Profound Hypoxemia Research Articles

Effects of profound hypoxemia on coagulation & fibrinolysis in normal individuals.

Hypoxia has been proposed to enhance, diminish, or have no effect on laboratory measures of coagulation or clinical thrombosis. Further, there usually are significant pathological or environmental factors concurrently present with hypoxia. Thus, the goal of the present investigation was to determine whether whole blood or plasmatic coagulation and fibrinolytic kinetics would change in response to progressive hypoxia to a systemic oxygenation (SpO2) of 70%. Healthy, conscious volunteers (n = 9) breathing a hypoxic mixture of gases during an in-vivo validation of noninvasive cerebral oximetry had blood samples collected and assessed with thrombelastography at normoxia and after SpO2 of 70%. A mild release of endogenous heparin-like activity occurred that diminished plasmatic coagulation, and a mild increase in clot lysis time also was noted. Further investigation to determine whether these phenomena occur in more chronic, less hypoxic states as sources of hypocoagulation or thrombophilia is needed.

CT measurement of airway wall thickness and emphysema in COPD: Correlation with pulmonary hypertension

Purpose Pulmonary hypertension (PH) is a common complication of COPD associated with increased mortality. The mechanisms coupling PH and bronchial obstruction are unknown; in particular PH appears unrelated to emphysema. We hypothesized that CT measurement of airway remodeling instead of emphysema may correlate with PH in COPD. Material and Method Data were retrieved from 60 COPD patients who had both right heart catheterization (RHC) and CT in a period of stability, and no other disease known to cause PH. CT measurement of airway wall thickness (WT) was assessed from the third to the fifth bronchial generation in 4 bronchial paths. Low lung area percentage (LAA %) was used to quantify emphysema extent. Results Thirty-four out of 60 COPD patients had PH (mean pulmonary arterial pressure [PAP m ] ≥ 25 mmHg). There was no difference between the two groups regarding age, sex, and spirometric results, whereas there was more profound hypoxemia in the PH group. WT measured at the fourth (WT4) and fifth generation (WT5) was increased in COPD with PH and correlated with PAP m ( r = 0.40; P = 0.01 and r = 0.63; P m and LAA % ( r = 0.13; P = 0.28). Conclusion This study demonstrates for the first time an association between structural alteration of bronchi and PH in COPD. Unlike quantification of emphysema, CT measurement of bronchial wall thickness correlates with PAP m and could estimate the severity of PH in COPD. Airway remodeling burden is not limited to airflow limitation to explain COPD severity and mortality ( Figure 1 ).

Computed tomographic measurement of airway remodeling and emphysema in advanced chronic obstructive pulmonary disease. Correlation with pulmonary hypertension.

Pulmonary hypertension (PH) is an established complication of advanced chronic obstructive pulmonary disease (COPD) associated with increased mortality. The mechanisms coupling PH and bronchial obstruction are unknown; in particular, PH appears to be unrelated to emphysema. We hypothesized that computed tomographic (CT) measurement of airway remodeling instead of emphysema may correlate with PH in COPD. We aimed to describe the clinical and CT characteristics of patients with COPD with or without PH and to correlate CT measurements of airway remodeling and emphysema with PH. Data were retrieved from 60 COPD patients who underwent both right heart catheterization and computed tomography in a period of stability and had no other disease known to cause PH. CT measurement of airway wall thickness (WT-Pi10) was used to assess airway remodeling and low lung area percentage (LAA%) to quantify emphysema extent. Thirty-four of the sixty patients with COPD had PH (mean pulmonary arterial pressure [PAPm] ≥ 25 mm Hg). There was no difference between the two groups regarding age, sex, and spirometric results, whereas there was more profound hypoxemia in the PH group. WT-Pi10 was increased in the patients with COPD and PH and correlated with PAPm (ρ = 0.62; P < 0.001). Conversely, there was no difference or correlation between PAPm and LAA% (ρ = 0.12; P = 0.33). In multivariate analysis (R(2) = 0.53), WT-Pi10 was the independent predictor most associated with PAPm elevation, as compared to hypoxia (PaO2) or pulmonary arterial enlargement (diameter ratio between the pulmonary arterial truncus and the ascending aorta). This study demonstrates, for the first time to our knowledge, an association between structural alterations of bronchi and PH in COPD. Unlike quantification of emphysema, CT measurement of airway remodeling correlates with PAPm and could be used to estimate the severity of PH in COPD. Airway remodeling burden is not limited to airflow limitation in the assessment of COPD severity and mortality.

Alveolar Proteinosis With Profound Hypoxemia at Presentation

Alveolar Proteinosis With Profound Hypoxemia at Presentation

Curable hypoxia in an octogenarian with an undiagnosed inherited condition: a case commentary

The accompanying case is an excellent illustration of why pulmonary arteriovenous malformations (PAVMs) have been considered very rare. Patients with PAVMs are generally asymptomatic and may be highly athletic, even in the presence of profound hypoxaemia due to right-to-left shunting through PAVMs. Data in papers published this year help explain why patients are so rarely symptomatic [1–3]; why some become symptomatic [1, 2]; and why, irrespective of respiratory symptoms, all PAVMs should be considered for treatment [4, 5]. PAVM development is usually complete by the end of puberty, and the octogenarian in this case would have spent decades undiagnosed with “silent” PAVMs and hypoxaemia. To understand how this could be the case, it is important to realise that, although this patient had low blood oxygen levels, his tissues were not more “hypoxic” than normal. Instead, as recently emphasised [1–3], PAVM patients use multiple mechanisms to maintain oxygen delivery. First, the relevant term for oxygen transport is not the arterial oxygen tension ( P aO2) or arterial oxygen saturation ( S aO2), but the arterial oxygen content ( C aO2) which also depends upon the concentration of haemoglobin [6]. Hypoxaemic PAVM patients generally utilise polycythaemic responses so that, irrespective of the S aO2, C aO2 on standing is preserved at just under 18 mL·dL−1 [1]. Secondly, the overall transport of oxygen to the tissues also depends on the volume of blood reaching the tissues in any given period (cardiac output) [6]. Cardiac output is the product of the heart rate and stroke volume, and both are increased in PAVM patients to compensate for hypoxaemia [2, 3]. For example, in the 165 PAVM patients reported …

Acute pulmonary injury with refractory hypoxaemia after implantation of Levitronix CentriMag ventricular assist device: successful treatment with veno-venous extracorporeal membrane oxygenation

Although acute pulmonary injury after cardiopulmonary bypass has been detailed in the literature, it was seldom mentioned in the context of following implantation of a ventricular assist device. We report on a 65-year-old male with end-stage ischemic cardiomyopathy who underwent implantation of Levitronix CentriMag (Levitronix, Waltham, MA) for cardiac support and was listed for heart transplantation. Acute pulmonary injury with profound hypoxaemia was noted 6h after the implantation. Despite optimal medical treatment and maximal ventilator support, refractory hypoxaemia persisted, and veno-venous extracorporeal membrane oxygenation (oxygenator: Affinity-NT; centrifugal pump: BPX-80 Bio-Pump, Medtronic, Minneapolis, MN, USA) was applied for ventilation support. The patient was weaned from the extracorporeal membrane oxygenation 4days later and from the ventilator on the next 2days. He underwent a successful orthotopic heart transplant after a total of 77days on Levitronix left ventricular device cardiac support.

Transtracheal oxygen and positive airway pressure: A salvage technique in overlap syndrome

The coexistence of sleep apnea-hypopnea syndrome (SAHS) with chronic obstructive pulmonary disease (COPD) occurs commonly. This so called overlap syndrome leads to more profound hypoxemia, hypercapnic respiratory failure, and pulmonary hypertension than each of these conditions independently. Not infrequently, these patients show profound hypoxemia, despite optimal continuous positive airway pressure (CPAP) therapy for their SAHS. We report a case where CPAP therapy with additional in-line oxygen supplementation failed to accomplish adequate oxygenation. Adding transtracheal oxygen therapy (TTOT) to CPAP therapy provided better results. We review the literature on transtracheal oxygen therapy and how this technique may play a significant role in these complicated patients with overlap syndrome, obviating the need for more invasive procedures, such as tracheostomy.

P143 Hypoxia induces hypothermia and sickness behaviour in mice following subcutaneous injection of live Staphylococcus aureus

Infections frequently cause or complicate illnesses associated with hypoxaemia and local tissue hypoxia. The influence of hypoxia on the interaction between host and pathogen is therefore of considerable interest. S....

Apnea Testing for Brain Death in Severe Acute Respiratory Distress Syndrome: A Possible Solution

A 42-year-old man with a subarachnoid hemorrhage complicated by anoxic brain injury, respiratory failure requiring mechanical ventilation, and severe acute respiratory distress syndrome (ARDS) presented a clinical conundrum for safe apnea testing in brain death determination due to profound hypoxemia. Case report. During brain death examination, despite meeting criteria for severe ARDS, apnea testing was successfully completed with the use of a pretest recruitment maneuver and 20 cm H(2)O CPAP valve. A recruitment maneuver and CPAP valve may be used in severe ARDS for safe apnea testing in brain death determination.

Targeting Aspiration Pneumonitis

Targeting Aspiration Pneumonitis

Détresse respiratoire aiguë due à Mycoplasma pneumoniae

Respiratory infections due to Mycoplasma pneumoniae are typically mild and subacute. We report the case of a 40-year-old man hospitalized for acute respiratory distress in the context of an acute infection with Mycoplasma pneumoniae. Radiological and pulmonary function test were consistent with an acute infectious bronchiolitis. The patient presented with isolated respiratory failure with profound hypoxemia requiring oxygen delivered at high concentration by face mask. The CT appearance of the lesions corresponded to a spread of bilateral micro-connected pulmonary nodules (a "tree-in-bud" pattern) associated with obstructive ventilatory disorder. The only pathogen identified by PCR on BAL and serology was Mycoplasma pneumoniae. The evolution was favorable with antibiotic therapy combined with corticosteroids. Mycoplasma pneumoniae may be responsible for severe respiratory illness in the form of bronchiolitis. In the setting of severe acute community pneumoniae antibiotic treatment which is also effective against Mycoplasma pneumonia should be considered. In this case, corticosteroids may be an effective adjunct by their action on the small airways.

The prediction of in-flight hypoxaemia using non-linear equations

Respiratory disease may cause profound hypoxaemia during flight. Previously derived linear equations poorly predict the need for supplemental oxygen during air travel. The current gold standard assessment is the hypoxic challenge test (HCT). Recent guidelines recommend HCT is performed for those patients with SpO2<95% at sea level. The HCT protocol is a costly and time consuming investigation. Retrospective clinical and HCT data from 138 patients were applied to previous linear equations to assess predictive value. Novel non-linear predictive models (NLMs) were constructed from these data. The linear equations and the NLMs were then applied prospectively to 44 patients undergoing HCT. Overall, 39% of historic patients had a positive HCT (PaO2N2<50mmHg). Existing linear equations varied in sensitivity (52-87%) and specificity (40-74%) at predicting positive HCT results. Seven novel NLMs (NLM1 to NLM7) were developed from the historic dataset. All NLMs predicted PaO2N2 more accurately than the original linear equations when tested prospectively. The best fit was observed using NLM2 which uses PaO2RA and PaCO2RA as input terms. The NLMs are applicable to a broad range of conditions. The novel NLMs represent a low cost option for the prediction of significant hypoxia during flight and perform better than SpO2 in identifying those patients who require more formal assessment with HCT.

Pulmonary vascular complications in portal hypertension and liver disease: A concise review

Chronic liver disease and/or portal hypertension may be associated with one of the two pulmonary vascular complications: portopulmonary hypertension and hepatopulmonary syndrome. These pulmonary vascular disorders are notoriously underdiagnosed; however, they have a substantial negative impact on survival and require special attention in order to understand their diagnostic approach and to select the best therapeutic options. Portopulmonary hypertension results from excessive vasoconstriction, vascular remodeling, and proliferative and thrombotic events within the pulmonary circulation that lead to progressive right ventricular failure and ultimately to death. On the other hand, abnormal intrapulmonary vascular dilations, profound hypoxemia, and a wide alveolar-arterial gradient are the hallmarks of the hepatopulmonary syndrome, resulting in difficult-to-treat hypoxemia. The aim of this review is to summarize the latest pathophysiologic concepts, diagnostic approach, therapy, and prognosis of portopulmonary hypertension and hepatopulmonary syndrome, as well as to discuss the role of liver transplantation as a definitive therapy in selected patients with these conditions.

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Case Reports: Hepatopulmonary syndrome (HPS) is defined as a clinical triad of chronic liver disease, abnormal pulmonary gas exchange resulting in arterial hypoxemia, and evidence of intrapulmonary vascular dilations producing a right to left intrapulmonary shunt. The only definitive treatment option is liver transplantation, with an anticipated improvement and subsequent resolution of hypoxemia weeks to months following transplantation. In light of an increasing trend to transplant patients with severe HPS characterized by profound hypoxemia, practical alternatives to high flow nasal cannula (HFNC) need to be considered in order to facilitate post-transplant patient mobilization and early discharge from the hospital while treating severe hypoxemia. To this end, we describe our experience with the application of transtracheal oxygen therapy in the management of post-operative hypoxemia following OLT for severe HPS in three patients. Persistent arterial hypoxemia in the immediate post-operative period required the use of high-flow nasal cannula (HFNC) oxygen. Although allograft function steadily improved, the patients’ hypoxemia did not improve in the immediate post-operative period, and they subsequently underwent placement of a transtracheal oxygen (TTO) catheter to facilitate mobilization and weaning from HFNC. Therapy with oxygen via the TTO catheter led to early patient mobilization and discharge, and rapid weaning and eventual liberation from supplemental oxygen. To our knowledge, this is the first report of such a management technique for this unique group of patients. Our observations highlight the utility of transtracheal oxygen therapy in the management of severe HPS after liver transplantation.

The use of ECMO for persistent pulmonary hypertension of the newborn: A decade of experience

PurposeDespite improvements in the management of persistent pulmonary hypertension of the newborn (PPHN), a number of infants with inadequate gas exchange are treated with extracorporeal membrane oxygenation (ECMO). The objectives of this study were to use the Extracorporeal Life Support Organization Registry to review the outcomes of neonates with PPHN receiving ECMO, and to identify pre-ECMO variables that may be associated with increased mortality. Materials and methodsThe study is a retrospective analysis of all patients with PPHN supported with ECMO and reported to the Extracorporeal Life Support Organization registry from 2000 to 2010. Prematurity was defined as <37 wk gestation. Univariate analysis was performed using Student's t-test or Fisher's exact test. Variables found to be statistically significant underwent multivariate analysis by logistic regression. Kaplan-Meier survival curves were generated to analyze the relationship between duration of ECMO support and patient survival. ResultsA total of 1569 neonates with PPHN received ECMO support during the study period, at an average age of 3.1 d of life and for a duration of 6.9 d. Survival among neonates with PPHN receiving ECMO support was 81%, and those receiving support for 7, 10, 14, and 21 d survived at rates of 88%, 78%, 55%, and 25%, respectively. By logistic regression, prematurity (P < 0.01), pre-ECMO pH ≤7.2 (P = 0.02), pre-ECMO SaO2 ≤65% (P = 0.01), and duration of ECMO ≥7 d (P < 0.001) were independent predictors of death in this group. An average of 2.2 complications occurred per patient, with cardiovascular, mechanical, and renal complications being the most common. ConclusionsNeonates with PPHN have high survival rates with ECMO support. Prematurity, acidosis, and profound hypoxemia are independently associated with increased mortality. Furthermore, prolonged ECMO support (>7 d) is associated with a higher risk of mortality in this cohort than in patients supported for <1 wk.

Recurrent lobar atelectasis in a child with cystic fibrosis

Cystic fibrosis pulmonary exacerbations in children usually manifest with increased cough and a fall in lung function. We report a challenging case where an 8-year-old girl has had frequent prolonged exacerbations over the last 3 years needing aggressive management, associated with multi-lobar collapse. She was born at term and presented with meconium ileus needing bowel resection and stoma formation which was reversed during first year of life. Cystic fibrosis was diagnosed on sweat testing, with a ΔF508 homozygous genotype. She has a younger brother aged 5 years, who also has cystic fibrosis. She was admitted as an infant with respiratory syncytial virus bronchiolitis at 7 months of age, requiring CPAP for few days. She was later admitted at 15 months of age with a pulmonary exacerbation, and a chest X-Ray showed left lower lobe collapse. Pseudomonas aeruginosa was isolated for the first time from bronchoalveolar lavage and she was treated with intravenous and nebulized antibiotics; she had a normal chest X-ray few weeks later. Nebulized dornase alpha (DNase) was started at 3 years of age and a gastrostomy inserted at age 6. A port-a-cath was inserted at age 7. Over the last 3 years she has had 2 to 3 pulmonary exacerbations per year requiring prolonged hospital admissions for up to 3 weeks. During these admissions she is treated with intravenous antibiotics, intensive physiotherapy, up to 4 times per day of nebulised hypertonic saline and twice daily DNase. In 2011 she had 5 hospital admissions for pulmonary exacerbations. Pulmonary exacerbations are preceded by trivial viral upper respiratory tract infection followed a few days later by acute onset of tachypnoea, dyspnoea and profound hypoxemia (oxygen saturations of 80–82% on admission). The chest X-ray shows lobar collapse with the left lower lobe most frequently involved as well as involvement of other lobes. Our approach is to treat her with humidified high flow oxygen, intravenous antibiotics, intensive physiotherapy and at least one early therapeutic bronchoscopy to re-inflate the collapsed lobe. Bronchoscopy is usually performed on the first or second day of admission and reveals very thick tenacious mucus, which is difficult to clear. We instill DNase during the procedure, and on some occasions she has chest physiotherapy under general anesthesia. Large mucus plugs can be removed, sometimes as bronchial casts. We believe that early bronchoscopy results in clinical and radiological improvement and she can be discharged home after 2 weeks with no respiratory distress and normal oxygen saturations (Figure 1). Open in a separate window Figure 1 Serial chest X-rays in a typical pulmonary exacerbation. a) X-ray on day of admission showing left, right lower & middle lobe collapse; b) X-ray 36 hr post bronchoscopy showing good inflation of right lung; c) X-ray 6 weeks later showing no lobar collapse

Severe refractory hypoxaemia in submassive pulmonary embolism: a surrogate marker of severe right ventricular dysfunction and indication for thrombolysis

The role of thrombolysis in pulmonary thromboembolism is controversial. We describe a case of life-threatening acute pulmonary embolism where thrombolysis was successfully administered because of extreme refractory hypoxaemia. We suggest that profound refractory hypoxaemia in this clinical setting was due to the combination of severe right ventricular dysfunction and shunting from pulmonary infarction. The shunt was not likely to have resolved in the short term, but right ventricular function and hypoxaemia improved with clot lysis. Similar clinical presentations should prompt active consideration of thrombolysis.

Tension pneumoperitoneum in a child resulting from high-frequency oscillatory ventilation: a case report and review of the literature

An 18-month-old male infant was placed on high-frequency oscillatory ventilation for profound hypoxemia and subsequently developed tension pneumoperitoneum. He underwent a bedside exploratory laparotomy for suspected perforated viscous. No intestinal perforation was identified, and a diagnosis of tension pneumoperitoneum secondary to pneumatosis cystoides intestinalis was made. To our knowledge, this is the only report of a pediatric patient developing tension pneumoperitoneum from high-frequency oscillatory ventilation. A review of the literature examines the differential diagnosis, physiology, and treatment of tension pneumoperitoneum.

Migrating Tumor

Migrating Tumor

Risk Factors for Persistent Pulmonary Hypertension of the Newborn

In utero, pulmonary blood flow is closely circumscribed and oxygenation and ventilation occur via the placental circulation. Within the first few breaths of air-breathing life, the perinatal pulmonary circulation undergoes a dramatic transition as pulmonary blood flow increases 10-fold and the pulmonary arterial blood pressure decreases by 50% within 24 hours of birth. With the loss of the placental circulation, the increase in pulmonary flow enables oxygen to enter the bloodstream. The physiologic mechanisms that account for the remarkable transition of the pulmonary circulation include establishment of an air-liquid interface, rhythmic distention of the lung, an increase in shear stress and elaboration of nitric oxide from the pulmonary endothelium. If the perinatal pulmonary circulation does not dilate, blood is shunted away from the lungs at the level of the patent foramen ovale and the ductus arteriosus leading to the profound and unremitting hypoxemia that characterizes persistent pulmonary hypertension of the newborn (PPHN), a syndrome without either optimally effective preventative or treatment strategies. Despite significant advances in treatment, PPHN remains a major cause of morbidity and mortality in neonatal centers across the globe. While there is information surrounding factors that might increase the risk of PPHN, knowledge remains incomplete. Cesarean section delivery, high maternal body mass index, maternal use of aspirin, nonsteroidal anti-inflammatory agents and maternal diabetes mellitus are among the factors associated with an increased risk for PPHN. Recent data suggest that maternal use of serotonin reuptake inhibitors might represent another important risk factor for PPHN.