CRUSH

PATHOPHYSIOLOGY
Our patient had many injuries. I do not intend examining all of these, but will highlight Crush Injury with references to Compartment Syndrome and Rhabdomyolysis. The pathophysiology of crush injury, apparently, is still poorly understood. 1What is it
Definitions
Crush Injury
There is a definite difference between an entrapped patient, and a patient with a crush injury. Bones may be fractured, but unless the limb and muscle is squashed there is no crush injury. "Case reports usually relate to patients that have been trapped by limbs. Such forces applied to head, chest and abdomen would not be compatible with survival 2 "The main injury is to the muscles. There is no distal pulse because of arterial occlusion, causing discolouration of the skin, ischaemia and eventual necrosis. Crush injury syndrome develops when the patient lives beyond the extrication."
Dr M. Michaelson (1992) states that the shortest duration reported in literature for crush injury is four hours.3 His opinion is markedly different to the training notes provided by the ASTC and other sources that quote 20 minutes as the minimum compression time. Apparently the Germans were the first to report crush injury during World War 1, but Bywaters 4 was the first to study the occurrence when he noticed that people who were trapped under the bombardment, although they seemed only slightly injured, died shortly after extrication.
Compartment Syndrome
This syndrome is very similar to crush syndrome but it is well described and well understood.5 It is caused by the rising of pressure within the muscle compartments. This pressure increases and occludes venous drainage from the compartment, which further elevates the compartment pressure. The result is muscle necrosis within the compartment. The best treatment for this condition is to release the pressure of the compartment through facsiotomy.
Rhabdomyolysis
Is the "disintegration of striated muscle fibres with excretion of myoglobin in the urine".6 This muscle breakdown and the release of muscle contents into the plasma can occur with crush injury syndrome and compartment syndrome. It is often detected by severe pain on the passive stretching of an injured muscle group. If diagnosed early, treatment can begin before rhabdomyolysis occurs.
CRUSH INJURY
Symptoms:
Signs:

Dizziness
Pale, cold and clammy skin

Faintness
Pulse slow at first - rapid and feeble

Nausea
Resps shallow and rapid

Thirst
Altered consc. level - coma
When muscle tissue is severely compressed, as in a crush injury, the cells are damaged and their contents spill out into the surrounding interstitial spaces. Potassium cations (K+) are freed and bicarbonate anions (HCO,-) are lost. They may escape into the circulation, raising the serum potassium level and producing metabolic acidosis. Ischaemic necrosis of the skeletal muscle will develop with prolonged arterial obstruction. Lactic acid is formed due to the resulting anaerobic metabolism.
Myoglobin, a large protein, escapes the broken muscle tissue leading to renal complications later and hypovolaemic shock may develop. If the patient survives the lifting weight, the crush injury becomes a syndrome. "There is no limb edema initially; the gross edema takes time to develop but, once developed, is most striking. In fact, it is so striking that it dominates the clinical picture."7
CRUSH SYNDROME
Definition
A syndrome is: "a combination of symptoms resulting from a single cause or so commonly occurring together as to constitute a distinct clinical picture".8 "Crush syndrome may be labelled traumatic rhabdomyolysis."9
So, we have a single cause, that of a crush injury to a limb, that results in the distinct clinical picture of:

Ischaemic Muscle Necrosis.

Hyperkalaemia.

Low serum calcium.

Low serum sodium.

Hypovolaemia.

Metabolic Acidosis/Lactic acid formation.

Myoglobinuria and Myoglobinaemia/Rhabdomyolysis.

Renal Failure.
Ischaemic Muscle Necrosis
This is caused by the death of muscle, in large sections or patches, as a result of lack of an oxygenated blood supply. The supply having been obstructed in this case by prolonged pressure to the tissue and vessels below the point of compression, where ischaemia develops into necrosis.
Hyperkalaemia
When K + is released from crushed cells and enters the circulatory system, it increases serum potassium levels, causing the heart to become extremely dilated and flaccid. K + is an electrolyte that slows the heart rate and reflects as a tall, peaked T wave and widening QRS complexes on an ECG. If the doses of K + are large enough, it can interfere with the conductivity of the heart muscle by blocking impulses through the AV node, causing fatal cardiac arrhythmias such as VF.
Low serum calcium
(Due to blood and fluid loss).
Low serum sodium
(Due to blood and fluid loss is allowed inside the crushed cells when K+ leaked out).
Hypovolaemia
Hypovolaemic shock is caused by loss of blood and body fluids from damaged blood vessels (veins, arteries and capillaries) into the crushed and ischaemic areas. There remains less circulating blood.
Metabolic acidosis/Lactic acid
When tissue is crushed, a loss of bicarbonate occurs, the pH level lowers. As blood is prevented from reaching the crush site, the cells are no longer able to obtain their supply of oxygen for aerobic metabolism. Anaerobic metabolism occurs, with the production of lactic acid as a by product. The pH of the blood lowers - it becomes more acidic. This is dangerous.
Myoglobinuria and Myoglobinaemia/Rhabdomyolysis
Remember from the definition earlier that rhabdomyolysis is muscle breakdown where myoglobin is released. Myoglobin is a large iron containing protein. It is usually found in skeletal and cardiac muscle. It acts as an intracellular carrier which aids the diffusion of oxygen throughout the muscle cell. It can also provide "a short-term store of oxygen which the cell can call upon during sudden changes in activity".10 It is not found in blood or urine unless tissue is damaged and it is allowed to diffuse into the bloodstream (myoglobinaemia) or into the kidneys and urinary system (myoglobinuria). It is usually witnessed as a brownish or dark blood discolouration when voiding. The molecules, being so large, block the fine tubules of the kidneys which also leads to renal failure.
Renal Failure
Prolonged hypotension caused by hypovolaemic shock may lead to extended vasoconstriction of the renal artery. This is perhaps the main cause of acute Renal Ischaemia and subsequent Renal Failure, but myoglobinaemia and myoglobinuria causing the blocking of the renal tubules leads to chronic renal failure.
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TREATMENT
There are two avenues of thought:
(1) Tourniquets, retrieval teams or doctors, and slow release of the weight only after everything has been prepared and set up. The great danger occurs when the crush victim is released and circulation of the ischaemic area begins again. Rapid blood flow into the crush site causing a sudden drop in BP and toxins flowing back to the heart and kidneys are of major concern.
While current recommended treatment consists of:

DRABC.

Oxygen therapy(1OO).

IV therapy (two lines - crystalliod solution initially, immediately followed by a colliod solution e.g. Haemaccel. Given until BP reaches an acceptable level).

Analgesia - beware that a renal condition is developing.

Monitor. ECG.

Maintain body temperature.

Reassurance.

Immobilisation of fractures where possible.

Other medical problems that may require treatment.

Some Ambulance services have approved the use of MAST Suits ... do not fit them over crushed limbs, lower torso is recommended to impede the circulation of toxins.
Management immediately prior to release:

Apply an arterial tourniquet.

Infusion rate increased.

ECG checked carefully.

10Omls of 8.4 Sodium bicarbonate infused prophylactically.

Reassurance to the patient that care will be taken.
It is stressed that the compression force be removed slowly.
Management immediately after release
Continue monitoring. If arrhythmias develop treat appropriately. Be on the lookout for peaked T waves, disappearing P waves, QRS widening, and a sine wave pattern forming leading to VF.
A Slowly release tourniquet and reapply it if necessary. & Continue IV.
Transport urgently to emergency department.
It is even suggested that, if a tourniquet cannot be fitted, pressure points be sought to stop arterial blood flow until the weight is lifted and a tourniquet can be placed.
(2) Too much time is wasted waiting for retrieval teams or doctors to arrive at the scene when patients should be released quickly, before more toxins develop. Dr John A. Chambers FRCS, Director of the Emergency Department, Dunedin Hospital, NZ, states, "Fear of sudden collapse and death shortly after extrication is rather over-emphasised and this happens very rarely. There are no proven advantages to be gained by releasing the crushing force slowly, using tourniquets above the crushed part or by waiting for the presence of a doctor before releasing the patient. The important factor is time and the patient should be released as soon as it is safely possible."11" His argument is controversial and contrary to current practice.
Dr Chambers recommends treatment for muscle crushed injury victims as follows:

& ABCS.

Combat hypovolaemia as necessary.

50Onils crystalloid per hour (to clear the renal tubules of myoglobin).

Analgesia prn.

Consider IV Diuretic, Bicarbonate, Calcium in consultation with doctor at the receiving hospital.
This treatment is very similar to the protocol developed by Dr M. Michaelson in Israel which is designed specifically to prevent acute renal failure in crush injury victims.
1. Combat hypovolaemia with crystalloids.
2. Infuse hourly 500 ml of crystalloids and 22.4 meq bicarbonate.
3. If diuresis is < 300ml/hr, give mannitol lg/kg per dose.
4. If blood pH is > 7.45, give 250 mg acetazolamide.
5. Monitor vital signs hourly, plus pH and volume.
6. Monitor every six hours osmolarity and electrolytes in blood and blood gases

BLAST
• Primary Blast Injury:
o These injuries are caused solely by the direct effect of blast overpressure on tissue. Since air is easily compressible by pressure while water is not, this almost always affects air-filled structures.
o Pulmonary barotrauma is the most common fatal primary blast injury. This includes pulmonary contusion, systemic air embolism and free-radical associated injuries including thrombosis, lipoxygenation and disseminated intravascular coagulation (DIC). ARDS may be a result of direct lung injury or shock due to other body injuries.
o An acute gas embolism (AGE), which is a form of pulmonary barotrauma, requires special attention. Air emboli most commonly occlude blood vessels in the brain or spinal cord. The resulting neurologic symptoms must be differentiated from the direct effect of trauma.
o Intestinal barotrauma is more common with in-water rather than air blast injuries. Although the colon is usually affected, any portion of the GI tract may be injured.
o The ear is the organ most frequently injured by primary blast injury. Acoustic barotrauma most commonly consists of TM rupture. Hemotympanum without perforation has also been reported. Ossicle fracture or dislocation may occur with very high energy explosions.
• Secondary Blast Injury:
o These injuries are caused by flying objects striking the patient.
o In many explosions, this mechanism is responsible for the majority of casualties. For example, the glass facade of the Murrow Federal Building in Oklahoma City shattered into thousands of heavy glass chunks, which were propelled through inhabited areas of the building with devastating results.
o The casings of military explosives (e.g. hand grenades) are specifically designed to fragment and maximize the damage caused by flying debris (a.k.a. shrapnel).
o Civilian terrorist bombers (e.g., Olympic Park in Atlanta) often deliberately place screws or other small metal objects around their weapons to increase secondary blast injuries.
• Tertiary Blast Injury:
o These injuries are caused by the patient flying through the air and striking other objects. They are generally only seen with high-energy explosions.
o Unless the explosion is of extremely high energy or is focused in some way (e.g., through a door or hatch), the victim must generally be very close to the explosion source.
o Together with secondary blast injuries, this was responsible for most of the pediatric casualties in Oklahoma City. There was a very high incidence of skull fractures (including 17 children with open brain injuries) and long bone injuries including traumatic amputations.
• Miscellaneous Blast-Related Injuries:
o These include other injuries caused by the explosion. They may include the following:
o Toxic inhalations and exposures, radiation exposure and burns (chemical or thermal)
o Asphyxiation in fires, including CO and CN poisoning following incomplete combustion, dust inhalation, including coal and asbestos exposure
o Crush injuries from collapsed structures and displaced heavy objects


MAŠČOBNA

Introduction
Fat embolism syndrome follows long bone fractures. Its classic presentation consists of an asymptomatic interval followed by pulmonary and neurologic manifestations combined with petechial hemorrhages. The syndrome follows a biphasic clinical course. The initial symptoms are probably caused by mechanical occlusion of multiple blood vessels with fat globules that are too large to pass through the capillaries. Unlike other embolic events, the vascular occlusion in fat embolism is often temporary or incomplete since fat globules do not completely obstruct capillary blood flow because of their fluidity and deformability. The late presentation is thought to be a result of hydrolysis of the fat to more irritating free fatty acids which then migrate to other organs via the systemic circulation.

Etiology
Many aspects of the fat embolism syndrome remain poorly understood, and disagreement about its etiology, pathophysiology, diagnosis and treatment persists. It is therefore difficult to determine the incidence of this complication. It ranges from less than 2 to 22 in different studies. Fat embolism has been associated with many nontraumatic disorders. It is most common after skeletal injury, and is most likely to occur in patients with multiple long bone and pelvic fractures. Patients with fractures involving the middle and proximal parts of the femoral shaft are more likely to experience fat embolism. Age also seems to be a factor in the development of FES: young men with fractures are at increased risk.

Fat embolism syndrome ( FES ) refers to the constellation of clinical manifestations that may develop after trauma, and specially after fractures, when fat droplets act as emboli, becoming impacted in the pulmonary microvasculature and other microvascular beds, especially in the brain. Embolism begins rather slowly and attains a maximum in about 48 hours. Open fractures furnish less emboli than closed fractures. Long bones, pelvis and ribs furnish more emboli; sterner and clavicle furnish less.
Other forms Other forms of trauma that rarely result in fat embolism include massive soft tissue injury, severe burns and liposuction. Nontraumatic settings occasionally lead to fat embolism. These include conditions associated with fatty liver, prolonged corticosteroids therapy, acute pancreatitis, osteomyelits, and conditions causing bone infarcts, such as sickle cell disease.
The principal clinical features of fat embolism syndrome are: Respiratory failure, Cerebral dysfunction and Petechiae
The source of fat droplets can be from disrupeted fat-containing tissues, or as a result from the release of some substance that alters fat emulsion in the plasma. As support for the last explanation, is the observation that intravascular coagulation occurs coincident with thrombocytopenia.
It is also clear that the syndrome is not simply a consequence of mechanical obstruction of small vessels by fat droplets. An important aspect of the pathogenesis of FES appears to be endothelial injury caused by fatty acids released from impacted fat droplets by lipoprotein lipase, with ensuring increased microvascular permeability and fluid leakage into interstitial spaces.
The onset of FES is sudden, with Restlessness and vague pain in the chest. Fever occurs, often in excess of 38,3 C (101 F), with a disproportionatelly pulse rate. Drowsiness with oliguria is almost pathognomonic; but the clinical diagnosis is definite if all the three following criteria are present within 72 hours after traumatic fracture.
1) Otherwise unexplained dyspnea, tachypnea, arterial hypoxemia with cyanosis and diffuse alveolar infiltrates on chest X-ray
2) Otherwise unexplained signs of cerebral dysfunction, such as confusion, delirium or coma.
3) Petechiae over the upper half of the body, conjunctive, oral mucosa and retinae.
Search for fat droplets in the urine, blood or CSF are occasionally helpful. In a recent study, large fat droplets were formed in brochoalveolar lavage cells of patients with definite fat embolism syndrome.
Other laboratories tests can be helpful are:platelet count, red blood cell count lipase and calcium serum dosage(which can be elevated and decrease respectively).
Management of fat embolism syndrome is supportive and consists primarily of ensuring good arterial oxygenation. Supplemental oxygen is given to maintain the arterial oxygen tension in the normal range. Restriction of fluid intake and the use of diuretics can be done (if systemic perfusion can be maintained), to minimize fluid accumulation in the lungs .
Prompt surgical stabilization of long bones fractures and correcting or preventing decreased systemic perfusion, reduce the risk of the syndrome.
The mortality rate from fat embolism syndrome is 10 percent or less and thus is clearly much lower then the 50 percent or greater mortality rate for most causes of the adult respiratory distress syndrome. Even severe respiratory failure associated with fat embolism seldom leads to death.
of trauma that rarely result