Page 672 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 54: Acute-on-Chronic Respiratory Failure 491

(2 mg every 6 hours), which may be as effective as an oral steroid regi- AECOPD and the probability of ACRF requiring intubation. This may
men in patients with a COPD exacerbation. 149,150 Notably, hyperglycemia in part be through a reduced influenza and pneumonia mortality. In
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was less common in the budesonide-treated patients. However, this 185 patients with a COPD exacerbation followed for up to 1 year, statin
approach is significantly more expensive. use was independently associated with a significant prolongation in time
to repeat hospitalization and intubation for AECOPD (HR for AECOPD
Antimicrobials Viral and bacterial lower respiratory tract infections are 164
equally common precipitants of AECOPD including patients who 0.19 [CI 0.06-0.14]; HR for intubation 0.14 [95% CI 0.10-0.30]). Meta-
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analysis has proved difficult because of significant heterogeneity among
require NIV or mechanical ventilation for ACRF. Viral/bacterial coin- 165
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fections occur in between 10% and 20% of cases. It is likely that inaccurate published studies. However in a systematic review, chronic statin use was
consistently associated with marked reductions in COPD-associated hos-
assessments of bacterial infections from studies of expectorated sputum
and underappreciation of the frequency of viral infections as a sole etiol- pitalization, need for ventilation and mortality. In the absence of evidence
suggesting therapeutic benefit of acute statin administration for ACRF
https://kat.cr/user/tahir99/
ogy confounded older studies investigating the effectiveness of antimi-
crobial treatment for patients with ACRF from COPD. Microbiological our practice is to continue chronically prescribed statins but not to initi-
ate therapy unless indicated for acute intercurrent cardiovascular disease.
studies of patients with AECOPD using protected specimen brush cul-
tures identified pathogens at >10 CFU/mL in the lower respiratory tract Magnesium While hypomagnesemia is a recognized independent associate
3
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of more than half of the 86 subjects; H influenza (30%) and P aeruginosa of recurrent admission for AECOPD, only a single small prospective
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(9%) were the most frequent isolates. Consistent with these observa- study of 72 subjects with AECOPD has demonstrated modest
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tions were data from a very large retrospective analysis of AECOPD improvement in PEFR with magnesium sulfate 1.2 g over 20 minutes
patients treated with antibiotics in the first two hospital days compared after β-agonist administration compared with placebo. PEFR improve-
with patients receiving antibiotics later or not at all. Early administration ment was 25.1 L/min better at 30 min and 7.4 L/min better at 45 min
of antibiotics was associated with reduced progression to respiratory after MgSO than placebo (p = 0.03). Since this has not been validated,
4
failure or hospital mortality. Patients with ACRF severe enough to and because of the concern that iatrogenic hypermagnesemia can poten-
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require MV are more likely than others to harbor gram-negative enteric tiate respiratory failure; magnesium sulfate is not part of our usual care
organisms and nonlactose fermenting gram-negative rods including P armamentarium.
aeruginosa, particularly if the patient has been recently hospitalized, Recognizing Impending Respiratory Failure Despite aggressive attempts to find
has documented bronchiectasis or frequent antibiotic treatments in the and reverse the causes of ACRF, some patients will progress to frank
preceding year. Since benefit has been demonstrated in several stud- respiratory failure. The decision to intubate requires clinical judgment
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ies and a trend toward benefit in some others, 12,154 inexpensive, oral, and is best assessed by a physician present at the bedside (Table 54-3).
broad-spectrum antibiotic (eg, ampicillin, doxycycline, trimethoprim- Assessment of respiratory failure based solely on results of arterial
sulfamethoxazole) should be provided in the absence of clinical features blood-gas studies or end-tidal CO monitoring is fraught with error.
2
of pneumonia. A stratified approach based on AECOPD severity and Certainly, a rising Pa CO 2 in a patient with progressively worsening
risk for pseudomonas has been proposed. Community-acquired pneu- symptoms and signs of distress should be interpreted as heralding
10
monia should be treated with a cephalosporin-macrolide combination respiratory arrest. However, the absolute level of the Pa CO 2 , isolated
or a high-dose, single-agent fluoroquinolone. High-dose quinolones or from other clinical data, may be less useful. Partitioning the acute and
antipseudomonal β-lactams should be considered for patients at risk for chronic components of the hypercarbic state by evaluating the metabolic
P aeruginosa and those with severe sepsis or shock. Consideration for acid-base compensation (pH, serum HCO , or strong ion difference) is
3
community- or institution -acquired methicillin-resistant Staphylococcus essential in analyzing elevated Pa CO 2 . While an occasional patient will be
aureus (MRSA) infection based on regional prevalence should prompt alert and conversant when the Pa CO 2 rises to 150 mm Hg most patients
empiric treatment with vancomycin or linezolid in appropriate patients with ACRF will progress to respiratory arrest long before progressive
with concomitant pneumonia. hypercarbia is clearly documented. ET CO 2 measurements estimated
While neuraminidase inhibitors (oseltamavir, zenamavir, peramavir) from a sampling nasal cannula are frequently confounded in dyspneic
are clearly effective and essential treatments for patients with acute COPD patients because patients fail to achieve end-expiratory plateau
respiratory failure from invasive influenza pneumonia, it remains (phase 4) in the presence of severe PEEPi, thus falsely underestimat-
unclear if these treatments afford meaningful survival improvement for ing true ET CO 2 . Furthermore, because of increased dead space frac-
patients with ACRF. Older patients who are at risk for ACRF were not tion in patients with COPD, the difference between ET CO 2 and arterial
disproportionately affected by 2009 H1N1 influenza epidemic, perhaps Pa CO 2 is increased to unpredictable degrees. Patients who have had an
because of persistent immunity from previous infection. COPD was unsuccessful attempt at stabilization with NIV are at particular risk
reported as a comorbidity in only 9.5% to 12.5% of patients requir- for underappreciated clinical instability. Predictors of NIV success or
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ing ICU admission and no data are available for patients with restrictive failure are summarized in Table 54-3. Most notably, lack of improve-
diseases such as IPF. ment in clinical and gas exchange measures within the first hour after
initiation of NIV should prompt urgent reevaluation as this strongly
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Anabolic Steroids Inflammation is not limited to the lung during an heralds decompensation.
AECOPD. Peripheral and diaphragmatic skeletal muscle weakness is Those patients may have very little tissue oxygen reserve, low effective
pronounced during ACRF and is associated with markers of systemic circulating volume, and are at substantial risk of cardiopulmonary arrest
inflammation such as IL-6 and IL-8. A combination of anabolic ste- if transition to intubation is delayed, potentially increasing the risk of
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roids (nandrolone decanoate, 25-50 mg IM every 2 weeks) and caloric death. Respiratory arrest may be complicated by aspiration or cardio-
8
supplementation (420 kcal/d supplement) raised the mouth pressure vascular instability, compromising future efforts to return the patient to
during a maximal static inspiratory maneuver in patients with clinically spontaneous breathing. Indeed, the survival of patients who are allowed
stable COPD but was ineffective in improving physiological function to progress to respiratory arrest is significantly lower than of patients
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or QOL as a replacement for dedicated rehabilitation. Similarly, COPD ventilated for acute deterioration of COPD who are intubated electively
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patients treated with oxandrolone experience a significant increase prior to arrest. The goal at this stage of management is to intubate the
in lean body mass. However, this effect may only be clinically useful in patient electively once mechanical ventilation becomes unavoidable. In
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patients receiving long-term oral steroids. We are aware of no trials some cases, this will require foregoing NIV and opting for immediate
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showing clinically important benefits in patients with ACRF. airway intubation for mechanical ventilation to avoid respiratory arrest.
HMG-CoA-Reductase Inhibitors (Statins) There is gathering evidence from retro- Useful bedside parameters of impending respiratory arrest include
spective studies that HMG-CoA-reductase inhibitors (statins) through respiratory rate, mentation, pattern of breathing, and the patient’s
putative immune-regulatory effects can modify both the likelihood of own assessment. The patient may be able to tell the physician whether
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