Proceedings

Sctional

of the Royal Society of

Medicine

801

Section of Urology
President-TERENCE J. MILLIN, M.A., M.Ch., F.R.C.S.
[May 19, 1949]

Management of the Patient with Anuria

By ASHTON MILLER, F.R.C.S.
IT is not my intention to go into the details of recent advances in the use of dialysis in the
treatment of urnmia, because this has been admirably done in this Section by Reid and
Darmady (1948). I am more concerned to consider the general management of a case of
renal failure and the indications for the use or avoidance of dialysis. During the past two
years I have had the opportunity in Bristol of observing ten cases of this type and this paper
represents conclusions reached after trying various methods of treatment. In all these
cases I have had the co-operation and help of Dr. G. K. McGowan of the Department of
Pathology, who has done a great amount of work in performing numerous blood chemical
analyses and in interpreting the results. There is no doubt that the clinical condition of the
anuric patient gives little indication of the real state of affairs. It has been said that such a
patient may appear to be "in vibrant health in the ward but be practically dead in the
laboratory", and this is no exaggeration for astronomical blood urea values are quite compatible with a conscious co-operative patient.
To treat renal failure one must be aware of its possible causes if only to make sure that
any such cause is not a continuing factor in its maintenance. Swift Joly classified 3 main
causes-Pre-renal, renal, and post-renal.
By pre-renal he meant the stoppage of urinary secretion resulting from a fall in bloodpressure below the level which can maintain an adequate filtration pressure in the glomeruli.
It has been shown that if the systolic blood-pressure in the afferent glomerular vessels falls
below 40-60 mm. of mercury then secretion of urine ceases; this is equivalent to a drop of
aortic systolic pressure to between 70 and 100 mm. of mercury, which can easily occur during
any prolonged or traumatic operation. Moreover, one-quarter of the cardiac output goes to
the kidneys, so that the effect on them of a drop in pressure is very great. The cause of the
drop in blood pressure may be a fall in the circulatory blood volume, such as occurs in shock,
himorrhage or dehydration, or to slowing of the circulation rate in cardiac failure.
By renal causes, he referred to any process in the kidney which stops secretion of urine in
the presence of an adequate filtration pressure, and this includes the various changes which
lead to tubular damage or blockage, such as all the varieties of Lucke's "Lower nephron
nephrosis" (1946), and poisons affecting the renal tubules. The mechanism of this variety
of anuria is still debated; some varieties have been shown to be due to tubular blockage,
such as that caused by mercury poisoning and, possibly, mismatched transfusion anuria, but
evidence of blockage in other cases is lacking and it seems probable that the glomerular filtrate
is reabsorbed direct into the blood owing to the absence of cells lining the tubules. It is seldom
an absolute anuria, but the very small amount of urine that is produced is usually of no significance. The third group of causes is post-renal, which implies ureteric obstruction. I
believe it is essential to include these causes in any discussion of anuria although they are
not strictly disturbances of secretion, because often it is not possible in the early stages to
determine whether the cause is renal or ureteric. For example, in sulphonamide anuria, the
most usual place for blockage to occur is at the lower ends of the ureters, but another type
may occasionally appear where the blockage appears to be in the tubules and the ureters are
unobstructed; as the treatment of these two varieties is different it is necessary to differentiate
them as early as possible. Again, after a pelvic operation during which there has been a fall
of blood-pressure, it is impossible to tell in the early stages whether anuria is due to accidental
ureteric obstruction or to a true pre-renal anuria caused by continued low blood-pressure.
The functions of the kidney which are lost are:
(1) The power of excreting water.-This means that the skin, lungs and bowel remain as
the only means by which the body can get rid of excess water and the total amount excreted
by these channels does not normally exceed 1,000 c.c. per day.
(2) The excretion of the products of protein breakdown of which urea forms the bulk and
is the most easily measured indicator.
(3) The maintenance of the normal electrolyte balance and osmotic pressure of the blood
by excretion of excess acid or base as required, and variation of amounts of fluid reabsorbed.
OCT.-UROL. 1

Proceedings of the Royal Society of Medicine

802

28

Spontaneous Recovery
It is usually about the eighth day after the onset of renal failure that urine secretion begins
again, and this is thought to be due to regeneration of the cells lining the tubules; the kidneys
are capable of supporting life about the fourteenth day or a little later. The first urine that
is produced is very dilute and is little more than a glomerular filtrate containing numerous
casts and much protein, but slowly the power of concentration returns until renal function
tests reach normal limits in some cases.
We can, therefore, resolve the course of the condition into three phases, as Muirhead
(1948) has suggested: the first, in which renal failure is determined and which lasts a few
hours or less, the second, in which life continues in the absence of renal function, the blood
urea mounting daily and electrolyte disturbances gradually increasing, and the third phase,
in which renal recovery starts and continues with resultant diuresis and excretion of large
quantities of salt in what is almost a glomerular filtrate. In other words, the kidneys recover
spontaneously or not at all by a normal process of healing of damaged epithelium.
If one accepts this explanation of the course of the condition, then obviously when the
kidneys are not working, fluids must not be given in excess of one litre each day and no attempt
should be made to force the kidneys to secrete which interferes with the water and salt balance,
or which prevents regeneration of tubular epithelium.

.1

_4

F?Aiva& ,cUW..Cno..ieq#9 #EC-OVERY

12
to
14.
~~~~
~~~~-8
DJqYS .

16

18

2O

FIG. 1.-Three-phase management.

We have come to the conclusion that these two principles are the basis of successful
management of temporary renal failure. As a result of unsuccessful efforts made in earlier
cases I can fully endorse Lattimer's view (1945) that patients who have been given excess
fluid in the early stages show a worse prognosis and take longer to show recovery of urine
secretion; and the striking results of Coller (1948) demonstrate this: out of 10 cases, the
first 5, treated by "forcing fluids", all died, while the second 5 all lived when fluids were
restricted. Giving excess fluid causes dilution of the body fluids, resulting 'in clinical
cedema; and it is useful to remember that cedema does not make its appearance until there
is considerable dilution, as the blood picture of this case shows; there was only moderate
clinical (edema:
P. P., AGED 20 YEARS. ANURIA 8 DAYS

Sodium
mg.%
275

(330)

Chloride
mg. %
360
(600)

Bicarb.
vols. %

Calcium
mg. %
6-8

Protein

Urea

mg.%

40
5-9
350
(60)
(10)
(6-5)
(30)
(Figures in brackets represent normal levels.)

Potassium Phosphate
mg. %
mg. %
28
(18)

7-5
(3)

Early Methods of Treatment

In our early cases every effort was made as soon as possible to persuade the kidney to
function not only by giving fluids, but also by administering diuretics; the most potent of
these is sodium sulphate in 4-285 % solution, which in ordinary circumstances can be relied
upon to produce a profuse diuresis. We did not realize, however, that if the kidney is not
producing urine, this solution cannot have any effect other than increasing the circulatory
blood volume, and the levels of sodium and sulphate in it; none is excreted except when it
is washed out in the glomerular filtrate as a foreign substance which is not reabsorbed in the
tubule. It was also found that administration of this salt made it difficult to determine the
chloride and bicarbonate levels of the blood. All other diuretics require secretion to be
proceeding to produce any result, and were therefore abandoned. Further activity was
directed towards increasing the blood supply of the glomeruli and tubules by one of
the methods of paralysing the sympathetic supply of the kidney. This can be done by
administering a spinal anesthetic, but as this must reach as high as the level of the

29

Section of Urology

803

sixth thoracic segment to be effective, it has been avoided for fear of the almost inevitable
drop in blood-pressure; epidural anesthesia has the same disadvantage, so lumbar paravertebral sympathetic block has been preferred. This has been performed in 5 cases at
varying stages of the condition without any effect on secretion, though we have achieved
vasodilatation in the leg. As with the tetra-ethyl ammonium salts, it is probable that by
the time that the need for their use is obvious, secondary tubular damage has already
occurred and vasodilatation will be without effect.
Decapsulation of the kidneys has been used in 3 cases, also without effect. There are two
reasons given for employing this operation, either to increase the blood supply of the renal
cortex or to remove the sympathetic supply to the renal cortical vessels. If anything a very
slight diminution in blood supply is all that is attained because the minute vessels passing into
the interstitial tissue from the cortex are torn, and any revascularization must be achieved
by the formation of granulation tissue which will take many days to be effective. The sympathetic supply enters the kidney along the renal vessels and the cortex contains no nerve tissue.
It has also been suggested that it may be used when there is great cedema present on the
supposition that it allows acedemra fluid to pass out from the substance of the kidney and so
diminishes the obstructive pressure on the glomeruli and tubules. Though fluid may drain
out and the intrarenal pressure may fall, aedema will still be present because the condition
is generalized and is the result of an overloaded circulation. The cases on which this operation
was tried included a patient with renal cortical necrosis and another with the lower nephron
syndrome resulting from incompatible blood transfusion; in the former case there had been
gross overhydration and generalized cedema was present, the operation being performed on
the fifth day of anuria with the blood urea 200 mg. %; this therefore represented a fair test
of the operation as the patient was still in a fairly good condition. Though much fluid
drained through the incisions, there was no decrease in the general cedema during the next
two days, no urine was produced, the blood urea rose to 230 mg.% and she became
comatose. Sections of the kidney taken at the time of the decapsulation and at autopsy later
showed a massive necrosis of the cortex exactly resembling an infarct of the kidney. It is
impossible to believe that the operation achieved anything helpful in this case. In the other
case renal failure was far advanced, the blood urea had reached 290 mg. % after seven days of
complete anuria; where now I would unhesitatingly use peritoneal dialysis, I performed a
quick bilateral decapsulation and the patient died four hours later. In a third case of advanced uraemia due to a sudden exacerbation of chronic nephritis with anuria, bilateral
decapsulation produced no result and the patient died a few hours afterwards. So that,
although it is true that the operation need not be formidable and can be done very expeditiously with minimal inhalation anesthesia, I am convinced that successes claimed for
it are fortuitous and I shall not advise it again.
A good example of such a coincidence occurred recently when a patient with renal failure
of six days' duration due to lower nephron nephrosis passed about 100 c.c. of urine immediately before I had arranged to do a bilateral lumbar sympathetic block. It was therefore
postponed, for a diuresis had commenced spontaneously; if I had arranged to do the block
in the morning instead of the afternoon we might naturally have imagined that it was the
cause of the diuresis.
Recent Principles of Treatment
Phase L-I have made it a rule that in the assessment of these cases cystoscopy and
catheterization of the ureters should be done as early as possible in every case in order to
distinguish renal from post-renal cases, in other words, to exclude ureteric obstruction.
This, I am sure, is of great importance. If obstruction is present, then unless it can be
relieved easily by some simple procedure such as catheterization of the lower ends of the
ureters to dislodge a plug of sulphonamide crystals, efforts should be directed towards
draining the part of the urinary tract above the obstruction as a life-saving measure, rather
than performing some definitive operation such as removal of a ureteric calculus or
reimplantation of a ureter into the bladder. I do not believe that one should leave ureteric
catheters indwelling for longer than six hours, there is a great danger that they may become
blocked and thus themselves cause obstruction. If drainage is required for a longer period
then I prefer to perform a nephrostomy.
Every effort is made to restore the circulating blood to as near a normal condition as
possible, for hemoglobin levels are often surprisingly low. Even in the case of anuria
due to mismatched transfusion, expert cross-matching will allow further blood to be given
with advantage.
As soon as convenient a biochemical blood analysis should be done. This allows gross
errors to be discovered and also sets a standard which enables one to assess any variations
that may occur. The blood sodium, chloride, bicarbonate and urea tests are adequate
in most cases.

Proceedings of the Royal Society of Medicine

804

30

Phase II.-The management of the second phase largely consists in catering for the reduced
fluid requirements of the body, giving low protein and high carbohydrate diet, and
watching the blood chemical results until the time comes to employ some method of artificial removal of waste products from the blood. I have no personal experience of external
dialysis by any type of artificial kidney, and my impression is that it is not less complicated
than methods of internal dialysis. The most effective of these is peritoneal dialysis, which
was therefore chosen as being easier and safer. That it is neither easy nor safe I would
hasten to assert, because it keeps a surgeon, a biochemist, and two nurses employed almost
full time, and the electrolyte changes occur with such rapidity that it is extraordinarily easy
to do more harm than good. But that it is a powerful therapeutic weapon we have no doubt
whatever.
There are two types of case in which it seems desirable to employ dialysis. First it may
be indicated in the patient in whom attempts to produce a diuresis have included the administration of excess of fluid with resultant cedema. If there is clinical pitting aedema present
it is unlikely that restitution of the normal fluid levels will occur simply by limiting fluid
intake by mouth over a period of a few days, and in any case it is necessary to restore the
blood values to normal as soon as possible if prolongation of the necessary recovery period
is to be avoided. The following is an example of this:
Hb.

G. D., AGED 40 YEARS. ANURIA 5 DAYS

Proteins Sodium Chloride Bicarb.
vols. %
%
mg. %
mg. %

Day

5
7
9

27
32

50
6-0

46
68

6-0

11

13
15
17
19

305
315
330

490

45

450

55

495

68

Urea
mg. %
188
225
204 Peritoneal
177 dialysis

171J

186
282
321

This patient had renal cortical necrosis resulting from an accidental haemorrhage associated with Rhesus sensitization, and had received fluids in large amounts so that after five
days of renal failure she had generalized cedema. Great clinical improvement occurred in
the first forty-eight hours of dialysis, and the aedema became negligible. Recovery of the
kidneys did not occur, however, and dialysis was discontinued on the 14th day; the patient
died on the twenty-eighth day after the onset of renal failure.
The second type of case is that in which the second phase is prolonged and renal function
does not return, so that the patient is in danger of death from accumulation of metabolic
products. Here dialysis is used simply to prolong life so that the kidneys may have a
greater chance of recovery as in the following case:
Day
5
6
7
8
9

F. S., AGED 60 YEARS. OLIGURIA FOR 4 DAYS

Urea
Proteins Sodium Chloride Bicarb.
vols. %
%
mg.%
mg.%
mg.%
42
436
530
6-3
306
58
502k Peritoneal
500
6-2
314
6-2
5-9

318

530

44
47

500f dialysis

475
500

This was a case of calculus anuria; secretion of urine started again but he developed
auricular fibrillation and died of cerebral thrombosis.
The indications in these types of case for the use of dialysis are of course not as yet finally
decided, but it has seemed that in the first variety the presence of generalized cedema is
sufficient indication. A blood dilution which has not reached the stage of gross cedema can
be dealt with by simple limitation of fluid intake for one or two days, but anything more
demands quicker and more effective methods. In the second type we watch the blood
urea value climbing day by day, with singularly little change in the clinical condition of
the patient, and any decision to use dialysis must be made on the results of blood analysis
alone, because death when it occurs may be very sudden.
I have been greatly impressed by the effect of dialysis upon the electrolyte content of the
blood, changes occur rapidly and it is possible to restore a patient to an almost normal
condition within a period of twenty-four hours; but it has not been possible to remove
sufficient urea to reduce the blood level to normal or anywhere near it. It has seemed that
the former function is often as important, if not more important, than the removal of urea.

31

Section of Urology

805

It has been found that a blood urea level of 200 mg. % in the presence of little or no excretion by the kidneys represents a level beyond which delay is dangerous. This is the present
basis of our treatment of these cases, though I would emphasize that with greater experience
I may alter my ideas.
Phase III.-We now come to the third phase, or the period of diuresis. The main thing
about this period is that although urine is being produced again, with the resultant vast
increase in morale both of patient and nursing staff, the patient is by no means out of
danger, and the strictest supervision of fluid and salt intake must continue if sudden death
is to be avoided. As we know, the first urine that is passed is simply a glomerular filtrate,
and this appears in larger and larger quantities, so that much fluid may be lost and the
patient passes fairly rapidly from one condition in which the fluid intake must be limited
to another in which the intake must be controlled by the amount that is excreted. The
volume may be enormous, but fortunately the patient feels thirsty so drinking is easy.
This fluid loss carries with it in solution sodium chloride in large quantities because tubular
reabsorption of this salt is inadequate, and this may have dangerous results. It is possible
by measuring the chloride content and the daily volume of the urine to work out exactly how
much salt is needed to replace that lost, and this may be given by mouth or intravenously.
As a rough guide we have found that half the daily total fluid excretion replaced as normal
saline by mouth should cover the amount lost and can be taken by the patient.
The figures from a successful example of this three-phase management are given below:
SULPHONAM1DE NEPHROSIS

Urea Fluid intake Urine

Chloride Bicarb.
ml.
ml.
vols. % mg. %
mg. %
Day
50
3,000
48
2
1,500
100
4
56
500
298
170
900
72
140
55
6
6-3
308
515
1,440
2,000
197
8
68
3,210
3,210
50
10
68
6-3
328
627
2,670
3,330
190
12
68
6,000
6,120
319
156
14
605
7-9
5,000
5,800
73
16
7,590
7,260
322
62
57
18
6*9
580
9,720
10,700
20
68
6,000
6,760
30
22
605
This was a woman aged 28, who, when 71 months pregnant, developea lobar pneumonia. She
was given in error a double dose of sulphathiazole, having 60 grammes in four days, and the next
day she developed hiamaturia followed by complete anuria. She was seen on the second day of
anuria and limitation of fluids commenced. Cystoscopy and catheterization of the ureters demonstrated no obstruction and no urine secretion. After the first blood analysis the fluid intake was
reduced to less than one litre daily for two days with resultant improvement in the figures on the
sixth day; on this day a medical induction produced a normal labour and a living child. Urine
production commenced shortly before labour, and a diuresis was well under way by the tenth day.
On the twentieth day she produced nearly 10 litres of urine and took by mouth 5 litres of normal saline
and over 5 litres of other fluid.
MANAGEMENT OF PATIENT W1TH ANURIA: SUMMARY
Phase I
(1) Remove cause; restore blood volume, blood-pressure and hemoglobin level by transfusion.
(2) Cystoscope and catheterize both ureters; if obstruction is found, relieve it or perform
nephrostomy.
(3) Estimate blood sodium, chloride, bicarbonate and urea.
Phase II
(1) Limit fluid intake to make up for insensible loss.
(2) Maintain adequate hemoglobin level by transfusion (packed cells are useful).
(3) Give low protein, high carbohydrate, diet.
(4) Check progress by estimating blood urea and bicarbonate on altemate days, at least.
(5) Employ dialysis if generalized cedema is present, or blood urea has risen to 200 mg. %.
Phase III
(1) Replace fluid excreted.
(2) Replace salt excreted.
(3) Check progress by estimating blood sodium, chloride, bicarbonate and urea every two to three
days until diuresis subsides.
REFERENCES
COLLER, F. A., et al. (1948) Ann. Surg., 128, 379.
DARMADY, E. M. (1948) Proc. R. Soc. Med., 41, 418.
LATTMER, J. K. (1945) J. Urol., 54, 312.
LUCKE', B. (1946) Milit. Surg., 99, 371.
MUIRHEAD, E. E., et al. (1948) Blood, 3, 101.
REID, R. W. (1948) Proc. R. Soc. Med., 41, 413.

Hb.
%
82

Proteins
%
6-3

Sodium
mg. %