12 the case of crushing cruiser

Information about 12 the case of crushing cruiser

Published on February 7, 2008

Author: Virginia

Source: authorstream.com

Content

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 Substances from 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 Substances from 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 Substances from 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 Substances from 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 Substances from 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.

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