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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Necrotizing tracheobronchitis (NTB) is a recently recognized cause of tracheal obstruction in the mechanically ventilated neonate. This process involves inflammation and necrosis of the mucosa of the distal trachea and mainstem bronchi. The sloughing of this material into the tracheal lumen results in plugging and acute respiratory distress. We documented this diagnosis in 19 infants. Four were diagnosed at autopsy. Fifteen had emergency bronchoscopy performed in the neonatal intensive care unit with removal of the obstructing debris. Ten of these 15 neonates survived (66.7%). The diagnosis of necrotizing tracheobronchitis should be suspected in those neonates requiring positive pressure ventilation in whom a sudden unexplained increase in ventilatory requirements develops. This is often associated with hypercarbia and a history of high-peak inspiratory pressures with or without hypoxia. Emergency bronchoscopy in these neonates is necessary both for diagnosis and treatment of the necrotizing tracheobronchitis.
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PMID:Necrotizing tracheobronchitis: a new indication for emergency bronchoscopy in the neonate. 404 64

Forty-five newborn infants in respiratory failure with respiratory distress syndrome were treated with intermittent negative pressure ventilation (INPV). There was a survival rate of 38% (17/45).All infants were initially treated without nasotracheal intubation. However, 24 of these developed a Paco(2) greater than 70 mm. Hg and were subsequently intubated. Intubation was followed by a decrease in the degree of hypercarbia in each instance and simultaneous increase in Pao(2).COMPLICATIONS ENCOUNTERED DURING VENTILATION WERE: emphysema (one patient), aspiration pneumonia (two patients), septicemia (two patients), misplaced nasotracheal tube (one patient).Follow-up of the 17 surviving patients for periods of four to 36 months disclosed two patients with post-intubation hoarseness. One infant initially had spastic quadriplegia with EEG abnormalities, both of which cleared by 5 months of age. In the remaining 14 infants, the results of physical, neurological and psychological examinations have remained within normal limits.
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PMID:Negative pressure artificial respiration: use in treatment of respiratory distress syndrome of the newborn. 526 98

Intrapulmonary occult bleeding is a serious complication of anticoagulants. Diagnostic difficulties are such that this complication is rarely described: 8 cases in the literature. The authors report two new cases. In both of these patients oral anticoagulant therapy resulted in a severe haemorrhagic syndrome on a clinical (melaena and/or epistaxis) and laboratory (haemoglobin less than 9 g/100 ml and prothrombin time less than 10 p. 100) basis. After a period of 24 to 48 hours, an acute respiratory distress syndrome developed. There was dyspnoea without major haemoptysis, a hypoxia/hypercapnia syndrome and, by X-ray, the rapid development of a diffuse micronodular miliary picture. The diagnosis of intrapulmonary occult bleeding was based upon fibroscopy with bronchoalveolar lavage (BAL) showing the pathological presence of large numbers of alveolar siderophages. However, the worsening of hypoxia brought about by bronchoalveolar lavage is such that careful consideration must be taken before the technique is used. Intrapulmonary occult bleeding must therefore be borne in mind in the presence of an imbalance in anticoagulant treatment complicated by respiratory distress and a reticulonodular radiological appearance.
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PMID:[Occult intrapulmonary hemorrhage caused by anticoagulants]. 611 3

Eleven observations of severe multicystic encephalopathy ( MCE ) in young infants and in a two-year-old child provide the basis for a summing-up and discussion of the various aspects of this characteristic polyetiologic phenomenon occurring in early infancy. In all cases the triggering causes or underlying disorders were different, although in five cases the common pathogenetic mechanism was a disturbance of circulation and/or respiration (acute respiratory distress syndrome). In two cases the basic disorders were a suppurative and a granulomatous meningoencephalitis. Carbon monoxide poisoning had occurred in one and diffuse meningocerebral angiomatosis in another two cases. In the eleventh case, one of a complicated twin birth, the exact cause of the MCE remained obscure. These cases together with those recorded in the literature demonstrate that the surprisingly constant pattern of damage in MCE , which results from different etiologic conditions, should be due to a specific mode of reaction of the infantile brain to a common pathogenetic mechanism. Anoxia with hypercapnia and the formation of brain edema are discussed as the basic events in the pathogenesis of MCE .
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PMID:Multicystic encephalopathy--a polyetiologic condition in early infancy: morphologic, pathogenetic and clinical aspects. 632 15

New developments in therapy for foals in respiratory distress are discussed. Therapy is based on preservation of the foal's life by maintenance of a patent airway, resuscitation with fluids and warmth, provision of humidified oxygen to raise the fractional concentration of inspired oxygen sufficient to avoid hypoxia and provision of ventilatory support when hypercapnia becomes critical. Ventilatory support described includes assisted and controlled ventilation, positive end expiratory pressure, continuous positive airway pressure and intermittent mandatory ventilation. The aims of these techniques are discussed together with their associated indications, disadvantages and complications. Secondary therapy includes coupage, airway hygiene, drug therapy and stress management. Knowledge of equine neonatology is limited in comparison with human neonatology. More information in basic physiology and pharmacology relating to equine neonatology is needed and the efficacy of various modes of therapy must be evaluated.
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PMID:Developments in management of the newborn foal in respiratory distress 2: Treatment. 638 14

When oxygen therapy is warranted, the minimum effective dose generally should be given. Hypoxemic patients who have normal baseline ABG may be treated initially with an intermediate to high FiO2 in the range of 35% to 100%, depending on the severity of the respiratory distress. The majority of patients with exacerbations of COPD who are not in extremis may be given an initial FiO2 of 28%, especially if their previous response to oxygen is known. When treating patients who have chronic severe hypercapnia (eg, those requiring chronic home oxygen), the initial FiO2 should be 24% even though renal compensation of the respiratory acidosis has occurred. Further mild elevation of the PaCO2, due mainly to the V/Q mismatch that oxygen therapy induces, may be sufficient to precipitate unacceptable hypercapnia. Patients with exacerbations of COPD who are obviously in extremis, with severe hypoxemia and acidosis, should start with an FiO2 of 24% unless they are being mechanically ventilated. The severity of the hypoxemia and acidosis is more predictive for the development of CO2 narcosis and respiratory failure than is the degree of hypercapnia in these patients. The FiO2 can be increased to 28% and incrementally higher if low FiO2 is tolerated. The use of a high FiO2 is subject to the following guidelines for prevention of clinically significant oxygen toxicity: 100% oxygen at atmospheric pressure is safe if given for less than six hours; 70% oxygen is probably safe for 24 hours; and after this time, 45% should be the approximate upper limit to the FiO2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oxygen therapy and oxygen toxicity. 641 43

Seven lambs (0.93 term gestation) were delivered by cesarean section with evidence of meconium in the amniotic fluid, meconium staining, and respiratory distress. The initial arterial blood gas and acid-base status indicated severe hypoxemia and acidosis. Three of these lambs developed pneumothoraces and died on control gas ventilation with positive end expiratory pressure. During the control period (90 min) with ventilatory support, there were no significant alterations in mean arterial oxygen tension (PaO2) and alveolar-arterial oxygen gradient (A-aDO2). The initial hypercarbia and acidosis were effectively controlled and corrected using mechanical ventilation and bicarbonate infusion. Fifteen min after the onset of fluorocarbon ventilation mean PaO2 significantly increased and A-aDo2 decreased. After 90 min of fluorocarbon ventilation, lambs were returned to gas ventilation. During this recovery period, PaO2 and A-aDo2 remained significantly improved compared with control gas values. Dynamic lung compliance increased, alveolar and peak tracheal pressure decreased and inspiratory elastic work of breathing decreased during liquid ventilation.
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PMID:Liquid ventilation: effects on pulmonary function in distressed meconium-stained lambs. 642 32

347 patients with idiopathic respiratory distress syndrome, born 1971 to 1976, were included into a prospective follow-up study. 71 patients (20%) died in the neonatal period, 197 out of 276 survivors (71%) had a complete follow-up for the first year of life, 112 survivors have so far been investigated up to the age of four years. According to neurological findings the patients were classified as normal, doubtful (age 6-12 months) or minimal brain dysfunction (4 years), mild cerebral paresis (CP), or severe cerebral damage, respectively. At the age of one year 3 patients (1.5%) had severe cerebral damage, 14 (7%) showed mild CP and another 56 (28%) had doubtful findings. Very low birth weight of very short period of gestation increased the risk for abnormal neurological findings only slightly. The need for mechanical ventilation, especially for more than 14 days, increases the risk for CP. Serious complications during the neonatal period, particularly implicating cerebral stress, significantly reduces medium-term prognosis. Perinatal asphyxia, neonatal acidosis, hypoxia or hypercapnia did not correlate with impaired cerebral prognosis. Preliminary findings at the age of four years demonstrate good correlation with neurological findings obtained at the age of 12 months. One patient initially classified as normal (2%) and 5 doubtful babies (15%) had developed mild CP. Another initially doubtful baby had severe cerebral damage at the age of four years. 62 out of 78 children tested (79%) showed normal intelligence, 14 (18%) had an IQ of 70--90, and 2 (3%) less than 70.
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PMID:Systematic follow-up of newborns with idiopathic respiratory distress syndrome. Results in 197 patients born 1971 to 1976. 703 Oct 20

One hundred and forty-six infants of 34 weeks' gestation or less were repeatedly scanned by means of real-time ultrasound to diagnose the presence of intraventricular haemorrhage (IVH), its severity, and the timing of onset of the condition. We describe a new method for grading the extent of the IVH which does not depend on ventricular size. IVH was clearly present in 52 (36%) of the 146 infants and in 32 (50%) of the 64 infants of 30 weeks' gestation or less. Repeated scans accurately timed the onset of IVH in 41 infants, and 32 (78%) had the first sign of IVH before 72 hours of age. Thirty-two clinical factors were analysed for possible correlation with the development of IVH: outborn compared with inborn, administration of sodium bicarbonate, hypothermia, intermittent positive pressure ventilation, continuous positive airways pressure, hypercapnia, severe acidosis, and respiratory distress syndrome all reached statistical significance. Analysis of variance showed that respiratory distress syndrome was the most important factor, but severe acidosis had some independent action on the development of IVH. Seventeen (81%) of 21 infants with hypercapnia (PCO2 greater than 6 kPa) together with severe acidosis (pH less than 7.1) developed IVH, of which more than half was moderate or severe in degree.
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PMID:Risk factors in the development of intraventricular haemorrhage in the preterm neonate. 709 4

Periventricular haemorrhage was diagnosed in vivo in 20 of 29 consecutively admitted infants of birthweight below 1500 g using an ultrasound scanner. Ten (51%) infants with haemorrhages survived. Mortality was related to the extent of the bleeding. Statistically significant associations with respiratory distress, ventilator therapy, metabolic acidosis, and hypercapnia were observed, lending support to their role in the pathogenesis of periventricular haemorrhage.
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PMID:Factors associated with periventricular haemorrhage in very low birthweight infants. 725 72


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