index terms:

Kidney
diseases
The abnormal nephrogram
nephrogram

. Ray B. Dyer, M.D.

. H. Alexander Munitz, M.B., B.Ch.

Robert Bechtold, M.D.
Robert H. Choplin, M.D.

Recognition of qualitative abnormalities in the nephro-

gram may be as important as the recognition of struc-
turai abnormalities for the det#{149}ctionof renal disease.

THIS EXHIBIT WAS DISPLAYED AT THE

71ST SCIENTIFIC ASSEMBLY AND AN-
NUAL MEETING OF THE RADIOLOGI-
CAL SOCIE1Y OF NORTH AMERICA
NOVEMBER 17-22. 1985. CHICAGO,
Introduction
ILLINOIS. IT WAS RECOMMENDED BY
THE URORADIOLOGY PANEL AND
WAS ACCEPTED FOR PUBLICATION The radiographic image of the contrast filled renal parenchyma,
AFTER PEER RE\.IEW AND RE\ASION the nephrogram, has long been utilized in the evaluation of structural
ON JUNE 6, 1986. abnormalities in the kidney. Further elucidation of certain disease proc-
esses may depend on the observation of qualitative abnormalities In
the nephrogram. In most cases, these abnormalities are due to antece-
dent pathology but, on occasion, are a direct result of the contrast
medium or of the diagnostic technique. It is necessary for the radiolo-
gist to recognize these latter abnormalities. An understanding of these
qualitative abnormalities is applicable to all radiographic modalities in
which a nephrogram is produced including angiography, intravenous
urography (lU) and computed tomography (CT).

The Normal N.phrogram

Striking images of the renal parenchyma occur during angiog-

raphy, when the renal vasculature is flooded with contrast medium.
Because current contrast materials are excreted almost exclusively by
glomerular filtration with little tubular secretion or resorption (20),
From the Department of contrast agents are cleared rapidly from the vascular system and
Radiology, Bowman Gray appear in the tubular filtrate. With rapid filming, the transition from
School of Medicine, Winston- . vascular opacification to tubular opacification can be perceived, and
Salem, North Carolina.
Address reprint requests
. this has allowed the division of the arfeniographic nephrogram into
. stages (4) (Figure 1). The first stage is a very transient vascular phase
to RB. Dyer, M.D., Department
of Radiology, Bowman Gray that has been subdivided into a cortical arteniogram, in which contrast
School of Medicine, 300 S. medium is observed in the interlobular arteries, and a glomerulogram
Hawthorne Road, Winston- in which the contrast agent is momentarily stagnant in the glomerular
Salem, NC 27103 tufts. This is followed by a cortical nephrogram, in which cortical capil-

Volume November,
6, Number#{243} #{149} 1986 #{149}
RadloGraphics I 039
 The abnormal nephrogram Dyer ci al.

E
a

#{149}a lanes, peritubular spaces, and tubular lumina of the cortex are
opacified. During the cortical nephrogram, the cortex is cleanly distin-
- guished from the medulla because of its greater inherent vasculanify
and because the contrast material is not yet present in the lumina of
the more distal tubules. This is followed by a general nephrognam during
z which contrast material is washed out of the cortical vessels and ex-
tracellular spaces and appears in the tubular lumina throughout the
cortex and medulla, with resultant loss of corticomedullary differentiation.

‘9_
An arteriographic vascular phase shows contrast medium in the interlobular
arteries with early glomenular filling.

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Dyer ci al. The abnormal nephrogram

z
0

a
z
0
V

I
3

Figure lB
An arteriographic cortical nephrogram demonstrates excellent cor-
ticomedullary differentiation.

At urography, following the injection of an intravenous bolus of

contrast material, there is little contribution to the nephrographic
density from contrast medium in vascular structures; the nephrographlc
image is due primarily to contrast material within the tubules (20).
Nevertheless, a radiograph obtained very soon after the bolus injection
may show corticomedullary differentiation (Figure 2). As with the
arteniographic nephrogram, this differentiation is rapidly lost as the
contrast agent progresses into distal tubular lumina. This same nephro-
graphic progression, from corticomedullary differentiation to homoge-
neous tubular nephrogram, can be distinguished with dynamic CT
imaging (Figure 3).
Regardless of the type of imaging, after the transient vascular
phase, the tubular nephrogram should become maximal within
minutes after the injection and should fade as the plasma concentra-
tion of the contrast medium decreases. To produce the normal
appearance, progression and regression of the nephnogram, the
processes of renal parenchymal perfusion, at a pressure sufficient to
allow normal glomerular filtration; normal tubular transit; and normal
tubular function are necessary. Aberrations of the above processes
may be reflected in qualitative abnormalities of the nephrogram.

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a

2B

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z
0

Figure 2A a
An initial tomogram after urographic
ticomedullary differentiation.
bolus injection demonstrates cor- z
0
V
3.
Figure 2B
A late tomogram. following unographic bolus injection, demonstrates loss of
corficomedullary differentiation owing to progression of the contrast mate-
rial into the tubules of the medullary portion of the kidney.
I

Figure 3A
This is an unenhanced image from a
dynamic CT sequence

Figure 3B
This image was taken 60 seconds after an
intravenous bolus injection of contrast mate-
rial. It shows opacification of the aorta and
renal vein with excellent renal corticomedul-
lary differentiation.

Figure 3C
This image illustrates the transition to
homogeneous density throughout the kidney
representing the tubular nephrogram.

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The abnormal nephrogram Dyer ci al.

impaired Perfusion

Vascular impairment, leading to reduced (28) in otherwise normal kidneys (Figure 4). It has
blood flow, may be associated with a variety of been attributed to reflex spasm in the renal
nephrographic abnormalities. While angiog- capillary bed related to direct catheter trauma
raphy represents the standard for evaluation of on to the pressure injection of highly concen-
the renal vasculature, aberrations in blood flow trated contrast medium into the renal artery.
may be observed on other types of images. Similar vascular alterations may be seen in
Transient rerouting of blood flow from the chronic renal disorders such as collagen
renal cortex to the renal medulla trrueta vascular disease, malignant nephnosclerosis,
shunting) (29) has been observed as a result of and chronic glomenulonephnitis, however.
catheterization and contrast medium injection

F..
This selective renal arterial injection demonstrates irregularity of the
peripheral vessels.

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V
a
Figure 4B
0
This late phase nephrogram shows a.
inhomogeneous opacification of V
the cortex as a result of Trueta 0
shunting in an otherwise normal C
U)
kidney. A repeat abdominal aorto- 0
3
gram, 30 minutes later, showed no
residual arterial spasm.

An exaggerated form of this irregular sclenoderma, and advanced hypertensive

cortical nephrogram, the spotted nephrognam, nephnosclenosis (32). Small areas of nonperfusion
(Figure 5) has been reported in patients with are difficult to demonstrate on intravenous
occlusive disease of small vessels related to a urography, but they are more readily ap-
number of causes, including necrotizing vas- preciated on CT images, owing to superior
culitis such as polyartenitis nodosa (30), contrast resolution (24) (Figure 6).

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0
U)

3
.

a.

aE

Figure 5A
A late arterial phase from an aorto-
gram shows bilateral spotted neph-
rognams in a patient with polyartenitis
nodosa.

Figure 5B
This is a late phase from a selective
renal arteniogram in the same patient;
it demonstrates occlusion of multiple
peripheral vessels with cortical irregu-
lanity.

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V
a
Figure 6A 0
In this patient with polyartenitis a.
nodosa, an enhanced CT scan V
shows wedge shaped defects 0
C
in the left kidney. U)
0
3

Figure 6B
This image represents a late arteriographic phase. It shows stagnation of
contrast material in multiple renal artery aneurysms bilaterally and areas of
nonperfusion more distally.
(Photo courtesy ot Thomas L Pope, Jr., M.D., Charlottesville, VA)

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 The abnormal nephrogram Dyer ci al.

Underperfusion related to renal artery from capsular vessels (Figure 9). Since the Initial
I stenosis (Figure 7) and nonperfusion related to descriptions in which the rim nephrogram was
renal artery occlusion from any cause (Figure 8) due to major renal artery obstruction from
: are associated with characteristic nephro- thrombosis or embolism, the rim nephrogram
aE graphic
described
findings (20). The rim nephrogram,
at urography (10) and subsequently
first has also been described with acute tubular
necrosis and renal vein thrombosis (13). In any
demonstrated by CT (11) is seen in severe renal case, the detection of a rim nephrogram
underperfusion; only a thin rim of peripheral indicates a severe aberration of blood flow to
renal cortex continues to receive vascular flow the kidney.

r ‘U

.v

.4

I A
.. .

I J4 -i-- ‘.‘ 1

Figure 7A
An early urographic tomogram reveals a small right kidney with decreased
nephnographic opacity in this patient with right renal artery stenosis.

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Figure 7B
This 20 minute radiograph shows hyperconcentration of contrast material in
the right collecting system and ureteral notching from collateral blood flow.

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0
U)
3
0 ‘:

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Dyer ci al. The abnormal nephrogram

Figure 8A
An early urographic film shows absence of a right neph-
rogram in this patient with hematuria following trauma.
Note the fracture of the L2 transverse process (arrow).

Figure 8B
The aortogram demonstrates abrupt termination of the
renal artery related to a traumatic thrombosis or sheening
avulsion of the vessel (curved arrow).

Figure 9A Figure 9B
This is an unenhanced CT scan of a patient with An enhanced scan shows a thin rim of enhance-
hematuria following blunt abdominal trauma. ment at the periphery of the right kidney.

Figure 9C
This selective right renal arteriogram demonstrates
traumatic thrombosis or avulsion of the distal right
Figure 9D
renal artery with proximal irregularity. Note the in-
This is the late arteniographic phase. Contrast
tact capsular vessel (arrows).
medium is present in a thin rim of tissue at the
periphery of the right kidney (arrowheads).

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0
U)
3
The rim nephrogram secondary to underperfusion should not be
0
a. confused with the rim nephrogram of urinary obstruction, which
represents the opacification of renal parenchyma that remains about
chronically dilated calyces (9) (Figure bO).
aE

This is the early arteriographic phase in a patient with a In this late arteriographic phase, a rim of contrast opacity is
staghorn calculus. It shows attenuation and splaying of seen in the thinned parenchyma surrounding markedly di-
the renal vasculature. lated calyces.

Of grave importance to the radiologist, is by the renin-angiotensin-aldosterone pathway.

the nephnographic appearance caused by a Slowed intratubulan transit coupled with hyper-
hypotensive reaction to contrast materials (17) concentration leads to persistence of the
(Figure bb). When the perfusion pressure drops nephrogram and to progressive increase in its
below that necessary for continued glomerulan opacity. Prolonged, bilateral dense nephro-
filtration, tubular stasis develops. Contrast grams, at times coupled with a decrease in
medium that is already present in the kidney renal size (16) demand immediate examination
becomes hyperconcentrated owing to in- of the patient to exclude the possibility of
creased salt and water resorption, mediated hypotension.

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Figure hA
This is an early tomogram made

I
after the bolus urographic injection
of contrast agent. It shows normal
nephrographic opacity.

,,

.1 Figure IIB
This tomogram, made approxi-
I
4 mately 3 minutes after the injection
of the contrast agent. shows the
normal progression to the pyelo-
graphic phase of the urogram.

‘. i
I

.,.

Figure IIC
This radiograph, exposed at 25
minutes, demonstrates loss of a
pyelogram, decrease in renal size,
. and recurrence of a nephrogram.

, No palpable blood pressure could

be obtained in this patient who de-
veloped a hypotensive reaction to
the contrast medium.

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0

q Renal vascular changes, Including shunting of blood from the

I cortex to the medulla and local areas of vascular spasm, may persist
. for long periods following a hypotensive episode (18). Areas of under-
. perfusion may be responsible for the persistent post shock nephnogram
a
#{149}g
(23) (Figure 12) which is occasionally
urography is performed following
seen in patients on whom
the resolution of a hypotensive
episode.

.3
This aortogram performed because of persistent blood loss,
shows severe vasospastic changes in all major aortic branches.
Systemic blood pressure, at this time, had been normal at 110/60 mm
Hg for four hours. Note the area of extravasation in the sub-
stance of the liver (arrow).

Figure 12A
This radiograph was obtained one hour after the injection
of a contrast medium in a patient who had sustained
trauma. Circumstances had prevented the patient’s trans-
port, and his blood pressure had been documented to
be below 70 mm Hg systolic for several hours. At the time
of the injection of the contrast agent, the patient was
normotensive. Note the compression ofthe bladder from
a large pelvic hematoma.

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Dyer ci al. The abnormal nephrogram

3
.
Vascular flow aberrations on the venous side may also produce
nephrographic abnormalities (8). Obstruction to venous oufflow may
decrease
interstitial
may impair

below
glomenular
edema,

(Figure
tubular
similar to that seen in acute
b3).
filtration
which frequently
transit,
and slow tubular
accompanies
and result in an obstructive
extrarenal obstruction
transit. In addition,
renal vein thrombosis,
nephrogram”
to be discussed I

Figure 13A
This five minute radiograph,
from the urogram of a patient
who had had an acute onset of
left flank pain. shows a persis-
tent nephrogram on the left
with poor filling of undilated
calyces.

Figure 13B
An inferior vena cavogram
shows clot extending from the
origin of the left renal vein.

Volume 6, Number November,

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The abnormal nephrogram Dyer ci al.

Impaired Tubular Transit

Obstruction to urine flow in the tubule or filtration is reduced but continues at a level
more distally in the collecting system may permitted by the continued resorption of water
Impair tubular transit. Unilateral extrarenal from the renal tubule (6). Slowed tubular transit
obstruction is the most frequently encountered results in hyperconcentration of the contrast
cause of a nephrographic abnormality (Figure medium. This produces the typical obstructive
14). Elevated renal pelvic pressure is transmitted nephrogram with progressive increase in the
in a retrograde fashion throughout the nephron. opacity of the nephrogram over minutes to
As a result of this opposing pressure, glomerular hours.

Figure l4A
This radiograph, exposed
one minute after a uro-
graphic bolus injection of
contrast material, shows
bilaterally symmetric neph-
rograms.

Figure 14B 4-

This eighty minute radio-

graph shows progressive in-
crease in the opacity of the
nephrogram on the right F.
owing to acute high grade , .. 1.;V ‘

obstruction from a distal

right ureteral stone.

L-4

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V
a
The segmental nephrogram (25) (Figure 15) The striated nephrogram is another qualita-
is an unusual variant of the obstructed nephro- tive nephrographic variation. It is due to visuali-
gram in which the nephnognam persists focally zation of medullary rays (3) in the renal panen-
in some portion of the kidney. This is usually seen chyma (Figure 16). The medullary rays consist of
when obstruction occurs in one limb of a dupli- bundles of renal tubules that extend from the
cated system. A segmental nephrogram has renal cortex to the renal medulla. Stniations are
been shown by CT, however, that was secondary most frequently encountered in the presence of
to calyceal obstruction from a transitional cell extrarenal obstruction, but they may be seen in
tumor that was not visible at urography (5). any condition that is associated with delayed
tubular transit and hyperconcentration of con-
trast material (3).

This is a 165 minute, erect radiograph of a patient

who had a right distal ureteral stone and a history
of multiple previous stone passages. Note the
linear stniations extending from the renal cortex to
the medulla.

Volume#{243},
Number#{243}#{149}
November, 198#{243}ROdIOGraphICS
#{149} I 057
 The abnormal nephrogram Dyer ci al

U)
C
a
I- Alterations of blood flow including hypoten- such as renal contusion (27) and acute
a sion (3) and renal vein thrombosis (31) have pyelonephnitis (2,12) have also been associated
3 been associated with the detection of these with the demonstration of stniations by angiog-
3 stniations. In these cases, blood laden with a naphy, unography and CT (Figure b7). The
contrast medium may be stagnant in penitubulan mechanism of the formation of stniations, in
capillaries; the stniations representing un- these cases, is felt to be an increase in paren-

I opacified
associated
urine in the tubular lumina.
with increased interstitial
Conditions
edema
chymal
resultant
pressure
tubular
opposing
stasis.
tubular transit, with

Figure h7
An enhanced CT scan of a patient with the clinical diagnosis of acute left
pyelonephnitis shows enlargement of the left kidney, multiple areas of de-
creased attenuation, and linear striations at “6 o’clock”.

In the normotensive patient, the occur- nephnon, were found in several patients during
nence of bilateral nephrognaphic abnormalities the diuretic phase of the renal failure which re-
should raise the question of a tubular obstructive suIted. The combination of Tamm-Horsfall and
process. Such an obstruction may occur in sev- Bence-Jones proteinunia has also been impli-
eral conditions. Protein precipitation has been cated in the development of acute renal failure
implicated as a cause of prolonged nephro- in patients with multiple myeloma following ex-
grams in a group of infants and children who posure to contrast agents. In these patients, pro-
became oligunic following intravenous urog- longed dense nephnograms, typical of a tubular
raphy (V. Large amounts of Tamm-Horsfall obstructive event, may be seen (Figure 18).
mucoprotein, a normal product of the proximal

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Dyer ci al. The abnormal nephrogram

This abdominal radiograph was obtained 24 hours after an enhanced CT

head scan in a patient with multiple myeloma. It shows faint persistence of
nephrograms bilaterally. The patient had developed anunia following the
enhanced CT head scan.

Uric acid nephropathy has been postu-

iated to occur as a result of intratubulan precipi-
tation of uric acid. Precipitation of the crystals
may be related to an increased plasma urate
concentration, excessive tubular secretion of
urate, and possibly to a lower percentage
resorption of the large urate load (19). These
factors, coupled with dehydration and the high
osmolanity of the contrast material administered,
may result in precipitation of the urate crystals.
On intravenous urography, “flash filling” of the
calyces may be seen, followed by an increas-
ingly more opaque nephrogram that may per-
sist for hours to days (19) (Figure 19). This excludes
an extrarenal obstructive process, and impli-
cates the contrast material as the cause of
Intratubular obstruction.

Volume 6, Number #{243}November,

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 The abnormal nephrogram Dyer ci al.

U)
C
a
I.- Figure 19
This radiograph was obtained 7 hours after the
a
3 injection of a contrast agent for urography in a
3
patient with hyperuricemia. It shows persistent
I.. nephrograms, enlargement of the kidneys, and
faint filling of undilated calyces.

aE

iL’% :‘

Prolonged nephrograms have also been reported in patients with

tubular obstruction as a result of myoglobmnunia (26). Patients with
myoglobinunia, and hyperproteinunic states may develop a striated
nephrogram, emphasizing the fact that any pathophysiologic condition
that produces delayed tubular transit may lead to visualization of the
medullary rays.

Abnormal Tubular Function

Acute tubular necrosis may result in Iwo nephrogram of increasing opacity is seen. In
different nephrographic patterns (7). In the these instances, the tubular damage may not
more common form, the nephrogram develops be as great, and oligunia is accounted for by
immediately and persists for days. It is postulated cortical underperfusion and reduced glomerular
that when tubular damage is great, transtubular filtration alone (Figure 20). Patchy areas of
diffusion from the penitubular capillaries allows increased opacity have recently been de-
rapid appearance of the contrast material in scnibed on CT in a patient with reversible, acute
the tubular lumina. This, coupled with decreased renal failure. They have been attributed to
glomerular filtration produces stasis in the patchy vasoconstniction (15).
tubules (7). Less commonly, a slowly developing

I 060 November,
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Dyer ci al. The abnormal nephrogram

Figure 20A
In this 15 minute radiograph from the a
urogram of a normotensive patient, -I
C
slowly increasing nephrograms are a.
seen bilaterally with poor opacifica- C
tion of the collecting systems. a
-‘I
C
3
0

0
3

- I
Figure 20B
as This 24 hour radiograph shows bilat-
eral nephrograms in this patient who
had been given an intravenous con-
trast agent prior to the return of labo-
ratory studies. The patient proved to
have acute tubular necrosis from the
ingestion of a toxin prior to the admin-
istration of the contrast agent.

‘:,

I,

Ss

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C
0
U
C
3
The radiologist must also be aware of diagnosis, as the finding of a persistent nephro-
U. radiographic findings associated with renal fail- gram may precede the development of oliguria,
a ure induced by a constrast medium. Abnormal or a detectable rise in serum creatinine. Con-
3
.0 persistence of the nephrogram during the trast medium induced acute renal failure has
3 course of a contrast study (21), or persistence of been attributed to tubular blockage from pre-
I-
a the nephrogram on a radiograph obtained 24 cipitation of proteins or uric acid, vasocon-
hours after such a study, should alert the striction, or sludging of red blood cells related to
0 radiologist to the development of renal failure the high osmolality of the contrast agent, and to
induced by contrast material (22) (Figure 21). The a direct toxic effect of the contrast material on
radiologist is in a unique position to suggest the the renal tubular epithelium (14).

Figure 21A Figure 21B

This radiograph of a nonmotensive patient with nor- This radiograph was exposed 24 hours after urography. Dur-
mal renal function was exposed 10 minutes after ing the interim, the patient had become oligunic and the
the injection of a contrast agent for urography. It BUN and creatinine had risen markedly. Following judicious
shows bilateral persistent nephrograms with poor medical management. renal function returned to normal.
opacification ofthe collecting systems, because of
nephropathy due to the contrast agent.

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Dyer ci al. The abnormal nephrogram

Conclusion

Qualitative or temporal abnormalities in the nephrogram may pro-

vide important clues to renal diseases that produce impaired vascular
flow, delayed tubular transit, or abnormal tubular function. Appreciation
of these abnormalities may be as important as the recognition of struc-
tural abnormalities for which the nephrogram is more commonly used.

References

1. Berdon WE, Schwartz RH, Becker J. Baker DH. Tamm-Horsfall 18. Kupic EA Abrams HL. Renal vascular alterations induced
prateinuria. Radiology 1969; 92:714-722. by hemorrhagic hypotension. Invest Radial 1968;
2. Berliner L. Bosniak MA. The striated nephrogram in acute 3:345-355.
pyelonephritis. Urol Radial 1982; 4:41-44. 19. Marlin DJ, Jaffe N. Prolonged nephrogram due to
3. Bigonglari LR. Patel 5K Appelman H, Thornbury JR. hyperuricaemia. Br J Radial 1971; 44:806-809.
Medullary rays. Visualization during excretory urography. 20. Newhouse JH, Pfister PC. The nephrogram. Radial Clin N
AiR 1975; 125(4):795-803. Amer 1979; 17(2):213-225.
4, Boijsen E. Anatomic and Physiologic Considerations. In: 21. Older PA Korobkin M. Cleeve DM, Schaaf P. Thompson
Abrams HL, ed. Abrams Angiography. 3d ed. Boston, W. Contrast-induced acute renal failure: Persistent
Little Brown and Co. 1983:1118-1119. nephrogram as clue to early detection. AIR 1980;
5. Breatnach ES. Stanley RJ, Lloyd K. Focal obstructive 134:339-342.
nephrogram: An unusual CT appearance of a transi- 22. Older PA Miller JP, Jackson DC, Johnsrude IS, Thompson
tional cell carcinoma. J Comput Assist Tomogr 1984; WM. Angiographically induced renal failure and its
8(5):1019-1022. radiographic detection. AiR 1976; 126:1039-1045.
6. Brenes LG, Forlano H, Koutouratsas N, Stouffer HM. 23. Pearl M, Lilienfeld PM. The post-shock nephrogram. J
Mechanism of the nephrographic effect during urinary Urol 1974; 111:391-393.
stasis. Acta Radiologica Diagnosis 1966; 4:14-20. 24. Pope TL, Buschi AJ. Moore TS, Williamson BRJ, Brenbridge
7, Cattell WR, Sensi M, Ackrill P. Fry 1K. The functional basis ANAG. CT features of renal polyarteritis nodosa. MR
for nephrographic pafferns in acute tubular necrosis. 1981; 136:986-987.
Invest Radial 1980; 15(#{243}):S79-S83. 25. Raghavaiah NV. Segmental nephrogram. J Urol 1978;
8. Coel MN, Tamer LB. Obstructive nephrogram due to 119:278-279.
renal vein thrombosis. Radiology 1971; 101:573-574. 26. Rosenberg HK Gefter WB, Lebowitz RL, Mahboubi S.
9, Elkin M. Obstructive uropathy and uremia. Radial Clin N Rosenberg H. Prolonged dense nephrograms in
Amer 1971; 10(3):447-465. battered children. Urology 1983; 21(3):325-329.
10. Frank PH, Nuttall J, Brander WL, Prosser D. The cortical rim 27. Rubin BE, Schllftman R. The striated nephrogram in renal
sign of renal infarction. Br J Radial 1974; 47:875-878. contusion. Urol Radial 1979; 1:119-121.
11. Glazer GM. London SS. CT appearance of global renal 28. Tadavarthy SM. Castaneda W. Amplatz K. Redistribution
infarction. J Camput Assist Tamogr 1981; 5(#{243}):847-850. of renal blood flow caused by contrast media.
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of acute inflammatory disease of the renal interstitium. 29. Trueta J, Barclay AE, Daniel PM, Franklin KJ, Pritchard
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Figure #{243}B
previously appeared in MR 1981; 13#{243}:986-987.

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