The diaphragm is the muscular separation between the chest and abdominal cavities that functions as a barrier and aids in respiration. Diaphragmatic hernia is a disruption of the diaphragm which allows abdominal organs to migrate into the chest cavity. Almost exclusively the result of blunt trauma to the abdomen, acquired or traumatic diaphragmatic hernia is a common injury in companion animals, with motor vehicle accidents being responsible for 85% of cases documented in one study. A rapid rise in intra-abdominal pressure following a forceful blow and failure of the epiglottis to remain closed, allowing the stabilizing effect of the air filled lungs to be lost acutely, is the classic explanation for diaphragmatic rupture. While diaphragmatic hernia can occur in any dog or cat, as most dogs and cats that suffer diaphragmatic hernias have been hit by a car or have experienced some other type of trauma, most dogs are young intact males, and most affected cats spend time outdoors. In most cases, acute diaphragmatic hernia results in significant respiratory difficulty. The trauma which caused the hernia may also result in rib fractures, lung lacerations, and lung bruising. These injuries may lead to pneumothorax, or hemothorax. If abdominal contents have entered the chest cavity, this can further compromise the ability to expand the lungs. If the initial insult is tolerated, a diaphragmatic hernia may be diagnosed later as an incidental finding in a relatively asymptomatic animal. For these reasons, the clinical signs of diaphragmatic hernia vary from none to severe respiratory compromise and shock. As mentioned previously, dyspnea is the most common clinical sign, and relates multifactorily to the presence of shock, chest wall dysfunction, the presence of air, fluid or viscera in the pleural space, decreased pulmonary compliance, edema, and cardiovascular dysfunction. Cardiac arrhythmias are present in approximately 12% of small animals with diaphragmatic hernia. Other common clinical signs include muffled heart and lung sounds, thoracic borborygmi, and evidence of trauma, such as abrasions. Chronically, abdominal organs, such as the liver or intestines can become adhered in the chest cavity and the animal may exhibit signs associated with liver or gastrointestinal disease such as vomiting or anorexia.
It is important to remember that loss of continuity of the diaphragm does not necessarily result in severe respiratory distress. The cause of respiratory impairment associated with diaphragmatic hernia is multifactorial. Hypovolemic shock, chest wall trauma, pleural fluid or air, pulmonary contusions, and cardiac dysfunction are factors that contribute to hypoventilation. Other injuries such as rib fractures or flail chest may compound mechanical dysfunction. Pulmonary compliance is decreased by pleural fluid, the presence of abdominal organs in the thorax, or pneumothorax. Pulmonary hemorrhage, edema, and atelectasis reduce total lung capacity and functional residual capacity. Myocardial contusion often accompanies other traumatic injuries and may decrease cardiac output. When myocardial injury is concomitant with impaired ventilation tissue hypoxia can result. Pain resulting from chest and abdominal contusion and accompanying injuries causes voluntary restriction of motion (thoracic excursion) and may therefore further compromise ventilatory capability.
Chest radiographs must be taken to diagnose the disease, and to look for any other abnormalities. In the normal animal, a diaphragmatic line, a cardiac silhouette, and air-filled lung fields are appreciated on chest radiographs. In the case of diaphragmatic hernia, loss of the diaphragmatic line, loss of the cardiac silhouette, displacement of lung fields, and presence of abdominal contents within the chest cavity may be noted on chest radiographs. Most cases of diaphragmatic hernia can be diagnosed from radiographs. However, fluid in the chest cavity can obscure the diaphragmatic line in the absence of a hernia. Repeating chest radiographs after thoracocentesis is advisable but may not definitively show a diaphragmatic hernia. In this case, ultrasound may be helpful to differentiate abdominal organs from pleural fluid. Ultrasonographic evaluation is useful to identify abdominal viscera on the thoracic side of the diaphragm especially in the presence of pleural fluid because it enhances sonographic evaluation. Ultrasound may identify abdominal organs, differentiate organs such as the spleen or liver from pleural fluid, and will sometimes identify the defect in the diaphragm. Contrast radiography, performed by injecting contrast material into the abdominal cavity, and MRI or CT evaluation may also be helpful.
Initial stabilization of diaphragmatic hernia patients consists of medical therapy for shock and respiratory distress, possible antimicrobial utilization and close observation. Adequate volume replacement is the best therapy for hypovolemic shock. However, volume overload can be as detrimental as hypovolemia, particularly in patients with traumatic diaphragmatic hernias because concurrent pathology such as atelectasis, pulmonary contusions, and physical compression of the lungs by fluid or organ entrapment predisposes patients to pulmonary edema. The resuscitation fluid of choice is the subject of much debate. Isotonic crystalloids have long been the mainstay of volume replacement in treating hypovolemic shock and probably remain the recommended fluid for initiating therapy; however, hypertonic saline, colloids, and combinations of these fluids offer many potential advantages in trauma patients, including effective low-volume resuscitation and less expansion of the interstitial space compared with traditional isotonic fluid therapy. Volume and speed of fluid replacement are dictated by cardiovascular parameters such as capillary refill time, pulse quality, mucous membrane color, and central venous pressure, as well as respiratory parameters such as ventilatory rate, auscultatory findings, and pulse oximetry.
Signs such as dyspnea, cyanosis, tachypnea, tachycardia, reduced mentation, and postural changes such as an “oxygen hungry” stance (i.e., abducted elbows, extended head and neck, and open-mouthed breathing) are suggestive of hypoxia and should be treated quickly. Various modes of oxygen delivery are available . The actual method chosen depends on a number of factors, including patient size and temperament, available equipment and desired level of oxygen to be delivered. In patients with marked shunting, delivery of even 100% oxygen does little to correct arterial hypoxemia because shunted blood is never exposed to the higher alveolar oxygen tensions and therefore continues to depress PaO2 while the blood perfusing ventilated alveoli is already almost fully saturated and improves only minimally with exposure to 100% oxygen. However, some elevation of arterial oxygen content occurs (mainly in the form of increased dissolved oxygen), making oxygen therapy a useful aid in immediately treating dyspneic patients with traumatic diaphragmatic hernias.
Removal of pleural effusion may also improve ventilation in selected cases. Antimicrobials may be used during the preoperative period to prevent infection-related pulmonary problems. Every patient with traumatic diaphragmatic hernia needs close observation, since rapid changes in ventilatory function may occur. Patients failing to respond adequately to pre-surgical management or rapidly deteriorate despite appropriate management should be taken to surgery as soon as possible.
The timing of anesthesia and surgical correction of diaphragmatic injury may have an important effect on the outcome of treatment. Approximately 15% of small animals with diaphragmatic hernia will die prior to surgery, and animals with diaphragmatic herniorrhaphy performed within the first 24 hours after injury have the highest mortality rate (33%). The timing of surgical repair depends upon the extent of the initial cardiopulmonary dysfunction, the presence or absence of organ entrapment, the degree of compromised pulmonary function, and whether or not the animal’s condition is improving, stable, or deteriorating. Diaphragmatic herniorrhaphy may require immediate surgery if aggressive supportive care cannot stabilize respiratory function. Acute dilatation of a herniated stomach or strangulated bowel are examples of situations where emergency surgery may be indicated. A herniated stomach can rapidly distend from aerophagia, decreasing pulmonary compliance and compress the caudal vena cava decreasing venous return resulting in a vicious cycle that can be rapidly fatal. A herniated parenchymal organ such as the spleen may tear as it passes through the diaphragm causing acute hemothorax and a patient that may deteriorate rapidly after an initial response to shock therapy. Most small animals with diaphragmatic hernia can be stabilized over 24 to 72 hours, therefore the presence of a diaphragmatic hernia, on its own, is not indication for emergency surgery. Accompanying thoracic injuries such as pulmonary contusion will improve dramatically in 24 to 48 hours. The goal of initial management is to improve the cardiorespiratory status of the patient to improve their capability of tolerating the stress of anesthesia and surgery.
Induction of anesthesia in the diaphragmatic hernia patient is done with as little stress as possible and with the goal of quick control of ventilation. Intravenous catheterization, appropriate intravenous fluid administration (crystalloid or colloid) and cardiorespiratory monitoring are important. Propofol is preferred because it allows rapid induction of anesthesia, quick intubation, and near immediate control of ventilation with assistance or by a mechanical ventilator. Isoflurane is preferred for maintenance of anesthesia because a surgical plane of anesthesia is attained more quickly, it is associated with decreased recovery time, subjects the patient to less cardiac depression, and does not sensitize the myocardium to arrhythmias. Assisted ventilation is required soon after induction because the patient usually has decreased pulmonary compliance secondary to the presence of air, fluid, or abdominal viscera within the pleural space. Inspiratory pressure should not exceed 20 cmH2O to limit potential barotrauma from pulmonary hyperinflation which may result in over-inflation of the lungs during surgery. Rupture of pulmonary parenchyma, intrapulmonary hemorrhage, plumonary edema, and rarely pneumothorax may result. Resolution of atelectic areas in chronically atelectic lungs during surgery may subject the lung to mechanical and reperfusion injury. Damage from reperfusion in the collapsed vascular channels may disrupt capillary integrity causing fluid to leak into the interstitium resulting in reexpansion pulmonary edema within several hours after surgery. Reexpansion of atelectic areas that will not inflate with 20 cm H2O will gradually re-expand over several hours with a continual negative pleural pressure of 10 cm H2O.
The preferred surgical approach is a ventral midline celiotomy, extending from the xiphoid process to a point caudal to the umbilicus. This exposure allows access to all regions of the diaphragm. The incision should be large enough to allow exploration of the abdominal cavity because injury to other abdominal organs may be present and treatable concomitantly. Most diaphragmatic tears are muscular and are located ventrally and may favor either the right or left side. The liver, small intestine and pancreas are most commonly prolopsed into the thoracic cavity when the diaphragm defect is on the right side, whereas the stomach, spleen, and small intestine prolapse on the left side. It is essential to examine the entire diaphragm because more than one tear may occur. Should additional exposure be required to retrieve abdominal viscera adhered to structures within the thoracic cavity, surgical exposure can be improved by enlarging the rent in the diaphragm, paracostal extension of the celiotomy, and by caudal midline sternotomy. Visibility of the diaphragmatic defect is enhanced by placing a pediatric Balfour retractor over the towel-protected abdominal incision. Abdominal or pleural fluid is removed by suction. The abdominal viscera are carefully retracted from the thorax using gentle traction. Final, definitive positioning of the viscera is delayed until the diaphragmatic defect is closed. Inspection of the lungs and pleural cavity is usually performed after the herniated contents have been retrieved from the pleural cavity. Closure of the diaphragm is achieved with either absorbable or nonabsorbable suture material, in a simple-interrupted or simple-continuous pattern. The least accessible part of the defect is closed first, taking care to avoid traumatizing the aorta, caudal vena cava, hepatic veins or esophagus. On closure of the diaphragmatic defect, residual air is removed from the pleural cavity either by thoracentesis performed through the diaphragm using a 20 gauge catheter, three-way stop-cock, and 35 ml syringe or by placing a thoracostomy tube. Exploration of the abdomen, with particular attention given to the previously displaced tissues, is performed. Any lesions requiring attention are repaired. Closure of the abdomen is achieved after definitive replacement of the abdominal viscera.
Postoperative considerations for the patient with a repaired diaphragmatic hernia include ventilatory support, analgesic administration, and close observation. Ventilatory support is continued until the patient is adequately ventilating spontaneously. Particular care is necessary when administering positive pressure ventilation during and after surgery, since trauma to the lungs from overzealous ventilation is a definite possibility. Re-expansion pulmonary edema following re-oxygenation of chronically collapsed lungs is a major cause of perioperative death, particularly in animals with long-standing diaphragmatic hernias. Reperfusion injury, with release of superoxide radicals which cannot be effectively scavenged, is thought to result in increased pulmonary capillary permeability and pulmonary edema. Spontaneous ventilation in the postoperative patient is assisted by maintaining the patient in a forequarters-elevated position and the appropriate use of analgesics. Analgesic administration is done to comfort the patient and to ease apprehension during recovery.
The prognosis for animals presenting with a traumatic diaphragmatic hernia is variable depending on other injuries incurred. Of the patients that survive to presentation, the timing of surgery will significantly affect prognosis. Animals that have surgery greater than 24 hours after trauma have a lower mortality rate than those having surgery within the first 24 hours owing to resolution of shock after appropriate medical stabilization. The proper utilization of medical stabilization followed by surgical intervention results in an overall success rate of over 90%. The most common complication following surgical intervention is the development or persistence of pneumothorax. While complications can occur in the immediate postoperative period, most are transient and self limiting and will resolve with conservative therapy.
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