Trauma may have local or polysystemic effects. With severe trauma (ie, automobile trauma), injuries to the respiratory and cardiovascular systems are common. Fractures or major vessel laceration result in the loss of large amounts of blood from the circulation. The net results are often inadequate gas exchange in the lungs and poor tissue perfusion resulting in low oxygen delivery to the tissues. Management of these critical patients depends on rapid, accurate diagnosis, and an understanding of the pathophysiology and treatment principles of both trauma and specific injuries.
Initial Presentation
A rapid initial survey of the animal is made, with particular attention given to the respiratory, cardiovascular and central nervous system. Any immediate threat to life should be eliminated. Injuries to multiple systems may exist, so priorities for treatment should be established. The goal of initial treatment is to ensure adequate delivery of oxygen to all tissues. This can be achieved by adherence to the following principles.
1. Assurance of a reliable airway.
2. Restoration of normal intrapleural pressure.
3. Assurance of normal function of bellows apparatus.
4. Maintain normal alveolar ventilation.
5. Maintain effective circulation, including adequate blood volume and hemoglobin concentration.
The overall management plan for the first two hours of acute care is:
1. Eliminating all immediate threats to life.
2. Initial examination and resuscitation.
3. Stabilization and re-evaluation.
Once the animal is stable, definitive repair of injuries can be considered.
Severe, immediate threats to life include airway obstruction or rupture, open pneumothorax, tension pneumothorax, severe hemorrhage, hypovolemic shock and CNS damage. If an animal presents comatose or stuporous after head trauma, it should be intubated and ventilated. The neck is extended and the pharynx cleared of any blood or excessive secretions. The maximum airway ventilation pressure should not exceed 20 cm H2O. If capnography is available, end tidal CO2 should be measured.
Stridor, a high pitched noise or inspiratory wheeze, is indicative of upper airway obstruction, possibly as a result of laryngeal or tracheal injury (commonly seen with bite wounds). Some animals with airway trauma will improve with supplemental oxygen. Oxygen can be provided with a face mask, oxygen cage or oxygen collar. Severely dyspneic animals generally do not tolerate placement of nasopharyngeal or transtracheal catheters for oxygen supplementation. Corticosteroids may be beneficial to decrease airway swelling. Anesthesia and intubation are indicated in animals that remain dyspneic in spite of medical treatment. Subcutaneous emphysema of the neck is suggestive of air leakage from the trachea. A tracheal tear is sometimes visible on survey radiographs. However, often an accurate anatomical diagnosis requires general anesthesia and either bronchoscopy or exploratory surgery. In either of these situations intubation must be carried out with extreme care to avoid worsening a tracheal tear or even avulsing the distal end of the trachea from the site of the tear. Emphysema of the thoracic wall suggests air leaking from the pleural space (ie, pneumothorax with air leaking out of the pleural cavity via penetrating wound). The primary concern in this situation is the pneumothorax which is treated by thoracocentesis initially. A chest tube is placed if the pneumothorax worsens in spite of treatment.
Increasing dyspnea, restlessness, decreased lung sounds and hyperresonance may indicate a tension pneumothorax. In this situation, a leaking area of lung is acting like a one way valve. During inspiration, the lung leaks air into the pleural space. During expiration, the lung seals, trapping the air. As the pneumothorax worsens breath by breath, the lungs collapse further and further. In addition, the more positive pleural pressure decreases venous return to the heart via the great veins. Immediate thoracocentesis is performed; a diagnosis of tension pneumothorax is suspected when the animal's condition fails to improve or when the clinician cannot aspirate enough air fast enough to generate negative pressure in the thorax. In this case, the animal is anesthetized, intubated and a chest tube placed immediately. Continuous suction drainage is often required.
Open pneumothorax is a true life threatening emergency. Animals present with a wound that sucks air when the skin obstructing the thoracic penetration is moved. Some animals will present in respiratory arrest. They should be intubated and ventilated immediately, and a chest tube inserted into the "sucking" chest wound. In animals with an open chest wound that are stable the wound is covered with a water soluble gel and the chest tapped. An occlusive dressing is then placed over the wound until definitive surgical exploration is performed.
Shock may be defined as poor tissue perfusion or inadequate cellular metabolism. Shock is often classified by cause as hypovolemic, cardiogenic, septic and possible neurogenic. Trauma associated hemorrhage results in decreased circulating blood volume. This hypovolemia is the primary factor in traumatic shock. Cardiac failure may also occur, particularly if the insult involved blunt chest trauma. Pain can activate the neurohormonal pathways (hypothalamic-pituitary-adrenal, etc.) which are key to the shock response.
In early shock, physiologic defense mechanisms result in:
1. Redistribution of blood to heart and brain.
2. Sympathetic stimulation to increase blood pressure and increase cardiac output.
3. Movement of extracellular fluid into the circulation.
4. Activation of renin-angiotensin-aldosterone and ADH systems to promote sodium and water retention.
In advanced shock, prolonged microcirculatory compromise leads to peripheral hypoxic cell death. Previous proximal arteriolar constriction causes severe damage to the tissues distal to the constriction. In advanced shock, postcapillary sphincter constriction occurs, resulting in stagnation of blood in the capillary beds. Capillary wall damage results in altered vascular permeability and loss of fluids and possibly protein. Cell membrane damage results in entry of sodium and water into the cell and leakage of potassium. Cells become "waterlogged" and cellular metabolism becomes anaerobic. Cell membrane potentials and cell function is disrupted.
The corner stone of hypovolemic shock treatment is rapid volume expansion to improve perfusion. One or more large bore IV catheters are placed and a warm balanced electrolyte solution is administered. The rate of volume administration is dependent on the degree of hypovolemia, the species of the animal, and the presence or absence of pulmonary contusions. For dogs and cats without evidence of pulmonary contusions, the initial fluid rate is 90 ml/kg/hr and 45 ml/kg/hr, respectively. Hemodilution is generally not a problem until the PVC is 25-30% or less. Oxygen transport is actually increased because of increased cardiac output and improved blood flow.
Current opinion favors less aggressive volume replacement in animals with severe pulmonary contusions to prevent massive pulmonary edema and respiratory failure. This "limited volume expansion" approach aims to improve circulatory function whilst maintaining adequate ventilation. Total solids (or colloid osmotic pressure), CVP, lung sounds, oxygen saturation and blood gases should be measured. Assisted ventilation may be required in some animals simply because of the severity of the pulmonary contusions. An initial fluid rate in animals with suspected pulmonary contusions is 10 -20 ml/kg in the first hour.
In addition to activation of "systemic" systems, many local systems are activated at the site(s) of trauma. The coagulation and complement systems, arachadonic acid cascades, and activated neutrophils all are essential components of healing and recovery. However, if these local responses amplify and become systemic, there is the potential for substantial damage to distant organs systems (Systemic inflammatory response - "SIRS" Multiple organ dysfunction - "MODS"). The activated neutrophil appears to be very important in causing distant organ injury after shock resuscitation. There has recently been renewed interest in hypertonic saline (HTS) resuscitation, because of the potential for HTS to modulate the inflammatory response. HTS resuscitation decreased PMN accumulation in the lungs and liver in hemorrhagic shock animal models. In vitro experiments that HTS administered before neutrophil "priming" (ie, by an initial trauma) decreased surface receptor expression, superoxide production, and elastase release. HTS after "priming" but before "activation"decreased the PMN respiratory burst and protease release. "Priming" and "activation" represent: i) The initial trauma; and ii) The subsequent surgery in a "two insult" model of SIRS and MODS. It remains to be seen if very early HTS resuscitation will translate into attenuation of SIRS and improved survival in clinical veterinary trauma patients.
The use of corticosteroids in hemorrhagic shock is controversial. Experimentally, they are useful within 2 hours of hemorrhagic shock onset only. They improve cardiac output, increase stroke volume, decrease peripheral vascular resistance, and increase oxygen availability. Their main mechanisms of action is thought to be inhibition of several of the inflammatory cascades (inhibition of prostaglandins, tumor necrosis factor [TNF] and interleukin [IL-1, IL-2] formation) and stabilization of lysosomal membranes, preventing release of damaging hydrolases. Corticosteroids may also have a role in preventing reperfusion injury. Doses extrapolated from experimental studies: Hydrocortisone: 50-100 mg/kg; Methylprednisolone: 15-30 Mg/kg; Dexamethasone: 4-8 mg/kg.
Examination and Continued Resuscitation.
Once an airway is secured, ventilation is adequate, volume replacement begun and obvious hemorrhage controlled, a complete and more thorough examination is done. It should be orderly so that no system is overlooked. Wounds are covered with sterile dressings, fractures immobilized and prophylactic antibiotics begun. Frequent monitoring is done and response to therapy evaluated.
Heart rate, respiration rate, pulse rate and strength, temperature (core and web), mucous membrane color, and capillary refill time are vital signs to measure. Physiologic monitoring should include urine output, EKG, PVC/TS/Dex. Ideally, blood pressure, central venous pressure (CVP), blood gases, and O2 saturation of hemoglobin should be monitored in critical patients. The rate of fluid administration is decreased once adequate cardiovascular response is observed (ie, improved mucous membrane color, decreased heart rate, improved blood pressure).
Animals with ongoing hemorrhage show initial improvement then become hemodynamically unstable when fluids are slowed. Diagnostic radiographs, thoracocentesis and abdominocentesis are performed to localize bleeding. (Hemorrhage does not clot when removed from the body). Only animals with severe ongoing hemorrhage not responsive to transfusion are considered for surgery before complete stabilization. Blood transfusions with either fresh whole blood, stored components, or autotransfusion are commenced. Other potential causes for poor response to volume replacement include cardiac arrhythmias, hypoxemia, acidosis, urinary tract damage and sepsis.
Moderate to severe ventilatory impairment is commonly secondary to pneumothorax or hemothorax and pulmonary contusions. Treatment includes lung re-expansion (chest drainage) oxygen support (Humidified nasal or transtracheal O2, or O2 cage) and airway clearance (nebulization, coupage).
Tissue oxygenation is impaired if the PCV drops rapidly to less than 25-30%. Hypoproteinemia predisposes to edema. Ideally, maintain the PCV between 25 and 30%, and the total solids between 4 and 5 gl dl. Albumin should be 2 gl dl or higher.
Stabilization and Re-evaluation.
Once cardiovascular and pulmonary function are controlled, the patient is reevaluated to avoid delayed or missed diagnosis and the need for definitive treatment. Monitoring and nursing care are continued. Specific attention is paid to fluid balance, PCV, TS, urine output, chest tubes, lungs and airway.
Occult injuries are not immediately evident. They include urinary leakage secondary to ruptured urinary bladder or lacerated urethra, ischemic necrosis or rupture of the bowel, and injury to the extrahepatic biliary tree. If the patient's clinical picture is not as expected, then additional diagnostic procedures, such as radiography (survey and contrast), laboratory measurements, and abdominocentesis with or without abdominal lavage are performed. Peritonitis may be responsible for the lack of response to therapy. Common signs of peritonitis are depression, shock, vomiting, diffuse abdominal pain, and the development of a peritoneal effusion.
Signs of septic peritonitis secondary to ischemic necrosis or rupture of the bowel can be noticed 6 to 24 hours after trauma. It should be emphasized that this is quite uncommon. Diagnosis is based on clinical signs (pain, vomition, fever), radiography (paralytic ileus, intraperitoneal free gas, loss of abdominal detail), and peritoneal fluid cytology of toxic neutrophils, bacteria, and intestinal debris.
Signs of urinary tract disruption include hematuria, dysuria, anuria, sublumbar pain, peritoneal effusion, plus those associated with uremia (vomition, dehydration, polydypsia). Clinical signs plus biochemical abnormalities (azotemia, hyponatremia, hyperkalemia) may be evident by 24 hours after trauma. A diagnosis of uroperitoneum is made based on clinical signs, lab findings, the presence of urine on abdominocentesis (when in doubt, submit a sample of peritoneal effusion for creatinine or BUN analysis) and catheterization. The specific site of injury is located with contrast radiography.
Bile peritonitis is an occult injury where signs may not develop until 2 weeks after injury. Signs include abdominal distention, icterus, anorexia. Diagnosis is based on clinical signs, history of trauma, laboratory findings (elevations in SAP, SGPT, and bilirubin). Specific sites of injury are located at laparotomy.