Issues in Pulmonary Anesthesiology
1Preventing Postoperative Pulmonary Complications: The Role of the Anesthesiologist
Warner, D.O and Weiskopf, R.B. Preventing Postoperative Pulmonary Complications: The Role of the Anesthesiologist, Anesthesiology 2000 May; 92(5): 1467-1472 (c) 2000 American Society of Anesthsiology
1Introduction: This article is a review of pulmonary complications and includes a discussion of significance of perioperative complications, causes, risk assessment, patient preparation and ultimately considers questions of prevention
This article begins with the recognition than one of the earliest victims of respiratory complications following surgery was the death of General "Stonewall" Jackson of pneumonia following apparently successful ether anesthesia in 1863.
Despite the intervening 230 years, postoperative pulmonary complications (PPC) continues to represent an important problem and a question is raised with respect to the role of the anesthesia provider and helping to prevent these problems.
One of the general problems in assessing PPC appears to be the variable definition.
For example there is relative unanimity for including pneumonia, bronchospasm, and respiratory failure.
But sometimes, other presentations are included such as unexplained fevers, abnormal breath sounds, productive cough, atelectasis, hypoxemia, and respiratory failure requiring mechanical ventilation.
Despite these different possible definitions of their appears general agreement that PPC is reasonably common and that the postoperative complication described as cardiac occurs with equal frequency to that of PPC.
In one study of adult men having elective abdominal surgery, PPC occurred somewhat more frequently than cardiac complication (about 10% versus about 6% respectively); a complication rate that was associated with longer hospital stays.
A number of examples of PPC appear related to abnormal respiratory muscle function.
Examples of this type include pneumonia and atelectasis.
Muscle function disruption may begin with anesthesia induction continuing into the postoperative timeframe. Anesthetics and other drugs used perioperatively influence central breathing regulation, having the effect of altering neuronal drives to respiratory muscles (e.g. diaphragm).
Given that breathing is a complex process which depends on several muscle groups coordinating their contractile behavior, such anesthetic-induced CNS effects might be expected to disrupt this process.
At moderate anesthesia doses, respiratory depression may be induced by altering timing/distribution of neuronal drives to respiratory muscles rather than an overall depression, which might be seen at high anesthetic doses.
An example of this effect is noted with 1.2 MAC halothane in which parasternal intercostal muscles are depressed but other muscles associated with respiration may exhibit increased activity (e.g. transversus abdominis).
Accordingly, perioperative dysfunction in this system is more likely due to disruption of coordinated muscle activity.
The consequence of this effect may be to reduce efficiency as reflected in hypoventilation.
Chest wall changes induce secondary effects such shows FRC reduction and atelectasis induction in dependent lung regions.
Regions of atelectasis and develop the commonly within a few minutes of anesthesia and can impair pulmonary gas exchange.
Chest wall distortion with atelectasis also occurs with respiratory musclinactivity during mechanical ventilation and even during positive and-expiratory pressure.
1Surgical Consequences:(see Fig. 2 below)
Consequences of surgical trauma result in intraoperative changes in breathing patterns to transition into the postoperative timeframe.
Factors that may be important include residual anesthetic effects.
Surgical trauma itself following thoracic abdominal surgery, are probably important in this regard and can be discussed in terms of three principal mechanisms.
(1) Respiratory muscle functional disruption because of incision with resultant reduced muscular function.
(2) Postoperative pain can induced voluntary respiratory motion limits and
(3) Visceral stimulation, for example, due to mechanical traction on the gallbladder or esophageal dilation appears to increase phrenic motoneuron output and changes other respiratory muscle activation patterns, the general consequence appears to reduce the extent of diaphragmatic dissent.
Therefore surgery and anesthesia collaborate in respiratory muscle contraction incoordination and as a result these effects can lead to reduction in FRC and vital capacity with atelectasis.
Such changes can persist for several days into the postoperative time. It is possible that atelectasis mainly to pneumonia (unproven).
The above pulmonary dysfunction may be reduced its endoscopic techniques are used which may minimize surgical trauma. In some common endoscopic methods such as laparoscopic cholecystectomy, abdominal viscera would still be stimulated (such as gallbladder traction) and as a consequence pulmonary muscular mechanics would still be influenced.
Bronchoconstriction can be induced by airway reflex stimulation during intubation or by drug-induced release of inflammatory mediators (e.g. cytokines).
Such bronchoconstriction, which increases airway resistance, may limit expiratory flow from the lung, even to the point of hyperinflation with barotrauma and impaired gas exchange.
Anesthetics themselves as well as tracheal intubation may degrade mucociliary transport.
Relatively long surgery with extended anesthesia may also attenuate lung inflammatory cell function which could manifest as increased susceptibility to postoperative infection.
Adverse effects on respiration may occur in a more direct way because of specific surgical or anesthetic procedures.
Cardiopulmonary bypass-induced acute lung injury
Barotrauma or surgical trauma-induced pneumothorax
Airway obstruction during spontaneous breathing-induced negative pressure pulmonary edema and finally
PPC risk factors include those that reference a specific surgical site, i.e. thoracic/abdominal surgery associated with highest risk, smoking, and the presence so preoperative pulmonary disease.
Postoperative pulmonary complications are not predicted by preoperative pulmonary function analysis, although the latter may predict pulmonary function following lung resection operations.
An example of this phenomenon is is seen in the fact that the extent of airway obstruction (FEV1 assessment) does not appear to be an independent risk factor for postoperative respiratory failure following abdominal surgery, even in patients who smoke.
Pulmonary function testing therefore appears more useful in developing interventions that optimize preoperative pulmonary function as opposed to a risk assessment procedure.
Spirometry in this context would be useful in assessing the asthmatic patient' s status rather than assessment of future risk.
A number methods have been implemented to possibly improve surgical outcome in patients with lung disease.
It is been difficult to demonstrate that these interventions improve outcome and some interventions may involve risk.
Nevertheless these interventions have included prolonged preoperative hospital stay in advance of surgery, application of β-2 adrenergic sympathomimetic agents, chest physiotherapy, aminophylline, antibiotics, and hydration.
Specific application of one or more of these interventions might be appropriate for a given patient rather than broad application of these interventions to all patients.
1aOne example would be recognition that for the asthmatic patient, minimization of preoperative airway inflammation using corticosteroids, would make not only theoretical sense but patients with more active inflammatory presentations have a higher likelihood of PPC.
This does not mean that all patients with asthma should receive routine systemic steroids prior to surgery.
However, if the airway inflammatory process appears active, such intervention in a particular patient would seem reasonable.
Smoking, by contrast is a significant concern and risk factor for PPC.
Specifically, when the patient should quit is somewhat controversial as a study even indicated that recent smoking cessation may possibly increased PPC risk
An important issue is that of preventing significant bronchoconstriction, for example, those that may occur subsequent to reflex-induced effects by laryngoscopy and endotracheal intubation.
These procedures sometimes can be avoided in patients with reactive airways.
Reduction in the airway reflex can occur by aerosol delivery of beta adrenergic agonists as well as antimuscarinic drugs (e.g. ipratropium bromide).
Avoidance of airway manipulation using regional anesthesia would appear reasonable, however, whether respiratory outcome is actually improved remains to be determined.
Severe respiratory disease may require use of breathing accessory muscles (e.g. abdominal muscles) and patients in this condition would not tolerate epidural or subarachnoid block-induction of accessory muscle paralysis.
Improved postoperative pulmonary function may follow from better postoperative pain management.
Regional analgesic methods may improve two of the three mechanisms noted in figure 2 above: pain and reflex inhibition of respiratory muscles.
An important question is whether such alteration of postoperative respiratory muscle function which presumably enhances lung expansion and may decrease the likelihood of atelectasis and pneumonia in fact occurs in this manner.
First let us consider epidural, local anesthetic blockade:
On one hand, this method increases tidal volume and vital capacity and there might be an expectation that these changes directly reflect diaphragmatic activity change following thoracic corrupter abdominal surgery.
These effects might be due to reduce pain and interruption of the afferent component in reflex circuits.
Local anesthetic blockade also however, paralyzes other respiratory muscles such as intercostal and abdominal muscles; such paralysis can change breathing patterns, complicating interpretation of influences on diaphragmatic activity.
Ultimately the effect of this type of block remains to be elucidated and appears complicated.
A number of research challenges need to be overcome before the answer of whether regional analgesic a actually translates to improve clinical outcome with respect to pulmonary issues can be decided.
Control of patient population, surgical methodology, analgesic regimens, whether or not epidural analgesia is instituted intraoperatively, combined with relatively low major PPC frequency contributed to the confounding nature of the problem.
1bMeta-analysis with respect to postoperative analgesic methods on pulmonary outcome has applied to many different surgical procedures has been undertaken.
In that study, postoperative epidural opioids appeared to significantly reduce atelectasis frequency but not other pulmonary complications, when compared to systemically administered narcotic.
Also, epidural local anesthetics reduced pulmonary infection and pulmonary complication incidence again compared to systemic opioids.
Given the general problems noted above, i.e. research methodological problems, these conclusions must be regarded as tentative.
1cIn a study that addressed many of the above research limitations, patients undergoing abdominal cancer surgery were randomized to receive either continuous epidural bupivacaine morphine or subcutaneous morphine infusion by catheter that simulated epidural placement.
In that study, epidural administration appear to provide postoperative analgesia which was considered excellent and superior to that obtained through subcutaneous morphine infusion.
However, the frequency of PPC was not altered, either in patients with normal or abnormal pulmonary systems.
Therefore, the use of regional techniques has yet to be demonstrated to consistently improve respiratory outcome.
Postoperative techniques to increase lung volume have been shown beneficial in preventing PPC; methods include intermittent positive pressure breathing, deep-breathing exercises, incentive spirometry* and chest physiotherapy.
All these approaches appear equally beneficial in reducing PPC frequency (by about a factor of 2 compared to know intervention).
This approach applies to at least two upper abdominal surgery.
*Incentive spirometry mimics natural sighing or yawning by encouraging the patient to take long, slow, deep breaths.
This objective is accomplished by using a device which provides patients with positive feedback when they inhale at a predetermined flowrate or volume and continue the inflation for at least 3 seconds.
The procedure increases transpulmonary pressure and inspiratory volumes, improves inspiratory muscle performance, and simulates normal pattern of pulmonary hyperinflation.
With repeated use, this procedure helps to maintain airway patency, preventing or reversing lung atelectasis.
1Warner, D.O and Weiskopf, R.B. Preventing Postoperative Pulmonary Complications: The Role of the Anesthesiologist, Anesthesiology 2000 May; 92(5): 1467-1472 (c) 2000 American Society of Anesthsiology--References 1a, 1b, & 1c second sourced from reference 1.
1aWarner DO, Warner, MA, Barnes, RD, Offord, KP, Schroeder, DR, Gray, DT, Yunginger, JW: Perioperative respiratory complications in patients with asthma. Anesthesiology 1996;85: 460-467.
1bBallantyne, JC, Carr, DB, deFarranti, S, Suarez, T, Lau, J, Chalmers, TC, Angelilo, IF, Mosteller, F: The comparative effects of postoperative analgesic therapies on pulmonary outcome; Cumulative meta-analyses of randomized, controlled trials. Anesth Analg 1998; 86: 598-612.
1cJayr, C, Thomas, H, Rey, A, Farhat, F, Lasser, P, Bourgain, JL: Postoperative pulmonary complications: Epidural analgesia using bupivacaine and opiods versus parenteral opioids. Anesthesiology 1993; 78: 666-676.