Acute Exacerbation of COPD: Non-invasive Positive Pressure Ventilation




© Springer International Publishing Switzerland 2017
Robert C. Hyzy (ed.)Evidence-Based Critical Care10.1007/978-3-319-43341-7_22


22. Acute Exacerbation of COPD: Non-invasive Positive Pressure Ventilation



Kristy A. Bauman 


(1)
Pulmonary and Critical Care Medicine, University of Michigan Health System, Ann Arbor, MI, USA

 



 

Kristy A. Bauman



Keywords
Acute exacerbation of COPDNon-invasive positive pressure ventilationHypercapnic respiratory failureDo-not-intubateBronchodilatorsSystemic corticosteroids



Case Presentation


A 73-year old male smoker with a past medical history of coronary artery disease, congestive heart failure and COPD on home oxygen arrived in the emergency department with difficulty breathing. He complained of gradually increasing shortness of breath on exertion for 1 week and cough with thick yellow sputum. He denied fever, chills, chest pain, orthopnea or paroxysmal nocturnal dyspnea. He had increased the use of his bronchodilators as directed by his primary care physician. This did not improve his symptoms. The morning of admission, he woke up and was unable to catch his breath. He called EMS. Upon arrival, he was afebrile with BP 160/80, HR 130, RR 36, sPO2 85 % on 4 L/min O2. Arterial blood gas (ABG) pH 7.24, pCO2 60, PO2 55, spO2 85 %. He was awake, yet lethargic, tachypneic and using accessory muscles of respiration. Chest auscultation revealed regular tachycardia, poor air movement, end-expiratory wheeze and no crackles. Chest x-ray demonstrated hyperinflation with no infiltrates.


Question

What is the immediate approach to this patient with acute respiratory failure?


Answer

Non-invasive positive pressure ventilation.

In the absence of absolute contraindication, all patients with acute hypercapnic respiratory failure due to an exacerbation of COPD should be treated with non-invasive positive pressure ventilation (NIPPV). This patient was initiated on NIPPV with pressure support of 12 cm H2O, PEEP 5 cm H2O, and FIO2 of 0.5 via a full face mask. Oxygen was titrated to maintain saturations of greater than 90 %. He was given two albuterol/ipratropium nebulized treatments in the first 30 min of his arrival, azithromycin 500 mg PO once, and solu-medrol 60 mg IV once. After 1 h, his respiratory rate decreased to 22 and he was no longer using accessory muscles. ABG on NIPPV demonstrated pH 7.33, pCO2 46, pO2 80, spO2 95 %. He was admitted to the intensive care unit for continued management. By hospital day 2, respiratory failure resolved and he was transferred to general care.


Principals of Management



Diagnosis


Acute exacerbations of COPD are characterized by sub-acute or acute worsening of chronic respiratory symptoms. Typical symptoms are dyspnea, cough, and increased sputum purulence and volume [1]. Severity of symptoms ranges from mild, which may improve without additional medical treatment, to severe resulting in respiratory failure or death. The hallmark of COPD exacerbations is airflow obstruction, dynamic hyperinflation and airways inflammation, often provoked by viral or bacterial infections or environmental triggers. COPD exacerbations are associated with reductions in quality of life, progression of lung disease, and increased risk of death. In a longitudinal study of 2138 COPD patients; mortality during follow-up was significantly higher in those with one or more hospitalized exacerbations during the first year of follow-up (15 %), as compared to 5 % in those without an event [2]. The predicted in hospital mortality of a COPD exacerbation is 10 % [3]. A severe exacerbation resulting in hypercapnic respiratory failure portends a 2-year mortality rate approaching 50 % [3]. Indications for ICU admission of a COPD exacerbation are given below [4]. The approach to treatment of an acute exacerbation of COPD with hypercapnic respiratory failure requiring intensive care unit admission follows.


Indications for ICU Admission





  • Severe dyspnea that responds inadequately to initial emergency therapy


  • Changes in mental status (confusion, lethargy, coma)


  • Persistent or worsening hypoxemia (PaO2 < 5.3 kPa, 40 mmHg) and/or severe/worsening respiratory acidosis (pH < 7.25) despite supplemental oxygen and noninvasive ventilation


  • Need for invasive mechanical ventilation


  • Hemodynamic instability—need for vasopressors


Bronchodilators


Short-acting beta adrenergic agonists (albuterol, levalbuterol) are potent bronchodilators with rapid onset of action and are first line therapy for acute exacerbation of COPD [5]. Typically, these are combined with short acting anticholinergic agents such as ipratropium bromide. Both drugs can be administered with equal efficacy via metered dose inhaler or nebulizer; however nebulized delivery is often preferred during an acute exacerbation of COPD due to ease of administration for persons in respiratory distress. Albuterol should be dosed at 2.5 mg/ 3 mL via nebulizer every 1–4 h or 4–8 puffs (90 mcg per puff) via MDI. Ipratropium bromide is dosed at 500 mcg by nebulizer every 4 h or 2–4 puffs (18 mcg per puff) via MDI every 4 h. There is no advantage to increasing the dose of nebulized albuterol to 5 mg and continuous nebulized beta-agonists are not recommended [6]. Side effects of beta-adrenergic agonists include tachycardia, anxiety, tremors, hypokalemia, and rarely lactic acidosis. Side effects of short acting anti-cholinergic agents include dry mouth, urinary retention and exacerbation of narrow-angle glaucoma. There is no role for methylxanthines such as aminophylline for treatment of hospitalized patients with COPD exacerbations [7, 8].


Systemic Corticosteroids


When added to bronchodilator therapy, systemic corticosteroids improve lung function, decrease treatment failure rates, prevent relapse, and decrease length of hospitalization [911]. There is no significant difference in clinical outcomes in hospitalized patients with a COPD exacerbation treated with oral versus intravenous corticosteroids [12]. The dose of corticosteroids and length of treatment varies widely in clinical trials. A randomized controlled trial (RCT) in patients with acute exacerbation of COPD treated in the emergency department randomized patients to either a 5 day course or a 14 day course of prednisone 40 mg daily. The study concluded that patients randomized to 5 days of treatment had similar rates of relapse within 6 months and this was non-inferior to a longer course [13]. Given the short and long term side effects of systemic corticosteroids, a reasonable approach to treatment is a 5 day course of 40 mg of prednisone for most patients [5]. In critically ill patients clinicians often prescribe higher doses with little evidence to support this practice. In an observational study of ICU patients with COPD exacerbations, doses of methylprednisolone <240 mg daily compared to >240 mg daily resulted in a slightly shorter hospital and ICU length of stay and duration of mechanical ventilation [14]. There was no mortality difference. There is not enough data to recommend an optimal dose of corticosteroids in the ICU setting.


Antibiotics


The majority of COPD exacerbations are due to bacterial or viral infections. There is evidence that viruses and bacteria act synergistically to provoke airways inflammation and exacerbation [15]. Additionally, new strains of airway bacteria have been shown to trigger a significant inflammatory response and resultant exacerbation [16]. GOLD and European Respiratory Society guidelines recommend antibiotics for all patients with a moderate to severe COPD exacerbation and for those requiring hospitalization [5, 17]. Antibiotics reduce the risk of treatment failure and length of hospital stay in persons with severe exacerbations [18]. For example, in a RCT of patients requiring intubation and mechanical ventilation, ofloxacin was compared to placebo and was found to decrease mortality (4 % vs 22 %), duration of mechanical ventilation and length of hospital stay [19]. The antibiotic regimen prescribed should target common bacterial pathogens, local patterns of resistance and risk factors for P. aeruginosa infection should be considered [20, 21]. Treatment courses of 3–7 days are appropriate in most cases. A meta-analysis comparing 5 days to greater than 7 of antibiotics (beta-lactams, macrolides, and fluoroquinolones) demonstrated no difference in outcomes and fewer drug related adverse events in those with 5 day course [22].


Non-invasive Positive Pressure Ventilation (NIPPV)


NIPPV refers to positive pressure ventilation through a nasal or oral interface as opposed to endotracheal tube or tracheostomy tube. NIPPV can be delivered through standard ICU ventilators or a variety of portable devices. Indications for NIPPV in COPD exacerbations are given below [4]. The most commonly used mode of ventilation employed in acute hypercapnic respiratory failure associated with COPD exacerbation is bilevel positive airway pressure (BPAP) where an inspiratory positive airway pressure (IPAP) and expiratory positive airway pressure (EPAP) is set. Pressure support, assist control and proportional assist ventilation are other options depending on the available device. There are few studies directly comparing NIPPV modes in acute hypercapnic respiratory failure. The goals of NIPPV are to reduce work of breathing, improve minute ventilation, correct hypercapnia and avoid endotracheal intubation while maximizing patient comfort. There are several available patient interfaces, full face mask, oronasal mask, nasal mask, and nasal pillows [23]. In a randomized trial of 26 patients with COPD exacerbations, NIPPV via full face mask, nasal mask or nasal pillows were compared [24]. The nasal mask was best tolerated while the full face mask provided the greatest physiologic improvement. A larger study comparing the nasal to orofacial mask found that more than half of patients with the nasal mask needed to be changed to the face mask most often due to air leak [25]. Based upon these studies, when initiating NIPPV for acute hypercapnic respiratory failure, full face mask or oronasal mask are the preferred approach. NIPPV should be initiated as soon as possible as delays may increase the likelihood of failure and need for endotracheal intubation [26]. Indications for invasive mechanical ventilation are shown below and include: cardiac/respiratory arrest, altered mental status, inability to clear secretions and protect the airway, non-respiratory organ failure, facial deformity or trauma, high risk of aspiration, recent esophageal surgery, anticipation of prolonged need for mechanical ventilation [4, 27]. Need for emergent intubation is an absolute contra-indication to NIPPV. Altered mental status due to hypercapnia is an exception. These patients should be closely monitored. Improved pH and PaCO2 within 30 min to 2 h predicts NIPPV success [28, 29]. If there is no improvement in mental status or physiologic variables within this time frame, the patient should be intubated or consider withdrawing NIPPV to oxygen therapy alone. There is high quality evidence that NIPPV for the treatment of acute hypercapnic respiratory failure in COPD improves important clinical outcomes. A meta-analysis including 14 randomized controlled trials and greater than 700 patients comparing standard therapy to NIPPV plus standard therapy in acute COPD exacerbation concluded that NPPV decreased mortality (11 % vs. 21 %), intubation rate (16 % vs. 33 %) and reduced hospital length of stay and complications related to treatment [30].

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Jul 20, 2017 | Posted by in Uncategorized | Comments Off on Acute Exacerbation of COPD: Non-invasive Positive Pressure Ventilation

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