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Nephrol Dial Transplant (2001) 16: Editorial Comments
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Nephrol Dial Transplant (2001) 16: 1311±1313
`Flash pulmonary oedema'Ða diagnosis for both the cardiologist and
the nephrologist?
S. Mansoor A. Shah and John E. Scoble
Renal Unit, Guy's and St Thomas' Hospital, London, UK
Introduction
The reason for the title is that since Pickering et al.
w1x ®rst described this condition in 1988, there have
been a number of papers con®rming this as a distinct
clinical entity w2±6x. However, it is unclear as to how
often it is recognized. This is probably because it falls
into a watershed between cardiology and nephrology.
These patients have pulmonary oedema but neither
Correspondence and offprint requests to: J. E. Scoble, Renal Unit,
Guy's and St Thomas' Hospital, St Thomas Street, London
3E1 9RT, UK.
#
severely impaired left ventricular function nor severely
impaired renal function.
Case description
The following case description illustrates the problem.
A 56-year-old female smoker with a 10 year history
of dif®cult to control hypertension presented to
hospital with acute shortness of breath and chest
tightness. On the following day her breathlessness
worsened with further chest discomfort. There were
some anterior lead electrocardiogram alterations suggestive of an anterior myocardial infarction and she
was treated with thrombolysis. There was no change
2001 European Renal Association±European Dialysis and Transplant Association
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Fig. 1. Renal angiogram showing bilateral proximal renal artery
narrowing, compatible with the diagnosis of ®bromuscular dysplasia.
Note the absence of atheromatous lesions of the aorta.
in the cardiac enzymes nor did her electrocardiogram
change. She was noted to have impaired renal function
with a plasma creatinine of 444 mmolul. She was treated
with diuretics and nitrates with improvement in her
shortness of breath and her plasma creatinine fell to
270 mmolul. She then underwent coronary angiography
which was entirely normal but a renal angiogram
was performed which is shown in Figure 1. The
aorta shows no evidence of atheromatous disease
and the angiogram was thought to be compatible
with ®bromuscular dysplasia in keeping with her early
onset hypertension. She underwent left renal angioplasty and right renal artery stenting. Her plasma
creatinine has fallen to below 100 mmolul since the
angioplasty and she has had no further attack of
shortness of breath 3 years later. She has been
reviewed by a cardiologist who has found no evidence
of ischaemic heart disease in any of the preceding
investigations.
Discussion
This case illustrates the dif®culty in diagnosing an
important and treatable acute pulmonary oedema.
The association of proven cardiac disease and pulmonary oedema even requiring ventilation can lead to
an incorrect diagnosis as in this case. In the ®rst series
the mean number of attacks of pulmonary oedema
was 2.3 before the diagnosis was made w1x. In the
Weatherford et al. series it was 2.5 prior to intervention w4x. The case of Kwan et al. had had 3 attacks
prior to investigation w12x. The patient reported
Nephrol Dial Transplant (2001) 16: Editorial Comments
by Farmer et al. w5x had been investigated for
dyspnoea prior to diagnosis but had been discharged
by a cardiology clinic as she had a good left ventricular dysfunction. She subsequently was admitted three
times with `¯ash pulmonary oedema', being ventilated
on two occasions. Diamond w2x reports one patient
who had ¯ash pulmonary oedema `frequently' after
coronary artery bypass grafting and on one occasion
had a respiratory arrest before the diagnosis was made!
All these reports show how late the diagnosis is made
because an echocardiogram showing good left ventricular function had led to a false sense of security in
the physician or more usually the cardiologist.
The original description occurred only in 1988 but
has now become recognized as a distinct clinical entity.
The reason for this is that all the individuals involved
in the original description w1x had signi®cant coronary
artery disease. In fact, in ®ve of the original series
of 11 a rise in plasma creatinine on an ACEI had
already occurred before the diagnosis of renovascular
disease was made. These patients did have signi®cant
heart disease. However, it is only because the speci®c
symptom of pulmonary oedema was improved by
angioplasty or renal artery bypass graft that the
relationship between the renal artery narrowing and
the pathophysiological condition was established. In
a second series in the original paper the correlation
was found with bilateral or unilateral disease with
a sole functioning kidney. A further review by the
same group w6x has shown that pulmonary oedema
occurred in 41% of patients with bilateral and 12% of
patients with unilateral disease. After stent placement,
22 out of 27 patients with bilateral disease improved
whereas only one of the three patients with unilateral
disease improved. Thus the observation in the original
paper that the syndrome occurs when all the functioning renal mass is supplied by a stenotic artery is
strongly supported. Others have suggested a stronger
correlation with renal artery occlusion combined with
stenosis w3x.
Following the original description, Missouris et al.
w7x described two cases where the presentation was
severe heart failure. In the ®rst case renovascular
disease was only suspected with an increase in plasma
creatinine with an ACEI. In each case the proof
of the diagnosis was the dramatic naturesis and
improvement in symptoms after the relief of renal
artery stenosis in single functioning kidneys. These
cases are, however, different from the original description as their symptoms were chronic. In many ways
this may be easy to understand and explain by the
mechanisms suggested by Pickering et al. w1x of the
blunting of the effect of a pressure naturesis due to
renal artery narrowing and decreased perfusion pressure to the kidney and tubule.
The importance of renovascular disease in chronic
congestive cardiac failure is unclear. There have
been no subsequent larger series reporting dramatic
improvement in stable congestive failure. However,
MacDowall et al. w8x have shown that in a general
medical clinic there is an incidence of over 30% of
Nephrol Dial Transplant (2001) 16: Editorial Comments
renovascular disease in patients presenting with
cardiac failure with a plasma creatinine of less than
300 mmolul. The only way to prove a causal relationship in such a situation is a positive response to
intervention and the Missouris et al. study represents
the only series at present of patients in heart failure
w7x. Khosla et al. w9x do however suggest a possible
improvement in New York Heart Association classi®cation of patients following intervention although
the same was also true in patients who had not
undergone intervention!
In fact, the original report does not include the
features we would now recognize for this condition
which are the acute and unprovoked nature of the
pulmonary oedema w1x. The abrupt nature of the
condition gives it its usual name: `¯ash pulmonary
oedema'. Planken and Ritveld w10x report two cases
where the precipitating factors were swimming and
central venous catheterization. Harker et al. w11x
reported a case where a patient with poor left ventricular function was precipitated into acute pulmonary
oedema by angioplasty to one renal artery in a patient
with bilateral renal artery stenosis. Interestingly,
Kwan et al. w12x report a case of Pulsus Alternans in
a patient with bilateral renovascular disease which was
cured by angioplasty. Pulsus Alternans is usually associated with impaired left ventricular systolic dysfunction
but occurred in this individual with a normal ejection
fraction. The patient in this report had been admitted
three times in pulmonary oedema in the 9 months
prior to investigation. The report indicates that these
changes were present when the patient was relatively
stable during investigation. This suggests that even
without the full blown episode of `¯ash pulmonary
oedema' subtle abnormalities of left ventricular dysfunction can be found. Weatherford et al. w4x in their
series of ®ve patients could not document an abnormality of systolic cardiac function prior to intervention. One common clinical feature not commented
in all the papers is that many patients experience their
`¯ash pulmonary oedema' only at night. The frequent
history is of a patient going to sleep without dyspnoea
but awoken in the night with shortness of breath
which may require ventilation. An unproved suggestion might be that these patients have severe renal
artery lesions which are non-critical during the
day with normal ambulant blood pressure, but with
a nocturnal dip in blood pressure the lesion becomes
critical provoking severe perturbation of the reninangiotensin system. As explained above, this is the
much more common clinical presentation rather than
one of stable congestive failure.
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Conclusion
Flash pulmonary oedema is an important diagnosis
to make. In many issues in renovascular disease there
is no good evidence base for either intervention or
non-intervention. However most authorities would
recognize `¯ash pulmonary oedema' as an absolute
indication for intervention. In our experience it rarely
occurs during the waking hours and it may present
a response to nocturnal hypotension in hypertensive
patients who maintain their nocturnal dipping of
blood pressure. Whatever the exact physiology it is
a rewarding condition to treat and one which we and
our cardiological colleagues would be wise to entertain.
References
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pulmonary oedema in hypertension due to bilateral renal
artery stenosis: treatment by angioplasty or surgical
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