Eats Beef From the Vietnam War Era and Amphetamine From 1940s

  • Journal List
  • Clin Kidney J
  • five.14(4); 2021 Apr
  • PMC8023192

Clin Kidney J. 2021 Apr; 14(4): 1088–1096.

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

Mirna Aleckovic-Halilovic

1 Department of Nephrology, Dialysis and Transplantation, Academy Hospital Tuzla, Tuzla, Bosnia and Herzegovina

Mirha Pjanic

1 Department of Nephrology, Dialysis and Transplantation, Academy Hospital Tuzla, Tuzla, Bosnia and herzegovina

Enisa Mesic

1 Department of Nephrology, Dialysis and Transplantation, University Infirmary Tuzla, Tuzla, Bosnia and Herzegovina

Joshua Storrar

ii Department of Renal Medicine, Lancashire Education Hospitals NHS Foundation Trust, Preston, UK

Alexander Woywodt

2 Department of Renal Medicine, Lancashire Teaching Hospitals NHS Foundation Trust, Preston, UK

Received 2020 Mar 23; Accustomed 2020 Apr 13.

Abstract

Rhabdomyolysis is a mutual cause of acute kidney injury, featuring muscle pain, weakness and nighttime urine and concurrent laboratory evidence of elevated musculus enzymes and myoglobinuria. Rhabdomyolysis is ofttimes seen in elderly and frail patients following prolonged immobilization, for example subsequently a fall, simply a variety of other causes are likewise well-described. What is unknown to near physicians dealing with such patients is the fascinating history of rhabdomyolysis. Cases of likely rhabdomyolysis accept been reported since biblical times and during antiquity, often in the context of poisoning. Every bit interesting is the link between rhabdomyolysis and armed conflict during the 20th century. Salient discoveries regarding the pathophysiology, diagnosis and treatment were fabricated during the two globe wars and in their backwash. 'Haff disease', a form of rhabdomyolysis offset described in 1920, has fascinated scientists and physicians alike, but the marine toxin causing it remains enigmatic fifty-fifty today. As a specialty, we have also learned a lot virtually the disease from 20th-century earthquakes, and networks of international help and cooperation take emerged. Finally, rhabdomyolysis has been described every bit 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.

Keywords: AKI, beat injury, history, rhabdomyolysis

INTRODUCTION

The term rhabdomyolysis derives from the Greek words ῥάβδος (rhabdos, rod), μῦς (mus, musculus) and λύσις (lusis, loosening), and describes a syndrome with disintegration of striated muscle and release of muscular cell constituents into the circulation [i]. Most cases are caused by trauma, prolonged immobilization or extreme concrete exertion [2]. Recreational drugs, medication and genetic myopathies are less normally implicated [iii] (Table 1). Astute kidney injury (AKI) is one of the almost astringent complications of rhabdomyolysis. AKI in rhabdomyolysis oft 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, belatedly diagnosis occurs even in contemporary clinical exercise often in conjunction with ane 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 likewise underscored by the fact that a PubMed search for 'Rhabdomyolysis' in the title and 'historical article' as publication type currently yields only 4 articles. None of them is published in a periodical within our own specialty. Here, nosotros provide a brief review of the history of rhabdomyolysis for the clinical nephrologist and for use during teaching. Nosotros draw interesting causes of rhabdomyolysis throughout human history, highlight upstanding dilemmas and describe how historical events helped our specialty diagnose, understand and treat AKI acquired by rhabdomyolysis.

Table ane.

Causes of rhabdomyolysis

Category Examples
Abnormal body temperature and related syndromes Heatstroke
Hypothermia
Malignant hyperthermia
Neuroleptic cancerous syndrome [four]
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 [x] Long-altitude running
Physical overexertion in sickle cell disease
Genetic syndromes (metabolic myopathies) [11, 12] Carnitine deficiency
Creatinine palmitoyltransferase deficiency
McArdle illness (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 corruption
Recreational drugs [nineteen, twenty] Amphetamine, Cocaine, Ecstasy, LSD
Toxins [3, 21] Snake and insect bite
Mushrooms
Haff disease
Hemlock (coturnism)
Carbon monoxide
Trauma and pinch Burns
Crush injuries and Immobilization
Ischaemic limb injury and vascular surgery [22]
High-voltage electric injury

CAUSES OF RHABDOMYOLYSIS SINCE ANTIQUITY: QUAIL AND HEMLOCK

The beginning (admitting 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:

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A wind sent by the Lord came up and blew quail in from the body of water; it dropped them all around the camp … The people were upwards all that twenty-four hour period and nighttime and all the side by side day gathering the quail … and they spread them out all around the camp. While the meat was nonetheless betwixt 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 peradventure most nephrologists volition 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 cherry-red hemp nettle (Galeopsis ladanum) [26] is non entirely articulate [27]. Coturnism is well described in artifact [27] and has been reported from effectually the Mediterranean throughout the 20th century, usually in autumn when the bird migrates in big numbers [24]. Rhabdomyolysis is a key feature of coturnism [24] and some authors accept suggested a genetic background that confers vulnerability to the toxin [28]. Much of our knowledge stems from the detailed clarification of the condition by Edmond Sergent in the 1940s [29, thirty]. Sergent, who at the time worked as director of the Morocco Institut Pasteur in Casablanca, described the instance of an Algerian hunter who had previously eaten quail without incident just and so developed astringent symptoms after some other repast involving quail [30]. Others accept suggested that Sergent viewed the biblical quail incident every bit one of transcendent mystery and they note that some questions around coturnism remain unresolved to the present day [30].

A like condition has been reported from Italy following consumption of skylarks, chaffinches and robins that have ingested plants from the hemlock family in jump [31]. Of note, the birds themselves are not susceptible to the agile alkaloids and they are heat stable. Other biblical accounts of poisoning have been linked to hemlock besides. Davies and Davies speculated whether the sudden and otherwise unexpected death of ii salubrious immature priests could be explained past their having inhaled incense contaminated with hemlock [32]. The use of plants from the hemlock family unit as a poison goes far dorsum in time. As a medicine, hemlock has multiple backdrop and was used since artifact well into the 18th century for a variety of weather including cancer [33] and whooping coughing [34]. The idea that 'hemlock' (Greek 'koneion') was the toxicant used in the suicide of Socrates is well known, although it has been attacked on linguistic likewise 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 equally carrot, fennel and parsnip. In that location is ofttimes confusion between water hemlock species (Cicuta and Oenanthe) and toxicant hemlock (Conium maculatum) [36]. Many contemporary incidents of accidental poisoning relate to the sometime, whereas the latter is implicated in intentional poisoning and Socrates' suicide. Many symptoms overlap simply differentiation between the two is important. Cicuta spp. (Effigy two) feature as their master toxins cicutoxin and oenanthotoxin, which human activity as (non-competitive) γ-aminobutyric acid antagonists in the central nervous arrangement, 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 all the same seen today [38], often as a result of 'foraging' [39]. Rhabdomyolysis is described in conjunction with both water [36] and poison [xl] hemlock and occurs due to seizure-induced muscle injury or as a result of directly myotoxicity. Roots of water hemlock are ingested past mistake for their sweet taste, which has been described every bit pleasant and similar to wild parsnip or wild carrot.

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

NINETEENTH TO Early on 20TH CENTURY: RHABDOMYOLYSIS DURING Armed services Conflict

To the best of our cognition, the outset description of rhabdomyolysis in state of war dates back to 1812 when Larrey, the smashing military surgeon of the Napoleonic ground forces, 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 High german surgeon Ludwig Frankenthal (1885–1944) who is credited with the kickoff report of traumatic rhabdomyolysis and AKI caused by war injuries, just this occurred almost a century later than Lerry'due south account, in 1916 [43]. A few years later on, Minami, a Japanese dermatologist who studied in Deutschland, under the supervision of the High german pathologist, Professor Ludwig Choice, described the kidneys of three German soldiers who died of traumatic injuries during Globe War I and suspected muscle harm as a likely culprit of the ensuing renal failure [44]. Minami's study is notable not only for its cute illustrations of the histopathology just as well for the clarity of its way 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 beat syndrome and its complications and a well-developed concept of pathogenesis in the German literature, the Allies entered World State of war II more or less oblivious of its beingness. It was Eric Bywaters (1910–2003), a Hammersmith hospital rheumatologist [45], who in 1940 rediscovered the syndrome in victims of the London Blitz [46]. L years later on Bywaters commented:

History … teaches usa that human being does non learn from history. … the medical machine in 1939 was not as fully prepared … as it might take been had it consulted its opponent's publications. [47]

In retrospect, 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 language military medical account of World War I described as many as 126 cases with this syndrome [49, 50].

Following their feel at Hammersmith, Bywaters and Beall described 4 victims of trauma-related beat out syndrome (Figure 3) with limb oedema, shock and oliguria with chocolate-brown 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 programme. Their arroyo involved vigorous rehydration preferably starting at the site of blow and alkalization of urine with the purpose of decreasing myoglobin precipitation in the renal tubules [52].

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Musculus of patient buried for vi h and surviving seven one/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 disharmonize. In their seminal 1966 newspaper, Fitts et al. reported a case of a young soldier who was buried under rubble for 20 h during the Vietnam War and sustained shell 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 earlier the crushed limbs are released [53]. A lot of experience was as well gathered during the Lebanese republic war in the 1980s [54]. Contemporary guidelines on the management of crush injury on the battlefield emphasize the early utilize of intravenous fluids [55]. However, fifty-fifty 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

Some other fascinating crusade of rhabdomyolysis was first described in the summer and fall of 1924 when physicians near the Prussian city of Königsberg (at present Kaliningrad in Russia) described an outbreak of an disease characterized by sudden, severe muscular rigidity and coffee-coloured urine [57]. A witness described the scenery in i of the coastal villages as follows:

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

Later chosen the Haff disease (from the High german word 'Haff'—shallow lagoon) the syndrome featured rhabdomyolysis in a person who had ingested freshwater fish, such equally burbot, crayfish or Atlantic salmon, inside 24 h earlier onset of illness. The fact that the victims were unremarkably fishermen immediately intrigued both public wellness officials and researchers, and a toxin in the aquatic nutrient chain was suspected more or less immediately. The affliction was observed simply in summer and fall and only on the declension of this particular part of the Baltic Sea, where it occurred in epidemics, small-scale clusters or sporadically [59, lx]. Several toxins were proposed as possible causes [61]. 1 hypothesis assumed that arsenic-containing waste matter derived from the nearby chemical manufacture led to the germination of arsenic gas just above the water surface, which was then inhaled by the victims during early morning line-fishing trips [58]. At some stage 600 gas masks were issued to fishermen. Former later the 'gas theory' was replaced by the 'eel theory' but this, too, remained controversial, not least because eel was the master source of income for these line-fishing communities. Eventually, no further cases were observed although the reasons for its disappearance remained as enigmatic as its actual cause [55]. Haff disease withal occurs [61–63], often associated with crayfish, only the exact nature of the toxin in the aquatic food concatenation remains unknown to the present solar 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 ii 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 nether diverse names and is consumed throughout the earth. 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 past 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 likely key gene for sometimes severe rhabdomyolysis to develop in individuals after repeated consumption of T. equestre and/or when the corporeality of mushrooms ingested exceeds a sure threshold and unmasks it [68].

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

SEISMO-NEPHROLOGY: EARTHQUAKES AND OTHER NATURAL DISASTERS

The history of rhabdomyolysis is not limited to state of war and homo conflict; crush injury also takes its cost in peacetime. Natural disasters such as earthquakes, hurricanes, tsunamis and cyclones are now well appreciated equally a cause of rhabdomyolysis, and the term 'disaster nephrology' [72] has been coined. In improver, seismo-nephrology [72] relates specifically to earthquake-associated renal injury. Antonino D'Antona [73] and Von Colmers [74] get-go described musculus destruction in victims of the 1909 Messina earthquake. Much of our current cognition about crush injury and rhabdomyolysis in this context stems from feel gained during of one of the greatest earthquakes of all time, which occurred in Tangshan, Communist china in 1976 with 242 769 dead and 164 851 injured [75], and a high per centum of victims suffering from some class of crush injury [76]. It has been reported that in the instance suddenly plummet of an eight-story building, 80% of the entrapped victims dice instantly from the straight effects of trauma, 10% survive with minor trauma, while 10% are desperately injured; of those, seven/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 Forcefulness' [79] and recommendations for the management of crush victims in mass disasters.

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(A) Makeshift dialysis facility in the All Marriage Surgical Scientific Centre in Yerevan, Soviet Commonwealth 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 at that place is restoration of blood flow one time victims are extracted from the rubble. Both mechanisms can coexist. The crush syndrome is the second most common cause of expiry in earthquake victims later asphyxia [72]. While rhabdomyolysis is the primary cause of AKI in these patients, there are other possible pre- and mail service-renal causes such every bit hypovolaemia from blood loss or aridity, too equally direct trauma to the kidneys and urinary tract.

Various studies, for example, involving victims of the Bam and Bingöl earthquakes (both in 2003) accept noted the benign effect of early handling 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 starting time in the 1940s and later reiterated following the Vietnam State of war [55], but the government for fluid assistants has evolved considerably and in parallel to growing experience with rhabdomyolysis overall. A detailed discussion of this topic is beyond the scope of our trivial article. Suffice to say that some studies advocate a fairly conservative approach (3 L over the first 24 h), whereas others suggest being more than aggressive (with upwards of 12 L in the same time catamenia) [81, 82].

Factors that increase the adventure of developing AKI and requirement for RRT include increased time under rubble, decreased book of fluid received and increased value of serum creatinine kinase [83]. However, it is still not easy to predict which patients are more probable to progress to a worse outcome. 1 small study assessed patients treated with crush syndrome in the Hanshin convulsion in Kobe, January 1996 [82]. It evaluated various laboratory markers such equally serum amylase, LDH and AST in these patients. There was a statistically pregnant divergence 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 attain. A key challenge for dialysis units but also for renal teams coming to help from away in the aftermath of an earthquake is the disrupted water supply. The fact that it is oft impossible for outside teams to appreciate the calibration of the disaster, permit lone to arrive in time to be of any use, has been highlighted elsewhere [78]. Branch work co-ordinated by the international renal societies has been extremely beneficial in several contempo earthquakes [79, 84].

RHABDOMYOLYSIS DUE TO TORTURE AND Like FORMS OF VIOLENCE

I 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 Clan's Tokyo Declaration of 1975 defines torture as:

The deliberate, systematic or wanton infliction of physical or mental suffering past one or more than persons acting lone or on the orders of any authorisation, to force another person to yield data, to make a confession, or for any other reason. [87]

As of today there is no uniformly accepted definition of torture, and different opinions be [88]. In full general, our noesis of the medical aspects of torture is rather express. 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 oft accept an understandable feeling of unease and discomfort regarding publishing information derived from treating the victims of man cruelty [85]. It is also important to bear in mind that medical practitioners take had diverse roles in torture, ranging from complicit witness, to bystander and facilitator, to perpetrator [ninety]. 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 await afterwards victims of torture [85]: what if medical practitioners provide care to prisoners, knowing that subsequently treatment they would merely be exposed to new abuse? Similarly, what if whatsoever attempt at publication would alert government and thereby deny futurity victims medical care?

Viewed against this background, the gruesome bear witness linking rhabdomyolysis and torture is quite considerable. Not surprisingly, victims of rhabdomyolysis due to torture and violence are predominantly immature 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 bachelor literature, the most prevalent types of physical torture and violence that victims underwent were fell beating of the whole body with sticks, rods made of metallic and guns, for several days, countless hours of 'sit-and-stand' exercise, electric shocks and hanging upside-downwardly with tied legs [89, 92, 93]. Another particular form of torture that causes rhabdomyolysis is reverse hanging in which victim's wrists are spring 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 every bit a sequel to torture and many patients are oliguric [86, 89, 91, 93, 95]. The presenting clinical, biochemical and radiological features practice non differ much from other aetiologies and some patients ofttimes lack obvious external bear witness of torture and violence [86, 89, 92, 93]. Aridity [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 claret 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 ∼xv% [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, ofttimes children, elderly or individuals with cognitive disabilities [95]. A detail form of violence observed in Southern Africa is chirapsia with the sjambok, a heavy whip made of rhinoceros hibernate (Effigy 5) [86, 91]. The soft tissue injury that ensues is ofttimes 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 afterwards the initial assessment. Finally, when assessing patients with rhabdomyolysis in conjunction with violent behaviour information technology is important to comport in mind that drugs may also be involved [100].

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A young patient who presented with AKI from rhabdomyolysis post-obit astringent 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 illness is closely linked to the history of the concluding 100 years (Figure 6). Nephrologists have learned a swell deal about rhabdomyolysis from studying victims of human conflict, peculiarly since Bywaters described the syndrome during the London Blitz in the 1940s [46]. It is sobering to larn that lessons already learned were ofttimes ignored, only to be relearned by a subsequent generation of physicians. Another interesting attribute of this topic is that the cause of one of the most enigmatic causes of rhabdomyolysis, the Haff affliction, remains unclear despite the fact that researchers have tried their hardest, with generations of theories existence proposed and afterward discarded. We can, yet, accept some alleviation from the fact that afterward on in the 20th century we accept fabricated peachy progress in elucidating the genetic basis of some cases of rhabdomyolysis. Another pitiful and oftentimes tragic aspect of the history of rhabdomyolysis is its link to earthquakes. Only a multinational effort supported past international organizations can bargain 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 manner, but we are conspicuously 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 upshot 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. Yet, it is equally linked to great examples of coordinated help and support for victims of natural disasters. Nosotros can only promise that future generations will exist more aware of the history of rhabdomyolysis, preserve and aggrandize the knowledge gained past their predecessors, and encounter cases more as an intellectual challenge during clinical exercise than as a sequel to human being violence and conflict.

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Time line: history and rhabdomyolysis intertwined from 1900 to present day. Bottom half: events relating to armed conflict and violence. Top half: events non associated with human conflict.

Conflict OF INTEREST STATEMENT

None declared.

REFERENCES

one. Vanholder R, Sever MS, Erek E. et al. Rhabdomyolysis. J Am Soc Nephrol 2000; xi: 1553–1561 [PubMed] [Google Scholar]

two. Bagley WH, Yang H, Shah KH.. Rhabdomyolysis. Int Emergency Med 2007; two: 210–218 [PubMed] [Google Scholar]

3. Huerta-Alardin AL, Varon J, Marik PE.. Bench-to-bedside review: rhabdomyolysis – an overview for clinicians. Critical Care (London) 2005; 9: 158–169 [PMC free commodity] [PubMed] [Google Scholar]

4. Eiser AR, Neff MS, Slifkin RF.. Astute myoglobinuric renal failure. A consequence of the neuroleptic cancerous syndrome. Arch Intern Med 1982; 142: 601–603 [PubMed] [Google Scholar]

6. Coffey RJ, Edgar TS, Francisco GE. et al. Precipitous withdrawal from intrathecal baclofen: recognition and management of a potentially life-threatening syndrome. Curvation Phys Med Rehabil 2002; 83: 735–741 [PubMed] [Google Scholar]

seven. Singhal PC, Kumar A, Desroches L. et al. Prevalence and predictors of rhabdomyolysis in patients with hypophosphatemia. Am J Med 1992; 92: 458–464 [PubMed] [Google Scholar]

8. Wang LM, Tsai ST, Ho LT. et al. Rhabdomyolysis in diabetic emergencies. Diabetes Res Clin Pract 1994; 26: 209–214 [PubMed] [Google Scholar]

nine. Kennedy L, Nagiah S.. A instance of severe rhabdomyolysis associated with secondary adrenal insufficiency and autoimmune hepatitis. BMJ Case Rep 2019; 12: e227343 [PMC free article] [PubMed] [Google Scholar]

10. Paternoster Thou, Capasso E, Di Lorenzo P. et al. Fatal exertional rhabdomyolysis. Literature review and our feel in forensic thanatology. Leg Med (Tokyo) 2018; 35: 12–17 [PubMed] [Google Scholar]

eleven. Scalco RS, Gardiner AR, Pitceathly RD. et al. Rhabdomyolysis: a genetic perspective. Orphanet J Rare Dis 2015; 10: 51. [PMC costless article] [PubMed] [Google Scholar]

12. Tonin P, Lewis P, Servidei Southward. et al. Metabolic causes of myoglobinuria. Ann Neurol 1990; 27: 181–185 [PubMed] [Google Scholar]

xiii. Kim HW, Choi JR, Jang SJ. et al. Recurrent rhabdomyolysis and myoglobinuric acute renal failure in a patient with polymyositis. Nephrol Dial Transplant 2005; 20: 2255–2258 [PubMed] [Google Scholar]

14. Hamel Y, Mamoune A, Mauvais FX. et al. Acute rhabdomyolysis and inflammation. J Inherit Metab Dis 2015; 38: 621–628 [PubMed] [Google Scholar]

15. Armstrong JH. Tropical pyomyositis and myoglobinuria. Arch Intern Med 1978; 138: 1145–1146 [PubMed] [Google Scholar]

xvi. Knochel JP, Moore GE.. Rhabdomyolysis in Malaria. Northward Engl J Med 1993; 329: 1206–1207 [PubMed] [Google Scholar]

17. Odolini South, Gobbi F, Zammarchi L. et al. Febrile rhabdomyolysis of unknown origin in refugees coming from West Africa through the Mediterranean. Int J Infect Dis 2017; 62: 77–fourscore [PubMed] [Google Scholar]

18. Vallone A, Marino R, Vento S.. Febrile rhabdomyolysis of unknown origin in refugees coming from Due west Africa through the Mediterranean to Calabria, Italy. Int J Infect Dis 2017; 63: 99–100 [PubMed] [Google Scholar]

19. Lau Hing Yim C, Wong EWW, Jellie LJ. et al. Illicit drug use and acute kidney injury in patients admitted to hospital with rhabdomyolysis. Intern Med J 2019; 49: 1285–1292 [PubMed] [Google Scholar]

20. Jermain DM, Crismon ML.. Psychotropic drug-related rhabdomyolysis. Ann Pharmacother 1992; 26: 948–954 [PubMed] [Google Scholar]

21. Daubert GP. Toxicant-induced rhabdomyolysis. In: Brent J, Burkhart Yard, Dargan P (eds). Disquisitional Care Toxicology: Diagnosis and Management of the Critically Poisoned Patient. Cham: Springer International Publishing, 2017, 679–690 [Google Scholar]

22. Adiseshiah M, Round JM, Jones DA.. Reperfusion injury in skeletal muscle: a prospective study in patients with acute limb ischaemia and claudicants treated by revascularization. Br J Surg 1992; 79: 1026–1029 [PubMed] [Google Scholar]

23. The Christian Standard Bible. Nashville, TN: LifeWay Christian Resource, 2017 [Google Scholar]

24. Tsironi M, Andriopoulos P, Xamodraka Eastward.. The patient with rhabdomyolysis: accept yous considered quail poisoning? Can Med Assoc J 2004; 171: 325–326 [PMC free article] [PubMed] [Google Scholar]

25. Rizzi D, Basile C, Di Maggio A. et al. Clinical spectrum of accidental hemlock poisoning: neurotoxic manifestations, rhabdomyolysis and acute tubular necrosis. Nephrol Punch Transplant 1991; 6: 939–943 [PubMed] [Google Scholar]

26. Aparicio R, Oñate JM, Arizcun A. et al. Epidemic rhabdomyolysis due to the eating of quail. A clinical, epidemiological and experimental study. Med Clin (Barc) 1999; 112: 143–146 [PubMed] [Google Scholar]

27. Grivetti LE. Coturnism. In: Jelliffe EFP, Jelliffe DB (eds). Agin Effects of Foods. Boston, MA: Springer US, 1982, 51–58 [Google Scholar]

28. Bellomo G, Gentili One thousand, Verdura C. et al. An unusual case of rhabdomyolysis. NDT Plus 2011; four: 173–174 [PMC costless article] [PubMed] [Google Scholar]

29. Sergent East. Les cailles empoisonneuses dans la bible, et en Algerie de nos jours. Arch Inst Pasteur Alger 1942; 161

30. Rutecki GW, Ognibene AJ, Geib JD.. Rhabdomyolysis in antiquity. From aboriginal descriptions to scientific explication. Pharos Alpha Omega Alpha Award Med Soc 1998; 61: 18–22 [PubMed] [Google Scholar]

31. Rizzi D, Basile C, Di Maggio A. et al. Rhabdomyolysis and acute tubular necrosis in coniine (hemlock) poisoning. Lancet 1989; 334: 1461–1462 [PubMed] [Google Scholar]

32. Davies ML, Davies TA.. Hemlock: murder before the Lord. Med Sci Law 1994; 34: 331–333 [PubMed] [Google Scholar]

33. Cave Due east. Account of the medical virtues of hemlock. The Gentleman's Magazine and Historical Relate 1761: 624–626 [Google Scholar]

34. Von Storck A. An Essay on the Medicinal Nature of Hemlock in Which Its Extraordinary Virtue and Efficacy, too Internally as Externally Used, in the Cure of Cancers, Schirrous and Oedematous Tumours, Malignant and Fistulous Ulcers, and Cataracts, are Demonstrated, and Explained. Translated from the Latin original. London: J. Nourse, 1760 [Google Scholar]

35. Dayan AD. What killed Socrates? Toxicological considerations and questions. Postgrad Med J 2009; 85: 34–37 [PubMed] [Google Scholar]

36. Schep LJ, Slaughter RJ, Becket Thou. et al. Poisoning due to h2o hemlock. Clin Toxicol 2009; 47: 270–278 [PubMed] [Google Scholar]

37. Clark GH, Fletcher J.. Farm Weeds of Canada. Ottawa, ON: Minister of Agronomics, 1906 [Google Scholar]

38. Foster PF, McFadden R, Trevino R. et al. Successful transplantation of donor organs from a hemlock poisoning victim. Transplantation 2003; 76: 874–876 [PubMed] [Google Scholar]

39. Lee MR, Dukan E, Milne I.. Three poisonous plants (Oenanthe, Cicuta, and Anamirta) that antagonise the result of gamma-aminobutyric acid in homo brain. J R Coll Physicians Edin 2020; l: 80–86 [PubMed] [Google Scholar]

forty. Karakasi MV, Tologkos South, Papadatou V. et al. Conium maculatum intoxication: literature review and case report on hemlock poisoning. Forensic Sci Rev 2019; 31: 23–36 [PubMed] [Google Scholar]

41. Larrey DJ. Memoires de Chirurgie Militaire et Campagnes. Paris: Smith and Buisson, 1812 [Google Scholar]

42. Kim SG, Woo J, Kang GW.. A case report on the acute and late complications associated with carbon monoxide poisoning: Acute kidney injury, rhabdomyolysis, and delayed leukoencephalopathy. Medicine (Baltimore) 2019; 98: e15551. [PMC costless commodity] [PubMed] [Google Scholar]

43. Frankenthal L. Die Folgen der Verletzungen durch Verschuttüng. Bruns Beitr Klin Chir 1918; 109: 572–587 [Google Scholar]

44. Minami S. Ueber Nierenveraenderungen nach Verschuettung. Virchows Arch Pathol Anat Physiol Klin Med 1923; 245: 247–267 [Google Scholar]

45. Dixon A. Eric George Lapthorne Bywaters [obituary]. BMJ 2003; 326: 1461 [Google Scholar]

46. Bywaters EG, Beall D.. Crush Injuries with impairment of renal part. Br Med J 1941; 1: 427–432 [PMC free article] [PubMed] [Google Scholar]

48. Callender GR, Coupal JF.. History of the Medical Department of the U.s. Army in the World State of war. Washington, DC: Government Printing Office, 1920 [Google Scholar]

49. Bywaters EGL, McMichael J.. Shell syndrome. In: Cope Z (ed). Surgery: History of the Second World War. London: Her Majesty's Stationery Office, 1954, 673–688 [Google Scholar]

50. Kayser F. Von Schjerning's Handbuch Der Arztlichen Erfahrungen im Weltkriege. Leipzig: JA Barth, 1922 [Google Scholar]

51. Mayon-White R, Solandt OM.. A case of limb compression ending fatally in uraemia. Br Med J 1941; 1: 434–435 [PMC free commodity] [PubMed] [Google Scholar]

52. Peiris D. A historical perspective on beat syndrome: the clinical awarding of its pathogenesis, established by the study of wartime crush injuries. J Clin Pathol 2017; 70: 277–281 [PubMed] [Google Scholar]

53. Fitts CT, Easterling RE, Switzer WE. et al. Crush injury. J Trauma 1966; vi: 507–515 [PubMed] [Google Scholar]

54. Michaelson M, Taitelman U, Bshouty Z. et al. Crush syndrome: experience from the Lebanon War, 1982. Isr J Med Sci 1984; 20: 305–307 [PubMed] [Google Scholar]

55. Greaves I, Porter K, Smith JE.. Consensus statement on the early management of trounce injury and prevention of beat out syndrome. J R Army Med Corps 2003; 149: 255–259 [PubMed] [Google Scholar]

56. Stewart IJ, Faulk TI, Sosnov JA. et al. Rhabdomyolysis among critically ill combat casualties: associations with acute kidney injury and bloodshed. J Trauma Acute Care Surg 2016; 80: 492–498 [PubMed] [Google Scholar]

57. Haffkrankheit ZB. In: Czerny A, Müller F, Pfaundler Mv. et al. (eds). Ergebnisse Der Inneren Medizin Und Kinderheilkunde: Siebenundfünfzigster Band. Berlin, Heidelberg: Springer Berlin Heidelberg, 1939, 138–182 [Google Scholar]

58. Juettemann A. Dice Geschichte des rätselhaften Phänomens "Haffkrankheit". ASU Zschr Med Praevent 2018; 53: 465–468 [Google Scholar]

59. Assmann H, Bielenstein H, Habs H. et al. Beobachtungen und Untersuchungen bei der Haffkrankheit 19321. Dtsch Med Wochenschr 1933; 59: 122–126 [Google Scholar]

60. Lentz O. Über die Haffkrankheit [About Haff disease]. Med Klin 1925; i: iv–eight [Google Scholar]

61. Bandeira Ac, Campos GS, Ribeiro GS. et al. Clinical and laboratory bear witness of Haff disease - case series from an outbreak in Salvador, Brazil, Dec 2016 to April 2017. Euro Surveill 2017; 22: 30552. [PMC free article] [PubMed] [Google Scholar]

62. Tolesani Júnior O, Roderjan CN, exercise Carmo Neto E. et al. Haff disease associated with the ingestion of the freshwater fish Mylossoma duriventre (pacu-manteiga). Rev Bras Ter Intensiva 2013; 25: 348–351 [PMC costless article] [PubMed] [Google Scholar]

63. Buchholz U, Mouzin E, Dickey R. et al. Haff disease: from the Baltic Body of water to the U.S. shore. Emerg Infect Dis 2000; half-dozen: 192–195 [PMC gratuitous article] [PubMed] [Google Scholar]

64. Diaz JH. Global incidence of rhabdomyolysis after cooked seafood consumption (Haff affliction). Clin Toxicol (Phila) 2015; 53: 421–426 [PubMed] [Google Scholar]

65. White J, Weinstein SA, De Haro L. et al. Mushroom poisoning: a proposed new clinical classification. Toxicon 2019; 157: 53–65 [PubMed] [Google Scholar]

66. Cho JT, Han JH.. A case of mushroom poisoning with Russula subnigricans: development of rhabdomyolysis, acute kidney injury, cardiogenic shock, and death. J Korean Med Sci 2016; 31: 1164–1167 [PMC free commodity] [PubMed] [Google Scholar]

67. Klimaszyk P, Rzymski P.. The yellow knight fights back: toxicological, epidemiological, and survey studies defend edibility of Tricholoma equestre. Toxins (Basel) 2018; 10: 468 [PMC gratuitous commodity] [PubMed] [Google Scholar]

68. Bedry R, Baudrimont I, Deffieux G. et al. Wild-mushroom intoxication as a cause of rhabdomyolysis. N Engl J Med 2001; 345: 798–802 [PubMed] [Google Scholar]

69. Ogundare O, Jumma O, Turnbull DM. et al. Searching for the needle in the Haystacks. Lancet 2009; 374: 850. [PubMed] [Google Scholar]

70. Emma F, Montini Thousand, Parikh SM. et al. Mitochondrial dysfunction in inherited renal affliction and astute kidney injury. Nat Rev Nephrol 2016; 12: 267–280 [PMC gratuitous article] [PubMed] [Google Scholar]

71. Conscious N, Laforet P, Voermans NC. et al. Phenotype and genotype of muscle ryanodine receptor rhabdomyolysis-myalgia syndrome. Acta Neurol Scand 2018; 137: 452–461 [PubMed] [Google Scholar]

72. Sever MS, Lameire N, Van Biesen Due west. et al. Disaster nephrology: a new concept for an erstwhile problem. Clin Kidney J 2015; viii: 300–309 [PMC complimentary article] [PubMed] [Google Scholar]

73. Natale Gaspare DS, Bisaccia C, de Santo 50.. The priority of Antonino D'Antona in describing rhabdomyolysis with astute kidney injury, following the Messina earthquake (Dec 28, 1908). Commentary. Ann I Super Sanita 2016; 52: i–3 [PubMed] [Google Scholar]

74. Von Colmers F. Ueber die durch das Erdbeben in Messina am 28. December. 1908 verursachten Verletzungen. Arch Klin Chirurg 1908; 90: 701–747 [Google Scholar]

75. Sheng ZY. Medical support in the Tangshan earthquake: a review of the management of mass casualties and certain major injuries. J Trauma 1987; 27: 1130–1135 [PubMed] [Google Scholar]

76. Soreide E, Grande CM.. Prehospital Trauma Care. New York, NY: Marcel Dekker, 2001 [Google Scholar]

77. Ron D, Taitelman U, Michaelson M. et al. Prevention of acute renal failure in traumatic rhabdomyolysis. Arch Intern Med 1984; 144: 277–280 [PubMed] [Google Scholar]

78. Tattersall JE, Mathias T, Richards NT. et al. Acute haemodialysis during the Armenian earthquake disaster. Injury 1990; 21: 25–28 [PubMed] [Google Scholar]

79. Vanholder R, Van Biesen W, Lameire N. et al.; International Guild of Nephrology/Renal Disaster Relief Task Force. The role of the International Gild of Nephrology/Renal Disaster Relief Job Force in the rescue of renal disaster victims. Contrib Nephrol 2007; 156: 325–332 [PubMed] [Google Scholar]

80. Omrani H, Najafi I, Bahrami M. et al. Astute kidney injury following traumatic rhabdomyolysis in Kermanshah earthquake victims; a cross-exclusive study. Am J Emerg Med 2020. doi: 10.1016/j.ajem.2020.01.043 [PubMed] [Google Scholar]

81. Gunal AI, Celiker H, Dogukan A. et al. Early and vigorous fluid resuscitation prevents acute renal failure in the beat out victims of catastrophic earthquakes. J Am Soc Nephrol 2004; 15: 1862–1867 [PubMed] [Google Scholar]

82. Hara I, Nakano Y, Okada H. et al. Treatment of trounce syndrome patients following the Slap-up Hanshin earthquake. Int J Urol 1997; 4: 202–204 [PubMed] [Google Scholar]

83. Iraj N, Saeed Due south, Mostafa H. et al. Safety fluid therapy in crushed victims of Bam convulsion. Am J Emergency Med 2011; 29: 738–742 [PubMed] [Google Scholar]

84. Vanholder R, Gibney Due north, Luyckx VA. et al. Renal Disaster Relief Task Force in Haiti earthquake. Lancet 2010; 375: 1162–1163 [PubMed] [Google Scholar]

85. Lameire N, Vermeersch E.. Nephrological and moral aspects of concrete torture. Nephrol Dial Transplant 1995; x: 160–161 [PubMed] [Google Scholar]

86. Muckart DJ, Abdool-Carrim AT.. Paint-induced nephropathy afterwards sjambok injuries. Southward Afr J Surg 1991; 29: 21–24 [PubMed] [Google Scholar]

88. Light-green D, Rasmussen A, Rosenfeld B.. Defining torture: a review of forty years of wellness scientific discipline research. J Traum Stress 2010; 23: 528–531 [PubMed] [Google Scholar]

89. Pollanen MS. Fatal rhabdomyolysis after torture by contrary hanging. Forensic Sci Med Pathol 2016; 12: 170–173 [PubMed] [Google Scholar]

91. Bowley DM, Buchan C, Khulu L. et al. Acute renal failure after penalty beatings. J R Soc Med 2002; 95: 300–301 [PMC free commodity] [PubMed] [Google Scholar]

92. Malik GH, Reshi AR, Najar MS. et al. Further observations on acute renal failure following physical torture. Nephrol Dial Transplant 1995; 10: 198–202 [PubMed] [Google Scholar]

93. Malik GH, Sirwal IA, Reshi AR. et al. Acute renal failure post-obit physical torture. Nephron 1993; 63: 434–437 [PubMed] [Google Scholar]

94. Knochel JP. Rhabdomyolysis and myoglobinuria. Annu Rev Med 1982; 33: 435–443 [PubMed] [Google Scholar]

95. Mukherji SK, Siegel MJ.. Rhabdomyolysis and renal failure in kid abuse. AJR Am J Roentgenol 1987; 148: 1203–1204 [PubMed] [Google Scholar]

96. Chaari A, Chakroun O, Ksibi H. et al. [Astute renal failure and rhabdomyolysis secondary to prolonged hunger strike. A case report]. Rev Med Interne 2009; xxx: 914–916 [PubMed] [Google Scholar]

97. Mercieca J, Brown EA.. Acute renal failure due to rhabdomyolysis associated with apply of a straitjacket in lysergide intoxication. Br Med J 1984; 288: 1949–1950 [PMC free article] [PubMed] [Google Scholar]

98. Lazarus SG, Wittkamp One thousand, Messner S.. Physical abuse leading to renal failure: a unique case of rhabdomyolysis. Clin Pediatr (Phila) 2014; 53: 701–703 [PubMed] [Google Scholar]

99. Peebles J, Losek JD.. Child concrete abuse and rhabdomyolysis: case report and literature review. Pediat Emerg Care 2007; 23: 474–477 [PubMed] [Google Scholar]

100. Reddy SK, Kornblum RN.. Rhabdomyolysis following fierce beliefs and blackout. J Forensic Sci 1987; 32: 550–553 [PubMed] [Google Scholar]


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