|Year : 2021 | Volume
| Issue : 3 | Page : 376-378
Left-sided massive hydrothorax in a DKD patient on CAPD using icodextrin
Maithrayie Kumaresan, Sandra Babu, Milly Matthew, Palaniappan Nagarajan, Georgi Abraham
MGM Healthcare, Chennai, Tamil Nadu, India
|Date of Submission||26-Apr-2021|
|Date of Acceptance||21-May-2021|
|Date of Web Publication||30-Sep-2021|
Dr. Georgi Abraham
MGM Healthcare, 15th Avenue, Harrington Road, Chennai 600015, Tamil Nadu.
Source of Support: None, Conflict of Interest: None
We report a case of a 51-year-old male patient with end-stage kidney disease secondary to diabetic kidney disease who presented with an atypical left-sided pleural effusion within 2 weeks of commencement on continuous ambulatory peritoneal dialysis (PD) using icodextrin dialysis solution. PD was withheld for the time being and the patient was switched to temporary hemodialysis and started on high-dose diuretics which led to the resolution of his symptoms. Here we discuss the clinical presentation, diagnostic techniques, and management options for treating hydrothorax in the PD population.
Keywords: CAPD, massive left-sided hydrothorax, ultrafiltration failure
|How to cite this article:|
Kumaresan M, Babu S, Matthew M, Nagarajan P, Abraham G. Left-sided massive hydrothorax in a DKD patient on CAPD using icodextrin. J Diabetol 2021;12:376-8
| Introduction|| |
Continuous ambulatory peritoneal dialysis (CAPD) is a simple home-based renal replacement therapy for diabetics with end-stage kidney disease (ESKD). Compared with maintenance hemodialysis, loss of residual renal function is slow in CAPD. Other than infections, mechanical complications such as hernias and leaks can lead to problems with ultrafiltration during dialysis. Massive hydrothorax is a rare complication and is estimated to occur in 1.6% of the patients on peritoneal dialysis (PD) and predominantly seen on the right side due to anatomical defects in the diaphragm, thus causing peritoneo-pleural leaks. Left-sided massive hydrothorax is extremely rare. However, we encountered a male patient with ESKD on CAPD for 2 weeks presenting with ultrafiltration failure and dyspnea secondary to a left-sided massive hydrothorax.
| Case Summary|| |
A 51-year-old male with ESKD secondary to diabetic kidney disease was started on CAPD on March 10, 2021. His diabetes mellitus was controlled on insulin Actrapid and Lantus. He was initiated on 2 L 7.5% icodextrin dialysate solution, 2–3 exchanges with a dwell time of 8–12 h, with the ultrafiltration volume varying from 100 to 700 cc. His residual urine output varied from 700 to 850 cc/day. He was well until 2 weeks, after which he noticed a diminution in the ultrafiltration rate. Shortly after, he presented to us with dry cough and shortness of breath. Vital signs were normal except for hypoxemia (SpO2 92% room air) requiring oxygen. Physical examination suggested left-sided massive pleural effusion. Laboratory investigations elicited serum albumin 3 g/dL, serum creatinine 9.62 mg/dL, hemoglobin 10.4 g/dL, and fasting blood sugar 93 mg/dL. Chest X-ray confirmed the presence of massive pleural effusion on the left side [Figure 1]A. As the patient had no signs of cardiac failure, pulmonary or pleural infections, PD was immediately withheld and he was switched over to temporary hemodialysis through the right internal jugular vein. Pre-hemodialysis weight was 90.5 kg and after the first session his weight dropped down to 86.3 kg. He was commenced on high-dose furosemide, and his symptoms and oxygen saturation improved significantly with dry peritoneum. No further investigations were done including paracentesis of the pleural fluid even for diagnostic applications such as glucose estimation as the patient was on icodextrin exchanges. The patient had a normal follow-up chest X-ray 3 weeks later and had no further dyspneic episodes [Figure 1]B.
|Figure 1: Chest radiograph PA view. (A) Marked left-sided hydrothorax. (B) Resolution of pleural effusion|
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| Discussion|| |
Pleural effusion due to pleuroperitoneal leak in patients undergoing CAPD was first described by Nakajima et al. in 1967. The development of pleuroperitoneal communications can be either due to a congenital or acquired diaphragmatic defect. A pressure gradient develops between the increased intra-abdominal compartment pressure (created by CAPD) and the physiological negative intrathoracic pressure. The normal intraperitoneal pressure in PD is 12 ± 2 cm of H2O. The intrathoracic pressure falls from −5 cm H2O at the end of expiration to about −10 cm H2O at the end of inspiration. The additional quantity of ultrafiltration volume further increases the intraperitoneal pressure, thereby opening up any defects in the diaphragm leading to peritoneo-pleural communication as in our patient. Most of the massive hydrothoraxes due to cardiac failure or chronic liver disease occur in the right side. The heart and the pericardial covering mask the left hemi-diaphragmatic defects, supporting this theory. The right-sided predominance is further validated by the presence of an embryological remnant processus vaginalis peritonei, which develops a recess between the peritoneum and the right hemithorax. However, a left posterolateral diaphragmatic defect arising from malformation of pleuroperitoneal fold referred to as Bochdalek hernia can also occur in 85% of the population [Figure 2].
The majority of hydrothorax cases occur within 30 days of commencing PD and up to 25% are asymptomatic. Moreover, a left-sided hydrothorax with dyspnea arises a speculation of cardiac failure, infective pathologies as well as other causes, resulting in unnecessary diagnostic procedures and imaging studies. Hence, before proceeding to invasive investigations, the presence of hydrothorax due to pleuro-peritoneal leak should always be ruled out in PD patients. Diagnosis of hydrothorax in PD relies on clinical, radiological, and biochemical findings. Shortness of breath, pleuritic chest pain, and decreased ultrafiltration volume is the classic triad. Pleural fluid analysis and thoracentesis usually suggest transudative fluids with markedly high glucose concentration while using dialysis fluid, which is either 1.5%, 2.5%, or 4.25% dextrose-containing solutions unlike the 7.5% icodextrin solution in our patient. Chest radiography denotes a massive pleural effusion. Other diagnostic techniques employed are nuclear medicine scan, intraperitoneal methylene blue administration, and high-resolution computed tomography. A range of conservative and invasive management options have been reported. Though most patients eventually require transition to permanent hemodialysis, temporary withholding of PD has sometimes resulted in its spontaneous resolution (40%). If the patient wishes to continue on PD or is unresponsive to conservative measures, treatment options include chemical or physical pleurodesis, laproscopic examination and closure of defect in diaphragm, and open thoracotomy or video-assisted thoracoscopic surgery, with success rates of returning to long-term PD reported in 48–88% of the cases. If surgery is intended to correct the diaphragmatic defect, prior thoracoscopy is recommended to verify whether the defect is visible and reparable.
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Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2]