12 the case of crushing cruiser

Case Presentation #12: 

Case Presentation #12 Jim Pointer, MD Alameda County EMS Medical Director

Complaint: 

Complaint It was a cold winter morning; dawn was breaking. A passerby turned a bend and was confronted with the wreak of a late model sedan. Inside the car, a young man was semi-conscious, upside down, trapped and badly injured. He had been there unnoticed for hours. You respond to the 9-1-1 call.

History: 

History Patient lost control of his car on a sweeping bend of a rural road and struck a tree. The car was found propped against a tree, nose down. Car was resting on both lower extremities. Environment was very dusty.

Primary Survey: 

Primary Survey Breathing: labored Skin: Pale, cool, clammy Vital Signs: B/P – unable to obtain, PR – 80, RR – 20, Pulse Ox – 98%

Secondary Survey: 

Secondary Survey HEENT: Extensive facial trauma Neck: ? Trauma Lungs: Clear Abdomen: Non-tender Back: Unable to assess Extremities: Bi-lateral femoral fractures, absent distal pulses Neuro: GCS - 9

Initial Treatment: 

Initial Treatment Oxygen: 100% - intubate if possible IV’s x 2 Normal Saline 20cc/hr Albuterol nebulizer Sodium Bicarb – 1 amp Extrication initiated COURSE: 30 minutes later, the car is lifted off, and the patient is extricated.

EKG #1: 

EKG #1 COURSE: 1 amp Calcium Chloride and one albuterol nebulizer treatment is administered. Patient is transported to a hospital with a hyperbaric chamber.

Pathophysiology : 

Pathophysiology Syndrome usually requires 4-6 hours of compression Mechanisms of muscle cell injury: Immediate cell disruption Direct pressure on muscle cells Vascular compromise (4 hour limit)

Release of Substancesfrom Injured Muscle: 

Release of Substances from Injured Muscle Amino acids & other organic acids: contribute to acidosis, aciduria, and dysrhythmia. Creatine phosphokinase (CPK) & other intracellular enzymes: serve as laboratory markers for crush injury. Free radicals, superoxides, peroxides: formed when oxygen is reintroduced into ischemic issue, causing further tissue damage.

Release of Substancesfrom Injured Muscle (cont.): 

Release of Substances from Injured Muscle (cont.) Histamines: vasodilation, bronchoconstriction Lactic acid: major contributor to acidosis and dysrhythmias. Leukotrienes: lung injury (adult respiratory distress syndrome [ARDS]), and hepatic injury.

Release of Substancesfrom Injured Muscle (cont.): 

Release of Substances from Injured Muscle (cont.) Lysozymes: cell-digesting enzymes that cause further cellular injury. Myoglobin: precipitates in kidney tubules, especially in the setting of acidosis with low urine pH; leads to renal failure. Nitric oxide: causes vasodilation which worsens hemodynamic shock.

Release of Substancesfrom Injured Muscle (cont.): 

Release of Substances from Injured Muscle (cont.) Phosphate: hyperphosphatemia causes precipitation of serum calcium, leading to hypocalcemia and dysrhythmias. Potassium: hyperkalemia causes dysrhythmias, especially when associated with acidosis and hypocalcemia.

Release of Substancesfrom Injured Muscle (cont.): 

Release of Substances from Injured Muscle (cont.) Prostaglandins: vasodilatation, lung injury. Purines (uric acid): may cause further renal damage (nephrotoxic). Thromboplastin: disseminated intravascular coagulation (DIC).

DIC / Third Spacing / Compartment Syndrome: 

DIC / Third Spacing / Compartment Syndrome Signs & Symptoms of Crush Injury (some or all of the following may be present): Skin Injury – may be subtle. Swelling – usually a delayed finding. Paralysis – may cause crush injury to be mistaken as a spinal cord injury Paresthesias, numbness – may mask degree of damage

DIC / Third Spacing / Compartment Syndrome (cont.): 

DIC / Third Spacing / Compartment Syndrome (cont.) Pain – often becomes severe upon release. Pulses – distal pulses may or may not be present. Myoglobinuria – the urine may become dark red or brown, indicating the presence of myoglobin.

Hyperkalemia: 

Hyperkalemia Mild hyperkalemia: 5.5-6.5 mEq/L peaked T waves Moderate hyperkalemia: 6.5-7.5 mEq/L prolonged PR interval, decreased P wave amplitude, depression or elevation of ST segment, slight widening of the QRS complex.

EKG #2: 

EKG #2

Hyperkalemia (cont.): 

Hyperkalemia (cont.) Severe hyperkalemia: 7.5-8.5 mEq/L further widening of the QRS due to bundle branch or intraventricular blocks, flat and wide P waves, Wenckebach, ventricular ectopics. Life-threatening hyperkalemia: >8.5 mEq/L loss of P waves, AV blocks, ventricular dysrhythmias, further widening of the QRS complex, eventually forming a sinusoid patern.

EKG #3: 

EKG #3

Treatment of Crush Injury: 

Treatment of Crush Injury Same principles as other trauma patients BEFORE RELEASE OF COMPRESSION: IV fluids at least 20cc/kg Sodium bicarb 50-100 mEq Albuterol nebulizer

Treatment of Crush Injury (cont.): 

Treatment of Crush Injury (cont.) AFTER RELEASE OF COMPRESSION: In addition to bicarb, other treatments may be needed to reverse hyperkalemia, depending on severity of injury Insulin & glucose Calcium – IV for life threatening dysrhythmias Beta-2 agonists – albuterol, alupent etc. Potassium-binding resins such as Kayexalate.

Treatment of Crush Injury (cont.): 

Treatment of Crush Injury (cont.) Dialysis – especially in patients with acute renal failure. Alkaline diuresis IV mannitol Wound Care Amputation Fasciotomy Hyperbaric chamber

Treatment of Crush Injury (cont.): 

Treatment of Crush Injury (cont.) AVOID PASG

Hyperbaric Oxygen Chamber: 

Hyperbaric Oxygen Chamber

Hyperbaric Oxygen Therapy: 

Hyperbaric Oxygen Therapy Before After

References: 

References Dickson JR: Crush Injury. Google.com 2001. Michaelson M: Crush Injury and crush syndrome. Western Journal of Surgery 1992; 16(5): 899-903. Gans L, Kennedy T: Management of unique clinical entities in disaster medicine. Emergency Medicine Clinical N/A; 14(2) 301-326.