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Correspondence to
Dilini Peiris, Department
of Chemical Pathology,
Basingstoke and North
Hampshire Hospital, Hampshire
Hospitals Foundation Trust,
Hampshire RG24 9NA, UK;
dilini.peiris@hotmail.co.uk
Received 29 June 2016
Revised 1 October 2016
Accepted 7 November 2016
Published Online First
5 December 2016
To cite: Peiris D. J Clin Pathol
2017;70:277–281.
A historical perspective on crush syndrome: the
clinical application of its pathogenesis, established
by the study of wartime crush injuries
Dilini Peiris
ABSTRACT
Crush syndrome is a fine example of how pathology can
play a direct role in revealing the best treatment and
management for diseases. It can occur when crush
injuries are sustained. Skeletal muscle becomes damaged
under the weight of a heavy object, and victims
experience severe shock and renal failure. The discovery
of the pathology of crush syndrome belongs to two
individuals: Seigo Minami and Eric Bywaters. They
separately helped to define the pathogenesis of crush
syndrome during World Wars I and II. Seigo Minami is
believed to have been the first to record the
pathogenesis of crush syndrome. In 1923, he described
the cases of three soldiers who died of renal failure
caused by crush injury during World War I. Using
microscopic studies to investigate the pathology of their
kidneys, he found the soldiers had died due to
‘autointoxication’ caused by rhabdomyolysis. This
discovery was not known to Eric Bywaters, who
described crush syndrome in 1941, having studied
victims of the London Blitz during World War II. He
defined the ‘autointoxication’ as the release of
rhabdomyolysis products via reperfusion. He therefore
established the need for emergency fluid replacement to
treat crush syndrome. The findings made by Minami and
Bywaters highlight a remarkable achievement in clinical
pathology, despite the adversity of war. It is these
findings on which current guidelines are based. By
reviewing their work, it is hoped that the role of
pathology can be better appreciated as a valuable
resource for delineating the treatment and management
of diseases.
INTRODUCTION
Crush syndrome is a medical condition that can be
caused by a ‘crush injury’,1 whereby skeletal muscle
becomes damaged under the weight of a heavy
object. It can be described as a reperfusion injury
caused by traumatic rhabdomyolysis. Victims
experience severe shock and renal failure, and
require emergency fluid replacement at the scene.
Such types of injury are a common occurrence in
traumatic events both natural and man-made.
These can range from earthquakes and hurricanes
to traffic collisions, house fires and inevitably,
wartime conflict. It is the latter that is the focus of
this review. As can be seen in figure 1, the destruc-
tion from bombing could cause individuals to be
buried under debris for several hours, while the
rescue effort would search for victims. It was these
situations that enabled the discovery of the patho-
genesis of crush syndrome.
Peiris D. J Clin Pathol 2017;70:277–281. doi:10.1136/jclinpath-2016-203984
Review
This discovery belongs to two individuals: Seigo
Minami and Eric Bywaters. Both individuals separ-
ately helped to define the pathogenesis of crush
syndrome during World Wars I and II in landmark
papers.
A BRIEF HISTORY OF THE DISCOVERY OF
CRUSH SYNDROME
Traditionally, the discovery of crush syndrome is
attributed to Bywaters, and is therefore also sometimes
referred to as Bywaters’ syndrome. However, there is
contention within the literature as to who was the first
to describe the syndrome. Bisaccia et al2 very recently
made a case for Antonino D’Antona, professor of
surgery and director of the division of surgery at the
University of Naples. Bisaccia has argued that
D’Antona produced the first medical reports during
the Messina-Reggio Calabria earthquake (1908). She
reports that D’Antona observed victims with circula-
tory shock who died as a result of uraemia, thus
linking crush syndrome to renal failure. However, it is
important to note that D’Antona did not provide
histological material, unlike Bywaters and Minami.
In actuality, after Bywaters’ landmark paper
regarding crush syndrome1 was published,
Bywaters found several accounts of crush syn-
drome, which had been previously described in
German literature. He found these having been in
disbelief about the fact that no one had reported
this syndrome before. He diligently reported these
findings in his letter to the British Medical Journal
in 19413 as reviewed by Almond.4 In this letter, he
credits six main individuals for what should have
been a collaborative discovery of crush syndrome:
1. F. Colmers
Colmers attended casualties of the
Messina-Reggio Calabria earthquake in Italy
(1908). He described 19 cases of patients who
appeared to have suffered from acute pressure
necrosis, 14 days after the events had occurred,
as the German expedition was unable to arrive
before then. In addition, he described one case
who had presented with haematuria and
oliguria.
2. L. Frankenthal
Frankenthal, who had volunteered as an army
surgeon during World War I,4 described three
soldiers who had been buried in 1916 during
World War I. Each presented with oedema,
haematuria and ischaemic muscle necrosis on
postmortem analysis.
3. A. Hackradt
Hackradt was a pathologist in Max Borst’s
laboratory, which incidentally had organised the
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Review
Figure 1 Bomb damage in London, England during World War II
(1944). Relief effort carried out by Civil Defence rescue workers. They
searched for victims who may have been buried under the debris
caused by a Flying Bomb—V1 attack. It was in such situations that
cases of crush syndrome often occurred. Image courtesy by Ministry of
Information Photo Division Photographer (Public domain), via
Wikimedia Commons.
war pathology service for Germany.4 In 1917, he described
tissue from a soldier who had been buried for 9 hours. This
victim presented with oedema of the leg, blisters and haema-
turia, with albumin and casts also present in the urine
passed. On postmortem analysis, kidney muscle necrosis and
tubular degeneration with blood casts was found.
4. A. Lewin
Lewin was a student under the German pathologist,
Professor Ludwig Pick. He had briefly described three cases
of crush syndrome in 1919, although these descriptions
were incomplete and unavailable to the public, and only
described the histopathology. Ludwig Pick, with his group,
which included Seigo Minami, made great contributions to
academic pathology and histological techniques. He there-
fore enabled the pathogenesis of crush syndrome to be
described fully by Minami with his tutelage.
5. K. Bredauer
Bredauer was a pathologist in Max Borst’s laboratory, who
described three further cases of crush syndrome in 1920.
6. S. Minami
Minami, who was an investigator in Professor Ludwig Pick’s
laboratory, summarised and compiled the literature from the
Table 1 Summary of crush syndrome cases studied by Seigo
Minami
Case Summary
1 A corporal of a Field Artillery Regiment, trapped for 13 hours
2 A corporal of a Field Artillery Regiment, trapped in a tunnel after a shell
explosion for an unknown duration
3 A sergeant, aged 36, who had been trapped in the same tunnel as case
2 after a shell explosion for an unknown duration
278
above individuals, and more completely investigated Lewin’s
three cases. Therefore, Bywaters primarily gave credit to
Minami in his letter, as he recognised that Minami had
made the work from the above individuals more accessible,
given that their material was previously inaccessible or only
presented in inaugural dissertations at the time.
In his letter, Bywaters explains the fact that crush syndrome
and its links with impaired renal function were well recognised
by German pathologists and clinicians so much so, that it had
been described in six textbooks of war surgery in Germany.
However, this had not been communicated to Great Britain or
the USA at the time.
Bywaters proposed several reasons for this gap in their
medical knowledge. First, he reasoned that war for Great
Britain involved fighting on foreign soil, which meant that the
wounded British would not be treated at their own hospitals.
However, an efficient pathology service had to be set up in
France. This was in contrast to the Germans, who were fighting
on their own borders and therefore had access to their own hos-
pital systems in areas of German occupation. Second, he com-
mented on differing scientific practices between Great Britain
and Germany. He pointed to how the Germans were well
versed in the practice of necropsy, which he encouraged to be
carried out on air-raid victims when possible.3 Bywaters recog-
nised the impact of war on scientific research, and emphasised
the importance of scientific communication between several dis-
ciplines for the progression of medicine. He mused that to
ignore German medicine because of the conflict would leave the
Allied countries at a loss, regardless of the decline in its
standard.
Despite Bywaters’ letter of his regret about not having found
the German literature before his landmark paper was published,
it is important to note that the individuals he mentioned
described symptoms related to crush syndrome previous to
1923. It was in fact Seigo Minami and Eric Bywaters who were
undeniably the first to articulate the pathogenesis of crush syn-
drome in relation to impaired renal function, and to communi-
cate this to the wider scientific community.
SEIGO MINAMI (1893–1975)
Seigo Minami was a Japanese dermatologist, who was the first
individual to officially establish the pathogenesis of crush syn-
drome in 1923, and make his findings available to the public,
when he was an investigator under the supervision of the
German pathologist, Professor Ludwig Pick. He described the
histopathology of the kidneys of three German soldiers who
died of traumatic injuries during World War I (table 1) in his
landmark paper ‘Renal Changes After Burial’ (Über Nieren
Veränderung nach Verschüttung)’.5 Despite the fact that the spe-
cimens Minami examined were from World War I, his findings
were actually made after the war had ended.
Case 1: A corporal of a Field Artillery Regiment, trapped for
13 hours
The patient presented with a traumatic injury to his left thigh.
The production of very cloudy urine was observed, and the
patient died just 7 days after hospital admission.
Case 2: A corporal of a Field Artillery Regiment, trapped in
a tunnel after a shell explosion for an unknown duration
The patient presented with a traumatic injury to his left thigh.
Haematuria and oliguria were observed by the fourth day after
hospital admission. Before death, red cells and hyaline casts
could be observed in the urine. The patient died on the sixth
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day after admission. Postmortem analysis showed grey muscle
necrosis and oedema of the lungs. Degeneration of the convo-
luted tubules was observed in the kidney, in addition to pigment
masses in the collecting tubules and in the Loops of Henle.
Review
Minami’s. It highlights the value of the discipline of histopath-
ology in deducing the pathogenesis of crush injury. When
Bywaters eventually found Minami’s work, it provided solid evi-
dence to corroborate Bywaters’ theories on crush injury and
renal failure.

Case 3: A sergeant, aged 36, who had been trapped in the

same tunnel as case 2 after a shell explosion, for an
unknown duration
The patient was admitted with swelling of the upper body. He
was producing very dark urine, and developing oliguria. The
patient died on the seventh day after admission.
Having carried out thorough microscopic studies to investi-
gate the histopathology of their kidneys, Minami theorised that
all three soldiers had died due to renal failure caused by a
physiological event that he defined as ‘autointoxication’. He
described this ‘autointoxication’ as the accumulation of toxic
protein degradation products in the blood, from rhabdomyolysis
(figure 2). He believed that it was these products that were
responsible for the diffuse damage of the renal parenchyma and
the nephrosis that he observed in the kidney sections of the sol-
diers. Minami proposed that the protein degradation products
were toxic in that they caused the release of histamine, which
would activate a number of pathways to induce lethal shock and
renal failure.
Detailed images of these histopathological sections can be
viewed in his paper.5 Therein Minami described how the kidney
sections reflected the serious affliction of the kidneys by the
presence of large masses of brown pigment and pigmented casts
which he predicted to be the products of ‘autointoxication’. He
noted the stark change in colour of muscle tissue sections when
normal and crush injury tissue were compared, as is represented
in figure 2. Importantly, he also confirmed that the pathology
observed was consistent with the clinical pictures reported for
the patients in all three of the cases he investigated.
To have theorised this concept without having been able to
monitor the actual victims was a remarkable accomplishment of
ERIC BYWATERS (1910–2003)
Eric Bywaters was a British physician who was the first to
describe ‘crush syndrome’ in 1941, in his landmark paper,
‘Crush injuries with an impairment of renal function’.1 In this
paper, Bywaters describes the cases of four victims of the London
Blitz during World War II (table 2). Figure 3 shows the way in
which victims would have been under debris caused by continu-
ous air raids during the war. All four patients were monitored
carefully from hospital admission to death.
Case 1: A female aged 17 years who was buried under
heavy masonry across the left leg for 9 hours
The patient was admitted with a traumatic injury to the left leg.
Fluid replacement was repeatedly administered to restore blood
pressure and urine flow, and to reduce oedema. Blood and urine
biochemistry was routinely monitored, but as the patient pro-
gressively worsened, the leg was amputated. Postoperation,
albumin was observed in the urine, as well as hyaline, granular
and red cell casts. Oliguria was noted, and while fluid replace-
ment momentarily restored urine flow, the patient’s blood pres-
sure suddenly collapsed, and she died 8 days after admission.
Case 2: A female aged 45 years who was crushed under a
building for 6 hours, with lacerations on both legs
The patient was admitted with a traumatic injury to both legs.
Raised haemoglobin levels were observed. Fluid replacement
was repeatedly administered to restore blood pressure, but this
was lost after a blood transfusion was given. Dark and turbid
urine was collected, which on analysis contained albumin and
both red cell and hyaline casts. Fluid replacement was repeatedly

Figure 2 The pathogenesis of crush syndrome. As summarised by Bywaters, crush injury victims suffer irreversible ischaemic muscle necrosis which
to a degree can be affected by temperature (the lower the temperature, the longer the ischaemic survival time). On extrication of the victim,
damaged muscle primarily absorbs sodium chloride from the returning blood (reperfusion). The muscle becomes swollen as a result, and
rhabdomyolysis occurs, leading to the release of degradation products into the circulation. Potassium disrupts cardiac rhythm and hypocalcaemia
can occur when calcium is later absorbed. The key component, myoglobin, is filtered at the glomerulus and acidic urine is produced. It is
precipitated in the distal convoluted tubules of the kidney, causing impaired reabsorption, and increasing intrarenal pressure, thus causing acute
kidney necrosis.

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Review
Table 2 Summary of crush syndrome cases studied by Eric
Bywaters
Case Summary
1 A female aged 17 years who was buried under heavy masonry across the
left leg for 9 hours
2 A female aged 45 years who was crushed under a building for 6 hours,
with lacerations on both legs
3 A male aged 34 years who was trapped under beams across his
shoulders, arms and thighs for 12 hours
4 A male aged 16 years who was buried under a collapsed house for
8 hours, with his left thigh crushed under masonry
administered to restore blood pressure, but this was lost after
a blood transfusion was given. The patient died just 6 days after
admission.
Case 3: A male aged 34 years who was trapped under
beams across his shoulders, arms and thighs for 12 hours
The patient was admitted with a traumatic injury to both his
arms and thighs. Albumin was identified in urine and anuria was
developing. A fasciotomy was performed, on the sixth day after
admission, blood pressure suddenly collapsed, and the patient
died the following day.
Case 4: A male aged 16 years who was buried under a
collapsed house for 8 hours, with his left thigh crushed
under masonry
The patient was admitted with a traumatic injury to the left
thigh. Fluid replacement was repeatedly administered, but there
was no improvement, even after a fasciotomy was performed,
and the patient died.
Figure 3 Civil Defence Training in Fulham, London (1942). Civil
Defence rescue workers practise the rescue of a woman trapped under
typical debris, including bricks, timber and wire for the purpose of
training. Image courtesy by Ministry of Information Photo Division
Photographer (Public domain), via Wikimedia Commons.
280
In all four cases, Bywaters observed a general pattern for the
course of crush syndrome pathophysiology through clinical, bio-
chemical and histopathological means:
1. Patient is buried for several hours with pressure on a limb.
2. Affected limb visibly swells.
3. Haemoglobin levels are raised.
4. Patient displays clinical signs of shock (blood pressure falls,
but can be restored by transfusions of serum, plasma and
blood).
5. Signs of renal damage are evident even postamputation.
6. Oliguria and dark urine containing albumin and myoglobin
is observed.
7. Patient exhibits thirstiness and vomiting.
8. Blood pressure remains slightly raised.
9. Blood urea and potassium become raised.
10. Sudden death of patient which occurs, often within a week
of admission, due to uraemia.
Autopsy analysis of the kidney lesions from crush injury
victims provided solid evidence of muscle necrosis, renal tubular
degenerative damage and the presence of a ‘brown pigment’.
This pigment was consistent with what Minami described,
which Bywaters later identified as ‘myohaemoglobin’ (myoglo-
bin). Myoglobin is found in myocytes, therefore, this would
have indicated the necrosis of muscle.6 These histopathological
investigations, together with the biochemical findings made for
each patient, elucidated the pathogenesis of this condition, for
which Bywaters and Beall coined the term ‘crush syndrome’.
In pursuing investigations into why myoglobin could be iden-
tified in kidney sections from crush injury victims, Bywaters
unknowingly defined the ‘autointoxication’ identified by
Minami as the release of chemical products of rhabdomyolysis
via reperfusion. Through blood and urine biochemistry analysis
he determined that myoglobin, lactic acid, creatine, creatine
kinase, phosphate, potassium and casts were the main culprits.
He proposed that the consequential damage caused to the
kidneys severely suppressed urine flow, thus increasing the tox-
icity of the blood, and further damaging the kidneys.
Bywaters hypothesised that myoglobin was implicit in his pro-
posal for the pathogenesis of crush syndrome. However, it was
unclear whether myoglobin was pathogenic by precipitating into
acidic urine as casts, or due to the kidney damage itself. To
determine the mechanism, Bywaters and Stead7 carried out a
series of experiments using rabbits. While a state of ‘circulatory
shock’ and ischaemic muscle necrosis could be induced in these
animals by compressing the leg muscles for a period of 4–
6 hours using rubber tubing, two effects of crush syndrome in
humans were not observed: myoglobin was not excreted by the
rabbits, and the kidneys of rabbits did not appear as severely
damaged. Bywaters reasoned that the lack of similarity may have
been due to the fact that rabbit muscle may not contain myoglo-
bin. To address this, Bywaters and Stead injected rabbits with
solutions of human myoglobin, in doses equivalent to those
measured in crush syndrome victims. Myoglobin was measured
by estimation; the alkaline haematin of myoglobin as ‘mg.
haemoglobin’ was compared with alkaline haematin from pre-
pared haemoglobin. They found that they could induce renal
damage this way, and that if the urine was acidic, this damage
would be more severe. Placing these studies in the context of
human crush syndrome victims, Bywaters reasoned that any
myoglobin that is excreted with acidic urine may have a role in
the pathogenesis of renal failure observed.
It was this discovery that enabled Bywaters to establish the
need for emergency fluid replacement to treat crush syndrome.
In his landmark paper, he described the use of recalcified
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plasma-saline (serum) followed by 5% glucose-saline.1 He con-
firmed that the management of crush syndrome should consist
of repeated rehydration, in addition to the alkalisation of urine
using fluids containing sodium bicarbonate. Bicarbonate could
decrease metabolic acidosis and decrease the precipitation of
myoglobin in the renal tubules, thus reducing the risk of renal
failure.8 He determined this in his investigations with Stead7
and from previous biochemical analyses of urine from affected
patients. He observed a dark and cloudy urine in patients, with
deposits of brown pigmented casts. In addition, he determined
that the urine was acidic and elicited a positive benzidine reac-
tion, indicating the presence of blood. Further analysis of urine
from seven patients suffering from crush syndrome using spec-
troscopy enabled Bywaters to identify the presence of myoglo-
bin. He confirmed this by ultrafiltration and ultracentrifuging.9
Importantly, when London was bombed again towards the
end of World War II, Bywaters estimated that as a result of the
research into the pathology of crush syndrome, and the applica-
tion of his findings in fluid replacement therapy, 95 of 186
patients with muscle crush syndrome were prevented from
developing acute renal failure.10
When Bywaters reviewed Minami’s paper, he identified that
Minami’s case 2 in particular was extremely similar to cases he
had described in his landmark paper. Therefore, Minami’s work
holds great significance in that it was vital for corroborating
Bywaters’ findings. Minami’s work was important to Bywaters
because it provided evidence of the same medical condition
being seen previously in World War I, in a different region. The
same conclusions had been drawn, in an independent study,
albeit by slightly different pathological means.
CRUSH SYNDROME TODAY
The findings of both Minami and Bywaters have been crucial in
informing current medical practice for the treatment and man-
agement of crush syndrome. With regard to the pathogenesis of
crush syndrome, they determined that victims had died of irre-
versible ischaemic muscle necrosis, as shown in figure 2. They
understood that extricating entrapped victims without immediate
treatment caused the return of circulation to the necrotic muscle.
Both individuals identified the pathogenesis of a very distinct
type of acute kidney injury (AKI), which requires specific and
rapid treatment, which could not have been determined without
extensive study into the mechanisms of the pathogenesis of
crush syndrome. While Minami examined posthumous kidney
tissue, Bywaters had the opportunity to monitor victims as they
were admitted. Given the fact that all four cases in his landmark
paper did not survive, he was able to determine that the renal
damage cause by crush injury in these patients was acute, and
that there was a narrow window for survival, so much so that
vigorous fluid replacement needed to be delivered to the patient
at the site of burial if there was to be a chance of survival.
The current consensus for the treatment and management of
crush syndrome is summarised by Sever and Vanholder,11 and
reflects Bywater’s suggestions. Sever and Vanholder have out-
lined that with regard to treatment, isotonic saline should be
administered given its effectiveness in volume replacement and
preventing AKI. In addition, sodium bicarbonate solutions com-
bined with half-isotonic saline can prevent the deposition of
rhabdomyolysis products such as myoglobin and uric acid. It is
recommended that fluid replacement should be started as soon
as possible, preferably during extrication if feasible. The initial
fluid replacement rate should be 1000 mL/hour, which should
be reduced by at least 50% after 2 hours. However, it is empha-
sised that this is not to be adopted as a uniform strategy, but
Peiris D. J Clin Pathol 2017;70:277–281. doi:10.1136/jclinpath-2016-203984
Review
rather that the patient’s individual circumstances should be con-
sidered, such as volume status and urine flow.
Despite the existence of this consensus, lack of knowledge
about this syndrome, in addition to the fact that crush injury
usually occurs in chaotic and traumatic situations, can hinder the
treatment of such victims. It is for this reason that the
International Society of Nephrology founded the Renal Disaster
Relief Task Force in 1989, initially as a relief effort for the
Armenian earthquake (1988). Lameire12 discusses the fact that this
body, which works closely with Médecins Sans Frontières (doctors
without borders), was set up on the basis of discoveries by Minami
and Bywater, and the research for the treatment and management
of crush syndrome that has been carried out since then.
Lameire12 describes how in comparison to the London Blitz
of 1940–1941, when crush syndrome was almost certainly fatal,
by 1999, the mortality rate for crush syndrome was reduced to
only 20%. This statistic on the mortality rate of crush syndrome
capitulates the significance of contributions by Minami and
Bywaters to our current knowledge of crush syndrome. It would
certainly be of interest to determine the current mortality rate
of crush syndrome globally; no doubt it will have decreased sig-
nificantly further from 1999.
CONCLUSIONS
The findings made by Minami and Bywaters highlight a remark-
able achievement in clinical pathology despite the adversity of
war. It is these findings on which current guidelines for the
treatment of crush syndrome are based, including the use of
fluid replacement and the treatment of this unique version of
AKI fuelled by rhabdomyolysis. This historical success therefore
highlights the significant role pathology can play in determining
the pathogenesis of a disease.
On reflection of the patch-worked nature of the discovery of
crush syndrome, it is important to note the importance of com-
munication and collaboration in pathology, as was discussed by
Bywaters after his discovery of Minami’s landmark paper.
The case of crush syndrome remains a clear example of how
pathology informs medical practice, and an inspiration for what
can be achieved by today’s pathologists when multiple disci-
plines of pathology are used for a common goal.
Handling editor Tahir Pillay
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
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A historical perspective on crush syndrome:

the clinical application of its pathogenesis,
established by the study of wartime crush
injuries
Dilini Peiris

J Clin Pathol2017 70: 277-281 originally published online December 5,

2016
doi: 10.1136/jclinpath-2016-203984

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