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Home , Respiratory failure

Acute after Abdominal Surgery

G. Ferreyra, V. Squadrone, and V.M. Ranieri

z Introduction

Each year, millions of patients undergo abdominal surgery. Despite advances in an- esthesia and surgical care, postoperative pulmonary complications are still a major problem in modern practice. Over the last three decades, extensive research has been focused on their prevention; however, they continue to produce increase in length of hospital stay, overall increased health care costs, and it is estimated that they account for 24% of all deaths occurring within 6 days of surgery [1]. The inci- dence rate of postoperative pulmonary complications in abdominal patients de- pends on the surgical site, presence of predictive risk factors, and the criteria used to define them. Unfortunately, there is no homogeneity to determine the frequency and variety of events due to a lack of uniform definition of postoperative pulmo- nary complications among different studies. Postoperative pulmonary complications are usually defined as events occurring in the postoperative period producing clini- cal disease or dysfunctions that adversely affect the clinical course (Table 1). The literature reports postoperative pulmonary complication rates of 6 to 80% [1±9]. The most severe form of postoperative pulmonary complication is respira- tory failure, a condition in which the fails in one or both of its functions: oxygenation and/or elimination of carbon dioxide. Acute respiratory failure due to postoperative pulmonary complications involves 10 to

Table 1. Some postoperative pulmonary complications

z z Hypoventilation (analgesic and/or residual neuromuscular blockade) z Bronchospasm z z z Chemical (aspiration of gastric contents) z Nosocomial z z Exacerbation of underlying pulmonary conditions (COPD) z Embolic phenomena (thrombus, fat, air) z ARDS z Tracheal laceration or rupture Acute Respiratory Failure after Abdominal Surgery 11

25% of postoperative abdominal patients and is associated with a 40 to 65% mor- tality rate [7±9]. Acute respiratory failure has been mostly defined as need for me- chanical ventilation. The data regarding the time at which is instituted vary broadly from a few hours after surgery to 5 days postoperatively [3, 4]. Patients who developacute respiratory failure and require endotracheal intuba- tion and prolonged mechanical have an increased morbidity and mortality [6]. Hypoxemia is the most common phenomenon responsible for acute respiratory failure and mechanical ventilation in postoperative abdominal patients. Most stud- ies have documented severe episodes of arterial oxygen desaturation in the early postoperative period that may persist for several days [10]. There are many defini- tions used depending on its severity. The incidence ranges from 41 to 68% [11]. The criteria for starting mechanical ventilation vary from a PaO2 lower than 60 mmHg [5] to a PaO2/FiO2 lower than 200 mmHg. Atelectasis and pneumonia are the most common underlying mechanisms responsible for postoperative hypox- emia. Atelectasis is defined as closure or collapse of alveoli and is often described in relation to radiologic findings and clinical symptoms. Pneumonia is usually ad- dressed with atelectasis together because many of the pathological changes with at- electasis may predispose a patient to pneumonia [12]. The incidence of pneumonia, considered as presence of clinical features consistent with collapse or consolidation plus an otherwise unexplained temperature above 38 oC and either a positive chest radiograph or evidence of infection from sputum microbiology, ranges between 2 and 19% [5, 13, 14]. Development of atelectasis within the perioperative period ranges between 80± 85%; in the postoperative period 20±70% of the episodes of severe hypoxemia are due to atelectasis [9, 13]. Development of postoperative atelectasis and pneumonia are associated with a 30 to 50% increased risk of developing acute respiratory fail- ure requiring mechanical ventilation [9, 15]. Atelectasis is considered one of the important mechanisms responsible for the development of acute lung injury (ALI) by reducing local alveolar lung tissue oxygen tension and increasing lung perme- ability. Recent data indicating that alveolar hypoxia may result in pulmonary vascu- lar leak and increased lung inflammation through macrophage recruitment support

Fig. 1. Mechanisms responsible for acute respiratory failure (ARF) in patients recovering from major ab- dominal surgery 12 G. Ferreyra et al.

this contention [16]. Moreover, atelectasis formation promotes both bacterial growth in the lung and translocation from the lung into the blood stream [12] (Fig. 1).

z Etiology of Postoperative Acute Respiratory Failure

The outcome of the surgical procedure depends on the correct management of the pre-, intra- and postoperative periods.

Preoperative Factors Risk factors in the preoperative period that may predispose to acute respiratory failure are listed in Table 2. In a case-control study in patients undergoing abdom- inal surgery, a multivariate analysis found, in order of importance, abnormal chest examination, abnormal chest radiograph, high cardiac-risk index, and presence of relevant co-morbidities were independently associated with an increased risk of acute respiratory failure [17].

Table 2. Preoperative risk factors for postoperative acute respiratory failure

General health and nutritional status: z age:(the risk increases over 70 years old) z ASA class z co-morbidity z obesity z low albumin z loss of body weight Respiratory status: z COPD, z smoke z sputum production z sleep disorders z presence of naso-gastric tube Surgical incision site and type of surgery: z Upper abdominal surgery:when the site is close to the diaphragm the risk is 10 to 40% more than in other sites z abdominal aortic aneurysm repair z emergency surgical procedures z open versus laparoscopic surgical approach Anesthesia: z longer than 2 hours z general vs peripheral anesthesia Acute Respiratory Failure after Abdominal Surgery 13

Perioperative Factors

Anesthesia. Around 90% of all patients who are anesthetized develop atelectasis. Moreover, these lesions occupy 15±20% of the lung before any surgery is performed [18]. Atelectasis produced by anesthesia is predominantly due to three factors: z loss of diaphragm muscle tone which no longer acts as a rigid wall between ab- domen and thoracic cavity; the abdominal pressure is hence transmitted to the thorax compressing the lung and causing compression atelectasis z with high inspiratory fraction of oxygen (FiO2) may promote atelecta- sis formation because of gas re-absorption z surfactant seems to be impeded during anesthesia reducing alveolar stability [3, 19, 20].

Surgery. Surgical manipulations cause structural abnormalities with increased per- meability and bowel wall edema, and motility disorders with accumulation of secre- tions and gas, both resulting in abdominal distension and increase in abdominal pressure [21].

Postoperative Factors

Pulmonary complications in the first hours after abdominal surgery are predomi- nantly due to atelectasis in the dependent regions of the lung, which are produced due to several factors during surgery. One of the basic mechanisms of development of atelectasis is the reduction in lung inflation, which is invariably affected after ab- dominal surgery. Despite that, there is no change in the percentage of forced ex- pired volume in the first second (FEV1) thus indicating the presence of a restrictive process [22]. There is an important reduction in inspiratory and expiratory reserve volume during the first days [23, 24] with a 30 to 40% reduction in functional resi- dual (FRC) [24, 25] and total lung (TLC) [26] capacities. All these factors are em- phasized by a prolonged recumbent position and residual pain producing impaired mucociliary clearance that combined with a weak cough effectiveness increases the risk of atelectasis and infections [27]. It has been suggested that chest wall and diaphragmatic dysfunction may be im- portant in the genesis of postoperative pulmonary complications. They contribute to the altered lung function due to a restriction in diaphragm movement. Ford et al. and others noted a decrease in trans-diaphragmatic pressure and diaphragm contribution to tidal volume after surgery, which did not reach the normal value even with active maximal inspirations and incentive spirometry done by the patient [23, 28]. Furthermore, the marked diaphragmatic dysfunction concomitant with a paradoxical movement of the diaphragm may persist for up to one week after upper abdominal surgery [23, 29]. In a recent study conducted in patients with su- pra-umbilical laparotomy, modifications in the diaphragm in the three days conse- cutive to surgery were found. These were compatible with an altered diaphragmatic excitability and or reduced central drive [30]. To date it is not clear if optimum control of postoperative pain by regional anesthesia may result in greater respirato- ry excursion or improvement in lung function [31]. This suggests that respiratory muscle dysfunction and respiratory failure may be produced by an alteration in central drive, even in the presence of enhanced pain control. It has been demon- strated that when animals breathe against severe inspiratory resistive loads, no 14 G. Ferreyra et al.

changes are observed in diaphragm force output, despite development of progres- sive and respiratory [32]. Pain is one of the factors responsible for decreased lung volumes provoking diminished respiratory performance. Optimum pain control using postoperative epidural analgesia may result in several benefits through a reduction in the in- cidence of pulmonary complications [33]. Hypoventilation, the result of a reduction in carbon dioxide elimination and eventually oxygenation is the consequence of a depression in respiratory drive caused by any anesthetic agent, an increase in abdominal pressure due to surgery, reduction of FRC and vital capacity, reduced respiratory muscle function, pain pro- voked from an abdominal incision, and an analgesic regime involving [34, 35]. Although there has been a significant decrease in the incidence of respiratory depression and hypoventilation over the course of the last two decades, a recent re- port found that the incidence of respiratory depression and consequent hypoventi- lation continue to be the same using patient controlled anesthesia vs epidural an- algesia [36].

z Treatment

Preoperative Considerable time and effort are devoted to prevention and treatment of acute res- piratory failure. There is no absolute consensus as to the most appropriate and ef- fective therapy, and considerable controversy exists. The goal is to identify patients with preexisting pathologies or predisposing factors that may affect the postopera- tive course. Smokers have a high risk of postoperative pulmonary complications even when they are not affected by chronic obstructive pulmonary disease (COPD). It has been shown that 8 weeks smoking abstinence is beneficial [37]. The treat- ment for COPD patients before surgery should include a combination of broncho- dilators, , and corticosteroids. The use of preoperative does not prevent the risk of postoperative pulmonary complications unless there is a current respiratory infection. Asthma patients should be free of wheezing, and if necessary the patient should receive corticosteroids [38]. A strict follow up should be done in patients with a diagnosis or suspicion of obstructive sleep apnea. Preoperative physiotherapy has been demonstrated to have beneficial effects on postoperative pulmonary complications [8]. In a recent randomized control trial, Fagevik Olsen and colleges studied the effect of preoperative chest physiotherapy vs no respiratory therapy in patients with and without high risk factors. The treat- ment, including breathing exercises with pursed lips, huffing, coughing and resis- tive training during inspiration and expiration, was associated with a reduction in postoperative pulmonary complications and improvement in oxygen saturation after abdominal surgery [7].

Intraoperative A recent study showed that reduction in oxygen concentration from 100 to 60% de- creased atelectasis [39]. Also, the application of positive end-expiratory pressure (PEEP) in the intraoperative period may play an important role in reopening the Acute Respiratory Failure after Abdominal Surgery 15 collapsed lung [40]. However, there is no evidence that it improves arterial oxyge- nation or lung function postoperatively [41].

Postoperative

Early treatment. In the postoperative period, there is evidence in favor of chest phy- siotherapy [42]. However, in many studies there is no definition of the specific chest physiotherapy intervention, which makes the evaluation of outcome difficult. Lung expansion maneuvers are the mainstay to reduce postoperative pulmonary complications. The techniques of percussion and postural drainage have shown no value as routine interventions; they may be of benefit in patients with established atelectasis or diseases causing secretion management problems [43]. Data regarding deep breathing and incentive spirometry are conflicting. Incentive spirometry is the technique to sustain maximal inspirations through a device. It is a widely used technique for prophylaxis and treatment of postoperative pulmonary complications [44], although there is not enough evidence to support its use. Most of the random- ized trials [45±47] have shown no effectiveness or at least no superiority of deep breathing, chest physiotherapy, or continuous (CPAP). is usually successful in preventing both continuous and episodic hypoxemia and can reduce tachycardia, particularly in the most hypoxemic patients [48]. However, oxygen therapy is rarely continued after the second postoperative night and the apparent incidence of hypoxemia may be greater in subsequent nights. A recent meta-analysis showed that although postoperative hypoxemia is more closely controlled with better oxygenation, there are no benefits regarding morbidity and mortality nor evidence of reduction in the incidence of acute respi- ratory failure [49]. Although the use of CPAP in post-abdominal surgery is rational, its effects on the treatment of atelectasis and on clinical outcomes are still not clear. From the 330 articles related to CPAP, only six randomized trials fit into the category of post- operative abdominal patients and most of them studied a small population. There is evidence that the application of CPAP in comparison with conservative phy- siotherapy and other techniques and when used for consecutive days after surgery, improves residual lung capacity and lung volumes in general more rapidly [24, 47, 48]. Furthermore, it may also diminish the development of atelectasis [43, 45, 46]. Stock et al. in a randomized study confirmed that after 72 hours of treatment only 22% of the CPAP grouphad atelectasis compared to 41% with physiotherapyand 42% with incentive spirometry [45]. In two subsequent randomized trials, the authors were not able to confirm a better outcome in physiologic effect or a reduc- tion in clinically relevant variables like pneumonia or a reduction in length of ICU stay in patients treated with CPAP [50, 51]. All these trials were characterized by the fact that treatment was applied only for a few hours and by the small number of patients included. Bohner et al. in a more recent study with a larger number of patients undergoing vascular abdominal surgery also found no correlation between CPAP and improvement in postoperative pulmonary complications [52]. However, there was a trend to a lower intubation rate in the grouptreated with CPAP. The limited scope of the foregoing randomized trials leaves unanswered questions about the utility of CPAP as a preventive treatment in acute respiratory failure. Delclaux and coworkers conducted a multicenter, randomized controlled trial comparing 16 G. Ferreyra et al.

CPAP with standard medical treatment. Although the authors reported better gas exchange in the CPAP groupin the first hours, no other benefit in reduction of en- dotracheal intubation rate and length of ICU and hospital stay was demonstrated thereafter. It may be that as these patients already had ALI they were more likely to require prolonged ventilator support and develop pulmonary complications [53]. Data addressing the use of non-invasive ventilation (NIV) in patients developing postoperative acute respiratory failure are sparse [53±58].

z Conclusion

Postoperative pulmonary complications remain a significant problem after abdom- inal surgery. Efforts should be focused on optimizing patient condition before and immediately after surgery when signs of acute respiratory failure are still not evi- dent. Physiotherapy, CPAP, and NIV seem to have a strong physiological rationale for reducing the development of atelectasis and increasing lung volumes to prevent acute respiratory failure when they are instituted early. Carefully conducted con- trolled clinical trials are necessary to draw valid conclusions relative to the clinical efficacy of these interventions in preventing and treating postoperative pulmonary complications in patients recovering from abdominal surgery.

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