Noninvasive Ventilation as a Temporizing Measure in Critical Fixed Central Airway Obstruction: A Case Report.

BACKGROUND: Critical central airway obstruction (CAO) requires emergent airway intervention, but current guidelines lack specific recommendations for airway management in the emergency department (ED) while awaiting rigid bronchoscopy. There are few reports of the use of noninvasive ventilation (NIV) in tracheomalacia, but its use as a temporizing treatment option in fixed, malignant CAO has not, to the best of our knowledge, been reported. CASE REPORT: An 84-year-old woman presented to the ED in respiratory distress, too breathless to speak and using her accessory muscles of respiration, with bilateral rhonchi throughout the lung fields. Point-of-care arterial blood gas revealed severe hypercapnia, and NIV was initiated to treat a presumed bronchitis with hypercapnic respiratory failure. Chest radiography revealed a paratracheal mass with tracheal deviation and compression. A diagnosis of critical CAO was made. While arranging for rigid bronchoscopic stenting, the patient was kept on NIV to good effect. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Recommendations for emergent treatment of life-threatening, critical CAO before bronchoscopic intervention are not well established. Furthermore, reports of NIV use in CAO are rare. We suggest that emergency physicians consider NIV as a temporizing measure for critical CAO while awaiting availability of bronchoscopy.

[Effects of acidification pretreatment for respiratory acidosis on the expression of matrix metalloproteinase-9 in rat lung tissues following ischemia/reperfusion].

OBJECTIVE: To establish rat model of lung ischemia/reperfusion (IR) in vivo, and to explore the effects of acidification pretreatment for respiratory acidosis on the expression of matrix metalloproteinase-9 (MMP-9) and the possible mechanisms.
 Methods: A total of 36 male Sprague-Dawley rats were divided into a sham group (S group), a IR group, and an experiment group (RA group) (n=12 in each group). The rat left lung hilum in the S group was dissociated, followed by perfusion without ischemia. After the left lung hilum in the IR group was blocked for 45 min, the rats were followed by reperfusion for 180 min. After left lung hilum in the RA group was dissociated, the respiratory parameters were adjusted so that pressure of end tidal carbon dioxide (PETCO2) reached 56-65 mmHg (1 mmHg=0.133 kPa) for 5 min, then the rats was subjected to IR. Lung tissue wet/dry (W/D) and lung permeability index (LPI) were calculated, while the lung histopathology was observed and the MMP-9 protein expression were measured.
 Results: Compared with the control group, the W/D and LPI in the IR group and the RA group increased after reperfusion (both P<0.05), and the levels of W/D and LPI in the group RA were lower than that in the IR group (P<0.05). LPI and pathology scores were significantly lower in the RA group than those in the IR group (both P<0.01). After IR, the expression of MMP9 in the lung tissues in the IR group and the RA group increased significantly (both P<0.01). The expression of MMP-9 protein in the RA group was significantly lower than that in the IR group (P<0.01).
 Conclusion: After lung IR injury, the expression of MMP-9 protein, vascular permeability and inflammatory exudation is increased. The acidification pretreatment for respiratory acidosis can inhibit the expression of MMP-9 protein and reduce inflammatory exudation after lung IR, showing a protective effect on lung IR injury.

Improved gas exchange and survival after KL-4 surfactant in newborn pigs with severe acute lung injury.

OBJECTIVE: To determine the effectiveness of artificial surfactant therapy using KL-4 surfactant in newborn pigs with hydrochloric acid (HCl)-induced acute lung injury (ALI). DESIGN: After induction of ALI via intratracheal HCl instillation, pigs were randomized to receive 5.8 ml/kg KL-4 surfactant or no surfactant prior to extubation to bubble CPAP. SETTING: Clinical laboratory. SUBJECTS: Spontaneously breathing newborn pigs (<1 week of age). INTERVENTIONS: Treatment with KL-4 surfactant on bubble CPAP with PEEP of 6 cmH(2)O for 3.5 hr after extubation compared with controls. MEASUREMENTS: Physiologic parameters and arterial blood gases were measured every 15 min. At the conclusion of the study, the lungs were excised for the analysis of histopathology and morphometric data. MAIN RESULTS: Pigs treated with KL-4 surfactant had arterial blood gases with less acidosis (P < 0.001), higher P(a)O(2) levels (P < 0.001), and lower P(a)CO(2) levels (P < 0.001). Pigs treated with KL-4 surfactant had improved survival compared with controls (6/12 KL-4, 2/12 control, P < 0.05). Postmortem morphometric data demonstrated that pigs treated with KL-4 surfactant had larger (P < 0.05) exchange units in the caudal-dorsal lung as compared to relatively atelectatic region in the control animals. CONCLUSIONS: In newborn pigs with severe HCl-induced ALI, treatment with KL-4 surfactant resulted in improved respiratory parameters, less dependent atelectasis, and improved short-term survival.

Correção dos distúrbios do equilíbrio ácido-básico na infância / Treatment of the acid-base disorders in childhood

Este artigo tem por objetivo abordar os aspectos mais relevantes da correção dos distúrbios ácido-básicos na infância. São abordados inicialmente alguns parâmetros úteis para a análise das gasometrias e interpretação dos distúrbios ácido-básicos. Ressalta-se a importância de buscar o diagnóstico etiológico do distúrbio ácido- básico através da análise dos dados clínicos e laboratoriais. São também discutidas a importância do cálculo do intervalo aniônico para indicar o mecanismo do distúrbio e orientar o tratamento, bem como a utilização do gradiente alvéolo-arterial de oxigênio para avaliar a hematose. Na segunda parte deste trabalho, aborda- se mais especificamente a correção dos distúrbios ácido-básicos, com ênfase na acidose metabólica por ser a alteração mais frequentemente observada na infância. São comentadas as indicações, os riscos e a forma de utilização do bicarbonato de sódio para correção das acidoses metabólicas. A seguir, é discutido de forma resumida o tratamento das alcaloses metabólicas, priorizando a correção das alcaloses cloreto-sensíveis por serem mais usualmente vistas em pediatria. Finalmente, são feitos comentários gerais sobre o tratamento dos distúrbios primariamente respiratórios - acidose e alcalose respiratória.

The aim of this paper is to establish some guidelines for the treatment of acid-base disorders in childhood. First, some useful guidelines for the blood gas analysis and the interpretation of acid-base disturbances are discussed. The etiology of the acid-base disorders must be investigated through clinical history and laboratorial features. The determination of the cause of the disarrangement is essential for an appropriate treatment. The use of anion gap calculation to define the mechanism of metabolic alterations is emphasized. The importance of the measurement of the alveolar-arterial gradient is also discussed, mostly related to respiratory diseases. In the second part of this paper, the treatment of each acid-base disturbance is reported in separate parts. Metabolic acidosis is more extensively discussed since it is the commonest acid-base disorder observed in children. The risks, indications and different forms of bicarbonate administration to correct the metabolic acidosis are descrised. The guidelines for the treatment of metabolic alkalosis are also summarized. The metabolic alkalosis is divided in two subtypes: chloride-sensitive and chloride-resistant disarrangement. Since the chloride-sensitive metabolic alkalosis is more frequent in childhood, it is more extensively discussed in this article than chloride-resistant disorders. Finally, general aspects about the treatment of the respiratory disturbances - acidosis and alkalosis — are briefly included.

Pre-operative coagulopathy management of a neonate with complex congenital heart disease: a case study.

Severe coagulation defects often develop in neonates undergoing cardiac surgery, both as a result of the surgical intervention, and as pre-existing defects in the hemostatic mechanisms. The following case report describes a newborn patient with complex congenital heart disease and respiratory failure whose pre-operative coagulopathy was aggressively managed prior to surgical correction. A 5-day-old, 2.5 kg child presented with interrupted aortic arch, ventricular septal defect, atrial septal defect, and patent ductus arteriosus. On admission, he was in respiratory arrest suffering from profound acidemia. In addition, the child was hypothermic (30.1 degrees C), septic (Streptococcus viridans), and coagulopathic (disseminated intravascular coagulation-DIC). The patient was immediately intubated and initial coagulation assessment revealed the following: prothrombin time (PT) 48.9 s (international normalized ratio (INR) 15.7), activated partial thromboplastin time (aPTT) >106 s, platelet count 30,000 mm(3), fibrinogen 15 mg dL(-1) and antithrombin III (AT-III) 10%. Before cardiac surgery could be performed, the patient's DIC was corrected with the administration of cryoprecipitate (15 ml), fresh frozen plasma (300 ml), and platelets (195 ml). In spite of the large transfusion of fresh frozen plasma, the AT-III activity, measured as a percentage, remained depressed at 33. Initial thromboelastographic (TEG) determination revealed an index of +2.02, and following 100 IU administration of an AT-III concentrate, declined to -2.32. Sequential TEG profiles were performed over several days, with the results used to guide both transfusion and medical therapy. The congenital heart defect correction was subsequently performed with satisfactory initial results, but the patient developed a fungal infection and expired on the 16th post-operative day. The present case describes techniques of coagulation management for a newborn with both a severe hemostatic defect and congenital heart disease.

Carbicarb: an effective substitute for NaHCO3 for the treatment of acidosis.

Carbicarb (Na2CO3 0.33 molar NaHCO3 0.33 molar), a mixture formulated to avoid the objections to sodium bicarbonate therapy, has been compared with 1 mol/L NaHCO3 and 1 mol/L NaCl in the treatment of mixed respiratory and metabolic acidosis (pH 7.17) produced by asphyxia in rats. In clinically appropriate doses, intravenous NaHCO3 raised arterial pH only 0.03 unit, elevated arterial carbon dioxide pressure, and doubled lactate concentration. With Carbicarb, the pH rise was three times as great and the blood lactate level was unchanged. The new drug should be effective in treating the acidosis of cardiopulmonary failure without raising blood carbon dioxide pressure or lactate levels and at lower sodium doses than required for NaHCO3.

Arterial blood gas tensions in acute severe asthma.

We have studied the serial changes in arterial blood gases in fourteen patients with acute severe asthma, all of whom received a standard therapeutic regime and had similar measurements made at identical time intervals under standard conditions. Hypoxaemia on admission was a constant finding, and the arterial oxygen tension often took a week or longer to return to a normal level. Treatment with 60% inspired oxygen provided a safe means of relieving hypoxaemia, provided that blood gases were measured before and during oxygen therapy. Most patients had a normal arterial carbon dioxide tension, which indicated the severity of their illness. Acid-base disturbances, when present, were mild and needed no specific treatment. Age, duration of the acute attack, and severity of airways obstruction were all unrelated to the changes in blood gas tension, and pulse rate was found to be a poor predictor of hypoxaemia in elderly asthmatics. Serial measurements of the arterial blood gases should be made in all patients with acute severe asthma.

Alteration of oxygen tension and oxyhemoglobin saturation. A hazard of sodium bicarbonate administration.

The administration of sodium bicarbonate solution, which has been advocated for the treatment of metabolic acidosis, may have detrimental side effects. We evaluated oxyhemoglobin saturation and oxygen tensions in eight anesthetized swine before and after freshwater near-drowning and after a rapid intravenous infusion of 7.5% sodium bicarbonate solution (8 mEq/kg). After freshwater aspiration, arterial and venous oxygen tensions and oxyhemoglobin saturation decreased. Administration of sodium bicarbonate resulted in decreased venous and increased arterial, oxygen tensions. Arterial, but not venous, oxyhemoglobin saturation increased. These findings suggest that sodium bicarbonate caused a distinct leftward shift in the oxyhemoglobin dissociation curve, which could impair tissue oxygenation. Therefore, to avoid detrimental effects, sodium bicarbonate should be administered slowly and in a dose sufficient just to correct metabolic acidosis.

Use of tolazoline in newborn infants with diaphragmatic hernia and severe cardiopulmonary disease. A preliminary report.

Two newborn infants with congenital diaphragmatic hernia, one of whom died, had significant improvement in arterial oxygen tension (Pao2) after intravenous administration of tolazoline (Priscoline) (1 to 2 mg. per kilogram). In both infants, systemic hypotension developed within minutes of administration of the drug and required pharmacologic and hemodynamic intervention. The response to tolazoline was more dramatic in the infant who survived, and his oxygen requirements were significantly reduced after the use of this drug. The infant who died also had a significant response to tolazoline. Tolazoline appears to be an important pharmacologic agent for use in the postoperative care of infants with diaphragmatic hernia and associated hypoxemia and acidosis.