Dry cough in a CAPD patient

Kay Herbrig1, Doreen Reimann1, Thomas Kittner2 and Peter Gross1

1 Nephrology, Department of Medicine, 2 Department of Radiology, Universitätsklinikum ‘C.G.Carus’, Dresden, Germany. Email: kay.herbrig@aol.com

Case

A 50-year-old female with end-stage renal disease (ESRD) treated by peritoneal dialysis (CAPD) complained of a dry cough. This had bothered her mainly at night. It had first started 2 weeks previously. There was no report of fever. She did not smoke.

Since childhood she had had reflux nephropathy and chronic pyelonephritis. She had undergone several operations including a partial nephrectomy on the left side 20 years ago and a total nephrectomy on the right side. The patient developed ESRD in 2001. She requested treatment by CAPD and did well. Her records indicated an 800–1200 ml ultrafiltration rate/day using dialysis solutions containing 2.27% glucose at daytime and 1.36% glucose over night. There were no problems with her compliance. Her residual renal function amounted to a daily urine production of ~600 ml. The ultrafiltration rate had been constant over the last months.

The medications consisted of nitrendipine, ramipril, furosemide, erythropoetin and calcitriol. The patient refused phosphate binders.

The physical examination showed a female in no acute distress. She was without ankle oedema or obvious signs of hypervolaemia. The supine blood pressure was 160/80 mmHg and she weighed 62 kg (height 1.72 m). She had no signs of dyspnoea. She coughed frequently. The breath sounds and the percussion note were both somewhat reduced on the right side.

The results of the laboratory evaluation showed the typical changes of a patient with ESRD.

The results of the laboratory evaluation were: glucose 4.98 mmol/l, potassium 3.54 mmol/l, creatinine 597 µmol/l, urea 8.9 mmol/l, calcium 2.05 mmol/l, phosphate 1.47 mmol/l, total protein 64.4 g/l, LDH 8.53 µmol/(lxs), CRP negative, haemoglobin 7.7 mmol/l, haematocrit 36%, white blood cells 4.7 GPt/l, platelet count 325 GPt/l. The arterial blood gas analysis showed following results: pH 7.475, pCO2 4.99 kPa, pO2 11.75 kPa, HCO3- 26.9 mmol/l, BE 3.3 mmol/l, O2 saturation 97%.

Ramipril was stopped but the dry cough persisted. A chest X-ray was ordered (Figure 1Go).



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Fig. 1.  Chest X-ray showing a pleural effusion with a pneumothorax on the right side.

 

Questions

Answers to the quiz on the preceding page

The chest X-ray showed a pleural effusion and a pneumothorax on the right side. A thoracic drainage was placed into the pleural effusion and 1.5 l of clear liquid was emptied. Samples were sent to the chemistry laboratory, to microbiology and to pathology for further studies. The following results were obtained: cell count 0.1 GPt/l; concentrations of: glucose 7.78 mmol/l (a simultaneous plasma glucose was not available, but usually the patient's serum concentration was ~5 mmol/l; fasting glucose concentration was 4.98), total protein 9.6 g/l (total protein in plasma 64.4 g/l), lactate dehydrogenase 0.83 µmol/(lxs) [LDH in plasma 8.53 µmol/(lxs)], total cholesterol 0.27 mmol/l, triglycerides 0.15 mmol/l. All laboratory tests are shown in Table 1Go.


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Table 1.  Laboratory tests of plasma and pleural effusion

 
The effusion contained no malignant cells and the culture grew out no microorganisms.

It was noticed that the placement of the thoracic drainage was followed by a marked decrease of the ultrafiltration rate of the patient. Therefore, we suspected a transdiaphragmatic leakage.

We emptied the peritoneal and pleural cavities completely. Immediately thereafter we filled the abdominal cavity with fresh dialysate containing methylene blue. Five minutes later the pleural drainage turned blue. The glucose concentration in the drainage fluid was 22.5 mmol/l. We tried to localize the suspected transdiaphragmatic leak by magnetic resonance imaging using gadolinum as contrast agent (dilution of gadolinum in dialysate 1:250). The contrast agent was given via the peritoneal catheter. The MRI study showed a slim collection of contrast medium in the ventral sinus phrenicocostalis on the right side (Figure 2Go). This suggested that the transdiaphragmatic leak could be in the ventral part of the peritoneum and the pleura.



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Fig. 2.  MRI study of the diaphragm showing a slim collection of contrast medium in the ventral part of the recessus phrenicocostalis on the patient's right side.

 
As a means of therapy peritoneal dialysis was temporarily halted and replaced by haemodialysis. The right pleural space was obliterated by induction of a talc pleurodesis. In this way we hope to preserve the patient's ability to resume CAPD later.

Pleural effusions and hydrothorax are rare complications of CAPD caused by a transdiaphragmatic leakage [1,2]. It is likely that fluid was slowly ‘sucked’ into the pleural space because of negative intrathoracic pressure. It is possible that a valve phenomenon may have contributed to this by preventing backflow from the pleural space to the abdominal cavity during phases of positive intrathoracic pressure. We do not know what caused the pneumothorax. It is possible that the latter originated—together with the peritoneo-pleural leakage—from some traumatic event such as violent coughing or sneezing. The fact that the patient had undergone multiple abdominal operations in the past might be a predisposition towards abnormal reactions of the tissues involved. We had no preceding evidence of mishandling of dialysate exchanges by the patient possibly introducing air into the abdominal cavity.

As described in the literature, in most cases the peritoneo-pleural leakage was diagnosed using peritoneo-pleural scintigraphy [1,3]. Using this method a transfer of the radioactive agent from the abdominal to the thoracic cavity can be detected. However, scintigraphy is not able to localize the defect in the diaphragma. In the present case the high glucose concentration in the drained pleural fluid and the blue discoloration of the pleural drainage upon addition of methylene blue to the abdominal dialysate suggested a transdiaphragmatic leakage. We used MRI for localizing it. In our patient, gadolinium contrast agent was given via the peritoneal catheter. There are no suggestions that gadolinium may be detrimental to the peritoneum. In this way a transdiaphragmatic leakage could be localized to the ventral part of the peritoneum and the corresponding pleura.

In the literature MRI has been used previously in attempts to visualize whether the abdominal cavity was suitable for peritoneal dialysis in patients with abdominal abnormalities [4]. MRI was also used by Urhahn et al. [5] trying to show transdiaphragmatic leakage of ascites in two cirrhotic patients, not on peritoneal dialysis.

Different therapeutic approaches to peritoneo-pleural leaks in peritoneal dialysis patients have been reported. Temporary discontinuation of CAPD, tetracycline instillation into the pleural space and surgical patch grafting of the diaphragmatic leak have all been described [6]. A novel method may be videoassisted talc pleurodesis [7]. This procedure may allow an identification of diaphragmatic defects amenable to repair and placement of talc under direct visualization. When these procedures are without success an alternative mode of dialysis must be considered.

Usually peritoneal dialysis patients report more dry and persistent cough than haemodialysis patients. A study by Min et al. [8] identified asthma, post-nasal drip, gastroesophageal reflux disease, chronic obstructive pulmonary disease, congestive heart failure, allergic rhinitis, pleural effusion and respiratory infection as frequent causes of cough in peritoneal dialysis patients.

This case presented an uncommon complication of peritoneal dialysis. In our experience MRI is a useful tool for localizing transdiaphragmatic leakage.

Conflict of interest statement. None declared.

References

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