NDT Advance Access originally published online on January 12, 2006
Nephrology Dialysis Transplantation 2006 21(3):807-810; doi:10.1093/ndt/gfk040
© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Teaching Point
(Section Editor: A. Meyrier)
Sudden onset of adult respiratory distress syndrome (ARDS) in a long standing chronic haemodialysis patient with lung calcification
Andrew Davenport
Consultant Renal Physician/Honorary Senior Lecturer, University College London Center for Nephrology, Royal Free Hospital, Pond Street, London NW3 2QG
Correspondence and offprint requests to: Andrew Davenport, Consultant Renal Physician/Honorary Senior Lecturer, University College London Center for Nephrology, Royal Free Hospital, Pond Street, London NW3 2QG. Email: andrew.davenport{at}rfh.nthames.nhs.uk, Andrew.Davenport{at}royalfree.nhs.uk
Keywords: ARDS; haemodialysis; hyperparathyroidism; lung calcification
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Introduction
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Patients with end-stage renal failure treated by haemodialysis
have a marked increased risk for cardiovascular death. These
patients have both an accelerated form of arteriosclerosis with
calcification in atheromatous intimal plaques and also medial
calcification due to Monckeberg's. In extreme cases soft tissue
calcification can lead to calciphylaxis resulting in skin ulceration,
amputation and death.
The present case describes a less frequently encountered problem due to vascular and soft tissue calcification, which presents management challenges to the renal physician.
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Case
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A 57-year-old Northern European Caucasoid man was admitted for
an elective parathyroidectomy. He had been on a regular thrice
weekly haemodialysis for 14 years due to hypertensive renal
disease. Both calcium-based phosphate binders and alfacalcidol
had been prescribed since 1992. Due to difficulties with phosphate
control, his calcium-based binders were switched to Alucaps®,
between 1994 and 1998, and then again to Renagel® from July
2001 until the current admission. His intact parathyroid hormone
(PTH) levels increased from 12.3 in 1994 (normal <7) to 42.4
in 1997, to 76.7 in 2000, to 93 pmol/l on admission. At times,
during episodes of iatrogenic hypercalcaemia the PTH fell to
around 30 pmol/l. From 1994 until admission for parathyroidectomy,
the average serum calcium was 2.60 mmol/l (9.86 mg/dl), phosphate
1.95 mmol/l (5.85 mg/dl), and calcium phosphate product 5.16
mmol
2/l
2 (57.7 mg
2/dl
2). A dual electron X-ray adsorption (DEXA)
scan had shown increasing total body calcium (
Table 1) and his
lateral spine X-ray showed aortic calcification (
Figure 1).
The patient was persuaded to accept a surgical parathyroidectomy.
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Table 1. Dual electron X-ray adsorption (DEXA) scan results. Bone mineral content (BMC), lean body mass (LBM), bone mineral density (BMD) g/cm2, Lumbar spine (L1–L4)
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The operation went smoothly but post-operatively, following
return to the ward, he was noted to have respiratory difficulty
with marked tachypnoea, and a reduced finger probe oxygen saturation
of 85%. The potassium had increased to 7.1 mmol/l with a normal
ionized calcium of 1.1 mmol/l. A chest X-ray (CXR) was thought
to show signs of pulmonary oedema (
Figure 2), and he was started
on continuous positive airway pressure (+5 cmH
2O) and then commenced
on haemodialysis, dialysate composition calcium 1.5 mmol/l,
potassium 3 mmol/l and temperature 35°C. Ultrafiltration
was attempted, but he became markedly hypotensive, systolic
blood pressure fell to 70 mmHg, followed by sudden onset of
atrial fibrillation at 130 min
–1, which spontaneously
resolved following cessation of dialysis. Although the troponin
I was elevated at 0.6 µg/l, the only ECG changes were
of minor antero-lateral ST wave depression, during the period
of atrial fibrillation. He maintained a peripheral oxygen saturation
of 95% on 6 l oxygen/minute with a PaO
2 of 14.5 kPa (108 mmHg)
and PaCO
2 of 4.82 kPa (36.2 mmHg). A further intermittent haemodialysis
was associated with systemic hypotension, necessitating termination,
and he was therefore treated by continuous haemofiltration.
A cardiac ECHO showed a normal-sized left ventricular cavity,
with an ejection fraction of 55% (compared to 60%, 2 years earlier).
The estimated mean right atrial pressure was 5 mmHg, with a
pulmonary artery systolic pressure of 21 mmHg. An isotopic lung
perfusion/ventilation scan excluded major pulmonary embolus.
Over the next few days his condition stabilized, continuous
haemofiltration was withdrawn and he returned to regular intermittent
haemodialysis.
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Fig. 2. Post-operative CXR showing bilateral interstitial shadowing predominantly within both middle and lower zones. The heart is enlarged with a cardiac to thoracic ratio of 14/30.
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Following recovery and discharge to home he underwent an adenosine
heart stress test which did not show any areas of absent or
reversible cardiac perfusion. As the CXR appearances remained
he had a computerized tomographic (CT) scan of his chest (
Figure 3)
revealing vascular calcification with ground glass appearance
due to interstitial lung calcification. Standard respiratory
function tests noted a restrictive pattern with reduced carbon
monoxide gas transfer (
Table 2,
Figure 4).
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Fig. 3. High-resolution CT of chest showing fairly heavy vascular calcification. Within the lungs, there are multiple symmetrical fairly extensive cloud-like areas of ground glass opacification, within which, particularly superiorly and posteriorly there are few high density foci of calcification.
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Table 2. Respiratory function tests performed on a day after haemodialysis day. Peak expiratory flow (PEF). Corrected total lung carbon monoxide transfer factor (TLCOc). Corrected transfer coefficient, corrected for patient's haemoglobin of 11.9 g/dl
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Fig. 4. Respiratory flow loop showing a restrictive pattern. Predicted flow volume loop (dotted line), actual flow loop (solid line).
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Discussion
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Although this patient had been well dialyzed for 14 years in
terms of small solute urea clearance, he had developed secondary
hyperparathyroidism with episodes of iatrogenic hypercalcaemia
and a persistently elevated calcium phosphate product. He had
been in receipt of calcium based phosphate binders for approximately
5 years, aluminium for 4 years and Renagel® for the last
3.5 years. For many years he had refused to consider a parathyroidectomy,
but was eventually persuaded.
Following surgery he developed respiratory distress with hypoxia, and this was initially thought to be due to pulmonary oedema, following clinical examination and review of the CXR. However, an attempt to remove fluid with ultrafiltration during haemodialysis resulted in profound hypotension and sudden onset atrial fibrillation. Typically, postoperatively respiratory compromise in the dialysis patient is often associated with excess intravenous fluid administration, acute heart failure due to a peri- or intra-operative myocardial event, or lung collapse. In this case the CXR was interpreted as showing pulmonary oedema. However, the cardiac ECHO measured a normal right atrial filling pressure, with no major left ventricular dysfunction, thereby excluding an acute myocardial infarct and left ventricular failure.The cardiac ECHO measured an increased pulmonary systolic pressure, compatible with both increased lung interstitial pressure and pulmonary arteriolar and or capillary pressures (non-cardiogenic pulmonary oedema). When ultrafiltration was attempted during intermittent haemodialysis, the patient developed sudden onset of atrial fibrillation. Atrial fibrillation is the most common arrhythmia which occurs during haemodialysis in acutely unwell patients with reduced cardiac filling pressures [1]. Further, intermittent haemodialysis was again associated with hypotension, and the patient required a change in dialysis modality to continuous haemofiltration, which was tolerated without cardiovascular instability. Others have reported that intra-dialytic hypotension is more common in patients treated by intermittent than continuous modalities [2].
Vascular and soft tissue calcification in haemodialysis patients has been noted for many years [3]. Previous studies have shown that calcium is not only deposited in the pulmonary vasculature, but also in the smaller bronchi and the interstitium, with deposition within the alveolar septa, resulting in lung fibrosis [4]. The most common type of lung interstitial calcium deposition is the Whilockite crystal pattern, (CaMg)3 (PO4)2, followed by calcium pyrophosphate [5]. Some studies have suggested that lung calcification can be detected in up to 40% of haemodialysis patients [6].
Earlier reports showed that lung calcification was more common in patients with persistently higher serum calcium levels, but no relationship was observed with the duration of haemodialysis, or the serum phosphate concentration, or calcium phosphate product, bicarbonate or pH [5]. Whereas, others noted a relationship not only with hypercalcaemia, but also the prescription of calcium based phosphate binders, duration of vitamin D therapy, peak calcium phosphate product and peak phosphate concentrations [6]. In this patient the serum calcium had been elevated on occasion, and was typically at or above the upper limit of normal. In addition DEXA scanning showed a progressive increase in total body calcium, and skeletal X-rays showed abdominal aortic calcification.
Typically pulmonary symptoms are uncommon, and this patient denied pre-existing exertional dyspnoea. Similarly, CXR findings have been reported to be unusual [8]. Previous reports have suggested a close relationship between pulmonary function tests in terms of changes to vital capacity, diffusing capacity and the severity of lung calcification [5]. However, lung histopathology studies have disputed this, showing that the degree of alveolar septal fibrosis and wall thickening, rather than mere presence of calcium deposits determined the magnitude of functional changes [7].
There is a very rare condition of alveolar microlithiasis, whereby tiny 0.2–5 mm calcified concretions, form in alveolar spaces along with some interstitial fibrosis. This leads to shunting at alveolar capillary bed, and over time the lungs stiffen, become restrictive, resulting in impaired gas transfer, with secondary pulmonary hypertension. In our case the respiratory function tests showed a restrictive flow loop pattern with reduced gas transfer. Unlike alveolar microlithiasis, which is a progressive condition, this patient's condition should stabilize provided that serum calcium and phosphate can be controlled following parathyroidectomy. Although there are reports from the paediatric haemodialysis field of cardiopulmonary calcification contributing to patient's death, due to non-cardiogenic pulmonary oedema and respiratory infection [7]. This particularly occurred following mechanical ventilation during general anaesthesia [8].
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Teaching points
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- Lung calcification can occur in haemodialysis patients due to both calcium deposition in the alveolar septal walls and the pulmonary vessels.
- In the severest cases this can lead to reduction in pulmonary function, typified by a restrictive pattern with reduction in vital capacity and gas transfer.
- Patients with lung calcification are more prone to non-cardiogenic pulmonary oedema.
Conflict of interest statement. None declared.
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References
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- Jaroszynski AJ, Glowniak A, Sodolski T, Zaluska W, Widomska-Czekajska T, Ksiazek A. Effect of haemodialysis on signal-averaged electrocardiogram P-wave parameters. Nephrol Dial Transplant 2005; doi: 10.1093/ndt/gfi175
- Manns M, Sigler MH, Teehan BP. Intradialytic renal haemodynamics – potential consequences for the management of the patient with acute renal failure. Nephrol Dial Transplant 1997; 12: 870–872[Free Full Text]
- Avram MM. The long Island College Hospital experience with a decade or longer of haemodialysis patients. In: Avram MM, (ed). Prevention of Kidney disease and long term survival. New York: Plenum 1982; 165–175
- Lee HY, Stretton TB, Barnes AM. The lungs in renal failure. Thorax 1975; 30: 46–53[Abstract/Free Full Text]
- Conger JD, Hammond WS, Alfrey AC, Contiguglia SR, Stanford RE, Huffer WE. Pulmonary calcification in chronic dialysis patients. Ann Intern Med 1975; 83: 330–336[Abstract/Free Full Text]
- Jarava C, Marti V, Gurpegui ML, Merello JL, Rdez-Quesada PB, Palma A. Pulmonary calcification in chronic dialysis patients. Nephrol Dial Transplant 1993; 8: 673–674[Free Full Text]
- Milliner DS, Zinsmeister AR, Lieberman E, Landing B. Soft tissue calcification in paediatric patients with end stage renal failure. Kidney Int 1990; 38: 931–936[Web of Science][Medline]
- Milliner DS, Lieberman E, Landing BH. Pulmonary calcinosis after renal transplantation in pediatric patients. Am J Kidney Dis 1986; 7: 495–501[Web of Science][Medline]
Received for publication: 25.11.05
Accepted in revised form: 11.12.05
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Introduction
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