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* From the Department of Medicine, Sound Shore Medical Center of Westchester, New Rochelle, NY.
Correspondence to: Robert D. Brandstetter, MD, FCCP, Department of Medicine, Sound Shore Medical Center of Westchester, 16 Guion Place, New Rochelle, NY 10802
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Key Words: atelectasis • complications • effusions • liver transplant
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1. On the second day following surgery, I was lying supine in bed at a 20° angle with a nasogastric tube in place, and I aspirated gastric contents. The refluxed liquid created intense esophageal pain, and although I struggled to a 45° sitting position to reduce laryngeal tracheal aspiration,1 it was too late.2 I experienced immediate laryngospasm and a new pain, now in the tracheobronchial tree. As frightened as I was, especially when I heard the pulse oximeter alarm ringing with the O2 saturation (O2 sat) falling < 90%, I knew I had to inspire slowly and calmly to overcome the acute upper airway vocal cord obstruction. To my surprise, I remembered the adverse pathophysiologic effect of the Mueller Maneuver.3 Having achieved this slow inspiratory air flow with an O2 sat of 83%, I then had bronchospasm and coughing. The expectorated secretions were an identical yellow color as the nasogastric tube drainage. Supplemental O2 was administered, along with inhaled bronchodilators and a return of the O2 sat to about 92%. The chest roentgenogram (CXR) was clear except for elevated diaphragms and a right pleural effusion secondary to postoperative ascites.4 Two days later, however, I developed fever with a change in sputum, and the CXR showed a right lower lobe (RLL) infiltrate and a moderate effusion. Antibiotic therapy was begun. The surgeons offered me the opportunity to review the CXR, and I initially declined, because I feared an extensive dense consolidation. Their cajoling efforts paid off, as the infiltrate was "not bad" and I managed to fall asleep that night without wondering whether or not I would wake up receiving ventilatory support.
2. My second encounter with breathing problems due to a change in body
position occurred when I attempted to lie on my right side. I became
dyspneic and tachypneic, with a fall in my O2 sat
to 82%. I immediately remembered, however, that the "bad lung
down" results in arterial desaturation secondary to gravitational
forces and resulting 
/
mismatch.5
By
changing to the left decubitus position with the good lung dependent,
my O2 sat recovered to > 92%. Whenever I
returned to bed, I managed to assume this preferred position to aid
breathing, although lying on my side was uncomfortable and painful due
to the extent of the transverse abdominal incision.
3. I could not believe it, but I experienced yet another respiratory embarrassment due to a different change in body position. Acknowledging the fluid resuscitation that I received during the transplant (28 U of packed RBCs, 24 U of fresh frozen plasma, 18 U of platelets, and 12 L of Ringer's lactate), I experienced tremendous third spacing, with massive peripheral edema and tense abdominal ascites. On one occasion, 4 days postoperatively, I raised my legs on a chair as the dependent ankle edema was quite painful. Within seconds, I had acute dyspnea and wheezing! My breathing had still been compromised by the presence of the effect of ascites on the diaphragm, as well as the pneumonia with pleural effusion. I initially thought that these were the explanations for the dyspnea.4 I called the nurse (who thought otherwise), and she administered IV furosemide, 40 mg. In < 1 min, even though there was no change in supplemental O2 or a change in my position, I experienced a curious sensation of warmth in my thoracic cavity and an immediate improvement in breathing. I was experiencing the venodilatation benefit of IV furosemide long before its diuretic effect!6 Once again I had then realized what I had done. The change in position of my legs up to the chair had increased my right ventricular preload, resulting in early pulmonary edema from this autotransfusion of vascular fluid.7 8 This phenomenon of respiratory distress with inadvertent change in leg position, and immediate improvement in breathing following IV furosemide occurred on at least two other occasions.
4. It was no surprise that I additionally suffered from the third-spacing, hemodynamic, "see-saw" effect of colloid replacement followed by IV furosemide "chaser." My serum albumin had fallen to 1.8 g/L secondary to the catabolic effects of infection, acute liver rejection, corticosteroids, and poor nutrition. The surgeons insisted that exogenous albumin was necessary to elevate the serum level. Well, each and every time I received the 250 mL of 5% albumin, I experienced worsening ascites as my abdomen became more tense.9 This would then be followed by light headedness and hypotension after the IV furosemide-induced venodilatation, and diuresis. I could not convince the surgeons to stop administering the albumin.6 Acknowledging that colloid can increase lung water in ARDS, I thanked God that I only had pneumonia and not an acute lung injury following the aspiration episode.
5. Another unique respiratory condition that I noticed was an altered breathing pattern associated with IV narcotic administration for postoperative pain.10 This pattern would occur about a couple of minutes following the IV narcotic, and it consisted of shallow periodic breathing and even central apneic episodes, as witnessed by observers. I actually knew that I was not breathing correctly, for when I would suddenly awake, I was dyspneic and frightened. I would then settle down, still free of pain, only to reexperience these periodic breathing patterns again, which were fortunately interrupted by the alarm of the pulse oximeter and my wakefulness. As we are all aware, the administration of IV narcotics has a remarkable influence on spontaneous breathing.
6. The last notable pulmonary complication that I suffered was RLL atelectasis on the 11th postoperative day. I had experienced an acute worsening of my baseline dyspnea as well as desaturation, even though the ascites was less and the CXR of the previous day had demonstrated a near resolution of the RLL infiltrate and effusion. The repeat CXR showed new RLL atelectasis. Although I had been reluctant to use incentive spirometers on my own patients, because of the controversy surrounding their effectiveness,11 the surgeons essentially "forced" me to cooperate in the use of an incentive spirometer for myself. With supervision and its appropriate use, the RLL radiologically reopened 6 h later. I, furthermore, personally learnt of the benefit of an appropriately supervised continuous positive airway pressure mask. This device reopened the RLL lobe when it collapsed again following liver biopsy and the need to be in the right decubitus position for 4 h to prevent hemorrhage. Both of these noninvasive techniques were accompanied by ambulation, under the threat of the surgeons to perform therapeutic bronchoscopy if the lobe did not reexpand!
It is more likely than not that each of us one day will become a patient. The transformation of physician to patient is probably incomplete in most instances. Anecdotally, we physicians do not make the best patients, as our knowledge is a double-edged sword and we are reluctant to give up control. This certainly may help or deter our physical and emotional healing process during a serious illness or following a major operation. Although I had clever and reassuring explanations for many of the morbid episodes that I experienced, the energy exerted in fear and anticipation was often of greater personal morbidity. I do believe that in the future, however, I will try to be a better patient to myself and to my physicians. This may be achieved by merely practicing what I preach to my own patients: "Trust me; you will soon be feeling better!"
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Received for publication May 3, 1999. Accepted for publication May 4, 1999.
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