Crush syndrome

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Crush syndrome
1985 Mexico Earthquake - Collapsed General Hospital.jpg
Collapsed building from 1985 Mexico earthquake. Earthquakes are a main cause of crush syndrome injuries.
Specialty Emergency medicine   OOjs UI icon edit-ltr-progressive.svg
Complications Kidney failure

Crush syndrome (also traumatic rhabdomyolysis or Bywaters' syndrome) is a medical condition characterized by major shock and kidney failure after a crushing injury to skeletal muscle. Crush injury is compression of the arms, legs, or other parts of the body that causes muscle swelling and/or neurological disturbances in the affected areas of the body, while crush syndrome is a localized crush injury with systemic manifestations. [1] Cases occur commonly in catastrophes such as earthquakes, to individuals that have been trapped under fallen or moving masonry.

Contents

People with crushing damage present some of the greatest challenges in field medicine, and may need a physician's attention on the site of their injury. Appropriate physiological preparation of the injured is mandatory. [2] It may be possible to free the patient without amputation; however, field amputations may be necessary in drastic situations.

Pathophysiology

Seigo Minami, a Japanese physician, first reported the crush syndrome in 1923. [2] [3] [4] He studied the pathology of three soldiers who died in World War I due to kidney failure. The renal changes were due to the buildup of excess myoglobin, resulting from the destruction of muscles from lack of oxygen. The progressive acute kidney failure is because of acute tubular necrosis.

The syndrome was later described by British physician Eric Bywaters in patients during the 1941 wartime bombing of London (the Blitz). [5] [6] It is a reperfusion injury that appears after the release of the crushing pressure. The mechanism is believed to be the release into the bloodstream of muscle breakdown products—notably myoglobin, potassium and phosphorus—that are the products of rhabdomyolysis (the breakdown of skeletal muscle damaged by ischemic conditions).

The specific action on the kidneys is not understood completely, but may be due partly to nephrotoxic metabolites of myoglobin.

The most devastating systemic effects can occur when the crushing pressure is suddenly released, without proper preparation of the patient, causing reperfusion syndrome. In addition to tissue directly suffering the crush mechanism, tissue is then subjected to sudden reoxygenation in the limbs and extremities. Without proper preparation, the patient, with pain control, may be cheerful before recovery, but then may suddenly die shortly thereafter. This sudden failure is called the "smiling death". [7]

These systemic effects are caused by a traumatic rhabdomyolysis. As muscle cells die, they absorb sodium, water, and calcium; the rhabdomyolysis releases potassium, myoglobin, phosphate, thromboplastin, creatine, and creatine kinase.[ citation needed ]

Crush syndrome can directly come from compartment syndrome, if the injury is left untreated. [8] Symptoms include the 5 Ps: pain, pallor, paresthesias (pins and needles), paralysis, and pulselessness. [9]

Treatment

There is no distinct treatment option that can undo the effects and damage from rhabdomyolysis because it is a necrosis. [10] However, the rate of the pathology that can lead to more complications can be decreased by acting early and consistently. [11] Overall treatment depends on preventing kidney failure (renal failure) which is done by rehydrating the patient. It also depends on making urine have a more basic pH (alkalinization of urine). [11]

Crush syndrome progression (MC most common,# fracture, MODS multiple organ dysfunction syndrome, RTN renal tubular necrosis). Acute compartment and crush syndrome.jpg
Crush syndrome progression (MC most common,# fracture, MODS multiple organ dysfunction syndrome, RTN renal tubular necrosis).

Immediate untreated crush syndrome death is caused by severe head injury, torso injury with damaged abdominal organs, and asphyxia (excessive loss of oxygen). Early untreated crush syndrome death is caused by hyperkalemia and by hypovolemic shock. Late untreated crush syndrome death is caused by renal failure, coagulopathy and hemorrhage, and sepsis. [11]

Due to the risk of crush syndrome, current recommendation to nonprofessional first-aiders (in the UK) is to not release those with a crush injury who have been trapped for more than 15 minutes. [12] Treatment consists of not releasing the tourniquet, overloading the patient with fluid using Dextran 4000 IU, and slow release of pressure. If pressure is released during first aid, then fluid is restricted and an input-output chart for the patient is maintained.[ citation needed ]

Field management

As mentioned, permissive hypotension (restrictive fluid therapy) is unwise. Careful fluid overload and administration of intravenous sodium bicarbonate is wise, especially if the crushing weight is on the patient for more than four hours, but often if it persists more than one hour. The San Francisco emergency services protocol calls for a basic adult dose of a 2 L bolus of normal saline followed by 500 mL/h, limited for "pediatric patients and patients with history of cardiac or renal dysfunction." [13]

Use of a tourniquet can stall the life-threatening consequences of a crush related injury and can be a second option if the person cannot immediately have the fluids that were lost be medically replaced back into the body. Tourniquet measures should be taken if the person has been entrapped for more than two hours. [14]

Initial hospital management

The clinician must protect the patient against hypotension, kidney failure, acidosis, hyperkalemia and hypocalcemia. Admission to an intensive care unit, preferably one experienced in trauma medicine, may be appropriate; even well-seeming patients need observation. Treat open wounds as surgically appropriate, with debridement, antibiotics and tetanus toxoid; apply ice to injured areas. Breathing and circulation must be checked and the patient should be given oxygen if eligible. Oral or intravenous fluids must be given depending on the measured amounts of electrolytes, arterial blood gases, and muscle enzymes. [11]

Intravenous hydration of up to 1.5 L/h should continue to prevent hypotension. A urinary output of at least 300 mL/h should be maintained with IV fluids and mannitol, and hemodialysis considered if an increase in urine is not achieved. Use intravenous sodium bicarbonate to keep the urine pH at 6.5 or greater, to prevent myoglobin and uric acid deposition in kidneys.

To prevent hyperkalemia/hypocalcemia, consider the following adult doses: [1]

Even so, abnormal heart rhythms may develop; electrocardiographic monitoring is advised, and specific treatment begun promptly.

Related Research Articles

<span class="mw-page-title-main">Rhabdomyolysis</span> Human disease (condition) in which damaged skeletal muscle breaks down rapidly

Rhabdomyolysis is a condition in which damaged skeletal muscle breaks down rapidly, often due to high intensity exercise over a short period. Symptoms may include muscle pains, weakness, vomiting, and confusion. There may be tea-colored urine or an irregular heartbeat. Some of the muscle breakdown products, such as the protein myoglobin, are harmful to the kidneys and can cause acute kidney injury.

<span class="mw-page-title-main">Kidney failure</span> Disease where the kidneys fail to adequately filter waste products from the blood

Kidney failure, also known as end-stage renal disease (ESRD), is a medical condition in which the kidneys can no longer adequately filter waste products from the blood, functioning at less than 15% of normal levels. Kidney failure is classified as either acute kidney failure, which develops rapidly and may resolve; and chronic kidney failure, which develops slowly and can often be irreversible. Symptoms may include leg swelling, feeling tired, vomiting, loss of appetite, and confusion. Complications of acute and chronic failure include uremia, hyperkalemia, and volume overload. Complications of chronic failure also include heart disease, high blood pressure, and anaemia.

Diuresis is the excretion of urine, especially when excessive (polyuria). The term collectively denotes the physiologic processes underpinning increased urine production by the kidneys during maintenance of fluid balance.

<span class="mw-page-title-main">Hypocalcemia</span> Low calcium levels in ones blood serum

Hypocalcemia is a medical condition characterized by low calcium levels in the blood serum. The normal range of blood calcium is typically between 2.1–2.6 mmol/L, while levels less than 2.1 mmol/L are defined as hypocalcemic. Mildly low levels that develop slowly often have no symptoms. Otherwise symptoms may include numbness, muscle spasms, seizures, confusion, or in extreme cases cardiac arrest.

<span class="mw-page-title-main">Acute kidney injury</span> Sudden decrease in kidney function that develops within 7 days

Acute kidney injury (AKI), previously called acute renal failure (ARF), is a sudden decrease in kidney function that develops within 7 days, as shown by an increase in serum creatinine or a decrease in urine output, or both.

Tumor lysis syndrome (TLS) is a group of metabolic abnormalities that can occur as a complication from the treatment of cancer, where large amounts of tumor cells are killed off (lysed) from the treatment, releasing their contents into the bloodstream. This occurs most commonly after the treatment of lymphomas and leukemias and in particular when treating non-Hodgkin lymphoma, acute myeloid leukemia, and acute lymphoblastic leukemia. This is a potentially fatal complication and patients at increased risk for TLS should be closely monitored while receiving chemotherapy and should receive preventive measures and treatments as necessary. TLS can also occur on its own although this is less common.

<span class="mw-page-title-main">Hyperkalemia</span> Excess potassium in the blood

Hyperkalemia is an elevated level of potassium (K+) in the blood. Normal potassium levels are between 3.5 and 5.0 mmol/L (3.5 and 5.0 mEq/L) with levels above 5.5 mmol/L defined as hyperkalemia. Typically hyperkalemia does not cause symptoms. Occasionally when severe it can cause palpitations, muscle pain, muscle weakness, or numbness. Hyperkalemia can cause an abnormal heart rhythm which can result in cardiac arrest and death.

<span class="mw-page-title-main">Electrolyte imbalance</span> Abnormality in the concentration of electrolytes in the body

Electrolyte imbalance, or water-electrolyte imbalance, is an abnormality in the concentration of electrolytes in the body. Electrolytes play a vital role in maintaining homeostasis in the body. They help to regulate heart and neurological function, fluid balance, oxygen delivery, acid–base balance and much more. Electrolyte imbalances can develop by consuming too little or too much electrolyte as well as excreting too little or too much electrolyte. Examples of electrolytes include calcium, chloride, magnesium, phosphate, potassium, and sodium.

<span class="mw-page-title-main">Hypovolemic shock</span> Medical emergency due to low blood volume

Hypovolemic shock is a form of shock caused by severe hypovolemia. It can be caused by severe dehydration or blood loss. Hypovolemic shock is a medical emergency; if left untreated, the insufficient blood flow can cause damage to organs, leading to multiple organ failure.

<span class="mw-page-title-main">Loop diuretic</span> Diuretics that act along the loop of Henle in the kidneys

Loop diuretics are pharmacological agents that primarily inhibit the Na-K-Cl cotransporter located on the luminal membrane of cells along the thick ascending limb of the loop of Henle. They are often used for the treatment of hypertension and edema secondary to congestive heart failure, liver cirrhosis, or chronic kidney disease. While thiazide diuretics are more effective in patients with normal kidney function, loop diuretics are more effective in patients with impaired kidney function.

Oliguria or hypouresis is the low output of urine specifically more than 80 ml/day but less than 400ml/day. The decreased output of urine may be a sign of dehydration, kidney failure, hypovolemic shock, hyperosmolar hyperglycemic nonketotic syndrome (HHNS), multiple organ dysfunction syndrome, urinary obstruction/urinary retention, diabetic ketoacidosis (DKA), pre-eclampsia, and urinary tract infections, among other conditions.

Cerebral salt-wasting syndrome (CSWS), also written cerebral salt wasting syndrome, is a rare endocrine condition featuring a low blood sodium concentration and dehydration in response to injury (trauma) or the presence of tumors in or surrounding the brain. In this condition, the kidney is functioning normally but excreting excessive sodium. The condition was initially described in 1950. Its cause and management remain controversial. In the current literature across several fields, including neurology, neurosurgery, nephrology, and critical care medicine, there is controversy over whether CSWS is a distinct condition, or a special form of syndrome of inappropriate antidiuretic hormone secretion (SIADH).

<span class="mw-page-title-main">Hepatorenal syndrome</span> Human disease

Hepatorenal syndrome (HRS) is a life-threatening medical condition that consists of rapid deterioration in kidney function in individuals with cirrhosis or fulminant liver failure. HRS is usually fatal unless a liver transplant is performed, although various treatments, such as dialysis, can prevent advancement of the condition.

<span class="mw-page-title-main">Hypoaldosteronism</span> Medical condition

Hypoaldosteronism is an endocrinological disorder characterized by decreased levels of the hormone aldosterone. Similarly, isolated hypoaldosteronism is the condition of having lowered aldosterone without corresponding changes in cortisol.

<span class="mw-page-title-main">Myoglobinuria</span> Presence of myoglobin in the urine

Myoglobinuria is the presence of myoglobin in the urine, which usually results from rhabdomyolysis or muscle injury. Myoglobin is present in muscle cells as a reserve of oxygen.

<span class="mw-page-title-main">Metabolic alkalosis</span> Abnormally high tissue pH due to metabolic dysfunction

Metabolic alkalosis is an acid-base disorder in which the pH of tissue is elevated beyond the normal range (7.35–7.45). This is the result of decreased hydrogen ion concentration, leading to increased bicarbonate, or alternatively a direct result of increased bicarbonate concentrations. The condition typically cannot last long if the kidneys are functioning properly.

Capillary leak syndrome, or vascular leak syndrome, is characterized by the escape of blood plasma through capillary walls, from the blood circulatory system to surrounding tissues, muscle compartments, organs or body cavities. It is a phenomenon most commonly witnessed in sepsis, and less frequently in autoimmune diseases, differentiation syndrome, engraftment syndrome, hemophagocytic lymphohistiocytosis, the ovarian hyperstimulation syndrome, viral hemorrhagic fevers, and snakebite and ricin poisoning. Pharmaceuticals, including the chemotherapy medications gemcitabine and denileukin diftitox, as well as certain interleukins and monoclonal antibodies, can also cause capillary leaks. These conditions and factors are sources of secondary capillary leak syndrome.

The Hs and Ts is a mnemonic used to aid in remembering the possible reversible causes of cardiac arrest. A variety of disease processes can lead to a cardiac arrest; however, they usually boil down to one or more of the "Hs and Ts".

Exertional rhabdomyolysis (ER) is the breakdown of muscle from extreme physical exertion. It is one of many types of rhabdomyolysis that can occur, and because of this, the exact prevalence and incidence are unclear.

Eric George Lapthorne Bywaters was a British physician.

References

  1. 1 2 "Blast Injuries: Crush Injury & Crush Syndrome" (PDF). Centers for Disease Control. Archived from the original (PDF) on 2016-03-04. Retrieved 2015-01-19.{{cite journal}}: Cite journal requires |journal= (help)
  2. 1 2 Minami, Seigo (1923). "Über Nierenveränderungen nach Verschüttung". Virchows Archiv für Pathologische Anatomie und Physiologie und für Klinische Medizin. 245 (1): 247–267. doi:10.1007/BF01992107. S2CID   28949830.
  3. ↑ Medical discoveries - Who and when- Schmidt JF. Springfield: CC Thomas, 1959. p.115.
  4. ↑ Morton's medical bibliography -An annotated check-list of texts illustrating History of medicine (Garrison-Morton). Aldershot: Solar Press; 1911. p.654.
  5. ↑ synd/3870 at Who Named It?
  6. ↑ Bywaters, E. G.; Beall, D. (1941). "Crush injuries with impairment of renal function". British Medical Journal . 1 (4185): 427–432. doi:10.1136/bmj.1.4185.427. PMC   2161734 . PMID   20783577.
  7. ↑ Nancy Caroline (2007). Nancy Caroline's Emergency Care in the Streets: Trauma Medical. Vol. 2 (6th ed.). Jones & Bartlett Learning. pp. 19–13. ISBN   9780763742393.
  8. ↑ Pallister, Ian (20 May 2016). "Management of Compartment Syndrome and Crush Syndrome". Orthopaedic Trauma in the Austere Environment. pp. 363–368. doi:10.1007/978-3-319-29122-2_28. ISBN   978-3-319-29120-8.
  9. ↑ "Compartment Syndrome - The 5 Ps". Ausmed. 17 May 2016. Archived from the original on 13 September 2022. Retrieved 6 January 2020.
  10. ↑ Sever, Mehmet (30 April 2011). "Management of Crush Syndrome Casualties after Disasters". Rambam Maimonides Medical Journal. 2 (2): e0039. doi:10.5041/RMMJ.10039. PMC   3678930 . PMID   23908797.
  11. 1 2 3 4 Smith, Jason (23 October 2002). "Crush Injury and Crush Syndrome". Ovid. 54.
  12. ↑ St John Ambulance UK First Aid Manual, 10th Edition, p. 118
  13. ↑ "Crush Syndrome" (PDF). San Francisco Emergency Medical Services Agency. 1 July 2002. Protocol: #P-101. Archived from the original (PDF) on 28 October 2011.{{cite journal}}: Cite journal requires |journal= (help)
  14. ↑ Walters, Thomas (28 December 2016). "Crush Syndrome - Prolonged Field Care" (PDF). Joint Trauma System Clinical Practice Guideline. Archived from the original (PDF) on 21 June 2022.
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