| 1 | General Principles of Trauma® Mark R. Brinker and Eugene C. Lou J. ADVANCED TRAUMA LIFE SUPPORT, should be kept warm. Warm fluids may be ‘A. Primary survey used to aid in maintaining a patient's body 1. Airway (with cervical spine protection) —The first principle of maintaining the airway with cervical spine protection is to prevent move- ment of the cervical spine. One must assume that the cervical spine is injured if the patient has sustained multiple trauma, has had a change in mental status, or has sustained any sort of blunt injury proximal to the clavicles. Breathing and ventilation —One must check for chest wall injuries that may compromise ventilation during the primary survey. These include pneumothorax, hemothorax, and flail chest (all of which impede normal ventilation). 3. Circulation (with bi control) Blood Volume and Cardiac Output— Hemorrhage is the number one cause of preventable death after an injury. ‘Therefore it is very important to rapidly recognize the signs of hemorrhage during the initial survey. Signs include decreased level of consciousness, loss of skin color, and rapid pulse. temperature. B. Resuscitation 1. Airway—A definitive airway must be estab- lished during resuscitation. . Breathing and ventilation—During resusci- tation, it is of utmost importance to verify that adequate tissue oxygenation is being achieved. Circulation a. Bleeding—Bleeding must be controlled. b. Intravenous Lines—A minimum of two large-bore peripheral intravenous (IV) lines must be established for fluid resuscitation. Fluid Resuscitation—Fluid resuscitation should be initiated with intravenous fluids. “The preferred initial fluid for resuscita- tion of a patient with hypovolemic trauma is lactated Ringer’s (warmed to 39° C). A rapid initial infusion of 2 to 3 Lis appropriate. If there is no response in the patient's vital signs to this rapid infusion, the next appropriate step is to give blood. b. Bleeding—To control bleeding in the ini- ‘Type-specific whole blood is the blood tial setting, the clinician should use manual replacement product of choice. Type O- pressure on open wounds; it is considered negative blood is the next best choice. The less ideal to use a tourniquet. indicator of adequate fluid resusci- 4. Disability—neurologic status ine output. a. Glasgow Coma scale (Table 1-1)—The C. Other studies and monitors Glasgow Coma scale is detailed scale for 1. ECG evaluating a patient's neurologic status. Itis 2. Urinary output a very useful scale but can be time consum- 3. Nasogastric tube ing in the acute setting. 4, Arterial blood gas (ABG) analysis b. AVPU—Use of the acronym AVPU is a 5. Pulse oxi more simple and rapid method of grossly 6 ic x-ray studies evaluating and characterizing a patient's neurologic status: A Alert V Response to vocal stimulus P_ Response to painful stimulus ‘U Unresponsive Exposure and environment—One must com- pletely undress the patient for a proper evalu- a. Cervical Spine Series—The cervical spine series must include the first thoracic verte- brae (T1) on the lateral film. If T] cannot be seen, the x-ray study must be repeated, or a swimmer’s view must be obtained. b. Anteroposterior Chest X-Ray Study ¢. Anteroposterior Pelvis X-Ray Study Secondary survey—The secondary survey is a head-to-toe evaluation involving a complete nev- ation. After the examination, the patient rologic examination (including the ‘Coma should be appropriately covered to maintain Scale). The se survey is not} jun body temperature. If necessary, the room til vital fanctions have been2 * General Principies oF TRAUMA Glasgow Coma Scale* Response to Assessment Eye Opening Spontaneous “To speech To pain None Best Motor Response ‘Obeys commands Localizes pain Normal withdrawal (Rexion) ‘Abnorinal withdrawal (flexion) —decorticate Exension—decerebrate None (flaccid) Verbal Response Oriented Confused conversation Inappropriate words Incomprehensible sounds None “To calculate 2 Glasgow Coms Seale score, add the score for Eye (Opening with the scores for Best Motor Responte and Verbal Re sponte. The best posible scores 15, and the worst posible sore 3. History: “AMPLE” Allergies Medicine: Past injuries, iffnesses, pregnancy Last meal Events/environment (mechanism of injury) (Table 1-2) . Examination—The clinician should examine the head and skull; maxillofacial area; neck; chest; abdomen; perineum, vagina, and rec- tum; musculoskeletal system; and neurologic system. Every orifice should be checked. I. SHOCK A. Steps in recognizing shock 2 Recognition of its presence—The patient ex- periences inadequore organ perfusion and tis- sue oxy a. Identification of the probable cause—Shock does not result from an isolated brain injury. B. Manifestations Tachycardia a. Infant— Tachycardia is a heart rate of more than 160 beats/min. b. Preschooler—Tichycardia is a heart rate of more than 140 beats/min, ¢. School-age Child—Tachycar rate of more than 120 beats/min. d. Adult—Tachycardia is a heart rate of more than 100 beats/min. Narrow pulse pressure—Narrow pulse pres- sure is due to vasoconstriction and indicates significant blood loss. is a heart C. Types 1 Hemorrbagic sbock—Hemorthagic shock is the most common type of shock occurring af- ter a traumatic injury. ‘Mechanisms of Injury and Related Suspected Injury Patterns ‘Mechanisms of Injury Suspected injury Patterns Frontal impact Cervical spine fracture Bent stering wheel ‘Anterior dal ches Bulls-eye facture, windscreen Pneumothorax ‘Traumatic aortic disruption Fractured spleen or liver Posterior fracture-dislocation of the hip, the knee Contralateral neck sprain Cervical spine fracture Lateral fil chest Pneumothorax “Traumatic sorte disruption Diaphragmatic Fraceured spe 4 Side impact, automobile Rear impact, automobile collision Ejection, vehicle om precludes meaningful prediction of injury patterns bur places the patent at greater risk from virtually all injury mechanisms ‘Mortality significantly increased Motor vehicle-pedestrian jead From American College of Surgeons, Committee on Traum: d- anced saa if suppor: Sradent massa, ed 6, Chicago, 1997, Amer- ican College of Surgeons. Classification of Hemorrhagic Shock Class Blood Volume Loss (%) Treatment 1 Upwois hid replacement u S030 hid replacement 1 301040 Fd replacernent and hood replacement v >40 (emergenly Fi replacement and fe threatening) "Hood replacement a. Blood Volume—The adult's blood volume is 7% of body weight. The child’s blood volume approximately 8% to 9% of body weight. b. Fluid. Replacement—Fluid replacement should be directed by the response to the initial fluid-replacement therapy (the fluid challenge). c. Classification (Table 1-3). d. Loss of Blood Volume (1) Long bone fracture—Long bone frac- ture can lead to the loss of 1% units of blood.GENERAL PRINCIPLES OF TRAUMA = 3, errr | Responses to Initial Fluid Resuscitation’ $____ Pees esate Need for Estimated Need for More Needfor _Blood Operative Early Presence Response _Vital Signs Blood Loss Ceystalloid Blood Preparation intervention of Surgeon Rapid _-Returntonormal Minimal (10% to 20%) Low Low ‘Type and Yes ross-match Transient Improve transiently; Moderate and ongoi Moderate to Type specific Yes recurrence of GOK 40x) ae high ope pees decreased ble pressure and increased heart rate None Remain abnormal Severe (>40%) High ‘Immediate Highly likely Yes blood release odie from American Collegeof Surgeons, Commins on Tenums: Aden vm life apport: Stadet mara cd 6, 1997, American Collage of 200 lof acated Ringer shan Se, 20 ml of ated Ringer in cle, 2) Femur fracture—Femur fracture can Iead to the loss of 3 units of blood. (3) Pelvic fracture—Pelvic fracture can lead to the loss of more than 3 units of blood. . Fluids (1) ‘Types—Isotonic fluids should be used initially. Lactated Ringer's is the fluid of choice. The neat best fluid is nor- mal saline. (However, normal saline can cause hyperchloremic acidosis if ven in large volumes.) (2 nial replacement The initial Nuid is 1 to 2 L for adults and 20 mV/kg for children, @) Total replacement—Three times the estimated ven i (4) Response to Fluids—In general, a fa- vorable response to fluid replacement therapy includes increased urinary out- put, improved level of consciousness, increased peripheral perfusion, and changes in vital signs (uch as increased blood pressure, increased pulse pres- sure, and decreased pulse rate). (@) Urinary outpur—Adequate uri- output in the adult is 0.5 mikg/hs. In the child adequate inary output is 2.0. 7 9 Bete eat Bi replacement therapy (Teble 1-4). 2. Nonbemorrbagic sbock a, Cardiogenic Shock—In the evaluation of cardiogenic shock, the electrocardiogram (ECG) and blood creatine phosphokinase evels with isoenzymes are important but may not be practical in the initial emer- gency setting. Cardiogenic shock is the result of myocardial dysfunction. Causes include blunt cardiac injury, cardiac tam- ponade, dysrhythmias, air embolus, and myocardial infarction. Symptoms include tachycardia, muffled heart sounds, jugular venous distention, and hypotension. ‘Tension Pneumothorax—Tension pneu- mothorax is a surgical emergency that re- quires immediate diagnosis and treatment. It arises when air enters the pleural space but cannot exit be€ause it is trapped by a flap-valve mechanism. This results in a rise in intrapleural pressure, causing col- lapse of the lung and a shift of the medi- astinum. Absent breath sounds are ob- served in tension pneumothorax but not cardiac (This helps the clinician distinguish these two condi- tions.) Symptoms include acute respira- tory distress, subcutaneous emphysema, absent breath sounds, hyperresonance to percussion on the ipsilateral side of the chest, and tracheal shift away from the side of injury. Treatment involves emergent placement of a needle or chest tube into the pleural space. ¢. Neurogenic Shock—Isolated head injuries do not cause shock. (The clinician must look for another source.) The symptoms are hypotension without tachyeardia and vasoconstriction. Treatment involves fluid resuscitation. Septic Shock—Septic shock may occur in patients with penetrating abdominal in- juries. Symptoms include tachycardia, vaso constriction, decreased urinary output, and decreased blood pressure. I. INJURIES BY LOCATION injuries s ~ A. Head 1, General—A total of 500,000 head injuries occur each year in the United States. Of these, approximately 80% can be classified as mild, 10% as moderate, and 10% as severe. Ap- proximately 20% of patients with head in-4 © Gewerat Principtss oF TRAUMA esaBRsSRsesas Figure 1-1. A normal intracranial pressure d nificant intracranial pathology. The intracrar juries have some lasting disability. Traumatic injuries to the brain typically elevate the in- tracranial pressure (which can impair brain function). The normal intracranial pressure is 10 mm Hg. A ter than 20 mm Hg is considered abnormal, and a change greater than 40 mm Hg is considered severe. A nor- mal intracranial pressure does not exclude a significant pathologic condition; the intracra- nial pressure can remain normal until the point of decompensation is reached (Figure 1-1). Patients with head injuries are at in- creased risk of developing heterotopic ossifi- cation. Continued neurologic compromise (uch as persistent limb spasticity) is associated with the recurrence of heterotopic ossification after resection. . Skull fractures—The existence of a skull frac- tare increases the chance of an intracranial hematoma 20 to 400 times. a, Basal Skull Fracture—Symptoms include periorbital ecchymosis (raccoon eyes), retroauricular ecchymosis (Battle’s sign), a cerebrospinal fluid leak, and cranial nerve VI palsy. . Intracranial lesions (Figure 1-2) a. Epidural Hematoma—Epidural_ hema- tomas are rare. They are typically found in the region of the temporal lobe. They are caused by a tear of the middle meningeal artery. Rapid bleeding leads to a mass ef- fect. Patients with this condition typi- cally have a lucid interval followed by sudden death. b. Subdural Hematoma—A subdural hema- toma is more common than an epidural hematoma, It can be of a global location in Volume-pressure curve Herniation Point of > decompensation Volume of mass ot exclude sig- pressure in a ‘trauma patient can remain normal, despite a significant mass le- sion, until the point of decompensation, where the exponential phase of the volume-pressure curve Is reached, (Modified from ‘Narayan RK. In Grossman RG, Hamilton WJ, eds: Principles of neu- rosurgery, Mew York, 1991, Raven.) the cranium. It is usually caused by a tear of a bridging vein. Subdural hematomas have a relatively high mortality rate. ¢. Intracerebral Hematoma and Contusion— Intracerebral hematoma and contusion are relatively common and are usually seen in association with a subdural hematoma. 4. Concussion (Table 1-5)—A concussion is a jarring injury to the brain that results in disturbance, to some degree, of cerebral function. €. Management of Head Injuries (1) Primary survey—The primary survey includes an evaluation of the patient’s airway, breathing, and circulation. 2) Neurologic examination—The neuro- logic examination includes a Glasgow ‘Coma Scale (see Table 1-1). @) Diagnostic procedures—In all patients with head injuries, a cervical spine xcray series should be obtained to eval- uate for possible injuries. A computed tomographic (CT) scan is useful for evaluating for intracranial pathologic conditions (see Figure 1-2). (4) Intravenous fluids—It is important to maintain normovolemia in a patient with a head injury. Hypotonic fluids and glucose are no longer recom- mended in the resuscitation of such a patient. These fluids can be harmful to the injured brain. One must also watch out for hyponatremia. (5) Hyperventilation—Hyperventilation can be used cautiously to decrease in- tracranial pressure by decreasing the patient’s partial pressure of carbon dioxide and increase cerebral vasocon- striction. The partial pressure of car- bon dioxide should be kept at 30 mm Hg and no less than 25 mm Hg to avoid cerebral ischemia, (©) Mannitol—Mannitol is used as a 20% solution and is given as a bolus of 1 g/kg for patients who have clinical signs of pupillary dilation, (1) Other medicativns—Furusemide (Lasix), steroids, anticonvulsants, and barbitu- rates are adjunctive medications that have been used with some success, but they should not be administered without consultation with a neurosurgeon. B. Thoracic injuries 1. General—Serious thoracic injuries have a mortality rate of approximately 10%. These injuries typically result in hypoxia, hyperca bia, and acidosis. Assessment for thoracic i juries must occur during the initial evaluation to identify potentially life-threatening injuries. ‘Major problems should be treated as they are identified. The patient with a scapular frac- ture after blunt trauma should be carefullyGEwERAL Principes OF TRauMA © 5 Figure 1-2. Computed tomographic scans showing various posttraumatic intracranial lesions. A, Normal appearance. B, Epidural kematoms. C. Frontotemporal contusion with shift. D, Sut dural hematoma with large shift. (Modified from Narayan RK. In Grossman RG, Hamilton WI, eds: Principles of neurosurgery, New York, 1991, Raven.) Severity Treatment Grade I (mild) No ls of consciousness Return to play as soon as asympromatic (long-term [No retrograde amnesia suspension of play fora third-time grade I concussion) Grade II (moderate) Loss of consciousness <5 minutes First epinde: Return to play after asymptomatic for Retrograde amnesia (There is always some permanent loss of I week ‘memory regarding the injury itself) Repeat episode: Long-term suspension of play Confusion and disorientation that resolve rapidly Grade III (severe) Prolonged unconsciousness Long-term suspension of play Permanent retrograde amnesia Confusion and dhorientation that persist6 * GENERAL PRINCIPLES OF TRAUMA evaluated (via chest x-ray study) for a pul- b. Life-Threatening Injuries monary contusion to the ipsilateral lung. (1) Simple pneumothorax—Simple pneu- 2. Bpes m may be associated with tho- a. Imminently Lethal Injuries racic spine fractures and scapular frac- 2) ‘Tension pneumothorax (see section on shock) @) Open pneumothorax—Open pneu- mothorsx isan open chest wal Sefeet classically known as the sucking cbest wound. Treatment is the placement of an occlusive dressing taped on three sides; this avoids the possibility of a tension pneumothorax arising. @) Flail chest—Flail chest is a chest wall segment with bony discontinuity from the rest of the thoracic cage. It usually results from multiple rib fractures, A flail chest disrupts chest wall motion, and there is paradoxical motion during respiration. Treatment is judicious fluid resuscitation and reexpansion of the lung with a definitive airway or intuba- tion as required. (4) Massive hemothorax—By definition, massive hemothorax involves more than 1500 ml of blood in the chest. Symptoms include shock, absent breath sounds, and dullness to percussion on the ipsilateral side. Treatment consists of restoration of biood volume, decom- pression of the chest withra large chest tube, and sometimes a thoracotomy. A is performed if more than 1500 ml of blood is evacuated from the chest or there is continued blood loss of more than 200 mV/hr for more than 2 hours and the patient exhibits hemo- dynamic instability. (S) Cardiac tamponade—Cardiac tampon- ade usually results from blunt chest wall trauma. By definition, it is the ac- cumulation of a very small amount of fluid in the pericardial sac. This fluid disrupts the Starling curve and can se~ verely affect normal hemodynamics. Symptoms of cardiac tamponade in- clude the classic Beck's triad (increased venous pressure, decreased arterial pressure, and muffled heart sounds). ‘Treatment consists of subxiphoid peri- cardiocentesis, (©) “Commotio cordis"—-Commotio cordis most commonly occurs in litde league baseball participants after a direct blow to the chest. Although the blow often appears to be of low velocity (in young athletes without history of cardiac abnormalities), the condition com- nionly results in sudden death; resus- citative attempts are usually not suc: cessful. No pathologic changes to the heart have been demonstrated in com- motio cordis. tures. Findings include decreased breath sounds and hyperresonance on percussion, An upright expiratory chest x-ray film may aid in making the diagnosis. Treatment involves the placement of a chest tube, @) Hemothorax—Hemothorax typically occurs as a result of a laceration of a Jung, the internal mammary artery, or an intercostal vessel. Treatment is sim- ilar to that of a massive hemothorax. ) Pulmonary —contusion—Pulmonary contusion can lead to respiratory fail- ure. Treatment consists of intubation and assisted ventilation if the patient is hyporemic. (@) Tracheobronchial injury—There is a very high mortality rate for tracheo- jal injuries, (5) Blunt cardiac injury—Bhunt cardiac in- jury can result in a cardiac contusion, valvular disruption, or rupture of a car- diac chamber. © Aortic disruption—Aortic disruption ‘occurs after a high-deceleration injury. Signs of aortic disruption on chest x-ray film include a widened mediastinum, obliteration of the aor- tic knob, deviation of the trachea to the right, obliteration of the space be- tween the pulmonary artery and the aorta, depression of the left main stem 10s, deviation of the esophagus (nasogastric tube) to the right, widened paratracheal stripe, widened paraspinal interfaces, presence of a pleural or api- cal cap, hemothorax on the left side, and fractures of the first or second rib or of the scapula. Q) Diaphragmatic injuries—Diaphrag- matic injuries commonly occur on the left side and are seen on chest x-ray films. (8) Penetrating mediastinal Surgical consultation is mandatory. 3. Pearls of wisdom—A simple pneumothorax can lead toa tension pneumothorax. A hemo- thorax can lead to an empyema if not diag- nosed. Diaphragmatic injuries are often missed and can lead to pulmonary compro- mise or entrapment of the peritoneal contents. A widened mediastinum must not be missed; the severity of injury (based on the mechanism of injury) must not be underesti- mated, The chest x-ray film should be care- fully checked. C. Abdominal injuries 1. Géneral—Abdominal injuries must be ruled out and can be difficult to recognize. They canbe from blunt injury, penetrating injury, or 0s fy un oy, engin inh, an automobile accident. The most common injury in the abdomen is of the spleen; the liver is the next most common. Penetrating in- juries can lead to hemorrhage and peritonitis. ‘The most common injuries in passengers restrained by lap belts are bowel injuries (devascularization from crushing or rup- ture) and lumbar spine fractures. Assessment a. History—It is important to gather infor- mation about the type of accident. In an tomobile accident, itis useful to determine whether there were any restraints or seat belts being used. In a penetrating-type in- jury, it is useful to determine the type of weapon involved. b. Signs of Abdominal Injury—Signs and symptoms include involuntary muscle guarding, rebound tenderness, and free air underneath the diaphragm as seen on chest x-ray film. c. Tests (Table 1-6) (1) Diagnostic peritoneal lavage (DPL)— DPL is deemed positive if there are at Teast 100,000 red blood cells per cubic millimeter, there are at least 500 white blood cells per cubic millimeter, or there is a positive Gram’: stain, Pelvic fractures can lead to false-positive re~ GENERAL PRINCIPLES OF TRAUMA ® 7 catheter should not be placed because it may lead to further dissection of the urethral tear. 2. Signs—Signs of pelvic injuries include blood 28 the urethral meatus; laceration and bleed- ing of the perineum, rectum, or vagina; ecchy- moa ofthe buttocks; and pelvic instability on examination. 3. Treatment—In addition to fluid resuscita- tion, unstable pelvic fractures in a hemo- dynamically unstable patient may require im- mediate skeletal stabilization. Traction, place- ment of a compression sheet (a laundry sheet tied around the bony pelvis), military anti- shock trousers, and emergency placement of an external fixator or pelvic clamp have all shown some success. Each of these devices is designed to close down the potential space for bleeding in an open-book-type pelvic fracture. If no improvement in hemodynamics oc- curs after placement of a pelvic clamp or external fixator, angiography with em- bolization of bleeding vessels is indicated. E. Vertebral injuries (see Chapters 24 through 26) 1. General—Injuries to the spine must be ex- cluded after trauma. Of all spinal injuries, 35% involve the cervical spine, 15% involve the thoracic spine, 15% involve the thoracolum- bar region, and 15% involve the lumbosacral ” a. Cervical Spine Injuries sults on DPL. (Thus in a patient with (1) Adantooccipital dislocation—Adan- a pelvic fracture, a DPL should be per- tooccipital dislocation accounts for ap- formed from a supraumbilical portal.) proximately 20% of all fatal cervical (2) Ulerasound spine injuries. GB) CT sean 2) Cl (atlas) fractures D. Pelvic injuries (see Chapter 13) G) Cl rotatory subluxation 1. General—Pelvic injuries are usually due to (4) C2 (axis) fractures high-energy trauma such as automobile acci- @) Odontoid fractures dents. Pelvic fractures can lead to a significant (b) Posterior element fractures loss of blood. Bleeding in a pelvic fracture is (5) Fractures and dislocations of the lower usually from disruption of venous plexuses and cervical spine (C3-C7). from bleeding cancellous bone surfaces. Occa- b. Thoracic Spine (T1-T10) Injuries—The sionally, massive bleeding can occur from ar- thoracic spine tends to be quite stable be- terial disruption. The incidence of urologic in- cause of the inherent stability added by the jury with high-energy fractures of the pelvis is rib cage. Displaced thoracic fractures com- approximately 30%. Blood in the urethral ‘monly cause neurologic injury because the meatus suggests a urethral tear; a Foley spinal canal is narrowest at this level. DPL vs. Ultrasound vs. CT in Blunt Abdominal Trauma PL Uttrasound Sean Indication Document bleeding if BP Document Suid if} BP Document orga injory if BP normal Advantages diagnosis and sensitive; Early diagnosis noninvasive and Most specific for injury, 92%-98% 98% aceurnte sen 864 97% sear Se nn nines dap isadvan ses injury tothe tor time; mises dia Sa ee, a, inva daphrag, bowel and tome pancreati injuries From American College of Surgeons, Committee on Tram: Advened rane Ife suport Student manual, ed 6, Chicago, 1997, American College of Surgeons DPL, Diagnostic peritoneal lavage; BP blood pressure.8 © Genenat Princptes oF TRAUMA Motor and Sensory Spinal Cord Levels Segmental Nerve Motor RootDermatome -Examination* _ Sensory Examination cs Deloid Lateral shoulder i ‘Thumb a ‘Middle Ginger a Linde finger 11 ‘Medial volar forearm nm Above nipple qn ‘Above nipple 1 Nipple Ts Chest 16 Chest Bul Chest Ts Xiphisternum 1p ‘Above umbilicus Tho ‘Umbiicus ™ Below umbilicus Tm! Symphysis pubis ui ‘Anterior thigh and knee L Hip flexors ‘Anterior thigh and knee B Quadriceps ‘Anterior thigh and knee 4 Tibialis anterior Medial aspect of leg Is Extensor hallucis First dorsal web space of Tongus the foot and lateral leg st Ankle plantar Lateral border of the flexors {foot and posterior leg 2 Posterior thigh 3 Ischial tuberosity area St erianal region Ss Perianal region ‘Monor grading sale: 0 Teal St 1 Palpable oF visible contraction, 2 Mosion with gravity eliminated, 3 Motion aguinst gravity but not resistance. '§ Motion ogunst resistance, bo es than normal strength. 5 Normal suengih. ¢. Thoracolumbar Spine (T11-L1) Injuries— Injuries at the ‘orasolumbay level can cause bowel and bladder dysfunction. 4, Lumbar Spine Injuries—Lumbar spine in- juries commonly result from seat-belt injuries. “The management of spinal in- with an adequate cervical spine x-ray series, which must include Ton the lat- eral x-ray film. It must be remembered that 10% of cervical spine fractures are associ- ated with a injury at a second level. tis necessary to keep the patient immobilized until there is certainty about the "ype of injury. F. Injuries of the nervous system 1. Spinal cord injuries a. Assessment (Table 1-7)—A thorough neuro- logic examination, including sensory and motor grading, is necessary (see 2). b. Spinal Cord Syndromes (exe Chapeer 3) ¢. Treatment—Treatment entails immobi- lization of the patient to prevent further neurologic insult. Patients with spinal TE Sk ‘Types of Peripheral Nerve Injuries Injury Pathophysiology Neurapraxia Reversible conduction block Good characterized by local ischemia and selective demyelination of the ‘axon sheath ‘More severe injury with disruption Fair (of the axon and myelin sheath but with an intact epineurium Complete nerve division with Poor disruption ofthe endoneurium Prognosis Axonotmesis Neurotmesis ‘Nerve Conduction Study Results Related to Trauma ‘Conduction Evoked Condition Latency Velocity Response Normal study Normal Upper extremities: >45 m/sec Biphasic Lower extremities: 40 mvsee Neurapraxia Proximal tolesion Absent Absent Abwent Distal tolesion Normal Normal Normal ‘Axonoumesis Proximal tolesion Absent Bsent Absent Distal tolesion Absent Absent Normal Neurotmesis Proximal tolesion Absent Absent Absent Distal tolesion __Absent_ Absent Absent Data from Jahss MH: Diordcr ofthe fot, Philadelphia, 1982, WB Saunders. Data from Miller MD, Brinker MR, eds: Review of = ‘epee, ed 3, Philadelphia, 2000, WB Saunders. cord injuries who come to medical at- tention less than 8 hours after the in- jury have the best chance for optimiz- ing their neurologic outcome if given methylprednisone. When there is less than 3 hours from the time of injury, patients should receive an initial bolus of 30 mg/kg of methylprednisone fol- lowed by an infusion of 5.4 mg/kg/hr for 24 hours. Patients between 3 and 8 hours from the time of injury should receive an initial bolus of 30 mg/kg fol- lowed by an infusion of 5.4 mg/kg/br for 48 hours, 2. Peripheral nerve injuries (Tables 1-8 through 1-10)—The most important prognostic factor for functional recovery after repair of a pe- ripheral nerve injury is the age of the patient, G. Skin and soft tissue injuries 1. Thermal injuries a. Burn Injuries (1) Assessment—lIt is imperative to rule out inhalation injury in a patient who———— a A Electromyographic Findings Related to Trauma Condition Insertional Activity Activity at Rest Minimal Contraction Interference Normal study, Normal Silence Biphasic and triphasic potentials. Complete ‘Neurapraxia| Normal Silence None None ‘Axonotmesis Tnereased Fibrilations and positive None None ‘Neurotmesis Increased Fibrillations and positive None None sharp waves. Dae om Jb MB Died of te fo, Paladin, 182, WD Senders. Data rom Miler MDs Rie of eon U5 indie 2, WB Slnaces ” has sustained a burn. Signs of inhala- Gon injury indude aca beans, singe- ing of the face and hair, carbon in the pharynx, and carbon in the sputum. It is also very important to remove all clothing to stop the burning process (which may be continuing from the clothing fibers). @) Definitions (@) First-degree bumn—A first-degree bum involves the epidermis. () Second: degree ‘bum—A second: legree burn involves the dermis. © Tinideres bumn—A third- degree bur involves the subcuta- neous tissues, (@ Fourth-degree burn—A fourth- degree burn involves the deep tissues. @) Calculation of the burned body surface area—Caleulation of the burned surface area involves using the “rule of nines” (Figure 1-3). This calculation is impor for assessing Nuid-replace- (4) Fhhid replacement requirements—A talof 204ml oflacsted Ringer’ is s0- ministered per kilogram of body weight per percent of bumed Moly outer area for second- and bm) n the first 24 hours. Half of this i Inthe first @ hours, and the remainder is over the next 16 hours. b. Cold Injuries a eset heat tissues should be ‘warmed in a warm water bath at me C(104° F). Local wound care along with tetanus immunization should be administered. Cold injuries are the most common cause of bilateral upper ‘extremity amputations. @ Frese. roabes weed Bon seve freezing caused by the intracellular formation of ice crystals and the oc- clusion of the microcirculation. Treat- ment is rapid rewarming in circulating warm (40° C [104° F}) water. Figure 1-3. The “rule of nines” is used in the management of se- vere burns to determine fluid replacement. tt also is useful as a practical guide for the evaluation of severe burns. The adult body fs generally divided Into surface areas of multiples of 9%. (From Rosen B Barkin RM, Hockenberger RS, et al, eds: Emergency med- cepts and clinical practice, ed 4, St Louis, 1998, Mosby.) fene10 © GeNenat Principtes oF TRAUMA ¢. Electrical Injuries (1) Ignition—Ignition involves a burn at the site of direct contact. @) Conductant—Conductant involves in- jury propagation along the neurovascu- lar structures. 3) Arc—High-voltage currents propagate along the flexor surfaces of the joints and lead to contractures. . Chemical Burns—The severity of injury de- pends on the amount and concentration of the agent, the duration of contact, the tissue penetrability of the agent, and the agent's mechanism of action. The most important aspect of treatment is copious irrigation. 2. Injection injuries —Injection injuries typically result from accidental high-pressure injection by paint or grease guns. These injuries may appear relatively benign but represent surgical emergencies because of their ability to rapidly destroy the soft tissues. 3. Wound bealing—Adequate soft tissue heal- ing after injury or surgery is promoted by a transcutaneous oxygen tension level higher than 30 mm Hg, an ischemic index (such as the ankle/brachial systolic index) of at least 0.45, an albumin level of at least 3.0 #/dl, and a total lymphocyte count higher than 1500 cells/mm’. These values may be improved by nutritional support, which can be given in the form of oral hyperalimentation. Oxygenated blood is a prerequisite for wound healing. The ischemic index is the ratio of the Doppler pressure at the level being tested to the brachial systolic pressure; itis generally ac- cepted that patients require an ischemic index of 0.45 at the surgical level to support wound healing. Doppler ultrasonography has histor cally been used as the measure of vascular i flow to predict wound healing in the ischemic limb. An absolute Doppler pressure of 70 mm He was originally described as the minimal in- flow to support wound healing. Doppler ul- trasonography measures arterial pressure in the upper and lower extremity; the area under the Doppler waveform tracing is a measure of blood flow. Values may be falsely elevated and not predictive in patients with peripheral vas- cular disease because of the noncompressibil- ity and noncompliance of the calcified periph- ral arteries. IV. COMPLICATIONS OF TRAUMA A. Pulmonary complications 1, Pulmonary embolism (PE)—PE should be sus- pected in postoperative patients with acute on- set of pleuritic pain, tachypnea, and tachycar- dia. The initial workup includes an ECG (right bundle branch block, right axis deviation in 25%s possible ST depression or T-wave inver- sion in lead IID), chest radiograph (hyperlucency rare), and ABG analysis (a normal partial pres sure of arterial oxygen does not exclude a PE). Amuclear medicine Yensladon-periion san be Pulmonary angiography is the gold bane is required for making the di- agnosis if there is any question. Heparin ther- apy (continuous IV infusion) is initiated for the patient with a proven PE and is monitored by the partial Stromal time (PTT). More aggressive (thrombolytic agents, vena caval filter, and other surgical measures) is re- quired in select cases. A total of 7 to 10 days of heparin therapy is followed by 3 months of oral warfarin therapy (monitored by the prothrom- bin time [PT]. . Adult respiratory distress syndrome (ARDS)— ARDS is acute respiratory failure secondary to pulmonary edema after trauma, shock, and in- fection, Etiologies include pulmonary infec- tion, sepsis, fat embolism, microembolism, as- ration, fluid overload, atelectasis, oxygen soxiciy, pulmonary contusion and head injury “Tachypnea, dyspnea, hypoxemia, and decrease Jung compliance are maifesatons, The clin- ical diagnosis of ARDS after a long bone fracture is best made using ABG analysis. Normal supportive care is often unsuccesfal, and a 50% mortality rate is common. Activa- tion of the complement system leads to further progression. Ventilation with positive end- expiratory pressure (PEEP) is important; steroids have not been proved efficacious. Early stabilization of long bone fractures (particularly the femur) decreases the risk of ARDS. }. Fat embolism syndrome—Fat embolism syn- drome is usually seen 24 to 72 hours after trauma (3% to 4% of patients with long bone fractures). It is fatal in 10% to 15% of cases. ‘The incidence of clinically significant fat ‘embolism is decreased by early skeletal sta- bilization. The onset of fat embolism syndrome + may be heralded by tachypnea, pulmonary ‘edema, tachycardia, hypoxemia, mental status changes, confusion, central nervous system de- pression, and petechiae. The fat embolism syn- drome may be caused by bone marrow fat (me- chanical theory), chylomicron changes as a result of stress (metabolic theory), or both. ‘Metabolism to free fatty acids, initiation of the clotting cascade, pulmonary capillary leakage, bronchoconstriction, and alveolar collapse re- sult in a ventilation-perfusion deficit (hypox- emia) consistent with ARDS. ‘Treatment in- cludes mechanical ventilation with high levels of PEEP. Steroids do not appear to have a pro- phylactic role. Prevention with early fracture stabilization is important. ia—Aspiration pneumonia can occur ” in patients with decreased mentation, supine positioning, and decreased gastrointestinal (GI) motility. Simple measures such as raising the'head of the bed and using antacids andmetoclopramide 3) can help avoid prob- lems. Appropriate Wee pul- monary toilet are required to treat established pneumonia. B. Circulatory complications 1. i sgulation involves a cascad- ing Sequence of enzymatic reactions tht be. ins wit i ing activity and Sencdel wid the formation ofs Bor clot as fibrinogen is converted to fibrin). Two in- terconnecting pathways have been described. a. Intrinsic Pathway—The intrinsic pathway is monitored via the PTT: The pathway is activated when factor XII makes contact with the collagen of damaged vessels. b. Extrinsic Pathway—The extrinsic pathway is monitored via the PT: The pathway is ctivated by the release of thromboplastin into the circulation secondary to cellular injury. Bleeding Time Test—The bleeding time test measures platelet function. The fi- brinolyti is. ible for dissolv- ing clos: Plasminogen coment pss min (with the help of tissue activators, factor XI, and thrombin); plasmin dis- solves the fibrin clot. 2. Thromboembolism—Thromboembolism is a ‘common problem in orthopaedic patients, es- pecially in those who sustain high- trau- matic injuries. The risk of thromboem- bolism is increased with a history of thromboembolism, obesity, malignancy, aging, heart failure, use of birth control pills, varicose veins, smoking, use of general anesthetics (in contrast to the use of continuous epidural anesthesia, which has a lower incidence of thromboem- boli), increased blood viscosity, immobiliza- tion, paralysis, and pregnancy. . Deep venous thrombosis (DVT)—Clinical suspicion is more helpful than the findings on physical examination (pain, swelling, ° Homans’ sign) for DVT. Useful studies in clude venography (the gold standard), which is 97% accurate (70% for iliac veins), iodine-125—labeled fibrinogen (operative site artifact causes false positive results); i dence armel oor ity); du- plex ultrasonography (B-mode), which is 90% accurate for DVT proximal to the trifurcation vessels; and Doppler imaging (immediate bedside tool, often best for the first study). Prophylaxis is the most important factor in decreasing morbidity and mortality, and the methods commonly used are listed in Table 1-11. The anticoagulation effects of war- farin (Coumadin) are via inhibition of he- patic enzymes, vitamin K epoxide, and perhaps vitamin K reductase. This inhibi- tion results in decreased carboxylation of the vitamin K-dependent proteins: factors UI (prothrombin), VII (the first to be af- fected), IX, and X. Warfarin does not act by directly binding vitamin K or the clot- ting factors. Its anticoagulation effects can be reversed with vitamin K or more rapidly with fresh frozen plasma. The di- agnosis of DVT after surgery requires the ini- tiation of heparin therapy (followed by later conversion to long-term warfarin therapy). Low-dose warfarin given to a patient ith a DVT interferes with the metabolifm of factors II (prothrombin), VI, IX, and X. ‘Treatment is recommended for all thigh DVT; however, the treatment of DVT oc- curring below the popliteal fossa is controver- sial. Preoperative identification of a DVT in a patient with lower extremity or pelvic trauma is an indication for placement of vena caval filter. Virchow’s triad of factors. involved in venous thrombosis includes stasis, hypercoagulability, and intimal injury. 4, Myocardial infarctic te chest pain, pain radiation, and ECG changes are classic signs and symptoms and warrant monitoring in an ‘Thromboembolism Prophylaxis Method Effect Advantages Disadvantages ‘Coagulation cascade: antithrombin I inhibitor Reversible, effecive Control, embolization Subcutaneous Antithrombin II inhibitor Reversible No eect in exeminy orgy Warfarin ‘Coagulation cascade: vitamin K Most effective, oral 3-5 days to full effect, cont Aspirin Inhibition of platelet aggregation ‘no monitoring Limited Dextran Dilution Eien Fluid overload, bleeding Pecoeiccomprenion Meth Inexpensive, no bleeding Bulky scapes (eno, Inkibison of cloning: formation Fixed dose, no monitoring Bleeding ‘alow-molecular- ‘of compleres between antithrombin ‘weight heparin IH and frctors Ha and Xa From Brinker MR. In Miller MD, Brinker MR, eds: Reva of erhypaedia, ed 3, Philadelphia, 2000, WB Saunders. See text for deal12. = GeNeRAL PRINCIPLES OF TRAUMA appropriate critical care environment where cardiac enzyme levels and the ECG can be monitored on a continuing basis. Risk factors include increased age, smoking, elevated cho- lesterol level, hypertension, aortic stenosis, a history of coronary artery disease, and a vari- ety of other factors. 5. Disseminated intravascular coas (DIG—DIC can arse fom cscs blac Joss in the trauma patient. It can also arise from burns, snake bites, shock, hemolysis from mismatched transfusions, and sepsis. DIC occurs when platelets have been con- sumed by the formation of microvascular thrombi. Laboratory values supporting the di- agnosis include decreased antithrombin III and fibrinogen levels, and increased fibrin split products, PT, and PTT, Treatment in- cludes correcting the underlying cause, with the adjunctive usage of heparin, platelets, and 1-desamino-8-D-arginine vasopressin. C. Soft tissue complications 1. Compartment — syndrome—Compartment syndrome represents elevated compartment pressures within a soft tissue envelope of an extremity and commonly’ follows significant trauma, Increased pressures lead to ischemia and may lead to irreversible injury to muscle and nerve. The classic clinical finding sug- gestive of compartment syndrome is pain out of proportion to what would be ex- pected, particularly with passive stretch- ing of the muscles of the compartment be- ing examined. For exomple, passive plantar flexion of the ankle and toes would be per- formed to examine the anterior compartment of the leg.) The earliest and most objective sign is a tense compartment. The five Ps of compartment syndrome are pain, pallor, paralysis, paresthesia, and pulselessness. A va- riety of methods have been described to measure compartment pressures. Compart- ment pressures higher than 30 mm Hg or within 10 to 36 mm Hg of the diastolic blood pressure suggest compartment syn- drome. Patients with altered sensorium (e.g., head injury, intoxication) cannot be adequately monitored with physical exam- ination, and therefore continuous mea- surement of compartment pressures with an indwelling catheter ic recommended. ‘Treatment involves emergent surgical release via fasciotomy. Compartinent syndrome after trauma can affect any of the compartments of the upper and lower extremity, including the buttock, thigh, leg, foot, arm, forearm, and hand. Chronic exercise-induced compart- ment syndrome is best confirmed via com- partment pressure measurements before and after exercise. 2. Decubitus ulcers—Decubitus ulcers are asso- ciated with advanced age, critical illness, and neurologic impairment. Common sites include the sacrum, heels, and buttocks, which may be a source of infection and increased morbidity. Prevention with constant changing of posi- tion, special mattresses, and treatment of sys- temic illness and malnutrition is essential. Once established, debridement and sometimes soft tissue transfers are required for treatment. " a. Cellulitis”-Celllits isan infection of the subcutaneous tissues. The infection is gen- erally deeper, and there are less distinct margins in cellulitis than in erysipelas. Clinical findings include erythema, tender- ness, warmth Iymphangits and Iyraphade- nopathy. Group A streptococcus is the most common organism; Stapbylococ- cus aureus infection is much less com- mon, Antimicrobial therapy includes the penicillinase resistant synthetic penicil- ins (PRSPs) (nafcillin and oxacillin), or for less severe cases, oral dicloxacillin. Alterna- tive treatment regimens include erythro- mycin, first-generation cephalosporins, amoxicillin/clavulanate (Augmentin), azi- thromycin, and clarithromycin. b, Erysipelas—Erysipelas is an infection of the superficial soft tissues characterized by a progressively enlarging, well-demarcated, red, raised, painful plaque. In nondiabetic patients the most common organism is group A streptococcus. The clinical pic- ture is similar to that of cellulitis, but the infection is more superficial and is well de- marcated; the treatment regimen is the same as that for cellulitis. In diabetic pa- tients with erysipelas, the most common or- ganisms are group A streptococcus, S. au- reus, Enterobacteriaceae. and clostridia (uncommon). Early and mild cases are best treated with a second- or third-generation cephalosporin or amoxicillin/clavulanate; severe cases may require imipenem (Pri- maxin), meropenem, or trovafloxacin. Dia- betic patients with erysipelas may require surgical debridement to rule out necrotiz~ ing fasciitis and obtain definitive cultures. Septic patients should have an x-ray evalu- ation to rule out gas in the soft tissues. ¢. Necrotizing Fasciitis (“Flesh-eating Bacte- ria”)}—Necrotizing fasciitis is an aggressive, life-threatening fascial infection that may be associated with an underlying vascular disease (particularly diabetes). Necrotizing fasciitis commonly occurs after surgery, trauma, or a streptococcal skin infecti ‘Many cases of acute necrotizing fasciitis in- volve several organisms. The most com- monly isolated organism is group A streptococcus. Clostridial or polymicro-= bial infections are also seen. Extensive surgical debridement (involving the entire length of the overlying celluli- tis) and IV antibiotics are required emergently. Initial antibiotic treatment is clindamycin plus penicillin G; alternative initial antibiotic treatment includes ceftri- axone or erythromycin tion of muscle thats grossly contaminated traumatic wounds (particularly those that are closed pri- marily). The clinical presentation ine cludes progressive pain, edema (distant fom the wound, and « foul-amelling serosaer guincous discharge. Radiographs typi- cally show widespread gas in the soft €s- sues. The gas facilitates rapid spread of the infection. Gas gangrene is classically caused by Clostridium perfringens or Clostridium sep- tiem, of other histotoxic Clartridiwm species (gram-positive, anaerobic, spore-forming rods that produce exotoxins). The exotoxins create local edema, necrosis of fat and mus- cle, and thrombosis of local vessels. Symp- toms include severe pain, high fevers, chills, tachycardia, confusion, and findings consis- tent with toxemia. Radical surgical de- bridement with fasciotomies is the pri- mary treatment; hyperbaric oxygen may be 2 useful adjuvant therapy, althoogh its effec tiveness remains inconclusive. Initial antibi- otic therapy should include ais in plus penicillin G. Alternative therapies include cefrriaxone and in, isan infec- found in : Toxic Shock Syndrome (1) Staphylococcal toxic shock syndrome— This form of toxic shock syndrome is a severe life-threatening condition caused by the toxin S. aureus. In or- thopaedics, this infection develops sec- ondary to the colonization of surgical ‘or traumatic wounds (even after minor trauma). The patient displays fever, hy- potension, and an erythematous macular rash with a serous exudate. (Gram-positive cocci are present) The wound may look very benign and be misleading in regards to the severity of the underlying condition. ‘Toxic shock syndrome can develop in ‘women in association with tampon use and colonization of the vagina with toxin-producing S. aureus. Toxic shock syndrome represents a tox- emia (1 tions includes irrigation, debridement, and IV antibi- otics. Initial treatment is with a PRSP (nafcillin or oxacillin); alternative an- me D. GI GENCRAL PRINCIPLES OF TRAUMA ® 13 tibiotic treatment includes a first-gen- eration cephalosporin. Patients with toxic shock syndrome may also require emergent fluid resuscitation. @) Streptococcal toxic shock syndrome— Streptococcal tori shock syndrome is commonly associated with e1 or necrotizing fasciitis, The offend: con ganism can be group A, B, C, or G Streptococcus pyogenes. Surgical Wound Infections—The most common offending organism is S. au- reus. Group A streptococcus and Entero- bacteriaceae are also common. There has been an increase in the incidence of Staphylococcus epidermidis wound infec- Bons The number of methiclin exert staphylococcal infections has also increased ‘over the past several years, and these infec- tions are best treated with vancomycin, (Al- ternatives to vancomycin for methicillin- resistant S. aureus include teicopla- nin, cotrimoxazole (Bactrim), doxycycline, minocycline, fusidic acid, fosfomycin, rif amy reported; the treatment for these organi is currently quinupristin/dalfopristin. Bite Injuries—Table 1-12 ‘Marine Injuries—Marine injuries involve or- isms that can cause indolent infections. Galtures may ake several weeks to grow on culture media. In the patient with a history ofa fiching (or another marine) injury who has an indolent, low-grade infection, atypi- cal mycobacteria (such as Mycobacterium mar inumt) should be considered. Ie is important to culture the specimen at 30° C (86° F). i. Puncture Wounds of the Foot—The most ‘common organism from the of a nail through the sole of a tennis s is Staphylococcus; the most characteristic organism is Pseudomonas aeruginosa. Pseudomonas (sram-negative rod) infections require aggressive debridement and appro- priate antibiotics (often, a two-antibiotic regimen). The initial antibiotic regimen should include ceftazidime or cefepime or tobramycin plus carbenicillin; an alterna- teint stiioge regimen might include ‘ciprofloxacin (except in children). The pro- phylactic antibiotic Seaunent for a patient with a recent (hours-old) puncture through the sole of a tennis shoe (without infection) remains controversial. Osteomyelitis de- velops in 1% to 2% of children who sus- i wound tions—GI complications can complicat range from ilens (treated with nasogatrc suction [tobe] and antacids) to upper GI bleedin, 1g- Postopera-14 ® GeneRat PRINGPLES OF TRAUMA Bite Injuries Source of Bite Organisms) Primary Antimicrobial (or Drug) Regimen Homan ‘Strepocceus viridans (100%) ‘Amoxicilin/clavalanate (Augmentin) Bocerides species > (Eikenlla~ cefoxitin or ampicillin} Coryncbacteriz species S.avrews Y jar rpecis species Dog S.viridenr Penicilin V or smpicilin Posteurela multocida ‘Consider antirabies treatment ‘Baceroides species Fusobacteriem species Car P muhocide Amoxicillin/clavalanate (Augmentin) or penicillin V S. sureur Possibly Pencil trent . Rat me ‘monlformis icin nn Anubis weament i nrindicned Pig Polymicrobial organisms (aerobes and anaerobes) Amouicilin/clavulanate (Augmentin) Skunk. raccoon, bat ? ‘Ampici Antirabies treatment is indicated Pit viper (snake) Prendomonas Antivenom therapy = Enterobacteriaceae efcinne OT S. epidermidis fetanus prophylaxis Clatridtam species Brown recluse sper = Dapsone Catfish sing “Toxins (may become secondarily infected) Amoxiclln/clavalanate (Augmentin) Nel frm Sno] P: Gl emir try, Miller MD. Brinker MR. eds: Recie= of orbapardis, 3, Philadelphia, 2000, WB Seunders tive ileus is common in diabetics with neuropa- thy. Upper GI bleeding is more likely in patients with a history of ulcers, use of nonsteroidal anti- inflammatory drugs, trauma, and smoking. Treat- ment includes lavage, antacids, and H,-blockers. Vasopressin (left gastric artery) may be required for more serious cases. E. Genitourinary complications 1, Urinary tract infections (UTD—The most common nosocomial infection, established UTIs should be adequately treated before surgery. Perioperative catheterization (re~ moved 24 hours after surgery) may reduce the rate of postoperative UTI. UTI can increase the chances of postoperative wound infections. Prolonged catheterization increases the inci- dence of UTIs. 2. Genitourinary injury—A retrograde ure- throgram best evaluates lower genitourinary injuries in patients with displaced anterior pelvis fractures. ‘The differential diagnoses af- tera direct blow to the scrotum are contusion, testicular rupture, epididymal rupture, and testicular torsion. Emergent urologic evalua- tion and consultation are required 3. Prostatic bypertrophy—Prostatic hypertrophy causes postoperative urinary retention. If the history, physical examination (prostate), and urine flow studies (<17 ml/sec peak flow rate) are suggestive, urologic consultation should be obtained. Dallas, 1994, Antimicrobial Therapy Ine. From Brinker MR. In 4. Acute tubular necrosis—Acute tubular necro- sis can cause renal failure in trauma patients. Alkalinization of the urine is important during the early treatment of this disorder. F. Meningococcemia—Meningococcemia can de- velop in patients with multiple infarcts, such as those with elecerical burns, G. Postsplenectomy infections—The most com- mon infections after splenectomy are streptococ- cal. These infections may be serious, V. OTHER TRAUMA-RELATED TOPICS A. Nutrition—Adequate nutrition should be en- sured before elective surgery. Malnutrition may be present in 50% of patients on a surgical ward. There are several indicators of nutsition (e.g,, an- ergy panels, albumin levels, transferrin level); a measurement of arm inuscle circumference is, the best indicator of nutritional status. Wound dehiscence and infection, pneumonia, and sepsis can result from poor nutrition. The lack of en- teral feeding can lead to atrophy of the in- testinal mucosae, leading in turn to bacterial translocation and the development of multi- ple organ system failure, Nutritional require- ments are significantly elevated as a result of stress and trauma. Full enteral or parenteral nu- ition should be provided for patients who can- not tolerate normal intake. Early elemental feed- ing through a jejunostomy tube can decrease complications in the patient with multipleGENERAL PRINCIPLES OF TRAUMA © 15 Compications/Other Aminoglycosides G-,PM ‘Auditory (most common) and vestibular toxicity are caused by dese pip re ir and vestibular Soy 2 scrumulaton nthe peri tn ont pleeSpenronl tac nro = Peele aa Eth aserber Cirsenctivecralhnpipenctin ——-Senaamerabes ledingdathess (rhein) palpi rst generation axis (surgical) hazolin is the drug of choice Second eneraon Some Gee col me = erie ee Hemlpc anemia (edi dts onl ‘Chloramphenicol ‘influenzae, anacrobes Bone mat J : = Gprotoen GTTethlinvene S curs “Tengen rson inch; nc reduce absorption of ciprofloxacin; theophylline eres crm coneeroatonech nek Cindanycin Gt, anzerobes Poonimenininoaeneeeane cn Eee Croce Imipenem G+, some G- : i Mediclivorctin/aftin Fence resane Same ne potin Penicillin: ‘Streprococei, G- eee (a r i, Gt is Plyny/nyatin & Noire Satonrant! ou Neely semi Temoycline faked ) i. ‘Stains teet ve (up foage 8) a moony ror vee Store expen Wi iV dle Cleseridivom difficile anne id From Brinker MR. In Miller MD, Brinker G-, gram negative; PM, polymicrobial : trauma. Enteral protein supplements have effective in patients at risk of develop- ing multiple organ system failure. B. Antibiotics 1, General—Antibiotics in orthopaedics may be used for (1) prophylactic treatment to prevent postoperative sepsis (for clean surgical cases, proper administration is 1 hour before surgery and continued for 24 hours after surgery), (2) initial care after an open traumatic wound, and 3) treatment of established infections. The perioperstive use of first-generation cephalosporins is efficacious in cases requirin grossly tures. Overal a eureus remains the leading cause of osteomyelitis and nongonococcal sep- tic arthritis, In general, the virulence of S.epi- dermidis infections is closely related to or- thopaedic hardware. Cli in achieves the highest antibiotic concentrations in bone; the concentration in bone neatly equals that of serum concentrations after IV adminis- ion. Clindamycin is bacteriostatic. tic-resistant bacteria—Two types of antibiotic resistance exist: MR, te: Rsoe f bata, 3, Philadephia, 2000, WB Swunder. ik G+, gram poste PON, pln GU genoa a. Intrinsic Resistance—Intrinsic resistance is the inherent feature of a cell that pre- vents antibiotics from acting on the cell (such as the absence of a metabolic path- ‘way or enzyme). b. Acquired Resistanco—A new resistant strain emerges from a population that was i ‘sensitive, (Acquired resistance is Rredised by plasmids fextrachromosomal genetic elements) and transposons.) 3. Antibiotic indications and side effects (Table 1-13). 4. Mechanism of action of antibiotics (Table 1-14). 5. Other forms of antibiotic delivery a. Andbions Bends Polyne Imethsery- late (PMMA) impregnated with antibiotics (usually an aminoglycoside) is useful when treating acute open wounds or established infections. Antibiotic powder is mixed with cement powder; the type of antibiotic to be used is guided by the microorganism present, and the dosage depends on the specific antibiotic selected and the type of PMMA used. Antibiotics that have used with PMMA for infection include tobramycin, gentamicin, cefazolin and cephalosporins, oxacillin, cloxacillin, methicillin, lincomycin, clindamycin, col- istin, fusidic acid (Fucidin), neomycin,16 = Genera Princess oF TRAUMA Mechanism of Action of Antibiotics Class of Antibiotic Examples Mechanism of Action Beta-lactam Terscylines Glycopeptides Rifampin i inding proteins on the surface of the bacterial cell Gen ab proceia synch amicin it protein synthesis ‘bramycin (The mechanism is via nding to. mic ribosomal RNA) Clindamycin Inhibit the dissociation of in peptidyl-tRNA from Clarithromycin ribosomes during Azithromycin translocation (The ‘mechanism is via binding to 50S ribosomal subunits.) Inhibit protein synthesis (on 70S and 80S ribosomes) ‘Vancomycin _Interfere with the inserion ‘Teicoplanin of glycan subunits into the cell wall. Inhibits RNA synthesis in bacteria Ciprofioxacin Inhibit DNA gyrase Levoforcin RNA, Ribonucleic acid; ¢RNA, transfer ribonucleic acid; DNA, de- onribonvelec acid kanamycin, and ampicillin. Chloram- phenicol and tetracycline appear to be activated during polymerization. Antibi- otics are eluted from PMMA beads with an exponential decline in elution over a 2- week period and then cease to be present in significant levels locally by 6 to 8 weeks. Local tissue concentrations of antibiotics are much higher than can be achieved with systemic administration and do not seem to cause problems in doses that are typically used. Extremely high local con- centrations of antibiotics can decrease cel- lular replication or even result in cell death. Increased surface area of PMMA (eg., with oval beads) enhances elution of antibiotics. Beads are inserted only after thorough debridement. Because PMMA itself is associated with a foreign body re- action, the beads should be removed. . Osmotic Pump—A method for delivering high concentrations of antibiotics lo- cally, an osmotic pump is used mainly for smotic pump ly osteomyelitis, C. Transfusion—Because of the possibility of dis- ase transmission, transfusion has become an im- portant issue. 1. Tr ion reactions a. Allergic Reaction—The allergic reaction is the most common; it occurs toward the end of transfusion. Symptoms include chills, pruritus, erythema, and urticaria, which usually subside spontaneously. Pretreat- ment with diphenhydramine (Benadryl) and hydrocortisone may be appropriate in patients with a history of allergic reactions. b. Febrile Reaction—Also common, febrile reactions occur after the initial 100 to 300 ml of packed red blood cells have been transfused. Chills and fever are caused by antibodies to foreign white blood cells. ‘Treatment is similar to that for an allergic reaction, ¢. Hemolytic Reaction—Less common but more serious than the other reactions, a he- molytic reaction occurs early in the trans- fusion. Symptoms include chills, fever, tachycardia, chest tightness, and flank pain. ‘Treatment consists of stopping the transfu- sion, administering IV fluids, having ap- propriate laboratory studies done, and monitoring the patient in an intensive care setting. 2, Transfusion risks—Risks include the trans- mission of hepatitis, human T-cell lym- photrophic virus, and human immunodefi- ciency virus (HIV) (1 in 400,000 to 600,000 per unit transfused). Donor deferral for high- Fisk individuals and more effective sgreening methods are helping manage these risks. D. Tetanus—Tetanus is a potentially lethal neu- ro ic disease caused by an exotoxin of Clostridium tetan, Prophylaxis against tet- anus requires classifying the patient’s wound (tetanus-prone or non-tetanus-prone) and a com- plete history of the patient’s immunizations. ‘Tetanus-prone wounds are more than 6 hours old; have an irregular configuration; are deeper than 1 cm; are the result ofa projectile injury, crush in- jury, burn, or frostbite; have devitalized tissue; and are grossly contaminated. Patients with tetanus- prone wounds who have an unknown tetanus sta- tus or have received fewer than three immuriza- tions require tetanus and diphtheria toxoids and tetanus immune globulin (human). Patients with tetanus-prone wounds who are fully immunized do not require immune globulin; however, tetanus toxoid should be administered if the wound is se- vere, the wound is more than 24 hours old, or the Patient has not received a booster within the past 5 years. The only type of patient with a non- tetanus-prone wound that requires any treatment is one with an unknown immunization history or a history of fewer than three doses of tetanus im- munization; these patients require tetanus toxoid, ‘The treatment of established tetanus is primarily to control the patient's muscle spasms with di- azepam. Initial antibiotic therapy includes peni- cillin G or doxycycline; alternative antibiotic ther- apy includes metronidazole. E. Rabies—Rabies is an acute infection charac-terized by irritation of the central nervous system that may be followed by paralysis and death. The organism involved is a neu- rotropic virus that may be present in the saliva of rabid animals. In the bites of dogs and cats, healthy animals should be observed for 10 days, and there is no need to start antirabies treatment. If the dog or cat begins to develop symptoms, then human rabies immune globulin with human diploid cell vaccine or rabies vac- cine absorbed (inactivated) should be started. For bites from dogs and cats who are suspected of being rabid or are known to be rabid, the pa- tient should be immediately vaccinated. Bites from skunks, raccoons, bats, foxes, and most res should be considered rabid, and the patient should be immunized immediately. Bites from the following animals rarely require an- tirabies treatment: mice, rats, chipmunks, ger- bils, guinea pigs, hamsters, squirrels, rabbits, and rodents. =. HIV infection—The incidence of HIV infection is relatively high in the homosexual male popula- tion and is becoming increasingly common in heterosexual patients. In addition, a large portion of the hemophiliac population is affected. The virus primarily affects the lymphocyte and macrophage cell lines and decreases the num ber of T-helper cells (formerly known as T4 lymphocytes, now known as CD4 cells). The di- agnosis of acquired immunodeficiency syn- drome requires one of the following scenar- ios: (1) an HIV-positive test plus one of the opportunistic (such as i carinii pneumonitis) or (2) an HIV-positive test plus a CD4 count of less than 200 cells/ul (normal uninfected individuals have a CD4 count of 700 to 1200 cells/l ). This disease has increased the importance of precautions for han- dling blood and body fluids during trauma man- agement and surgery. The risk of seroconversion from a contaminated needle stick is 0.3%; the risk increases if the exposure involves a larger amount of blood. The risk of seroconversion from mu- cous membrane exposure is 0.09%. Unfortu- nately, blood donated for transfusion that tests negative for the HIV antibody may transmit HIV to the blood recipient because there is a delay (in the donor) between infec- tion with HJV and the development of a de- tectable antibody. The risk of transmission of HIV via a blood transfusion is 1 in 400,000 0 600,000 per unit transfused. HIV positivity is not a contraindication to performing required surgical procedures. HIV-positive patients (even those who are asymptomsaci) with traumatic orthopaedic injuries (especially open fractures) or those undergoing certain orthopaedic surgical procedures appear to be at increased risk for de- veloping wound infections as well as non-wound- related complications (e.g., UTI, pneumonia). GeNeRaL Princitss OF TRAUMA © 17 G. Hepatitis —Three types are commonly recog- nized. 1. Hepatitis A—Hepatitis A is common in areas with poor sanitation and public health con- cerns (fecal-orel transmission). Surgical or traumatic transmission is not a major problem. 2. Hepatitis B—Approximately 200,000 people in the United States are infected with the hep- atitis B virus each year, and there are more than 1 million carriers. Screening and the use of a vaccine have reduced the risk of transmis sion for health care workers. Immune globulin is administered after exposure in nonvacci- nated individuals. Neither vaccine nor im- mune globulin administration has been docu- mented as causing HIV transmission. 3. Hepatitis C—Hepatitis C is the most com- mon transfusion-associated hepatitis and is also associated with IV drug abuse. H. Missile ballistics—Gunshot wounds are typically classified as high velocity (22000 fr/sec) or low ve- locity (<2000 fr/sec). Low-velocity guns, such as handguns, tend to cause laceration, and such wounds can be treated by debridement of the en- try and exit wounds. High-velocity guns, such as assault rifles, have far more energy transferred to the tissues (KE = ¥MV*). A cavitation effect oc- curs that is 10 to 14 times the diameter of the mis- sile. These wounds may require multiple debride- ments. Missiles designed to expand and fragment, such 5 gunshot shells, hollow points, and partially jacketed bullets, cause more destruction than fally jacketed bullets. Temporary nerve injuries can oc- Cur from the blast effect of mises, and arterial injuries should always be suspected when a patient has weak or absent pulses and an expanding hematoma. Low-velocity missiles usually do not become hot enough to be sterile and can intro- duce foreign material from clothing into the wounds. (For further details, see Chapter 24,) 1. Hypothermia—Treatment for hypothermia of the body (defined as core temperature of less than 35° C (95° F}) can include passive external rewarming (such as blankets, clothing, and warmed IV fluids) and active core rewarming (such as peritoneal lavage, pleural lavage, and oth- ers) for cases of severe hypothermia. Hypother- mia isa serious, life-threatening condition that is made worse by surgery and anesthesia. When possible, surgical intervention should be delayed until the hypothermic state is corrected, VI. COMMONLY USED GRADING SYSTEMS IN TRAUMA PATIENTS ‘A. Glasgow coma scale (see Table 1-1) B. Revised trauma score (Table 1-15) C. Mangled extremity severity score (Table 1-16) D. Gustilo classification of open fractures (sec Chapter 2) E. Tscheme classification of soft tissue injuries (see Chapter 2)18 * GenERaL PRINGPLES OF TRAUMA Revised Trauma Score’ RANEY RY Test ‘Question Numbers, Parameter Measurement Score 1998 OSAE—Adule Reconstructive Hi Respiratory rate 10-29 4 1998 OSAE—Pediatric “ 230 3 Orthopaedics 69 2 1998 OSAE—Sports Medicine 1s 1 ————— None o 1997 OITE, 61, 64, 74, 129, 131, 193, 231, Systolic blood pressure 290 4 259,259 76-89 3 1997 OSAE—Adule Spine 50.75 2 1997 OSAE—Foor and Ankle oa 149) i 1997 OSAE—Musculoskeletal 2,9, 15,38, 39, 44, 49, 51,54, No pulse ° ‘Tuma 59, 60, 65, 78, 95 ‘Add Glasgow Coma Bes 4 1997 OSAE—Orthopaedic 38, 103 converted score ou 3 Basic Science 68 2 45 1 1996 OITE, 75, 100, 202, 224 1 ° 1996 OSAE—Anatomy-Imaging 1996 OSAE—Musculoskeletal B “To calculate a Revised Trauma Score, add the scores for Respiratory ‘ate, Systolic blood pressure, and the converted Glasgow Coma Seve Tumors and Diseases 1996 OSAE—Shoulder and Elbow 5 1995 OTE 29, 104, 190, 224 1995 OSAE—Adule Reconstructive Hip/Knee 1995 OSAE—Pediatrie 1B Orthopaedics 1995 OSAE—Sports Medicine 1,70, 91, 98 Points Skeleta/Soft Tissue Injury Low energy (stab, simple fracture, “civilian” 1 ‘gunshot wound) Medium energy (open or multiple fraczures, dislocation) High energy (close-range shotgun or “military” 3 gunshot wound, crush injury) Very high energy (same as above but with gross 4 ‘contamination, soft tissue avulsion) Limb Ischemia Pulse reduced or absent but normal perfusion 1 Polsslesness, paresthesia, diminished 2 capillary refi Cool, paralyzed, insensate, numb 3 Shock Systolic blood pressure always >90 mm Hg ° 1 Hypotensive wansienty Persistent hypotension Age (Years) 30 ° 30-50 1 >50 iy nee eee ceneeeee En “To calelate a Mangled Extremity Severity Scores the sors seciSot Tanto Linb uch Shas sat SUGGESTED READINGS ct fishy story, JAMA 247:1314, re Ee en pat rhe eae er teres So cussion, Phys Sports Med 14:75-83, 1986. ciao Th XT, Chiu HS, et al: Post-traumatic fat embolism: Its eee veer ote pata eo 1994 OTE, 65, 102, 139, 144, 173, 219 1994 OSAE—Adule Spine 3 1994 OSAE—Foot and Ankle 7 1994 OSAE—Musculoskeletal 12, 22, 24, 35, 43, 51, 54, 56, Trauma 58, 85, 95 Duis JH, Nisten MWA, Klausen H), etal Fat embolism in patients ‘with an isolated fracture of the femoral shaft, 7 Trauma 28:383-390, 1988. Heeppensall RB, Sapega AA, Score R, et ak: The comparunentsyndcome: An experimental and clinical sy of muscular energy metabolism us- ing phosphorous nuclear magnetic resonance spectroscopy. Clin Or- thep 226 158-155, 1988. ‘Masen FA, Winguise A, Krugmice RB: Diagnosis and management of compartnent syndrome, J Bane Joint Surg 62A:286-291, 1980. Rosner RABaird RA, Malerick MM Fat tore shock syndrome as 2 complica of orthopaedic unger ease report, 7 Bane Join Surg 4952-959, 19, Salzman EW, Harris WH: Prevention of venous thromboembolism in ‘orthopaedic patients, J Bone Joins Surg 54A:903-913, 1976, Seldon 1: Thee eype3 of meive injures, Brain 66:238-293, 1993 Thompeom 128, Flynn TC Miller PW ta: The significance of seapu- Ine facture, Trane 30028-9797, HN Whitesides TE: Haney TC, Morimoto Ky ota: Tissue pressure mea- surements ava determinant forthe need of asiotomy, Clin Ortbop Tiss D5. Recent Anicles Anderson PA. Rivara FP, Maier RV. etal The epidemiology of seatbelt- associated injuries, J Trauma 31:60-67, 1991. Estes NAM: Sudden death in young children, N Engl J Med 333:380- 381, 1995. Garland DE: \ clinical perspective on common forms of acquired het- ‘rotrophic ossification, Clin Orthop 263:13-29, 199 WISE Ben RE: Sabon ven ome A cetining challenge, Surgery 108:1-9, 1990. Johansen K, Daines M, Howey T, et ak Objective criteria accurately pre- dict amputation following lower extremity wauma, J Trenme 30(5):568.572, 1990, Manoli A: Compartment syndromes ofthe foot: Current concepts, Foot ‘Ankle 10340.544, 199,