Intensive Care Med (1990) 16:405-407

Intensive Care Medicine 9 Springer-Verlag1990

Case reports Pulmonary embolism in end stage renal disease K. G u n t u p a l l i , O. S o f t e r a n d P. Baciewicz Department of Medicine, Emory University, School of Medicine and Veterans Administration Medical Center, Atlanta, GA, USA Received: 7 November 1989; accepted: 26 February 1990

Case reports

years. Significant co-morbid conditions included chronic obstructive pulmonary disease with recurrent respiratory infections and hypertension. Two days prior to admission, his routine dialysis procedure was complicated by hypotension, necessitating discontinuation of the treatment. Hypotension recurred during the next hemodialysis treatment and was associated with chest pain, requiring admission for further evaluation. On physical examination the patient was not in acute distress. Blood pressure was 70/40mmHg with pulsus paradoxus 12 mmHg, temperature 98.6~ (37 ~ respiratory rate 24/rain, pulse rate 90/min, and irregular. The internal jugular veins were distended. Cardiac auscultation revealed normal heart sounds but with pericardial friction rub. There was dullness to percussion at both lung bases and rales on auscultation. The remainder of the physical examination was unremarkable. Laboratory results included: hematocrit 31.3, white blood cell count 4.6• blood urea nitrogen 63mg/dl, creatinine 7.gmg/dl, glucose 146mg/dl, sodium 134mmol/1, potassium 5.2 retool/l, chloride 99 mmol, bicarbonate 23 mmol/t. Arterial blood gases revealed pH 7.33, PaO2 46 mmHg and PaCO2 37 mmHg breathing room air. Chest X-ray demonstrated cardiomegaly and bilateral pleural effusions, left larger than right. The electrocardiogram revealed atrial fibrillation without acute ST-Tsegment changes. Echocardiograp)y demonstrated a small hemodynamically insignificant posterior pericardial effusion and normal left ventricular function. Poor right ventricular function with dilation of the right ventricle was also noted. The latter finding was not reported in a previous study done 8 months earlier. There was no evidence of cardiac tamponade. In view of the persistent hypotension, a pulmonary artery catheter was inserted; the right atrial pressure was 30 mmHg, the pulmonary artery pressure was 77/24 mmHg. A ventilation perfusion scan was performed. This revealed areas of matched ventilation and perfusion abnormalities at the right lung base interpreted as low probability for pulmonary emboli. Marked decrease in perfusion and ventilation on the left was attributed to a large left pleural effusion. However, in view of the new onset right ventricular dysfunction, pulmonary hypertension, and systemic hypotension, a pulmonary angiogram was performed. Abrupt cut-off of multiple branches to the right lower and middle lobes were demonstrated at angiography (Fig. 1). Therapy with intravenous heparin sulfate was initiated. The patient experienced gradual cardiovascular improvement, with no hypotension during hemodialysis. However, on the 12th day the patient suffered unexpected eardiopulmonary arrest that culminated in his death. Postmortem examination was not performed. Hence, the immediate cause of death remained uncertain.

Case 1

Case 2

w.G. was a 64-year-oldblack male with a history of diabetes mellitus and ESRD. He was on hemodialysis three times a week for the past 10

R.T. was a 61-year-oldmale with ESRD on chronic ambulatory peritoneal dialysis who presented to the hospital with fever, chills and abdomi-

Abstract. Clinically significant p u l m o n a r y e m b o l i s m is considered to be rare i n patients with e n d stage renal disease. Two cases with l o n g s t a n d i n g renal disease o n dialysis, are reported where p u l m o n a r y e m b o l i s m c o n t r i b u t e d significantly to m o r b i d i t y a n d mortality. O n e p a t i e n t h a d h y p o t e n s i o n d u r i n g dialysis. T h e differential diagnosis o f sustained h y p o t e n s i o n d u r i n g dialysis or i n the I C U s h o u l d i n c l u d e p u l m o n a r y embolism. Establishing the diagnosis m a y require p u l m o n a r y angiography. Key words: P u l m o n a r y e m b o l i s m - E n d stage renal disease

T h e true incidence o f p u l m o n a r y e m b o l i s m is u n c e r t a i n because the disorder frequently remains u n d i a g n o s e d . Fatal p u l m o n a r y e m b o l i s m a n d n o n - f a t a l e m b o l i s m occurs i n 3 - 5 a n d 1 5 - 2 0 cases per 1000 hospital admissions, respectively [ 1 - 3]. T h e incidence o f p u l m o n a r y e m b o l i i n patients with chronic renal failure is reported to be lower c o m p a r e d to the general p o p u l a t i o n . F u r t h e r m o r e , clinically significantly p u l m o n a r y emboli are considered rare in patients with e n d stage renal disease (ESRD) treated with dialysis [ 4 - 5]. P r i o r reports of p u l m o n a r y emboli i n patients with E S R D have b e e n ascribed to endocarditis or c o m p l i c a t i o n s o f vascular access [ 6 - 1 8 ] . We report two patients with E S R D requiring dialysis i n w h o m m a j o r p u l m o n a r y emboli, u n r e l a t e d to dialysis, vascular access or endocarditis played a significant role i n their demise. These two patients are m e m b e r s o f a group o f 120 patients c u r r e n t l y o n dialysis therapy at the VA Medical Center. T h e criteria for i n i t i a t i o n o f chronic dialysis i n E S R D patients includes a slowly progressive increase in s e r u m creatinine > 1 0 m g / d l , or a creatinine clearance < 10 m l / m i n .

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Fig. 1. Pulmonary angiogram showing pulmonary emboli to the right lower and middle lobes (Case 1) nal pain. The past medical history was significant for chronic obstructive pulmonary disease and coronary artery disease. He underwent coronary artery bypass grafting twice. On examination, his temperature was 100.2~ (37.9~ pulse 92/rain and regular with a blood pressure of 160/100 mmHg. Lungs were clear to auscultation. A grade II/VI ejection systolic murmur was heard at the apex. The abdomen was distended with rebound tenderness. Bowel sounds were markedly reduced. Laboratory examination revealed a hematrocfit of 49%, white blood cell count l l.6x 103/mm with normal differential, blood urea nitrogen 54 mg/dl, and creatinine 12.2mg/di. Electrolytes revealed a sodium 146retool/l, potassium 3.9 retool/l, chloride 93 retool/l, and bicarbonate 25 mmol/l. Peritoneal fluid was cloudy with cells 21xl0~/mm with 99% segmented neutrophils. Gram stain of the peritoneal fluid demonstrated gram-negative rods and the culture subsequently grew Serratia marcescens. He was treated with amikacin, dose adjusted to ESRD. Fever, abdominal pain and marked small and large bowel distension persisted over the

Fig. 2. Picture taken at post mortem showing pulmonary emboli in the main, right and left pulmonary arteries (Case 2)

K.K. Guntupalli et al.: Pulmonary embolism in end stage renal disease next few days. On the 7th hospital day, the course was further complicated by acute shortness of breath and a new right pulmonary infiltrate. Hypoxemia (PaO 2 60 mmHg on room air, alveolar arterial oxygen tension gradient 42 mmHg) was noted and a presumptive diagnosis of pneumonia was made. On the 10th day, because of persistent abdominal distension and worsening peritoneal signs, a laparotomy was performed. Purulent material was found throughout the abdominal cavity without evidence of perforation or necrosis of the gut. Approximately i2 h after surgery, the patient suffered a cardioputmonary arrest from which he could not be resuscitated. Postmortem examination revealed multiple large emboli wedged in the right and left main puImonary arteries (Fig. 2). Multiple small emboli were also evident within all lobes of the lungs. These were recent in appearance without adherence to the vessel walls. No pneumonia was identified. Because of the reported low incidence of pulmonary emboli in chronic renal failure patients, the records of 80 patients with ESRD (serum creatinine > 10mg/dl or receiving dialysis therapy) autopsied between 1970-1987 at the Veterans Administration Medical Center, Decatur, Georgia, were reviewed retrospectively for the presence of major pulmonary emboli. Patients with acute renal failure were excluded because of the potential contributions of comorbid conditions. Three more cases were identified where the examining pathologist or the attending clinician believed that the emboli were significant contributors to the demise of the patient. In two of the three patients predisposing factors were present, metastatic carcinoma of the prostate in one and previous pulmonary emboli related to venous stasis of the lower extremities in the other.

Discussion

The incidence of pulmonary emboli in the USA is estimated to be 600000 cases per year with an overall mortality of approximately 30O7o [1-31. The great majority of deaths occur among patients where the diagnosis is not established and, hence, treatment not instituted [3]. Confirmation of the diagnosis of pulmonary emboli is often difficult and may require pulmonary arteriography in some cases [41. In contrast to the prevalence of pulmonary emboli in the general population, major pulmonary embolization is considered to be rare, or non-existant in patients with advanced renal disease [4]. In a retrospective review of 2,255 autopsy records of general population, Mossey et al. observed that the overall evidence of pulmonary embolism was 32.3 %. Ninety-five of these patients had chronic renal failure (serum creatinine > 5 mg/dl). By contrast, microscopic clinically insignificant pulmonary emboli were found in only 9.5% in patients with chronic renal failure. It is suggested that the platelet dysfunction associated with uremia reduced significant thrombotic tendency and, therefore, the occurrence of pulmonary emboli. The lower prevalence of venous thrombosis and pulmonary emboli in patients with ESRD lends support to this hypothesis. In another autopsy series of 326 cases of ESRD patients on dialysis, only two cases of major pulmonary emboli were identified [51. In both of these cases, hypotension was not a presenting manifestation. Clinically significant pulmonary emboti have, however, previously been described in patients with ESRD [6-18]. In these reported cases the occurrence of emboli was related to the dialysis procedure, arteriovenous shunts or indwelling vascular catheters. Berlyne et at. reported three cases of pulmonary emboli during dialysis

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K.K. Guntupalli et al.: Pulmonary embolism in end stage renal disease

presenting with pleuritic chest pain and hemoptysis [10]. Two cases of symptomatic pulmonary emboli associated with clotted arteriovenous shunt have also been reported [12]. Infected external arteriovenous fistulae were the source of emboli in other cases [6-7, 14, 16]. Kjellstrand et al. reported a case of pulmonary embolism following femoral vein catheterization for hemodialysis access [11]. Cotton fiber embolization and embolization of microaggregates generated during extracorporeal circulation have also been described [19-20]. Pulmonary calcification in the chronic renal failure patients at times may also mimic pulmonary emboli [22]. In contrast to the present two patients presenting with hypotension during dialysis, in most of the above reports, the presenting symptoms were of pleuritic chest pain and hemoptysis. In some earlier cases, further confirmatory diagnostic tests were not done. Septic pulmonary emboli can be diagnosed circumstantially when an infected access site along with multiple bilateral pulmonary nodular densities exists. However, in the absence of this classic picture, thrombotic pulmonary emboli should also be considered in the differential diagnosis of patients with acute shortness of breath, hypotension, or hypoxemia as seen in the non-renal failure patients. Reports of major emboli in chronic renal failure have only been retrospective by autopsy studies. In the present report, apart from a sedentary lifestyle and chronic atrial fibrillation in the first patient, and hospitalization and immobility in the second, no other predisposing factors for the development of pulmonary emboli were identified. Furthermore, review of the autopsy records of chronic renal disease patients identified an additional patient who developed a major pulmonary embolus without any specific underlying predisposing condition. It is of interest that two of the three cases identified in our report had hypotension during dialysis as the sole manifestation of pulmonary embolism. Prolonged immobilization, serious acute illness, such as sepsis and other predisposing medical conditions (e. g., atrial fibrillation) as in the present cases, are well known predisposing factors for pulmonary embolism. Hence, in presence of these comorbid conditions (which may exist in ESRD patients as well), false pulmonary embolus could develop as illustrated in the present report. We propose that major pulmonary emboli do occur in patients with ESRD, unrelated to dialysis or vascular access problems. The differential diagnosis of unexplained hypotension in ESRD patients on dialysis should include pulmonary embolism. Establishing this diagnosis may be difficult and may require pulmonary arteriography.

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Dr. K.K. Guntupalli Baylor College of Medicine Smith Tower 6550 Fannin Street Suite 1236 Houston, TX 77030 USA

Pulmonary embolism in end stage renal disease.

Clinically significant pulmonary embolism is considered to be rare in patients with end stage renal disease. Two cases with long standing renal diseas...
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