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“Sweet” hydrothorax complicating chronic peritoneal dialysis
European Journal of Internal Medicine 17 (2006) 583 – 584 www.elsevier.com/locate/ejim
Brief report
“Sweet” hydrothorax complicating chronic peritoneal dialysis B. Smolin ⁎, I. Henig, Y. Levy Department of Internal Medicine D, Rambam Health Care Campus and Rappaport Faculty of Medicine, Technion Haifa Bat Galim 35254, Israel Received 16 April 2006; received in revised form 22 May 2006; accepted 22 May 2006
Abstract Massive pleural effusion occurring during continuous peritoneal dialysis (PD) is a rare, life-endangering complication of this procedure. We describe a case of a patient with type 2 diabetic end-stage renal disease (ESRD) treated by PD who had new-onset dyspnea, right pleural effusion, and uncontrolled hyperglycemia. Respiratory distress and pleural effusion progressed quickly during the course of dialysis. A large volume of a “sweet” fluid with a high glucose content was evacuated from the pleural space. Immediate improvement in the patient's condition and glucose control followed discontinuation of PD and initiation of hemodialysis. © 2006 European Federation of Internal Medicine. Published by Elsevier B.V. Keywords: Peritoneal dialysis; Hydrothorax; Type 2 diabetes mellitus
1. Introduction Pleural effusion is a typical diagnostic challenge in internal medicine. In end-stage renal disease (ESRD) patients, the development of excessive pleural fluid is relatively common, with the majority of cases caused by a volume overload, congestive heart failure, infection, or malignancy. Hydrothorax complicating peritoneal dialysis (PD) is reported occasionally in nephrology journals. Nevertheless, the issue remains unfamiliar to internists because most PD patients are treated in PD units. However, in many medical centers, general practitioners encounter a growing number of ESRD patients, increasing the need to be aware of complications related to PD. We report on an unusual case of life-threatening extensive pleural effusion in a patient with diabetes mellitus (DM) who was treated by PD. 2. Case report A 75-year-old woman presented to the emergency room because of severe dyspnea. Her previous medical history included well-controlled type 2 diabetes, hypertension,
⁎ Corresponding author. Fax: +972 4 8543286. E-mail address: [email protected] (B. Smolin).
ischemic heart disease, s/p coronary artery bypass grafting, and ESRD treated by PD. Respiratory distress began 3 days before admission and worsened during periods of her regular PD. The dyspnea was only partially relieved by sitting in bed. It was associated with chest discomfort and profound weakness, without fever, cough, nausea, diaphoresis, or palpitations. It was the patient's first ever episode of such a dyspnea and she denied prior episodes of orthopnea and paroxysmal nocturnal dyspnea (PND). Concomitantly, diabetes became uncontrolled, with blood glucose exceeding 500 mg%/dl. It was unexplained since she continued regular subcutaneous insulin treatment and diet. In the emergency room, the patient was in moderate respiratory distress with a respiratory rate of 24/min, blood pressure 200/90 mm Hg, a regular heart beat (64 bpm), temperature 37 °C, and O2 saturation of 90% while breathing room air. Lung auscultation revealed decreased respiration on the right side, and a chest X-ray taken upon arrival revealed right pleural effusion with signs of pulmonary congestion (Fig. 1A). ECG findings were consistent with sinus bradycardia 55/min and LVH, without new abnormalities compared to an old record. Blood count, cardiac troponin, and electrolytes were unremarkable. Creatinine was 5.12 mg/dl and BUN 21 mg/dl. Plasma glucose was 238–609 mg/dl with pH and HCO3 in the normal range. Intravenous furosemide and subcutaneous insulin were
0953-6205/$ - see front matter © 2006 European Federation of Internal Medicine. Published by Elsevier B.V. doi:10.1016/j.ejim.2006.05.005
584
B. Smolin et al. / European Journal of Internal Medicine 17 (2006) 583–584
Fig. 1. (A) Chest X-rays on admission and (B) concomitant to PD (8 h later). Note the extensive involvement of the right hemithorax in this patient.
administered. A working diagnosis of congestive heart failure and uncontrolled DM was suggested. In the hours that followed, during regular PD, the patient's condition and respiratory distress worsened considerably. PD was stopped. A repeat chest X-ray revealed a significant increase in the amount of pleural fluid with secondary atelectasis of the right lung (Fig. 1B). An emergency pleural paracentesis was performed and 2000 ml of dialysate fluid was evacuated from the pleural space, followed by an immediate improvement in the patient's respiratory distress. High blood glucose (609–587 mg/dl) rapidly returned to normal values as well. The gross appearance of the fluid that was removed was very unusual, as it looked like pure “water”. Its laboratory characteristics—glucose 822 mg/dl, pH 7.56, total protein 0.2 g/dl, albumin 0.1 g/dl, and LDH 13 U/dlconfirmed the definition of dialysate fluid. Thus, free movement of the dialysate fluid from the peritoneal to the pleural spaces with consequent respiratory distress and absorption of the dialysate glucose to the blood were evident. Consequently, PD was converted to hemodialysis, followed by a complete return to the patient's previous stable metabolic and functional state. She was discharged on day 7 with a blood glucose of 238 mg/dl. 3. Discussion Massive hydrothorax occurring during continuous PD is a rare, but serious, complication of this procedure. It may appear at any time during the course of treatment and may be responsible for the development of severe dyspnea during PD [1]. As in our case, the pleural fluid appears to arise from the peritoneal dialysate, depending on the time coincidence of its appearance and its chemical composition [2]. Most of the time, it is right-sided and, for some reason, more frequent in female than in male patients [3]. In some cases, there may be traumatic diaphragmatic fenestrations, but the majority of cases appear to be due to a less well-defined communication between the peritoneal and pleural spaces [2]. Treatment
consists of prompt discontinuation of PD and immediate thoracentesis, depending on the severity of the clinical condition [2]. Along with a permanent switch to hemodialysis, a large follow-up study from Japan showed that in nearly half (46%) of PD patients who developed this complication, hydrothorax was fully resolved following just a brief interruption of PD or the combined use of a small exchange volume in a semi-sitting position and pleurodesis with tetracycline or other agents [1]. There are also reports on thoracotomy or video-assisted thoracic surgery performed to locate and close the diaphragmatic defects in order to return the patients to continuous ambulatory peritoneal dialysis (CAPD) [4,5]. Another point to be emphasized in our case is that the accumulation and retention of dialysate in the pleural space led to severe hyperglycemia. This point has never been highlighted previously, perhaps because the elevated blood glucose levels were attributed to respiratory distress only. Other reasons for this unexpected extreme hyperglycemia, such as ischemia or infection, were excluded in our patient. Since, prior to this complication, the patient had near-normal glucose levels for years and since, after fluid evacuation, glucose promptly dropped to normal levels, we suggest that the direct absorption of glucose from the pleural space to blood is a tentative additional explanation. In summary, hydrothorax complicating PD due to a mechanical shift of dialysate fluid to the pleural space should be included in the differential diagnosis of dyspnea and pleural effusion in ESRD patients. Severe hyperglycemia may be explained by direct absorption of the glucose from the retained dialysate. 4. Learning points • Pleural effusion is common in patients with end-stage renal disease. • Hydrothorax complicating peritoneal dialysis is rare. • Hydrothorax may be a life-threatening complication. • Severe hyperglycemia may follow in diabetic patients. • Prompt recognition and treatment are necessary. References [1] Nomoto Y, Suga T, Nakajima K, Sakai H, Osawa G, Ota K, et al. Acute hydrothorax in continuous ambulatory PD—a collaborative study of 161 centers. Am J Nephrol 1989;9(5):363–7. [2] Rudnick MR, Coyle JF, Beck LH, McCurdy DK. Acute massive hydrothorax complicating PD, report of 2 cases and a review of the literature. Clin Nephrol Jul 1979;12(1):38–44. [3] Lepage S, Bisson G, Verreault J, Plante GE. Massive hydrothorax complicating PD. Isotopic investigation (peritoneopleural scintigraphy). Clin Nucl Med Jun 1993;18(6):498–501. [4] Jagasia MH, Cole FH, Stegman MH, Deaton P, Kennedy L. Videoassisted talc pleurodesis in the management of pleural effusion secondary to continuous ambulatory PD: a report of three cases. Am J Kidney Dis Nov 1996;28(5):772–4. [5] Szeto CC, Chow KM. Pathogenesis and management of hydrothorax complicating PD. Curr Opin Pulm Jul 2004;10(4):315–9.
Brief report
“Sweet” hydrothorax complicating chronic peritoneal dialysis B. Smolin ⁎, I. Henig, Y. Levy Department of Internal Medicine D, Rambam Health Care Campus and Rappaport Faculty of Medicine, Technion Haifa Bat Galim 35254, Israel Received 16 April 2006; received in revised form 22 May 2006; accepted 22 May 2006
Abstract Massive pleural effusion occurring during continuous peritoneal dialysis (PD) is a rare, life-endangering complication of this procedure. We describe a case of a patient with type 2 diabetic end-stage renal disease (ESRD) treated by PD who had new-onset dyspnea, right pleural effusion, and uncontrolled hyperglycemia. Respiratory distress and pleural effusion progressed quickly during the course of dialysis. A large volume of a “sweet” fluid with a high glucose content was evacuated from the pleural space. Immediate improvement in the patient's condition and glucose control followed discontinuation of PD and initiation of hemodialysis. © 2006 European Federation of Internal Medicine. Published by Elsevier B.V. Keywords: Peritoneal dialysis; Hydrothorax; Type 2 diabetes mellitus
1. Introduction Pleural effusion is a typical diagnostic challenge in internal medicine. In end-stage renal disease (ESRD) patients, the development of excessive pleural fluid is relatively common, with the majority of cases caused by a volume overload, congestive heart failure, infection, or malignancy. Hydrothorax complicating peritoneal dialysis (PD) is reported occasionally in nephrology journals. Nevertheless, the issue remains unfamiliar to internists because most PD patients are treated in PD units. However, in many medical centers, general practitioners encounter a growing number of ESRD patients, increasing the need to be aware of complications related to PD. We report on an unusual case of life-threatening extensive pleural effusion in a patient with diabetes mellitus (DM) who was treated by PD. 2. Case report A 75-year-old woman presented to the emergency room because of severe dyspnea. Her previous medical history included well-controlled type 2 diabetes, hypertension,
⁎ Corresponding author. Fax: +972 4 8543286. E-mail address: [email protected] (B. Smolin).
ischemic heart disease, s/p coronary artery bypass grafting, and ESRD treated by PD. Respiratory distress began 3 days before admission and worsened during periods of her regular PD. The dyspnea was only partially relieved by sitting in bed. It was associated with chest discomfort and profound weakness, without fever, cough, nausea, diaphoresis, or palpitations. It was the patient's first ever episode of such a dyspnea and she denied prior episodes of orthopnea and paroxysmal nocturnal dyspnea (PND). Concomitantly, diabetes became uncontrolled, with blood glucose exceeding 500 mg%/dl. It was unexplained since she continued regular subcutaneous insulin treatment and diet. In the emergency room, the patient was in moderate respiratory distress with a respiratory rate of 24/min, blood pressure 200/90 mm Hg, a regular heart beat (64 bpm), temperature 37 °C, and O2 saturation of 90% while breathing room air. Lung auscultation revealed decreased respiration on the right side, and a chest X-ray taken upon arrival revealed right pleural effusion with signs of pulmonary congestion (Fig. 1A). ECG findings were consistent with sinus bradycardia 55/min and LVH, without new abnormalities compared to an old record. Blood count, cardiac troponin, and electrolytes were unremarkable. Creatinine was 5.12 mg/dl and BUN 21 mg/dl. Plasma glucose was 238–609 mg/dl with pH and HCO3 in the normal range. Intravenous furosemide and subcutaneous insulin were
0953-6205/$ - see front matter © 2006 European Federation of Internal Medicine. Published by Elsevier B.V. doi:10.1016/j.ejim.2006.05.005
584
B. Smolin et al. / European Journal of Internal Medicine 17 (2006) 583–584
Fig. 1. (A) Chest X-rays on admission and (B) concomitant to PD (8 h later). Note the extensive involvement of the right hemithorax in this patient.
administered. A working diagnosis of congestive heart failure and uncontrolled DM was suggested. In the hours that followed, during regular PD, the patient's condition and respiratory distress worsened considerably. PD was stopped. A repeat chest X-ray revealed a significant increase in the amount of pleural fluid with secondary atelectasis of the right lung (Fig. 1B). An emergency pleural paracentesis was performed and 2000 ml of dialysate fluid was evacuated from the pleural space, followed by an immediate improvement in the patient's respiratory distress. High blood glucose (609–587 mg/dl) rapidly returned to normal values as well. The gross appearance of the fluid that was removed was very unusual, as it looked like pure “water”. Its laboratory characteristics—glucose 822 mg/dl, pH 7.56, total protein 0.2 g/dl, albumin 0.1 g/dl, and LDH 13 U/dlconfirmed the definition of dialysate fluid. Thus, free movement of the dialysate fluid from the peritoneal to the pleural spaces with consequent respiratory distress and absorption of the dialysate glucose to the blood were evident. Consequently, PD was converted to hemodialysis, followed by a complete return to the patient's previous stable metabolic and functional state. She was discharged on day 7 with a blood glucose of 238 mg/dl. 3. Discussion Massive hydrothorax occurring during continuous PD is a rare, but serious, complication of this procedure. It may appear at any time during the course of treatment and may be responsible for the development of severe dyspnea during PD [1]. As in our case, the pleural fluid appears to arise from the peritoneal dialysate, depending on the time coincidence of its appearance and its chemical composition [2]. Most of the time, it is right-sided and, for some reason, more frequent in female than in male patients [3]. In some cases, there may be traumatic diaphragmatic fenestrations, but the majority of cases appear to be due to a less well-defined communication between the peritoneal and pleural spaces [2]. Treatment
consists of prompt discontinuation of PD and immediate thoracentesis, depending on the severity of the clinical condition [2]. Along with a permanent switch to hemodialysis, a large follow-up study from Japan showed that in nearly half (46%) of PD patients who developed this complication, hydrothorax was fully resolved following just a brief interruption of PD or the combined use of a small exchange volume in a semi-sitting position and pleurodesis with tetracycline or other agents [1]. There are also reports on thoracotomy or video-assisted thoracic surgery performed to locate and close the diaphragmatic defects in order to return the patients to continuous ambulatory peritoneal dialysis (CAPD) [4,5]. Another point to be emphasized in our case is that the accumulation and retention of dialysate in the pleural space led to severe hyperglycemia. This point has never been highlighted previously, perhaps because the elevated blood glucose levels were attributed to respiratory distress only. Other reasons for this unexpected extreme hyperglycemia, such as ischemia or infection, were excluded in our patient. Since, prior to this complication, the patient had near-normal glucose levels for years and since, after fluid evacuation, glucose promptly dropped to normal levels, we suggest that the direct absorption of glucose from the pleural space to blood is a tentative additional explanation. In summary, hydrothorax complicating PD due to a mechanical shift of dialysate fluid to the pleural space should be included in the differential diagnosis of dyspnea and pleural effusion in ESRD patients. Severe hyperglycemia may be explained by direct absorption of the glucose from the retained dialysate. 4. Learning points • Pleural effusion is common in patients with end-stage renal disease. • Hydrothorax complicating peritoneal dialysis is rare. • Hydrothorax may be a life-threatening complication. • Severe hyperglycemia may follow in diabetic patients. • Prompt recognition and treatment are necessary. References [1] Nomoto Y, Suga T, Nakajima K, Sakai H, Osawa G, Ota K, et al. Acute hydrothorax in continuous ambulatory PD—a collaborative study of 161 centers. Am J Nephrol 1989;9(5):363–7. [2] Rudnick MR, Coyle JF, Beck LH, McCurdy DK. Acute massive hydrothorax complicating PD, report of 2 cases and a review of the literature. Clin Nephrol Jul 1979;12(1):38–44. [3] Lepage S, Bisson G, Verreault J, Plante GE. Massive hydrothorax complicating PD. Isotopic investigation (peritoneopleural scintigraphy). Clin Nucl Med Jun 1993;18(6):498–501. [4] Jagasia MH, Cole FH, Stegman MH, Deaton P, Kennedy L. Videoassisted talc pleurodesis in the management of pleural effusion secondary to continuous ambulatory PD: a report of three cases. Am J Kidney Dis Nov 1996;28(5):772–4. [5] Szeto CC, Chow KM. Pathogenesis and management of hydrothorax complicating PD. Curr Opin Pulm Jul 2004;10(4):315–9.