As long as diseases are allowed to become surgical ultimates, just so long will we have postoperative pulmonary complications. Too, it is not insignificant that respiratory infections themselves have remained essentially unsolved in all respects to date.
For many years general anaesthesia (inhalation anaesthesia) received the brunt of the blame for these most undesirable occurrences, but since the advent of widely used local and spinal anaesthesia, no such simple explanation could be acceptable; for these methods showed similar if not higher incidences of pulmonary disorders postoperatively. A review of some facts regarding this dilemma in matter of causation, prevention and treatment will be especially interesting to surgeon and internist alike.
The majority of major surgical procedures are followed by two or three days rise in temperature. Although this is usually ascribed to the absorption of foreign material, etc., at the operative site, a fair number of these patients do slow slight cough and not rarely some upper back pain. Very frequently we pass over such a transitory picture without recognizing that many such instances do represent a mild degree of postoperative respiratory disease.
It is now generally felt that the difference of the above situation from that of a downright pneumonic one, or even from that of the dramatic pulmonary atelectasis, is only a matter of degree. All grades of such states have their origin in similar factors and are favorably or adversely affected by our management of surgical cases.
The following notations from the recent literature may seem confusing but many generalities are agreed upon. We present in brief a few summaries we have gleaned from modern work:
1. Respiratory infections following surgery are associated with aspiratory, embolic or atelectatic phenomena and are lobular in type.
2. In a series of 100 tonsil cases, under general anaesthesia, the following comments were made: 72 out of 78 with no cough but with the cough reflex still present showed aspiration of blood and mucus, whereas in 18 out of 22 that were coughing, no blood or mucus was found in the lung. It seems reasonable to assume then that cough is an efficient expellent but that the reflex invoking it often is not adequate to prevent aspiration.
3. Infections from the bronchi readily extend into the atelectatic areas so frequently found in the lung after laparotomy.
4. Postoperative pulmonary complications appear early after surgery and more especially after upper abdominal manipulations. The symptoms are most frequently at the bases and are characterized by bronchial hypersecretion.
5. All abdominal operations are followed by diaphragmatic paresis and reduced thoracic amplitude. Hypoventilation is thereby basic to all postoperative pulmonary disorders. The fact that the symptoms occur early and in the lung bases follows in logical sequence. Whether or not symptoms arise depends on the patient and possible pre-operative pulmonary disease.
6. Hypoventilation can be avoided by:.
(a) Careful surgery.
(b) Carbogen inhalations intra- and post-operatively.
(c) Sufficient opiates.
(d) Avoidance of tight bandaging.
(e) Postural exercises and frequent changes of. position after surgery.
7. Postoperative atelectasis and pneumonia are stages of the same process. If the obstruction causing atelectasis is relieved early the symptoms disappear, but if secretion plugging the bronchus is from virulent pneumococci and hence very thick, a pneumonic state will be seen.
8. Postoperative pulmonary complications represent pulmonary collapse of varying degrees associated with multiple emboli. Postoperative pneumonia is merely a diagnostic error for atelectasis. The two prominent factors are viscid secretions and inhibited coughing.
9. Bronchoscopic drainage of heavy secretion was followed by immediate relief of symptoms and also by the reinflation of the collapsed lung areas distal to the obstruction.
10. Profound preoperative narcosis increases the liability of the patient aspirating mucus in the induction stage of general anaesthesia.
11. Atropine does not dry up secretions. It merely thickens them to a point where they are more difficulty expectorated and much more likely to cause bronchial occlusion.
12. On prevention and treatment.
(a) Eradicate nose and throat disease.
(b) Moderate sedation sparing atropine.
(c) Prevention of aspiration.
(d) Uniform depth of anaesthesia.
(e) Gentle surgery.
(f) Postoperatively deep breathing, dressings, and. sedation must be adjusted to prevent hypoventilation.
(g) In actual atelectasis carbogen inhalations,. production of cough by any means, or if necessary. the bronchoscopy.
13. In a reported series of 500 cases done by one surgeon, one assistant, and one anaesthetist, there was a morbidity of. 9 percent and a mortality of. 2 percent. They ascribed their good results not to mild preoperative analgesia for this was deep; not to the choice of anaesthetic for it was nitrous oxide, oxygen, and ether. Rather, they felt that careful, even anaesthesia, prevention of anoxemia, gentle surgery, sterile anaesthetic apparatus, and great care of the details (transportation, room temperature, drafts, etc.) was responsible for this remarkably low incidence of infection.
14. In one series of 300 cases, it was noted that spinal anaesthesia was slightly better than inhalation anaesthesia as regards pulmonary disease. In this group it was stated that hypoventilation was the main causative factor with accumulation of bronchial secretions and cough inhibition running a close second. Also, it was stated that probably all these cases are atelectatic to a degree but the diagnosis was hard to make. As to prevention, carbogen and frequent change of posture were advised. No other treatment was mentioned except that in a wet type of chest ephedrine in full doses was thought to be helpful.
15. One author stated that postoperative major atelectasis was fairly common and that it was often mistaken for massive pulmonary embolus or frank pneumonia. He noted that artificial pneumothorax dramatically relieved the symptoms.
16. An English writer states that postoperative pneumonia is the result of multiple emboli, that the causes were trauma, mobilization, and sepsis in the surgical field. He gave a doubtfully equal place to aspiratory phenomenon.
From this review we may conclude then that several factors are preeminent. The most prominent of these are: hypoventilation, multiple minute emboli, aspiration, and atelectasis.
Hypoventilation results from excessive autonomic stimulation especially in rough peritoneal handling and exploratory procedures. It is most notable in upper abdominal work. Its presence is basic to the development of all other pneumonic changes.
Multiple emboli. These occur in all surgery but especially in pelvic work and in the surgery of infected areas. With adequate pulmonary ventilation no serious results accrue from these emboli, but with hypoventilation the ground work is set for a pulmonary complication.
Aspiration has been shown to be a common occurrence despite the presence of a cough reflex. Aspiration alone does not seem to be a major cause for trouble, but when associated with other factors is probably the greatest of all exciting agencies.
Aspiratory phenomenon are favored by poorly induced uneven, or too deep inhalation anaesthesia. Heavy preoperative sedation preceding spinal or local can probably be assumed as likely to have similar results.
Atelectasis has been shown to be far more common then previously believed. Minor and minute multiple atelectatic areas are observed in all less serious cases of postoperative pulmonary disability and major lobar atelectasis is frequently thought to be a lobar pneumonia or a massive pulmonary embolus. This latter is a serious error, for whereas lobar pneumonia or pulmonary embolus are highly disastrous conditions, the relief of obstruction brings a quick cure to the atelectasis patient.
Frequent x-ray pictures will do much to prevent this mistake. The development of atelectasis is seen only when Hypoventilation and emboli or aspiration give rise to local bronchitis. The resulting secretions provide the obstruction necessary for its occasion. Pneumococci which give rise to viscid secretions (apparently in direct proportion to virulence) are the most usual bacteria found.
Aside from these major tenets three minor ones must also be considered:.
1. Preoperative pulmonary disease is frequently blamed for trouble. While it is doubtless important to know of preexisting lung disease, in that one may be doubly careful, many case series were practically uninfluenced by the occasional presence of such cases.
2. Preoperative nasal or buccal foci of infection were considered quite important where any danger of aspiration might be expected.
3. Postoperative inhibition of coughing either by excessive sedation, or unrelieved pain, or tight abdominal binding, predisposed to hypoventilation. Such inhibition ranks with operative trauma in the etiology of decreased vital capacity.
DIAGNOSIS.
All cases of postoperative pulmonary complications occur within one to four days, develop rapidly, are noted at the lung bases, and are accompanied by increased bronchial secretions.
