Your unit is called to the structural collapse of a home. Upon your arrival the medical branch director advises you there is one patient identified, trapped in the basement. Rescue personnel advise you he’s been trapped for approximately four hours, and it will take another hour to extricate him. In the interim they have gained access to the patient so you can begin your assessment and treatment.
You identify that the patient is a 36-year-old male, awake and talking to you and trapped under a pile of heavy rubble from the waist down. The patient has no prior medical history, appears anxious, and says he is in tremendous pain. He further says he feels cold. His airway is patent, and he does not appear to be in any significant respiratory distress. There is no visible bleeding noted. His current vital signs are heart rate 120, strong and regular; blood pressure 130/80; and respiratory rate 24.
You consult with your partner to develop a game plan for treatment. Based on the assessment of your patient, you concur he should be treated for crush syndrome and needs pain management.
Crush injury occurs as a result of direct physical crushing of the muscles by a heavy weight and usually involves compression of the legs, arms, and/or trunk. Crush injuries are typically associated with accidents but can occur in nontraumatic patients as well; patients who have been immobilized for a long time—like a patient unconscious following a stroke, drug overdose, or even just intoxication who has been in the same position for a long period—are susceptible to crush injury if pressure areas are not protected.
Crush injury can be broken down into two manifestations: compartment syndrome, a localized injury, and crush syndrome, a systemic injury.
Compartment syndrome occurs due to an increase in pressure within a closed compartment. This causes a decrease in perfusion and function of the tissues within that space. Compartment syndrome starts as early as when the compartment pressure exceeds capillary pressure and becomes clinically evident when the compartment pressure exceeds venous pressure. This results in lack of outflow, which worsens the compartment pressure as blood and edema back up in the space.
Early examination findings will show pain disproportionate to the injury and paresthesia. Pain is worse with passive stretching of the muscles in the compartment (e.g., dorsiflexion of the foot for a compartment syndrome of the calf). Late signs may reveal pallor and paralysis. Pulselessness is the last sign, occurring when the pressure finally exceeds arterial pressure. It usually results in the need for amputation because the nerves and muscles are dead. A fasciotomy is the treatment for a compartment syndrome and must be done emergently when one is diagnosed.
Crush syndrome is a reperfusion injury that leads to traumatic rhabdomyolysis. Once pressure is released, the muscle cell contents, such as potassium and myoglobin, are released systemically. Generally this occurs between 4–6 hours but may occur with entrapment of greater than one hour.
The pressure on the muscle causes damage to the muscle sarcolemma, the covering of the muscle fibers. The job of the sarcolemma is to keep certain contents inside the cell and certain contents outside. Once damage to the sarcolemma occurs, the permeability of the membrane increases, and cellular contents start to leak out, which can have a devastating effect on the body.
When the muscle is compressed, tissue perfusion is decreased, and the tissue becomes ischemic. The cell is unable to consume oxygen, causing it to switch from aerobic to anaerobic metabolism. Due to the lack of oxygen consumption, cells generate large amounts of lactic acid, which results in metabolic acidosis.
In normal cells there is more sodium and less potassium on the outside of the cell. Due to the damage to the cellular membrane during a crush injury, sodium, water, and calcium rush into the cell, causing swelling, while simultaneously potassium, myoglobin, purines, and other toxins leak out of the cells and into the surrounding tissue. All of this is maintained inside the compressed area. However, once the force is released, these cell contents are released into the systemic circulation.
As with any patient, and particularly in this case, scene safety is a priority. Due to the dangerous nature of most crush scenes, only specialized personnel with appropriate PPE should enter the area. This includes PPE for the patient, if possible, such as a helmet, eye protection, and, if oxygen is not available or necessary, then a face mask/N95 particulate mask. Evaluate the ABCs and use c-spine precautions if necessary, as well as tourniquets if appropriate. It is also important to keep the patient warm with warm fluids and heating blankets to prevent hypothermia.
Treatment of compartment and crush syndromes is focused on three different modalities: hypovolemic shock, acute renal failure, and metabolic abnormalities (such as acidosis and hyperkalemia).
Hypovolemic shock can occur due to bleeding from the original mechanism of injury.
Renal failure occurs when the limb is released from being under pressure. Free myoglobin, released from the crushed muscle cells, is too big to cross the glomerulus of the kidney. This results in plugging of the holes in the glomerulus and therefore a decrease in the glomerular filtration rate. This in turn prevents urine formation and therefore results in renal failure. High levels of acids and phosphates build and can further directly damage the kidneys. The release of lactic acid can also cause metabolic acidosis, which can result in hypotension if the levels get too high. It is important to monitor the patient’s urine output and color if possible; patients may have myoglobinuria, which causes the urine to be a reddish-brownish color and can be detected on a urine dipstick.
Once potassium is released into the systemic circulation, the resulting hyperkalemia can cause lethal dysrhythmias that lead to death if not treated promptly. Patients should have a cardiac monitor attached and a 12-lead ECG evaluated. Depending on potassium levels, ECG changes may be evident. On the 12-lead you should initially look for peaked T-waves and prolonged PR intervals. As the potassium levels increase, you will notice a widening of the QRS complexes into sine waves, which can then deteriorate into ventricular fibrillation. During the 2010 Haiti earthquake, point-of-care devices (e.g., i-STAT) were invaluable providing direct electrolyte and creatinine measurements in disaster field conditions.
Pain management will provide some comfort for the patient and reduce anxiety during the extrication process. Ketamine, if available, is a great choice for pain management. A typical dose is 0.3–0.5 mg/kg IV or 1–2 mg/kg IM/IN. The medication has a short duration, so reassess and monitor the patient frequently.
Ketamine causes the patient to have a sympathetic response, which increases their pulse and blood pressure and can cause bronchodilation. And while it generally maintains the respiratory drive, if given too fast, it may cause apnea. Other alternatives may include fentanyl or morphine.
Isotonic fluids can replace loss of extracellular fluid and help diurese extra potassium and avoid acute renal failure. Start fluid repletion before extrication of entrapped subjects with crush syndrome if possible.
Third-spacing at the site of muscle injury can worsen hypovolemia, so patients with rhabdomyolysis may require fluid resuscitation to initiate and maintain a vigorous diuresis. It is recommended to initially administer between 1–2 L/hr of isotonic solution prior to extrication, with reevaluation after the first hour.
Mannitol is a controversial treatment. It is thought that its antioxidizing and vasodilatory effects could aid in preventing renal failure. Mannitol may also decrease muscle intracompartmental pressure due to its tonicity.
Mannitol also expands extracellular volume, increasing urine output and preventing renal tubular cast formation, but despite these properties there does not appear to be any conclusive evidence showing its benefits.
Mannitol is contraindicated in heart failure, hypotension, and end-stage renal failure. Consider it on a case-by-case basis, as it has many contraindications and requires close monitoring of the patient.
It used to be thought that alkalinization of the urine by giving sodium bicarbonate would prevent precipitation of the myoglobin in the renal tubules and therefore protect the kidney. However, this has not been borne out in studies, and therefore most centers no longer use this therapy. However, it is indicated as a treatment for management of hyperkalemia because it shifts potassium into the cell and lowers serum potassium levels.
The goal of treating hyperkalemia is to protect the myocardium and drive potassium back into the cells. Calcium chloride helps protect the myocardium by antagonizing the membrane action of potassium. Albuterol, insulin, and sodium bicarbonate drive potassium back into the cell. Dextrose should be given to prevent hypoglycemia from insulin administration.
Now that we have reviewed the syndrome and its treatment, let’s get back to our patient who's trapped in the structural collapse. You and your partner have completed your initial assessment and applied a c-collar and provided supplemental oxygen.
Based upon what we have learned above, the remainder of your treatment would include establishing an IV with a large-bore catheter (16/18g) and giving a liter of 0.9% normal saline. You would then administer 24 mg ketamine IV to alleviate the patient’s pain.
Once the patient is freed from the rubble and brought to the ambulance, a second IV line would be established, and you would administer a sodium bicarbonate solution with 44 or 88 mEq mixed with a liter of D5W.
Upon reassessment the patient has become altered in mentation and displays peaked T-waves on his ECG, so you also would administer 1 g calcium chloride, 20 mg albuterol via nebulizer using a 0.5% concentration, 10 units of insulin, and 25 g of D50. Prepare for a possible cardiac arrest by placing defibrillation pads and readying for CPR.
Meir Shubowitz is a paramedic in New York City. He served for three years as a combat paramedic with the Israel Defense Force at the rank of staff sergeant.