Crush syndrome

Crush syndrome
ICD-10	T79.5
ICD-9	958.5
DiseasesDB	13135
MeSH	D003444

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Synonyms and keywords: Bywaters' syndrome; traumatic rhabdomyolysis

Overview

Being a common occurrence in victims of natural disasters and human wars, crush syndrome is still a rare finding in daily practice. Falling short to direct-fatal trauma, crush syndrome is the second most common cause of mortality after a disaster. It is the sequalae that follows when an individual or a part of him/her has been crushed between two heavy objects and although it has a wide range of presentation like shock, trouble breathing, electrolyte disturbances and irregular beating of the heart, the main culprit behind these findings is the extensive damage to the kidneys as a result of the trauma the person was subjected to. This can be prevented with aggressive fluid resuscitation, but the sheer number of incoming trauma patients during a calamity plays a major role in creating logistic problems for the response teams and hence it becomes important to diagnose it earlier rather than later.

Definition and related terms

• Crush syndrome : also known as traumatic rhabdomyolysis or reperfusion syndrome, it is defined as the systemic features of a crush injury leading to renal failure.
• Crush injury : the damage caused to muscle cells due to pressure applied on them locally, for a prolonged period of time.
• Rhabdomyolysis : the breakdown and release of muscular tissue (myoglobin) into the bloodstream resulting in renal damage and the subsequent build up of toxic compounds in the blood.
• Compartment syndrome : the raised pressure (>20 mm of Hg) within a localized region causing decreased local circulation which can lead to ischemia and necrosis of that osteo-musculo-fascial compartment. This can later lead to release of necrosed muscle tissue into the blood which damages the kidney and can present with features similar to crush syndrome.

Historical perspective

The first reported relations between compressive trauma and renal damage were after the 1909 earthquake in Sicily and World War I. In the year 1923, a physician named Seigo Minami reported crush syndrome after observing three soldiers who died due to renal failure as a result of injuries sustained during World War I. Having this background knowledge, the incidence of crush syndrome was then observed in increasing numbers during World War II. During the London air raids many individuals experienced similar injuries, wherein Bywaters and Beall discussed the presentations of the syndrome. Statistically, out of 100 people with crush injuries, about 80 succumb to fatal head trauma or are not able to breathe underneath the rubble. Out of the remaining 20 that do reach the hospital, about 10 recover completely while 7 out of the other 10 proceed into developing signs of crush syndrome. A series of 11 cases where studied and differences between similar syndromes like crush and compartment syndrome were delineated in 1975. Main focus of managing crush syndrome is now to diagnose it earlier, to finalize a standard treatment with fluids to be administered to patients and to identify those who have extensive renal damage and would now require kidney replacement.

Pathophysiology

The complete pathogenesis of crush syndrome involves primarily two main events which in turn have several smaller steps that participate in their development. The trauma causes compression of a limb or region of the body, which if is present for two to three hours, leads to the process of rhabdomyolysis. This in turn, causes renal damage and eventually renal failure if allowed to proceed.

• 1. Compression induced rhabdomyolysis :
  • Increased local pressure causes the sarcolemma membrane to become permeable.
  • Substances move down their concentration gradient from the extracellular to the intracellular compartment and vice versa.
  • Water, sodium-Na+ and calcium-Ca2+ enter the cell while potassium-K+ and myoglobin enter the extracellular compartment.
  • As intracellular Ca2+ rises, muscular contraction ensues, emptying the cell’s ATP stores.
  • The ATP deficient cell causes mitochondrial damage along with release of enzymes like proteases and phospholipases.
  • These enzymes and oxidative stress, damage the phospholipids present in the cell membrane and as a result cause lysis of the muscle cell.
  • Toxic metabolites which were accumulating inside the cell are then released into the extracellular compartment.
  • These substances induce damage to the capillaries present in the area leading to leaking, which causes increased compartmental pressure due to third spacing of fluids.
  • Increased pressure in the compartment results in occlusion of these vessels and further depletion of energy sources like ATP and glycogen.
  • Decreased circulation causes reduced oxygen saturation of myoglobin.

The real damage ensues when circulation is re-established which allows leukocytes to attack this region and release all these toxins to the rest of the body.

• 2. Renal injury following rhabdomyolysis : A plethora of mechanisms are now aimed at damaging the kidney, once the injured area has been re-perfused. Most of the released metabolites and compounds are toxic to the kidney and hence lead to acute kidney injury (AKI).
  • The collection of fluid in the injured area causes decreased intra-vascular volume and consequently reduces the blood supply to the kidney. This leads to the pre-renal subtype of AKI.
  • Toxins and cytokines released upon re-perfusion causes constriction of renal vessels, further aggravating the pre-renal AKI via hypoperfusion.
  • K+ released from the damaged muscle effects the heart by causing decreased output, contributing to renal ischemia.
  • Myoglobin levels rise in the blood which upon reaching the kidney form casts in the tubular system causing renal damage and AKI.
  • Proteins released from damaged cellular membranes accumulate in renal tubules causing obstruction and further potentiate renal injury.
  • Increased serum phosphorus levels depress cardiac contraction and combine with Ca2+ to form precipitates in renal tubules which induces renal inflammation.
  • Lastly, damaged tissue can release thromboplastin into the blood stream which can activate the disseminated intravascular coagulation pathway (DIC), further decreasing renal blood supply.

Diagnosis

Early recognition of crush syndrome can tremendously improve the patient’s prognosis and the overall course of his/her stay at the hospital. Local findings mentioned below should alarm the physician to then look for any suspicious systemic features of crush syndrome. If systemic features are present as well, certain investigations can then lead to the confirmation of crush syndrome as the diagnosis.

• 1. Local features :
  • Pain which is proportionately more in intensity than the severity of the injury .
  • Swollen muscles or tense skin above the injured area.
  • Abnormal sensation in the injured area.
  • Pallor or deficiency of the natural colour of the skin.
  • Paralysis or inability to move the affected area.
  • Decreased sensation or absence of pulse adjacent to the injured region.
  • Feeling of increased pressure or heaviness in the injured area elicited by the victim.

• 2. Systemic features :
  • Trouble breathing or shortness of breath.
  • Decreased urine output or reddish tinge to the urine.
  • Hypotension as a feature of hypovolemic shock.
  • Irregular heart-beat or arrythmia due to increased K+ levels.
  • Neurological abnormalities like light-headedness or dizziness.
  • Fever and generalised malaise, which point to development of an infection in the injured area.

• 3. Investigations :
  • Brownish discoloration of the urine due to presence of myoglobin.
  • Visible blood in the urine or hematuria.
  • Raised protein levels in the urine or proteinuria.
  • Increased serum creatinine kinase (>1000 IU per litre).
  • Hyperuricemia
  • Raised serum lactate levels.
  • Hyperkalemia and hyperphosphatemia.
  • Hypocalcemia is seen often and sometimes hypercalcemia due to stress can also be encountered.
  • ECG may show rhythm abnormalities due to electrolyte disturbances
  • Compartment pressures may be raised above 20 mm of Hg.

Treatment

Since most of the crush syndrome patients have experienced major trauma and injuries, it is essential to transfer victims away from the disaster site and to nearby medical centers for prompt treatment. Keeping an eye on the cardiovascular and renal status form the mainstay of successful management. Medical and para-medical staff should be well trained in recognizing the signs of crush syndrome as history is often unavailable in these scenarios. Treatment in the form of resuscitation should begin as soon as the victim makes contact with a health personnel.

• 1. Fluid resuscitation :
  • Fluids should be administered early into the management.
  • There is no fixed amount or rate at which fluids should be given, but fluids need to be given within 6 hours of the trauma.
  • Normal saline (NS) is the fluid of choice. If intravenous cannulation is successful before removing the victim from underneath the rubble, fluid should be administered at a rate of one litre per hour. This rate should be continued during the extrication and can be reduced to 500 ml per hour if extrication takes longer than 2 hours.
  • Ringer’s Lactate, Plasmalyte A and Hartmann’s solution contain potassium and should be avoided in patients with signs of crush syndrome.
  • Bicarbonate, lactate and citrate can be used to combat metabolic acidosis. For every litre of NS infused, 50 mmol of bicarbonate can be administered along with it.
  • Infusing larger doses of bicarbonate may exacerbate hypocalcemia by decreasing the amount of ionized calcium in the serum.
  • Regular checks on blood pressure, respiratory rate and urine output should be performed to assess whether fluid replacement is proceeding adequately or not.
  • Insulin along with a glucose drip can be used to prevent the ongoing influx of K+ into the bloodstream.
  • Blood transfusion may also be required according to the severity of injuries met by the patient.
• 2. Renal function management :
  • Urine output in a diagnosed crush syndrome case should be around 300 ml/hr as maintain kidney function is now of utmost priority.
  • As third spacing of fluid at the site on injury can be as high as 4 litres, approximately 12 litres of fluid per day is required for adequate renal function.
  • Mannitol may be added to NS in patients with urine output > 20 ml per hour - in the amount of 50 ml of 20% mannitol. It aids in decreasing raised pressures at the local site of injury, maintains an alkaline pH of the urine which prevents tubular obstruction caused by casts and thus allows adequate blood supply to reach the kidneys.
  • Mannitol is not an alternative to NS and is rather used as an adjunctive treatment option, especially in patients with crush syndrome also developing compartment syndrome.
• 3. Renal dialysis :
  • Dialysis has a firm foothold in management of crush injury.
  • As complications of trauma induced AKI occur more frequently than its other causes, dialysis is required more often.
  • Serum urea, creatinine and urine output are important factors used to decide whether dialysis is required or not. Serum K+ levels exceeding 7 meq/L is another indication for dialysis treatment.
  • Early initiation of dialysis in trauma induced AKI may improve overall survival.
  • Peritoneal dialysis, intermittent haemodialysis and continuous renal replacement therapy and some of the options used in trauma patients. Out of these, intermittent dialysis is the most used modality for crush syndrome victims.
  • Intermittent dialysis provides quick elimination of the excess potassium build up in the body and the same dialysing machine may be used for multiple patients in a day. It may be used for individuals with bleeding disorders as it can be used with minimal anticoagulation.
  • Dialysis may be required for two-three times daily upto a span of 10-15 days.
• 4. Hyperbaric oxygen :
  • Administering oxygen at high pressure and concentration can help in increasing oxygen saturation of the injured tissue.
  • Improved oxygen supply will in turn lead to healing of vessels and cessation of fluid loss from the vessels in form of capillary leak.
  • Presence of oxygen discourages proliferation of anaerobic bacteria in damaged muscle tissue.
  • A pressure of 2.5 atmospheres is required to be administered for a week long regimen lasting 90 minutes daily.
• 5. Surgical options :
  • Debridement of dead and necrosing tissue is essential to prevent further progression of crush syndrome.
  • A fasciotomy may be required if compartmental pressures are above 30mm of Hg.
  • Performing a fasciotomy earlier rather than later is always considered a good practice, as a late fasciotomy may further require an amputation to halt the ongoing insult to the victim’s systems.
  • Surgically opening these injured sites to relieve pressure is essential and after debridement is complete, these sites are kept open for a while to prevent repeat rise in compartmental pressures. They are later closed by suturing and healing by secondary intention.
• 6. Prevention of infection :
  • Broad spectrum antibiotics may be used to prevent development of localised infection due to exposure of the wound to the external environment.
  • A tetanus shot may also be administered

Relation to disasters

• Disasters have occurred numerous times over the course of human history and earthquakes are especially notorious for causing structures like buildings and houses to collapse.
• These heavy structures may either cause injury to vital organs of the body like the brain and heart or may incite damage to non-vital organs like limbs and extremities by compressing them with their weight. Therefore, earthquake victims form majority of crush syndrome cases.
• Although it may not be possible to prevent mortality stemming from injuries to vital organs, victims with crush injuries can be prevented from developing features of crush syndrome.

Location	Year	Magnitude	Deaths	Crush syndrome	Dialysis
Spital, Armenia	1988	6.7	25,000	600	225-385
Kobe, Japan	1995	6.9	5,000	372	123	2008
Marmara, Turkey	1999	7.6	17,118	639	477
Gujarat, India	2001	7.6	20,085	124	96
Bam, Iran	2003	6.6	35	31,000	118	229
Kashmir, India	2005	7.6	33	86,000	65	113
Sichuan, China	2008	7.9	87,587

• Table 1 shows the major earthquakes that have occurred over past years and the number of crush syndrome cases seen in each one of them.
• Utmost importance should be given to starting fluids in these patients, preferably before the extrication begins. The fluids should be continued to maintain adequate urine output, since most of the pathogenesis of crush syndrome stems from kidney failure.
• The lack of kidney function causes unwanted toxins and compounds to accumulate in the blood which sets forth the development of systemic inflammation and other events like arrythmias, heart failure, acute respiratory distress and shock.
• The challenge in situations like earthquakes is to procure enough medical personnel and equipment required to safely extricate and transport crush injury victims to the hospital while administering fluid en route. Unavailability of transport, personnel or medicines are the common logistic problems disaster response teams face during these times.