From quail to earthquakes and human conflict: a historical perspective of rhabdomyolysis

Abstract

Rhabdomyolysis is a common cause of acute kidney injury, featuring muscle pain, weakness and dark urine and concurrent laboratory evidence of elevated muscle enzymes and myoglobinuria. Rhabdomyolysis is often seen in elderly and frail patients following prolonged immobilization, for example after a fall, but a variety of other causes are also well-described. What is unknown to most physicians dealing with such patients is the fascinating history of rhabdomyolysis. Cases of probable rhabdomyolysis have been reported since biblical times and during antiquity, often in the context of poisoning. Equally interesting is the link between rhabdomyolysis and armed conflict during the 20th century. Salient discoveries regarding the pathophysiology, diagnosis and treatment were made during the two world wars and in their aftermath. ‘Haff disease’, a form of rhabdomyolysis first described in 1920, has fascinated scientists and physicians alike, but the marine toxin causing it remains enigmatic even today. As a specialty, we have also learned a lot about the disease from 20th-century earthquakes, and networks of international help and cooperation have emerged. Finally, rhabdomyolysis has been described as a sequel to torture and similar forms of violence. Clinicians should be aware that rhabdomyolysis and the development of renal medicine are deeply intertwined with human history.

INTRODUCTION

The term rhabdomyolysis derives from the Greek words ῥάβδος (rhabdos, rod), μῦς (mus, muscle) and λύσις (lusis, loosening), and describes a syndrome with disintegration of striated muscle and release of muscular cell constituents into the circulation [1]. Most cases are caused by trauma, prolonged immobilization or extreme physical exertion [2]. Recreational drugs, medication and genetic myopathies are less commonly implicated [3] (Table 1). Acute kidney injury (AKI) is one of the most severe complications of rhabdomyolysis. AKI in rhabdomyolysis often leads to rapid release of potassium and phosphate from muscle, leading to a need for higher doses of renal replacement therapy (RRT) than is required for other forms of AKI. The diagnosis is often straightforward, usually when there is an obvious cause such as prolonged immobilization or trauma. However, late diagnosis occurs even in contemporary clinical practice often in conjunction with one of the rarer causes (Table 1). Common and unusual causes of rhabdomyolysis are well known to nephrologists and to renal faculty, and are also regularly taught during ward rounds and in case presentations. What is much less known even among seasoned renal educators is the fascinating and thought-provoking history of rhabdomyolysis from biblical times to the late 20th century. This is also underscored by the fact that a PubMed search for ‘Rhabdomyolysis’ in the title and ‘historical article’ as publication type currently yields only four articles. None of them is published in a journal within our own specialty. Here, we provide a brief review of the history of rhabdomyolysis for the clinical nephrologist and for use during teaching. We describe interesting causes of rhabdomyolysis throughout human history, highlight ethical dilemmas and describe how historical events helped our specialty diagnose, understand and treat AKI caused by rhabdomyolysis.

Table 1.

Causes of rhabdomyolysis

Category	Examples
Abnormal body temperature and related syndromes	Heatstroke
	Hypothermia
	Malignant hyperthermia
	Neuroleptic malignant syndrome [4]
Drugs [5]	Antimalarials
	Baclofen withdrawal (abrupt) [6]
	Colchicine
	Corticosteroids
	Cyclosporine
	Fluconazole
	Neuromuscular blocking agents
	Statins and fibrates
Electrolyte abnormalities	Hypophosphatemia (particularly in conjunction with alcohol) [7], hypokalaemia, hypocalcaemia, hyponatraemia, hypernatraemia
	Diabetic ketoacidosis [8]
Endocrine disorders [9]	Hypothyroidism
	Non-ketotic hyperosmolar syndrome
	Thyrotoxicosis
Exertion [10]	Long-distance running
	Physical overexertion in sickle cell disease
Genetic syndromes (metabolic myopathies) [11, 12]	Carnitine deficiency
	Creatinine palmitoyltransferase deficiency
	McArdle disease (myophosphorylase deficiency), mitochondrial respiratory chain deficiencies, phosphofructokinase deficiency
Immune-mediated myopathies [13, 14]	Dermatomyositis
	Polymyositis
Infections	Bacteria [15]: Streptococcus, Salmonella, Legionella, Staphylococcus, Listeria, Tetanus
	Viruses: Influenza, Adenovirus, Coxsackie, Herpes Cytomegalovirus, Epstein-Barr virus, Human Immunodeficiency Virus
	Malaria [16]
Miscellaneous	Alcoholism
	Cardioversion
	Sepsis
	Unexplained rhabdomyolysis in migrants [17, 18]
Physical violence	Beating, torture, child abuse
Recreational drugs [19, 20]	Amphetamine, Cocaine, Ecstasy, LSD
Toxins [3, 21]	Snake and insect bite
	Mushrooms
	Haff disease
	Hemlock (coturnism)
	Carbon monoxide
Trauma and compression	Burns
	Crush injuries and Immobilization
	Ischaemic limb injury and vascular surgery [22]
	High-voltage electrical injury

Adapted from Vanholder et al. [1].

CAUSES OF RHABDOMYOLYSIS SINCE ANTIQUITY: QUAIL AND HEMLOCK

The first (albeit vague) mention of possible rhabdomyolysis is often credited to the Bible. In numbers 11:31, the Israelites are hungry and god sends quail (Coturnix coturnix; Figure 1), which the people collect and eat with considerable greed:

FIGURE 1.

Coturnix coturnix (common quail). Image in the public domain via Royal Society of the Protection of Birds at https://www.rspb.org.uk/birds-and-wildlife/wildlife-guides/bird-a-z/quail/ (4 March 2020, date last accessed).

A wind sent by the Lord came up and blew quail in from the sea; it dropped them all around the camp … The people were up all that day and night and all the next day gathering the quail … and they spread them out all around the camp. While the meat was still between their teeth, before it was chewed, the Lord’s anger burned against the people, and the Lord struck them with a very severe plague. [23]

Quail poisoning (coturnism) is a well-described cause of rhabdomyolysis [24], although perhaps most nephrologists will be unaware of the link. Toxins ingested with contaminated quail meat are believed to be the cause [25]. Whether the toxins are from hemlock or other plants such as henbane (Hyoscyamus niger) or red hemp nettle (Galeopsis ladanum) [26] is not entirely clear [27]. Coturnism is well described in antiquity [27] and has been reported from around the Mediterranean throughout the 20th century, usually in fall when the bird migrates in large numbers [24]. Rhabdomyolysis is a key feature of coturnism [24] and some authors have suggested a genetic background that confers vulnerability to the toxin [28]. Much of our knowledge stems from the detailed description of the condition by Edmond Sergent in the 1940s [29, 30]. Sergent, who at the time worked as director of the Morocco Institut Pasteur in Casablanca, described the case of an Algerian hunter who had previously eaten quail without incident but then developed severe symptoms after another meal involving quail [30]. Others have suggested that Sergent viewed the biblical quail incident as one of transcendent mystery and they note that some questions around coturnism remain unresolved to the present day [30].

A similar condition has been reported from Italy following consumption of skylarks, chaffinches and robins that have ingested plants from the hemlock family in spring [31]. Of note, the birds themselves are not susceptible to the active alkaloids and they are heat stable. Other biblical accounts of poisoning have been linked to hemlock as well. Davies and Davies speculated whether the sudden and otherwise unexpected death of two healthy young priests could be explained by their having inhaled incense contaminated with hemlock [32]. The use of plants from the hemlock family as a poison goes far back in time. As a medicine, hemlock has multiple properties and was used since antiquity well into the 18th century for a variety of conditions including cancer [33] and whooping cough [34]. The idea that ‘hemlock’ (Greek ‘koneion’) was the poison used in the suicide of Socrates is well known, although it has been attacked on linguistic as well as on medical grounds [35]. In Plato’s account of events, Socrates’ muscles are described as cold and stiff but clear evidence of rhabdomyolysis is lacking [35].

In trying to link muscular toxicity to hemlock, it is important to appreciate that hemlock species are a member of the order Umbelliferae, which also includes many edible plants such as carrot, fennel and parsnip. There is often confusion between water hemlock species (Cicuta and Oenanthe) and poison hemlock (Conium maculatum) [36]. Many contemporary incidents of accidental poisoning relate to the former, whereas the latter is implicated in intentional poisoning and Socrates’ suicide. Many symptoms overlap but differentiation between the two is important. Cicuta spp. (Figure 2) feature as their principal toxins cicutoxin and oenanthotoxin, which act as (non-competitive) γ-aminobutyric acid antagonists in the central nervous system, resulting in seizures [36]. In contrast, C. maculatum results in respiratory paralysis, secondary to muscle weakness [36] and rhabdomyolysis attributed to its main alkaloid coniine. Accidental hemlock poisoning is still seen today [38], often as a result of ‘foraging’ [39]. Rhabdomyolysis is described in conjunction with both water [36] and poison [40] hemlock and occurs due to seizure-induced muscle injury or as a result of direct myotoxicity. Roots of water hemlock are ingested by mistake for their sweet taste, which has been described as pleasant and similar to wild parsnip or wild carrot.

FIGURE 2.

Spotted water hemlock (Cicuta maculata), from Clark and Fletcher [37] (image in the public domain).

NINETEENTH TO EARLY 20TH CENTURY: RHABDOMYOLYSIS DURING MILITARY CONFLICT

To the best of our knowledge, the first description of rhabdomyolysis in war dates back to 1812 when Larrey, the great military surgeon of the Napoleonic army, described muscle necrosis in carbon monoxide poisoning during the occupation of Berlin [41]. Carbon monoxide remains a well-described cause of rhabdomyolysis to the present day [42]. It is often German surgeon Ludwig Frankenthal (1885–1944) who is credited with the first report of traumatic rhabdomyolysis and AKI caused by war injuries, but this occurred almost a century later than Lerry's account, in 1916 [43]. A few years later, Minami, a Japanese dermatologist who studied in Germany, under the supervision of the German pathologist, Professor Ludwig Pick, described the kidneys of three German soldiers who died of traumatic injuries during World War I and suspected muscle damage as a likely culprit of the ensuing renal failure [44]. Minami’s report is notable not only for its beautiful illustrations of the histopathology but also for the clarity of its style and language. In his conclusion Minami states

… This is caused by the acute breakdown of muscular protein where multiple necrosis has occurred, which is seen in all cases of this group. [44] (Authors’ translation).

Despite such detailed reports of crush syndrome and its complications and a well-developed concept of pathogenesis in the German literature, the Allies entered World War II more or less oblivious of its existence. It was Eric Bywaters (1910–2003), a Hammersmith hospital rheumatologist [45], who in 1940 rediscovered the syndrome in victims of the London Blitz [46]. Fifty years later Bywaters commented:

History … teaches us that man does not learn from history. … the medical machine in 1939 was not as fully prepared … as it might have been had it consulted its opponent’s publications. [47]

In hindsight, it is quite remarkable that until Bywaters' 1941 publication this potentially lethal entity was largely unknown to the British and American medical literature, including textbooks of military medicine [48]. It is noteworthy that the official German military medical account of World War I described as many as 126 cases with this syndrome [49, 50].

Following their experience at Hammersmith, Bywaters and Beall described four victims of trauma-related crush syndrome (Figure 3) with limb oedema, shock and oliguria with brownish urine. All four patients died in about a week with nitrogen retention and necropsy revealing pigment casts, polymorphonuclear invasion and acute tubular necrosis [46]. Blood transfusion was initially considered as a contributing factor. However, Mayon-White and Solandt, describing a similar patient who had never received blood, refuted this assumption [51]. In 1943, using animal models, Bywaters and Stead identified myoglobin as the offending agent and formulated a treatment plan. Their approach involved vigorous rehydration preferably starting at the site of accident and alkalization of urine with the purpose of decreasing myoglobin precipitation in the renal tubules [52].

FIGURE 3.

Muscle of patient buried for 6 h and surviving 7 1/2 days showing oedema and necrotic lateral muscles of the leg. From Bywaters [47], with permission.

Rhabdomyolysis has remained an important topic in military medicine during more recent armed conflict. In their seminal 1966 paper, Fitts et al. reported a case of a young soldier who was buried under rubble for 20 h during the Vietnam War and sustained crush injury, extensive muscle necrosis and rhabdomyolysis [53]. The case illustrates the advances made since Bywaters’ reports and the patient survived following extensive debridement of necrotic muscle and haemodialysis in several military facilities [53]. The authors emphasize that due to the advent of dialysis more patients with rhabdomyolysis may survive, and also recommend intravenous fluids even before the crushed limbs are released [53]. A lot of experience was also gathered during the Lebanon war in the 1980s [54]. Contemporary guidelines on the management of crush injury on the battlefield emphasize the early use of intravenous fluids [55]. However, even on 20th-century battlefields, rhabdomyolysis is associated with mortality as described in recent studies of the Iraq and Afghanistan wars [56].

UNUSUAL CAUSES OF RHABDOMYOLYSIS IN THE 20TH CENTURY: HAFF-KRANKHEIT, MUSHROOMS AND GENETIC DISORDERS

Another fascinating cause of rhabdomyolysis was first described in the summer and fall of 1924 when physicians near the Prussian city of Königsberg (now Kaliningrad in Russia) described an outbreak of an illness characterized by sudden, severe muscular rigidity and coffee-coloured urine [57]. A witness described the scenery in one of the coastal villages as follows:

It was an unbelievably saddening thing to watch: Strong men being carried from their fishing boats to their homes – completely stiff and utterly helpless. (Authors’ translation) [58]

Later called the Haff disease (from the German word ‘Haff’—shallow lagoon) the syndrome featured rhabdomyolysis in a person who had ingested freshwater fish, such as burbot, crayfish or Atlantic salmon, within 24 h before onset of illness. The fact that the victims were usually fishermen immediately intrigued both public health officials and researchers, and a toxin in the aquatic food chain was suspected more or less immediately. The disease was observed only in summer and fall and only on the coast of this particular part of the Baltic Sea, where it occurred in epidemics, small clusters or sporadically [59, 60]. Several toxins were proposed as possible causes [61]. One hypothesis assumed that arsenic-containing waste derived from the nearby chemical industry led to the formation of arsenic gas just above the water surface, which was then inhaled by the victims during early morning fishing trips [58]. At some stage 600 gas masks were issued to fishermen. Sometime later the ‘gas theory’ was replaced by the ‘eel theory’ but this, too, remained controversial, not least because eel was the main source of income for these fishing communities. Eventually, no further cases were observed although the reasons for its disappearance remained as enigmatic as its actual cause [55]. Haff disease still occurs [61–63], often associated with crayfish, but the exact nature of the toxin in the aquatic food chain remains unknown to the present day [64].

Mushroom poisoning is another cause of rhabdomyolysis that has emerged in the 20th century. A recent classification of mushroom poisoning proposed by White et al. [65] includes two subgroups with muscular toxicity, namely 3A with a rapid onset (caused by Russula spp.) and 3B with a delayed onset (Tricholoma spp.). There are reports of Russula subnigricans causing delayed-onset rhabdomyolysis with AKI in the severely poisoned patient [66]. Tricholoma equestre is known under various names and is consumed throughout the world. Since there are controversial opinions on its edibility and ability to cause rhabdomyolysis [67], a group of French authors investigated the rhabdomyolysis apparently induced in 12 humans by several consecutive meals of T. equestre by administering equivalent doses of extracts of this mushroom to mice. They concluded that a genetic muscular susceptibility was a probable key factor for sometimes severe rhabdomyolysis to develop in individuals after repeated consumption of T. equestre and/or when the amount of mushrooms ingested exceeds a certain threshold and unmasks it [68].

Another interesting cause of rhabdomyolysis also became evident in the late 20th century: genetic disorders. A typical patient develops rhabdomyolysis after moderate exercise in a scenario that one would not normally associate with rhabdomyolysis [69]. A whole host of genetic conditions that predispose to rhabdomyolysis have now been identified, many of which are mitochondrial [70]. A more recent discovery is that mutations in the ryanodine receptor 1 gene predispose to rhabdomyolysis and also, interestingly, to malignant hyperthermia [71]. The diagnosis of an inherited myopathy in a patient with rhabdomyolysis requires a high degree of suspicion and often involves muscle biopsies and tests in specialized centres. Even other forms of rhabdomyolysis may have a more subtle genetic background [70].

SEISMO-NEPHROLOGY: EARTHQUAKES AND OTHER NATURAL DISASTERS

The history of rhabdomyolysis is not limited to war and human conflict; crush injury also takes its toll in peacetime. Natural disasters such as earthquakes, hurricanes, tsunamis and cyclones are now well appreciated as a cause of rhabdomyolysis, and the term 'disaster nephrology' [72] has been coined. In addition, seismo-nephrology [72] relates specifically to earthquake-associated renal injury. Antonino D’Antona [73] and Von Colmers [74] first described muscle destruction in victims of the 1909 Messina earthquake. Much of our current knowledge about crush injury and rhabdomyolysis in this context stems from experience gained during of one of the greatest earthquakes of all time, which occurred in Tangshan, China in 1976 with 242 769 dead and 164 851 injured [75], and a high percentage of victims suffering from some form of crush injury [76]. It has been reported that in the case of a sudden collapse of an eight-story building, 80% of the entrapped victims die instantly from the direct effects of trauma, 10% survive with minor trauma, while 10% are badly injured; of those, 7/10 develop crush syndrome [77]. But it was not before the Armenian earthquake in 1988 (Figure 4)—and an additional 150 000 deaths—that this entity received attention through the establishment of the International Society of Nephrology’s ‘Renal Disaster Relief Task Force’ [79] and recommendations for the management of crush victims in mass disasters.

FIGURE 4.

(A) Makeshift dialysis facility in the All Union Surgical Scientific Centre in Yerevan, Soviet Republic of Armenia, 1988. From Tattersall et al. [78] with permission. (B) Improvised dialysis facility using the NxStage device following the Haiti earthquake. With permission from NxStage, Lawrence, MA, USA.

As a renal community, we have learned a considerable amount about the pathogenesis of AKI and crush syndrome in earthquake victims. Rhabdomyolysis can occur either as a sequel to crush injury from direct trauma or due to the ischaemia reperfusion injury that occurs when there is restoration of blood flow once victims are extracted from the rubble. Both mechanisms can coexist. The crush syndrome is the second most common cause of death in earthquake victims after asphyxia [72]. While rhabdomyolysis is the primary cause of AKI in these patients, there are other possible pre- and post-renal causes such as hypovolaemia from blood loss or dehydration, as well as direct trauma to the kidneys and urinary tract.

Various studies, for example, involving victims of the Bam and Bingöl earthquakes (both in 2003) have noted the beneficial effect of early treatment at the disaster scene with intravenous fluids [80–83]. This helps to reduce the incidence of AKI and ultimately requirement for RRT. This concept had been proposed first in the 1940s and later reiterated following the Vietnam War [55], but the regime for fluid administration has evolved considerably and in parallel to growing experience with rhabdomyolysis overall. A detailed discussion of this topic is beyond the scope of our little article. Suffice to say that some studies advocate a fairly conservative approach (3 L over the first 24 h), whereas others suggest being more aggressive (with upwards of 12 L in the same time period) [81, 82].

Factors that increase the risk of developing AKI and requirement for RRT include increased time under rubble, decreased volume of fluid received and increased value of serum creatinine kinase [83]. However, it is still not easy to predict which patients are more likely to progress to a worse outcome. One small study assessed patients treated with crush syndrome in the Hanshin earthquake in Kobe, January 1996 [82]. It evaluated various laboratory markers such as serum amylase, LDH and AST in these patients. There was a statistically significant difference in the level of amylase between those who survived (lower level) and those who died. The cause for this was not established [82].

Compared with war injuries, earthquakes affect a vast number of victims—often in rural areas—without prepared and efficient pre-hospital and hospital services. As such, optimal managements for these patients are difficult if not impossible to achieve. A key challenge for dialysis units but also for renal teams coming to help from abroad in the aftermath of an earthquake is the disrupted water supply. The fact that it is often impossible for outside teams to appreciate the scale of the disaster, let alone to arrive in time to be of any use, has been highlighted elsewhere [78]. Co-operative work co-ordinated by the international renal societies has been extremely beneficial in several recent earthquakes [79, 84].

RHABDOMYOLYSIS DUE TO TORTURE AND SIMILAR FORMS OF VIOLENCE

One of the saddest aspects of this condition is when it occurs as a sequel to torture [85] or to other forms of violence [86]. The World Medical Association’s Tokyo Declaration of 1975 defines torture as:

The deliberate, systematic or wanton infliction of physical or mental suffering by one or more persons acting alone or on the orders of any authority, to force another person to yield information, to make a confession, or for any other reason. [87]

As of today there is no uniformly accepted definition of torture, and different opinions exist [88]. In general, our knowledge of the medical aspects of torture is rather limited. There are several reasons for this, including the lack of autopsy data following such deaths in captivity, especially in times of socio-political instability [89]. Secondly, medical practitioners often have an understandable feeling of unease and discomfort regarding publishing data derived from treating the victims of human cruelty [85]. It is also important to bear in mind that medical practitioners have had various roles in torture, ranging from complicit witness, to bystander and facilitator, to perpetrator [90]. There is considerable dilemma in publishing reports of torture, although in many cases one has to admire the courage and dedication of the authors [85]. Lameire and Vermeersch have highlighted a number of ethical dilemmas for doctors who look after victims of torture [85]: what if medical practitioners provide care to prisoners, knowing that after treatment they would only be exposed to new abuse? Similarly, what if any attempt at publication would alert authorities and thereby deny future victims medical care?

Viewed against this background, the gruesome evidence linking rhabdomyolysis and torture is quite considerable. Not surprisingly, victims of rhabdomyolysis due to torture and violence are predominantly young males, well active and with good muscular fitness at the time they were detained [89, 91–93]. Some authors have speculated that muscular individuals are more prone to rhabdomyolysis due to the larger quantities of muscle breakdown products released into the bloodstream [94]. According to the cases described in available literature, the most prevalent types of physical torture and violence that victims underwent were brutal beating of the whole body with sticks, rods made of metal and guns, for several days, endless hours of ‘sit-and-stand’ exercise, electric shocks and hanging upside-down with tied legs [89, 92, 93]. Another particular form of torture that causes rhabdomyolysis is reverse hanging in which victim’s wrists are bound behind the back, and the victim is suspended for several hours with overstretching of the muscles and ischaemic necrosis [89].

AKI is common in rhabdomyolysis as a sequel to torture and many patients are oliguric [86, 89, 91, 93, 95]. The presenting clinical, biochemical and radiological features do not differ much from other aetiologies and some patients often lack obvious external evidence of torture and violence [86, 89, 92, 93]. Dehydration [92, 93], hunger strike [96] and the use of straightjackets [97] may also contribute to AKI and rhabdomyolysis. In some cases a combination of rhabdomyolysis and haemolysis could have caused AKI [92]. Haemoglobinuria can occur as a result of mechanical trauma to the red blood cells due to the repetitive physical trauma of microcirculation of the soles during beating in a way that is similar to that seen in March haemoglobinuria [92]. The majority of reported patients required dialysis [91–93] and fatalities are not uncommon with mortality rates ∼15% [86, 91–93]. Some authors have emphasized the importance of early recognition and timely management of potentially reversible condition [92].

Rhabdomyolysis can also occur in victims of domestic or other violence, often children, elderly or individuals with cognitive disabilities [95]. A particular form of violence observed in Southern Africa is beating with the sjambok, a heavy whip made of rhinoceros hide (Figure 5) [86, 91]. The soft tissue injury that ensues is often invisible and the extent of damage is underestimated [86, 91]. Lazarus et al. described rhabdomyolysis due to child abuse [98], and other similar reports do exist [99]. A high degree of suspicion is required in cases of rhabdomyolysis where the cause is not entirely obvious after the initial assessment. Finally, when assessing patients with rhabdomyolysis in conjunction with violent behaviour it is important to bear in mind that drugs may also be involved [100].

FIGURE 5.

A young patient who presented with AKI from rhabdomyolysis following severe traumatic (‘sjambok’) injuries. He recovered fully after receiving dialysis in our ICU. Courtesy of Prof Ikechi Okpechi, Division of Nephrology and Hypertension, University of Cape Town, South Africa.

CONCLUSION

Rhabdomyolysis has been described since antiquity and our understanding of the disease is closely linked to the history of the last 100 years (Figure 6). Nephrologists have learned a great deal about rhabdomyolysis from studying victims of human conflict, particularly since Bywaters described the syndrome during the London Blitz in the 1940s [46]. It is sobering to learn that lessons already learned were often ignored, only to be relearned by a subsequent generation of physicians. Another interesting aspect of this topic is that the cause of one of the most enigmatic causes of rhabdomyolysis, the Haff disease, remains unclear despite the fact that researchers have tried their hardest, with generations of theories being proposed and later discarded. We can, however, take some consolation from the fact that later on in the 20th century we have made great progress in elucidating the genetic basis of some cases of rhabdomyolysis. Another sad and often tragic aspect of the history of rhabdomyolysis is its link to earthquakes. Only a multinational effort supported by international organizations can deal with large numbers of rhabdomyolysis victims requiring RRT in a disaster setting such as the earthquakes in Turkey or Haiti [84]. Much of this knowledge has been acquired the hard way, but we are clearly much better prepared for our encounter with such patients in the setting of catastrophe or conflict. Some of the history of rhabdomyolysis makes for grim and uncomfortable reading, particularly when the disease occurs as a consequence of torture and violence. In this sense, the history of our specialty is very much intertwined with some of the darkest chapters of 20th-century history and with human conflict. However, it is equally linked to great examples of coordinated help and support for victims of natural disasters. We can only hope that future generations will be more aware of the history of rhabdomyolysis, preserve and expand the knowledge gained by their predecessors, and encounter cases more as an intellectual challenge during clinical practice than as a sequel to human violence and conflict.

FIGURE 6.

Time line: history and rhabdomyolysis intertwined from 1900 to present day. Bottom half: events relating to armed conflict and violence. Top half: events not associated with human conflict.

CONFLICT OF INTEREST STATEMENT

None declared.