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Case Report
Severe gastroparesis causing postoperative respiratory complications in a heart-lung recipient
1Department of Cardiothoracic Surgery, Chaohu First People's Hospital, Chaohu; 2Department of Cardiac Surgery, the Affiliated Provincial Hospital of Anhui Medical University, Hefei, PR China
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Abstract
Heart-lung transplantation is reserved for selected patients who have end-stage cardiac and pulmonary disease. Gastroparesis,
which is associated with aspiration, is commonly seen after transplantation. Here, we present a case in
which gastric contents aspiration leads to Pseudomonas aeruginosa pulmonary infection, 11 months after the heart
lung transplantation. We strongly recommend that early diagnosis and aggressive management of post-transplantation
gastroparesis is essential to prevent lung allograft injury and pulmonary infections.
Key words
heart-lung transplantation; gastroparesis; Pseudomonas aeruginosa; pulmonary infection
J Thorac Dis 2010;2:121-123. DOI: 10.3978/j.issn.2072-1439.2010.02.02.003
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Introduction
Heart-lung and lung transplantation has become an
acceptable treatment option for end-stage lung disease,
and the number of transplants being performed in the
world is increasing. Among the possible complications,
gastroparesis is a frequent complication of lung or heartlung
transplantation that may lead to micro aspiration
into the lung allograft (1). Gastroparesis also leads to
poor absorption of immunosuppressant medications and
aspiration pneumonia (1).
The respiratory infections have been reported as one
of the complications of gastroparesis and it remains
an important cause of postoperative mortality, but the
microbiological consequences have rarely been evaluated.
In the case reported here, pseudomonas aeruginosa
infection of the lungs led to catastrophic consequences 11
months after the transplant.
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Case report
A 29-year-old man with primary pulmonary hypertension
underwent heart-lung transplantation on June 8, 2005 (2). He had no reflux disease or gastroparesis prior to
transplantation. The patient was extubated on postoperative
day 2. Perioperative antibiotics were administered
routinely as infection prophylaxis. The patient received
post-operative immunosuppression with cyclosporine A,
mycophenolate mofetil and prednisone. By postoperative
day 8, he complained of early satiety, epigastric pain,
belching and bloating. A gastric scintigraphy revealed
an estimated gastric emptying half-life of 390 minutes
(normal, 45-100 min). At the time of scintigraphy, he was
not taking any medications affecting the study (these
medications were stopped 4 days before scintigraphy),
except for the immunosuppressive scheme. Conservative
treatment was started that is administration of promotility
agents (cisapride and metoclopramide), high-dose proton
pump inhibitors and frequent small meals with the patient
in an upright position. But this did not significantly
attenuate his symptoms which resulted in a 5-kg weight
loss within the first 2 months (from 65 kg to 60 kg).
Within the next 9 months, recurrent bouts of vomiting
led to 2 episodes of aspiration requiring hospitalization,
and he continued to experience bloating, early satiety,
belching and sporadic bucking. After 11 months, he
presented with sudden onset shortness of breath, fever
(temperature 39.3℃) and productive cough associated with
greenish sputum. Laboratory tests yielded white blood
cells 6830 mm3 (85% neutrophils, 3.7% lymphocytes,
10.7% monocyte). In emergency room, patient was
found to be in respiratory distress leading to emergent
intubation to maintain the saturations. New radiographic
infiltrates appeared in pulmonary parenchyma and some
purulent bronchial secretion was extracted by consecutive endotracheal suction on admission. The culture yielded
Pseudomonas aeruginosa. This is the sign of pneumonia
(3). Bronchoscopy also revealed some mucus pluggings
and food particles at the entrances to the left main bronchi,
which also yielded Pseudomonas aeruginosa after culture
(Fig. 1). The patient (weight 55 kg) was treated with
imipenim/cilastin (1 g three times a day). However, his
condition deteriorated rapidly and he died 1 week later. No
postmortem examination could be performed.
Figure 1 Bronchoscopy revealed some mucus
pluggings and food particles in trachea and
at the entrances to the left main bronchi,
which yielded Pseudomonas aeruginosa after
culture.
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Discussion
Gastroparesis in the heart-lung recipient can cause the
undesirable symptoms and several respiratory distress
due to aspiration pneumonia (4). The mechanism of
posttransplant gastroparesis is thought to be multifactorial
(5).
Gastroparesis might predispose to microaspiration and
pulmonary infections (4), which was main cause in our
case. Frequent nausea, vomiting, and gastroesophageal
ref lux can lead to aspiration pneumonitis. Laryngeal
exposure to acid and aspiration of gastric contents may lead
to severe respiratory disorders. The mechanism involved
in the complication of bacterial pneumonia in patients
with aspiration of gastric contents, however, remains
uncertain. The effect of this aspiration is generally thought
to be caused by gastric acid because the gastric contents
introduced into the lungs can cause severe pulmonary
injury, which is indistinguishable from that caused by the
aspiration of an equivalent amount of gastric acid (6).
Bacterial pneumonia is the result of infection of the
lower respiratory tract by microorganisms of the oral
and pharyngeal regions. Pseudomonas aeruginosa is an
opportunistic pathogen which colonizes at oropharynx
and is one of the potential pathogens isolated from sputum
samples from patients with respiratory aspiration of gastric
contents (7). Bacterial adherence to the airway epithelium
is the first step of bronchopulmonary infections. Acid aspiration can worsen bacterial infection by a mechanism
involving bacterial cell adherence to the airway epithelium.
Ramphal et al. Ramphal et al previously repor ted
Pseudomonas aeruginosa can adhere efficiently to acidinjured
tracheal epithelium, but not to uninjured epithelium
(8). The authors suggested that acid injury could expose
binding sites or change the surface structure of the cell
membrane, thus permitting adherence of a nonmucoid
strain of Pseudomonas aeruginosa by pili and subsequently
leading to bacterial pneumonia (9). In our case, respiratory
aspiration of gastric contents induced airway epithelial
injury and enhanced Pseudomonas aeruginosa adherence
to the acid-injured epithelium, which led to the subsequent
development of bacterial pneumonia. Further, this case was
further complicated by the essential immunosuppressive
therapy.
Gastrointestinal complications may be an important
factor of respiratory infections or mortality during the
peri-operative period (10) and the consequences of such
complication are well described in the literatures but the
microbiological consequences have rarely been evaluated.
The main finding in this case is Pseudomonas aeruginosa
pulmonary infection in the heart-lung transplant recipient
with the complication of gastroparesis. However, no further
attempts were made to obtain an etiologic diagnosis.
The diagnosis of Pseudomonas aeruginosa pneumonia
was not clearly proven. Nevertheless, colonization with
Pseudomonas aeruginosa was considered clinically
significant and antibiotic therapy was initiated by the
clinician (11).
Heart-lung recipients with gastroparesis are at increased
risk for aspiration pneumonitis. In order to avoid the
morbidity of gastroparesis in this subset of fragile
patients, it may be prudent to perform a prophylactic
management, including surgery. Alternatively, a high
suspicion of gastroparesis should be maintained early in
the postoperative course.
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References
Cite this article as: Tao YQ, Yan ZY, Sha JM, Zhu ZY, Lei H. Severe gastroparesis causing postoperative respiratory complications in a heart-lung recipient. J Thorac Dis 2010;2(2):121-123. doi: 10.3978/j.issn.2072-1439.2010.02.02.003
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