[Lethal Pressure Crush 47
Sharif Garmon
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Background: Crush syndrome (CS) is characterized by ischemia/reperfusion-induced rhabdomyolysis and the subsequent onset of systemic inflammation. CS is associated with a high mortality, even when patients are treated with conventional therapy. We hypothesized that treatment of lethal CS rat model with dexamethasone (DEX) have therapeutic effects on the laboratory findings and clinical course and outcome.
Methods: To create a CS model, anesthetized rats were subjected to bilateral hind limb compression with rubber tourniquets for 5 hours and randomly divided into three groups as follows: saline-treated CS group, CS groups treated with low (0.1 mg/kg) and high doses (5.0 mg/kg) of DEX. Saline for the CS group or DEX for the DEX-treated CS groups was intravenously administered immediately before reperfusion. Under continuous monitoring and recording of arterial blood pressures, blood and tissue samples were collected for histologic and biochemical analysis at designated period before and after reperfusion.
Results: Ischemic compression of rat hind limbs reduced the nitrite content in the crushed muscle, and the subsequent reperfusion induced reactive oxygen species-mediated circulatory collapse and systemic inflammation, finally resulting in a mortality rate of 76% by 48 hours after reperfusion. A single injection of high-dose DEX immediately before reperfusion activated endothelial nitric oxide synthase (eNOS) by sequential phosphorylation through the nongenomic phosphoinositide 3-kinase (PI3K)-Akt-eNOS signaling pathway. DEX also exhibited anti-inflammatory effects by modulating proinflammatory and anti-inflammatory mediators, consequently suppressing myeloperoxidase activities and subsequent systemic inflammation, showing a complete recovery of the rats from lethal CS.
Crush syndrome is a medical condition characterized by significant systemic symptoms resulting from toxins released by crushed muscle tissue. Crush injuries are commonly seen in severe trauma, and include direct soft tissue destruction, bony injury and limb ischemia.
For example, intra-compartmental pressures as little as 40 mmHg, lasting greater than eight hours, can precipitate this syndrome. Knowing that muscle compartment pressures can reach up to 240 mmHg in a trauma setting, you can imagine how quickly this syndrome can develop. (See Figure 1.)
This hypoxia forces metabolism down the anaerobic pathway, resulting in increased lactic acid formation. Additional toxin release from the limb will remain localized at the site of trauma, as venous return proximal to the injury site is impeded.
Once the cause of crush injury and pressure is relieved, all toxins from the damaged tissue cellular components will be released systemically. This systemic release can ultimately be fatal, which should prompt extreme caution and early care when managing a patient with a potential crush injury.
The major detrimental components released during crush injury are myoglobin and potassium. Myoglobin can collect in the kidney faster than it can be eliminated, causing injury to the renal tubular cells, leading to acute renal failure. Potassium leaking from damaged cells will increase intravascular potassium, potentially leading to fatal dysrhythmias.
Examples of other toxins released from damaged cells include: lactic acid, histamine, nitric oxide and thromboplastin. Lactic acid causes metabolic acidosis and, like potassium, can lead to cardiac dysrhythmias. Histamine release causes vasodilation and bronchoconstriction, resulting in dyspnea and possible respiratory distress. Nitric oxide can worsen hypovolemic shock by causing vasodilation. Thromboplastin can lead to disseminated intravascular coagulation.
Several other toxins have also been identified to cause electrolyte disturbances and can have a negative effect, including uric acid, calcium, intracellular enzymes, leukotrienes and phosphate. As many of the toxins released cause vasodilatation, this results in increased capillary bed leakage, edema, third spacing of fluids and hypotension.
Early prehospital resuscitation with IV normal saline is vital to preventing mortality. Patients have been seen going into cardiac arrest just seconds after being rescued from their confinement. Early causes of arrest are commonly due to hypovolemia, hyperkalemia and severe metabolic acidosis, as previously mentioned.
Management of the crush injury patient begins as soon as safely possible, ideally while the patient is still entrapped. If the prehospital provider can safely access the patient, they should always begin with trauma triage, vital signs and cardiac monitoring.
Always remember to treat pain early. Use of the intranasal route for analgesia, via a mucosal atomization device (MAD) or nebulizer (if no MAD is available), should be utilized prior to obtaining IV access.
Fentanyl is a great choice for pain control due to its decreased effect on blood pressure, but will likely need to be re-dosed multiple times during a prolonged extrication. Use of nephrotoxic drugs, such as ketorolac or other NSAIDs, should be avoided.
Due to confinement and positioning, if IV access poses a challenge, early utilization of intraosseous (IO) access is recommended. Initial management includes aggressive fluid hydration with normal saline for treatment of hypovolemia and to prevent acute renal failure from excess rhabdomyolysis.
Patients with significant comorbidities, or known congestive heart failure, should still receive fluids but must be monitored closely for fluid overload. Particularly, if you note the patient becoming dyspneic or developing crackles/rales during lung auscultation, the IV fluid administration rate should be titrated down.
Once extrication is successful, cardiac monitoring is paramount. Early and ongoing ECG monitoring for hyperkalemia is essential so therapy can be initiated immediately. Any ECG signs of hyperkalemia warrant treatment with calcium chloride, beta agonist (albuterol), insulin/glucose and sodium bicarbonate.4
If renal failure progresses, dialysis may be indicated. Additional infections secondary to the trauma site may lead to sepsis. Compartment syndrome, particularly of the lower limbs, is also a common sequela of crush injury, which may require fasciotomy or even amputation of the limb.
Some rescuers have been hesitant to make progress on extrication due to the patient calling out in pain with any movement of the entrapping material and ketamine may be required to facilitate timely extrication.
A humoral IO line is started, and your patient has already received 2 L of normal saline. Two tourniquets have been placed above the injury site on standby and are not fully engaged. You prepare bicarbonate, calcium chloride, albuterol, insulin, D50, fentanyl, ketamine and more IV fluid.
Crush injury compartment syndrome is a condition that results from bleeding or swelling after an injury. The acute syndrome occurs when pressure builds up inside an enclosed muscle space within the body, like the compartments of the foot. This high pressure is dangerous, and it can impede blood flow to and from affected tissues. In many cases, crush injury compartment syndrome will require emergency surgery to prevent permanent injury, which can include severe tissue damage, loss of body function, or even death.
While acute compartment syndrome most commonly occurs during bone breaks and foot crush injuries, there are several types of compartment syndrome. The chronic form of this condition develops over days or weeks, and it may be caused by vigorous, regular exercise. This typically affects the lower leg, buttock, or thigh. By contrast, abdominal compartment syndrome also develops after a severe injury, surgery, or during critical illness, and it can affect the liver, bowels, kidneys, and other organs.
Around 75 percent of the time, crush injury compartment syndrome is caused by a broken bone, but burns, crush injuries, too-tight bandaging, surgery to blood vessels, blood clots, and prolonged limb compression (such as that experienced while unconscious) can also cause the condition. Crush injury compartment syndrome can develop rapidly over the course of hours or days. There are many symptoms, but the most common are listed below:
A physical exam is typically needed to diagnose crush injury compartment syndrome. In many cases, the doctor will need to measure the pressure inside the affected body part. This typically involves inserting a needle, which is attached to a pressure monitor, into the suspected area. Plastic catheters may also be placed to continuously monitor the pressure.
Importantly, compartment syndrome symptoms often have a delayed presentation. One study found that patients did not experience symptoms for the first 6 hours after the injury-causing accident. However, they were admitted in the operating room approximately 24 hours after the initial injury with signs of foot crush compartment syndrome. Your physician will be aware of the possibility of developing compartment syndrome after the initial trauma, but keep an eye on the injury. You may be discharged from the hospital within hours with instructions to return if symptoms begin to present.
If you are diagnosed with crush injury compartment syndrome, you may require immediate surgery to reduce the compartment pressure. Other treatments typically include providing fluids intravenously, providing oxygen through the nose or mouth, taking pain medications, and/or keeping the body part below the level of the heart, which will improve blood flow.
While a foot crush injury may sound like an easy condition to diagnose, your doctor will need to identify several symptoms before providing a definitive diagnosis. Each accident and injury cause is different, which means there is wide variety of symptom experiences. That said, the most common foot crush injury symptoms are listed below.
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