scholarly journals Inhaled high molecular weight hyaluronan ameliorates respiratory failure in acute COPD exacerbation: a pilot study

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Flavia Galdi ◽  
Claudio Pedone ◽  
Christopher A. McGee ◽  
Margaret George ◽  
Annette B. Rice ◽  
...  

Abstract Background Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) carry significant morbidity and mortality. AECOPD treatment remains limited. High molecular weight hyaluronan (HMW-HA) is a glycosaminoglycan sugar, which is a physiological constituent of the lung extracellular matrix and has notable anti-inflammatory and hydrating properties. Research question We hypothesized that inhaled HMW-HA will improve outcomes in AECOPD. Methods We conducted a single center, randomized, placebo-controlled, double-blind study to investigate the effect of inhaled HMW-HA in patients with severe AECOPD necessitating non-invasive positive-pressure ventilation (NIPPV). Primary endpoint was time until liberation from NIPPV. Results Out of 44 screened patients, 41 were included in the study (21 for placebo and 20 for HMW-HA). Patients treated with HMW-HA had significantly shorter duration of NIPPV. HMW-HA treated patients also had lower measured peak airway pressures on the ventilator and lower systemic inflammation markers after liberation from NIPPV. In vitro testing showed that HMW-HA significantly improved mucociliary transport in air–liquid interface cultures of primary bronchial cells from COPD patients and healthy primary cells exposed to cigarette smoke extract. Interpretation Inhaled HMW-HA shortens the duration of respiratory failure and need for non-invasive ventilation in patients with AECOPD. Beneficial effects of HMW-HA on mucociliary clearance and inflammation may account for some of the effects (NCT02674880, www.clinicaltrials.gov).

Author(s):  
Giulia Spoletini ◽  
Nicholas S. Hill

Non-invasive ventilation (NIV) has been increasingly used over the past decades to avoid endotracheal intubation (ETI) in critical care settings. In selected patients with acute respiratory failure, NIV improves the overall clinical status more rapidly than standard oxygen therapy, avoids ETI and its complications, reduces length of hospital stay, and improves survival. NIV is primarily indicated in respiratory failure due to acute exacerbations of chronic obstructive pulmonary disease, cardiogenic pulmonary oedema and associated with immunocompromised states. Weaker evidence supports its use in other forms of acute hypercapnic and hypoxaemic respiratory failure. Candidates for NIV should be carefully selected taking into consideration the risk factors for NIV failure. Patients on NIV who are unstable or have risk factors for NIV failure should be monitored in an intensive or intermediate care units by experienced personnel to avoid delay when intubation is needed. Stable NIV patients can be monitored on regular wards.


Author(s):  
Terry Robinson ◽  
Jane Scullion

Non-invasive positive pressure ventilation (NiPPV) is an effective form of ventilatory assistance. It was first used at the beginning of the twentieth century; since then, there has been growing interest in its role in treating type 2 (hypercapnic) respiratory failure. In the last 20 years NiPPV has had an important role in the management of acute exacerbations of chronic obstructive pulmonary disease (COPD), but its use is not limited to those with COPD. Initially, NiPPV was used mainly to support patients with neuromuscular disease, poliomyelitis, and pulmonary oedema. Since then many different groups of patients have been found to benefit from NiPPV, including patients requiring bridging pre-transplant, post-surgical respiratory support, and weaning from mechanical ventilation. NiPPV is also increasingly used to support patients with spinal injury. This chapter describes types 1 and 2 of chronic respiratory failure, types of ventilators and interfaces, and the British Thoracic Society indications for use and contraindications are all covered. Nursing care considerations and service provision are both included.


1961 ◽  
Vol 06 (01) ◽  
pp. 015-024 ◽  
Author(s):  
Sven Erik Bergentz ◽  
Oddvar Eiken ◽  
Inga Marie Nilsson

Summary1. Infusions of low molecular weight dextran (Mw = 42 000) to dogs in doses of 1—1.5 g per kg body weight did not produce any significant changes in the coagulation mechanism.2. Infusions of high molecular weight dextran (Mw = 1 000 000) to dogs in doses of 1—1.5 g per kg body weight produced severe defects in the coagulation mechanism, namely prolongation of bleeding time and coagulation time, thrombocytopenia, pathological prothrombin consumption, decrease of fibrinogen, prothrombin and factor VII, factor V and AHG.3. Heparin treatment of the dogs was found to prevent the decrease of fibrinogen, prothrombin and factor VII, and factor V otherwise occurring after injection of high molecular weight dextran. Thrombocytopenia was not prevented.4. In in vitro experiments an interaction between fibrinogen and dextran of high and low molecular weight was found to take place in systems comprising pure fibrinogen. No such interaction occurred in the presence of plasma.5. It is concluded that the coagulation defects induced by infusions of high molecular weight dextran are due to intravascular coagulation.


1967 ◽  
Vol 18 (03/04) ◽  
pp. 766-778 ◽  
Author(s):  
H. J Knieriem ◽  
A. B Chandler

SummaryThe effect of the administration of warfarin sodium (Coumadin®) on the duration of platelet aggregation in vitro was studied. Coumadin was given for 4 consecutive days to 10 healthy adults who were followed over a period of 9 days. The duration of adenosine diphosphate-induced platelet aggregation in platelet-rich plasma, the prothrombin time, and the platelet count of platelet-rich plasma were measured. Four other healthy adults received placebos and participated in a double-blind study with those receiving Coumadin.Although administration of Coumadin caused a prolongation of the prothrombin time to 2 or 21/2 times the normal value, a decrease in the duration of platelet aggregation was not observed. In most individuals who received Coumadin an increase in the duration of platelet aggregation occurred. The effect of Coumadin on platelet aggregation was not consistently related to the prothrombin time or to the platelet count. In the placebo group there was a distinct relation between the duration of platelet aggregation and the platelet count in platelet-rich plasma.The mean increase in the duration of platelet aggregation when compared to the control value before medication with Coumadin was 37.7%. In the placebo group there was a mean increase of 8.4%. The difference between the two groups is significant (p <0.001). Increased duration of platelet aggregation also occurred in two individuals who received Coumadin over a period of 10 and 16 days respectively.


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