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Theme: General movement trauma on organism. Shock, collapse, syncope




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Ф КГМУ 4/3-04/01

ИП № 6 УМС при КазГМА

от 14 июня 2007 г.


KARAGANDA STATE MEDICAL UNIVERSITY


Department of surgical diseases 1,

military field surgery, with physiotherapy and therapeutic physical training


LECTURE


Theme: « General movement trauma on organism. Shock, collapse, syncope.

Terminal conditions »


Discipline: General surgery


Specialty: 051301 – general medicine


Course: 3


Time: 1 hour


Karaganda - 2010 y.


Discussed and confirmed at the meeting of the Department


Protocol № _____ of "____" _________ 2010 y.


Head of the Department of surgical diseases 1,

military field surgery, with physiotherapy

and therapeutic physical training: Shakeyev K.T.


^ The theme: « General movement trauma on organism. Shock, collapse, syncope. Terminal conditions »


The purpose: to Care of the injured patient begins with the primary survey. Identifying and treating all immediately life-threatening injuries is the first priority. Resuscitation is begun simultaneously with the primary survey. The secondary survey follows the rapid initial evaluation and involves a detailed head-to-toe assessment. In the definitive care phase, all injuries are prioritized and treated. The patient's ultimate outcome is directly related to the length of time between injury and definitive care.


The lecture plan:

  1. idea wound shock

  2. theory shock

  3. classification shock

  4. clinic, principle treatment

  5. terminal disease

  6. syncope.

  7. collapse.


The lecture Theses.

Thoracic Trauma

Thoracic trauma accounts for one-fourth of trauma deaths and is second only to head trauma as the most common type of fatal injury. Although some of these injuries are immediately or rapidly fatal, others can be treated with simple interventions if they are recognized. Knowing the signs and symptoms of these injuries and having a high index of suspicion is the key to early recognition. Of thoracic injuries, 85% can be treated with simple maneuvers that are taught in medical school. The other 15% usually require operative intervention. It is convenient to divide these injuries into groups according to their severity (Table 9-2).

^ Immediately Lethal Thoracic Injuries

Airway obstruction, the first entity in this category, was previously discussed. Tension pneumothorax, the second type, occurs when there is a continuous buildup of air in the pleural space, with no means of escape. As the intrapleural pressure rises, the ipsilateral lung collapses, the mediastinum is displaced to the opposite side, and the contralateral lung is compressed. On the injured side, the intrapleural pressure becomes positive relative to the uninjured side, and can exceed ambient pressure. The mediastinum and trachea are pushed to the contralateral side. As a result, compression, distortion, and kinking of the superior and inferior vena cavae occur. Venous return to the heart is significantly

Table 9-2. Categories of Thoracic Trauma decreased, and as a result, oxygen delivery is compromised. Unless this condition is rapidly treated, death ensues. Tension pneumothorax should never be diagnosed by chest x-ray; it is a clinical diagnosis that is made by physical examination. Waiting for x-ray confirmation may lead to the patient's death. Physical signs include respiratory distress, tachycardia, hypotension, jugular venous distension, and contralateral tracheal deviation. On the injured side, breath sounds are absent or markedly decreased, with hyperresonance (tym-pany) to percussion (Table 9-3). If tension pneumothorax is suspected, rapid decompression with a needle is indicated. A 14-gauge (or larger), 5-cm-long, over-the-needle catheter is inserted into the pleural cavity through the second intercostal space (just over the top of the third rib) in the midclavicular line. A rush of air from the needle signifies decompression of the tension. The needle is removed, but the catheter is left in place to prevent recurrence. Needle decompression is a rapid, temporary treatment that converts a tension pneumothorax into a simple pneumothorax.

Immediately Lethal Injuries

Potentially Lethal Injuries

Nonlethal Injuries

Airway obstruction

Pulmonary

Simple




contusion

pneumothorax

Tension

Myocardial

Simple

pneumothorax

contusion

hemothorax

Open pneumothorax

Traumatic aortic

Scapula and rib




rupture

fractures

Massive

Traumatic




hemothorax

diaphragmatic







rupture




Flail chest

Tracheobronchial tree







disruption




Cardiac tamponade

Esophageal injury




Definitive treatment requires a chest tube thoracos-tomy, placement of a polyethylene tube into the pleural cavity, often through the fifth intercostal space in the midaxillary line (Figure 9-4G). The tube is placed to establish a closed intercostal drainage system to remove air, fluid, and blood from the pleural space, thus allowing the lung to expand. The external end of the chest tube is attached to a water seal, which acts as a one-way valve that lets air escape from the pleural cavity. Suction is commonly applied to the water seal to ensure adequate evacuation of the pleural cavity and expansion of the lung. The suction pressure is commonly set at '20 cm H20.

Open pneumothorax, or a sucking chest wound, occurs when a large chest wall defect permits equilibration of intrapleural and atmospheric pressures. This situation leads to lung collapse. As the patient breathes, air is heard or seen bubbling from the wound. If the size of the opening in the chest wall is two-thirds the diameter of the trachea or larger, resistance to flow is lower

Table 9-3. Signs of Tension Pneumothorax and Cardiac Tamponade

Tension Pneumothorax

Cardiac Tamponade

Respiratory distress

Respiratory distress

Tachycardia

Tachycardia

Hypotension

Hypotension

Jugular venous distension (elevated CVP)a

Jugular venous distension (elevated CVP)a

Ipsilateral absent or markedly decreased breath sounds

Muffled or distant heart sounds

Ipsilateral hyperresonance to percussion (tympany)

Pulsus paradoxus > 10 mm Hg

Contralateral tracheal deviation




*ln the hypovolemic patient, this sign may not be present. CVR central venous pressure.

through the injury than through the trachea. Air then moves preferentially in and out of the pleural space instead of into the trachea, thus preventing effective ventilation. Therefore, this wound is immediately life-threatening. The fastest and easiest way to stop this abnormal air movement is to cover the wound with an impermeable dressing (e.g., Vaseline gauze, plastic wrap), taped on three sides, to create a one-way flap valve. During expiration, as pressure in the pleural space increases, air can escape under the open side of the dressing. During inspiration, as pressure in the pleural space decreases, the dressing is sucked down, occluding the wound and preventing air from entering the pleural space. It is crucial not to tape the dressing on all four sides because doing so might convert an open pneumothorax to a tension pneumothorax. Definitive care involves placement of a chest tube and closure of the chest wall defect.

Massive hemothorax is the rapid loss of more than 1500 mL blood into the thoracic cavity. It is a class III or greater hemorrhage into the chest. Diagnosis is made when a hypotensive patient has decreased or absent breath sounds and dullness to percussion on one side of the chest. Initial management is the same as that of any patient who is in hemorrhagic shock. A portable supine chest x-ray usually shows complete opacification on the injured side. Treatment typically begins with the insertion of a large (#36-40 French) chest tube. An autotrans-fusion device should be set up, if available. If 1500 mL blood is immediately evacuated, the patient will probably require an emergent thoracotomy. If less than 1500 mL blood is initially evacuated and bleeding continues at a rate of 200 mL/hr or more, thoracotomy may still be required. Sometimes, there is no further significant blood loss from the chest tube, and thoracotomy is avoided. A post-chest tube chest radiograph should be obtained to verify complete drainage of the hemothorax.

Flail chest occurs when consecutive ribs are fractured in multiple places (i.e., each rib is fractured in at least two places). This free-floating, or flail, segment of the chest wall moves paradoxically with inspiration and expiration. Paradoxical motion occurs because the flail segment is not in bony continuity with the rest of the thoracic cage. As the patient inhales, the ribs rise and the diaphragm descends, creating negative pressure in the pleural space. The uninjured chest wall expands, but the flail segment, responding to the negative intrapleural pressure, moves inward. Similarly, as the patient exhales, the normal ribs retract, but the flail segment moves outward. Seeing or palpating this paradoxical motion makes the diagnosis. The ventilatory insufficiency that is seen in flail chest is not simply caused by the abnormal chest wall motion. What is more important is the underlying lung injury in combination with hypoventilation. A significant amount of force is required to break multiple ribs in multiple places. Some of this energy is transmitted through the chest wall into the underlying lung, causing a pulmonary contusion, which involves extensive intraparenchymal hemorrhage and alveolar collapse. As a result, a ventilation-perfusion mismatch occurs and results in hypoxemia.

The pain associated with multiple rib fractures causes the patient to splint the injured chest wall by inhibiting its movement during ventilation. Hypoventilation is the consequence. Patients with significant ventilatory impairment need mechanical ventilation to prevent hypoxia and hypercarbia. Positive end-expiratory pressure (PEEP) may also be required to maintain adequate oxygenation. Optimization of intravascular volume and myocardial performance often requires placement of a central venous or pulmonary artery catheter. Definitive treatment requires reexpansion of the lung, adequate oxygenation, judicious use of fluids, and adequate analgesia to improve ventilation.

Cardiac tamponade as a result of trauma occurs when blood accumulates within the pericardial sac and compresses the heart. It is associated with blunt and penetrating injuries to the heart (e.g., a car accident that thrusts the driver's sternum into the steering wheel). Even isolated injuries to the small pericardial and coronary vessels can cause tamponade. In blunt trauma, the site that is most likely to be injured has the thinnest wall, the right atrial appendage. However, rupture of other cardiac chambers, including the great vessel, can also occur. When blood leaks into the fibrous, nondis-tensible pericardium, it compresses the cardiac chambers and restricts ventricular filling in diastole. As a result, stroke volume and cardiac output decrease. The increased pressure within the pericardial sac is transmitted to each cardiac chamber, resulting in equalization of the right atrial, right ventricular diastolic, pulmonary artery diastolic, pulmonary capillary wedge, left atrial, left ventricular diastolic, and intrapericardial pressures. Three classic clinical signs, known as Beck's triad, are related to these hemodynamics: (1) muffled (distant) heart sounds; (2) elevated central venous pressure (jugular venous distension); and (3) hypotension. Other signs include pulsus paradoxus (a decrease of > 10 mm Hg in systolic blood pressure during inspiration) and Kussmaul's sign (an increase in CVP with inspiration). Muffled heart sounds and pulsus paradoxus may be difficult to elicit in a noisy emergency department. Distended neck veins associated with elevated CVP may not be present in the hypovolemic patient. Cardiac tamponade and tension pneumothorax are included in the differential diagnosis in patients who are pulseless, but have cardiac electric activity (see Table 9-3).

The initial treatment of a patient who is suspected of having cardiac tamponade is administration of intravenous fluids. Raising CVP higher than the intrapericardial pressure temporarily increases cardiac output, allowing time to prepare for definitive therapy. Measuring CVP after placement of a central venous catheter and setting up bedside echocardiography are helpful steps in confirming the clinical diagnosis. However, pericardiocentesis should not be delayed for these diagnostic adjuncts. A 16- to 18-gauge, 15-cm-long, over-the-needle catheter attached to a 30- to 60-mL syringe is used for the procedure. The patient's electrocardiogram (ECG) reading is monitored with standard leads or a precordial lead that can be attached to the needle with a sterile alligator clip. The needle is inserted 1 to 2 cm to the left and inferior to the xiphochondral junction at a 45° angle to the skin. The needle is directed toward the tip of the left scapula and slowly advanced while the syringe is aspirated. Return of blood into the syringe signifies entry into the pericardium. Removal of as little as 10 mL blood can significantly improve cardiac function. The catheter (not the needle) is advanced into the pericardial sac, the needle is withdrawn, and the catheter is anchored in place and capped with a three-way stopcock to allow for repeat aspirations, if necessary. Pericardiocentesis can be negative if the blood is clotted. If the needle enters the heart, the ECG reading will show an injury pattern (i.e., ST-T wave changes, QRS widens and enlarges). If a precordial ECG lead is attached to the needle, the tracing inverts when the epicardium is entered. Pericardiocentesis is a temporizing maneuver. Definitive therapy requires opening the pericardium, finding the source of bleeding, and repairing it. This repair requires a qualified surgeon. If one is available, then it becomes a clinical decision as to whether to first perform the pericardiocentesis followed by operative exposure of the heart or to proceed directly to the operating room without pericardiocentesis. In extreme cases, there may not be time to go to the operating room, and a left anterior thoracotomy must be done in the emergency room.

^ Potentially Lethal Thoracic Injuries

Pulmonary contusion is an injury to the lung parenchyma that causes interstitial hemorrhage, alveolar collapse, and extravasation of blood and plasma into alveoli. It causes a ventilation-perfusion mismatch that results in hypoxemia. Physical examination may show a blunt or penetrating injury to the chest. Blunt injuries are associated with chest wall contusions, rib fractures, sternal fractures, and flail chest. The radiographic appearance is that of a poorly defined infiltrate that develops over time. These findings on chest x-ray are usually present within 1 hour of injury, but may take as long as 6 hours to become visible. Treatment includes observation, supplemental oxygen, or mechanical ventilation in patients who have pulmonary insufficiency.

Myocardial contusion is a difficult diagnosis to make. The diagnosis of blunt cardiac injury requires a high index of suspicion, especially in patients who have had deceleration or crush injuries to the anterior chest. These injuries are associated with motor vehicle accidents that involve the driver's sternum being propelled into the steering wheel. Fractures of the sternum or ribs may be present. The anterior myocardium (right ventricle) is primarily involved, and when severely injured, may lead to right-sided heart failure, hypotension, arrhythmia, and rarely, myocardial rupture. Management of this type of severe injury requires ECG monitoring, creatine kinase isoenzymes, echocardiography, and CVP monitoring. Making the diagnosis by ECG is often difficult because the weaker right ventricular electric activity is overshadowed by the stronger left ventricle. However, ECG changes (i.e., depression or elevation of the ST segment) or elevation of the creatine kinase myocardial band (CK-MB) fraction to greater than 6% of the total CK can be helpful in identifying patients with significant injury. Myocardial contusion should be considered in any patient who has blunt chest trauma and subsequently has arrhythmia. Echocardiography may show abnormal ventricular wall motion. Cardiac monitoring for 24 hours is usually all that is necessary in the susceptible, but asymptomatic patient. Longer monitoring is essential for patients who have arrhythmia, heart failure, elevated CK-MB, or abnormal ventricular wall motion.

Traumatic aortic rupture is a common cause of immediate death in abrupt deceleration injuries associated with motor vehicle accidents or falls from great heights. For survivors, salvage is possible with early diagnosis and treatment. Shear forces work on the aorta at sites of anatomic fixation. Common sites are just distal to the origin of the left subclavian at the ligamentum arterio-sum, at the root of the aorta near the aortic valve, and at the diaphragmatic hiatus. The mechanical forces associated with this type of injury work on the aorta at sites of anatomic fixation. In a horizontal deceleration, seen in motor vehicle accidents, the heart and aortic arch continue to move forward, while motion of the descending aorta is limited because of its posterior attachments. In a vertical deceleration, seen in falls from great heights, the heart, weighted with blood, moves rapidly downward, stretching the aortic arch and causing injury in this location. Anterior-posterior compression of the chest and abdomen can also result in fracture or dislocation of the lower thoracic spine, which can injure the aorta at the diaphragmatic hiatus. The forces involved in these types of injury are complex and interrelated. For example, in motor vehicle accidents, the body moves forward, the heart and aortic arch decelerate at a different rate than the descending aorta, the chest hits the steering wheel (causing anterior-posterior compression, and the heart is displaced caudally and to the left. As a result, the aorta is exposed to shearing, bending, and torsion stresses that are beyond its ability to maintain structural integrity. If the initial tear involves the intima and media, the aortic blood is contained by the aortic adventitia and a pseudoaneurysm forms. If the initial tear involves all three layers of the aortic wall, the patient exsanguinates into the chest. Ruptures at the aortic root carry a high mortality rate; those at the diaphragmatic hiatus are rare. Of the survivors, most have injuries at the ligamentum arteriosum. Specific symptoms include severe chest or back pain. Radiographic signs that suggest aortic disruption are listed in Table 9-4. Often, however, there are no specific symptoms or signs. Having a high index of suspicion in patients with deceleration trauma may be the only indication for further evaluation. Arte-riography is the diagnostic procedure of choice. Computed tomography (CT) is not an optimal study to diagnose this condition. More useful diagnostic studies include transesophageal echocardiography and spiral CT scan arteriography. Rapid operative repair is necessary if these patients are to survive. Preoperative preparation includes control of blood pressure. Hypotension

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