of life. The newborns were divided into two groups based on the clinical observations during the first hour of life, the blood pH and the base deficit: Group 1: 30 calves without respiratory distress syndrome (vital, non asphyxial); they did not develop any diseases in the course of the experiment. Group 2: 14 calves with respiratory distress syndrome (asphyxial; 9 of these animals died in the course of the experiment. No significant differences between the vital and asphyxial calves were found in respect to the enzymes AST, GLDH, gamma-GT, CK as well as total bilirubin values measured during the first week of life. These blood parameters were within the normal range for calves delivered at term. The results do not indicate any disorder in liver and muscle functions in prematurely born calves with or without respiratory distress syndrome.

[Creatinine, urea and mineral levels during the first week of life in healthy premature calves and calves with a delayed asphyxia syndrome]. / Kreatinin-, Harnstoff- und Mineralstoffgehalte bei frühgeborenen gesunden oder an einer Spätasphyxie erkrankten Kälbern im Verlauf der ersten Lebenswoche.

The physical condition of 44 calves delivered by caesarean section before term was monitored by clinical and repeated laboratory examinations (analysis of creatinine, urea, sodium, potassium, chloride, and inorganic phosphorus) during the first seven days of life. The newborns were divided into two groups based on the clinical observations during the first hour of life, the blood pH and the base deficit: Group 1: 30 calves without respiratory distress syndrome (vital, non asphyxial); they did not develop any diseases in the course of the experiment. Group 2: 14 calves with respiratory distress syndrome (asphyxial); 9 of these animals died in the course of the experiment. The analysis of the parameters creatinine, urea, sodium, potassium, chloride, and inorganic phosphorus did not reveal any disturbance in kidney function in vital or in asphyxial prematurely born calves. All findings corresponded to those in calves born at term. So these parameters are not very meaningful in relation to metabolic disorders in respiratory distress syndrome.

[Changes in the blood coagulation potential of premature calves with and without respiratory distress syndrome]. / Veränderungen im Blutgerinnungspotential frühgeborener Kälber mit und ohne Atemnotsyndrom.

In 46 newborn calves with and without respiratory distress syndrome which had been delivered prematurely by caesarean section a blood coagulation profile was established. These animals were compared with 26 healthy, 5- to 8-day-old calves. Prematurely delivered calves showed a lower average plasma fibrinogen concentration than animals delivered in due time. Calves which developed a respiratory distress syndrome had a slightly prolonged prothrombin time and partial thromboplastin time as well as a lower antithrombin III activity already immediately postnatum compared with healthy prematures and some-day-old calves. It has to be assumed that in calves with respiratory distress syndrome--in analogy to pulmonary immaturity--the blood clotting mechanism is not yet fully developed. In healthy prematures and surviving asphyctic calves hemostasis remains largely stable during the first day of life, whereas plasma fibrinogen concentration increases. In the calves not surviving the examination period prothrombin time and partial thromboplastin time postnatum became significantly longer. Only in these severely asphyctic calves the presence of a consumption coagulopathy seems likely. A secondary reactive fibrinolysis was not observed.

Developments in management of the newborn foal in respiratory distress 1: Evaluation.

Developments in evaluation of newborn foals with respiratory distress are discussed. Major causes of respiratory distress are outlined and discussed in terms of the similar respiratory signs exhibited by foals with this clinical syndrome. History, physical examination, clinical pathology, chest radiography and blood gas analyses are discussed as important elements of the evaluation of the condition of these foals. Foals with respiratory disease are grouped into three major categories on the basis of clinical signs and arterial blood gas profiles. The evaluation of foals with respiratory distress is designed not only to reach an accurate diagnosis of the aetiology but also to define the foal's need for respiratory support.