Theresa W. Fossum, DVM, MS, PhD, DACVS
Texas A&M University College of Veterinary Medicine, College Station, TX, USA
Diaphragmatic hernias are commonly recognized by small animal clinicians and may be congenital or occur secondary to trauma. Congenital pleuroperitoneal hernias are seldom diagnosed in small animals because many affected animals die at birth or shortly thereafter. Most diaphragmatic hernias in dogs and cats are caused by trauma, particularly motor vehicle accidents. The abrupt increase in intraabdominal pressure accompanying forceful blows to the abdominal wall causes the lungs to rapidly deflate (if the glottis is open), producing a large pleuroperitoneal pressure gradient. Alternately, the pressure gradient that occurs between the thorax and the abdomen may cause the diaphragm to tear. The tears occur at the weakest points of the diaphragm, generally the muscular portions. Location and size of the tear or tears depend on the position of the animal at the time of impact and the location of the viscera. Traumatic diaphragmatic hernias are often associated with significant respiratory embarrassment; however, chronic diaphragmatic hernias in asymptomatic animals are not uncommon. Diaphragmatic hernias may also occur in animals with connective tissue disorders.
Signalment. There is no breed predisposition for traumatic diaphragmatic hernias. Young males have historically thought to be more commonly affected; however, a recent study of traumatic diaphragmatic hernias identified no sex predilection.
History. The duration of a diaphragmatic hernia may range from a few hours to years. Many (15% to 25%) are diagnosed weeks after the injury. The animals may be presented in shock acutely after the trauma (see below), or the hernia may be an incidental finding. Animals sustaining trauma often suffer from associated injuries (e.g., fractures). With a chronic diaphragmatic hernia, the clinical signs most often are referable to either the respiratory (i.e., dyspnea, exercise intolerance) or the gastrointestinal systems (i.e., anorexia, vomiting, diarrhea, weight loss, pain after ingestion of food) or they may be nonspecific (e.g., depression). Many animals with chronic hernias are not dyspneic at the time of diagnosis.
Physical Examination Findings
Animals with recent traumatic diaphragmatic hernias frequently are in shock when presented for treatment; therefore, clinical signs may include pale or cyanotic mucous membranes, tachypnea, tachycardia, and/or oliguria. Cardiac arrhythmias are common and associated with significant morbidity. Other clinical signs depend on which organs have herniated and may be attributed to the gastrointestinal, respiratory, or cardiovascular system. The liver is the most commonly herniated organ, a condition that often is associated with hydrothorax caused by entrapment and venous occlusion.
Definitive diagnosis of pleuroperitoneal diaphragmatic hernia usually is made by radiography or ultrasonography. If significant pleural effusion is present, thoracentesis may be necessary for diagnostic radiographs. Radiographic signs of diaphragmatic hernia may include loss of the diaphragmatic line, loss of the cardiac silhouette, dorsal or lateral displacement of lung fields, presence of gas or a barium-filled stomach or intestines in the thoracic cavity, pleural effusion, and/or failure to observe the stomach or liver in the abdomen. It may be difficult to diagnose diaphragmatic hernias radiographically if only a small portion of the liver is herniated. In a recent study, thoracic radiographs revealed evidence of diaphragmatic hernia in only 66% of affected animals. Ultrasound examination of the diaphragmatic silhouette may help when herniation is not obvious radiographically (i.e., hepatic herniation, pleural effusion). Ultrasonography may be particularly difficult if severe pulmonary contusions are present which make the lung appear ultrasonographically similar to liver, if only omentum is herniated, or if adhesions between the liver and lung are present. Also, care should be taken not to mistake a normal mirror-image artifact (usually seen as apparent liver parenchyma on the thoracic side of the diaphragmatic line) for herniated liver.
Positive contrast celiography occasionally may be helpful. Prewarmed water-soluble iodinated contrast agent is injected into the peritoneal cavity at a dosage of 1.1 ml/kg (the dose is doubled if ascites is present), the patient is gently rolled from side to side or the pelvis is elevated, and films are taken immediately after the injection and manipulation. Criteria used in evaluating these images should include the presence of contrast medium in the pleural cavity, absence of a normal liver lobe outline in t he abdomen, and incomplete visualization of thee abdominal surface of the diaphragm. Positive-contrast celiograms should be interpreted cautiously, because omental and fibrous adhesions may seal the defect, resulting in false negative studies.
Chronic diaphragmatic hernias may have a higher mortality than acute diaphragmatic hernia s; however, the prognosis with both groups is good to excellent with surgery (see below under Prognosis). If pulmonary contusions are severe, surgical repair of diaphragmatic hernias should be delayed until the patient's condition has been stabilized; however, herniorrhaphy should not be delayed unnecessarily. Animals with gastric herniation should be evaluated carefully for gastric distention and should be operated on as soon as they can safely be anesthetized, because acute gastric distention within the thorax may cause rapid, fatal respiratory impairment.
Prophylactic antibiotics should be given before induction of anesthesia in animals with hepatic herniation. Massive release of toxins into the circulation may occur with hepatic strangulation or vascular compromise. Premedicating such patients with steroids may be beneficial. An ECG should be performed on all trauma patients before surgery.
From: Fossum TW, Small Animal Surgery, Mosby Publishing Co., St. Louis, Mo, 2007.
Make a ventral midline abdominal incision; if greater exposure is needed, extend the incision cranially through thee sternum. Replace the abdominal organs in the abdominal cavity ((if necessary, enlarge thee diaphragmatic defect). If adhesions are present, dissect the tissues gently from the thoracic structures to prevent pneumothorax or bleeding. With chronic hernias, débride the edge of the defect before closure. Close thee diaphragmatic defect in a simple continuous suture pattern. If the diaphragm is avulsed from the ribs, incorporate a rib in the continuous suture for added strength (Figure 1). Remove air from thee pleural cavity after closing the defect. If continued pneumothorax or effusion is likely, place a chest tube. Explore the entire abdominal cavity for associated injury (i.e.,, compromise of the vasculature to the intestine or splenic, renal, or bladder trauma) and repair any defects. An abdominal flap graft has been reported for repair of chronic diaphragmatic hernia in dogs. The graft is obtained from thee peritoneum and transverse abdominal muscle caudal to the diaphragm. The graft is elevated, placed over the defect, and sutured to the diaphragm.
Postoperative Care and Assessment
Patients should be monitored postoperatively for hypoventilation, and oxygen should be provided if necessary. Reexpansion pulmonary edema (PPE) is a possible complication associated with rapid lung reexpansion after repair of a diaphragmatic hernia. Postoperative analgesics should be provided.
Signalment. Traumatic pneumothorax is most common in young dogs because they are mo re likely to be hit by cars or receive other trauma that may result in pulmonary damage. For similar reasons, males may be more commonly affected than females. Although traumatic pneumothorax occurs in cats, it is less common than in dogs. Spontaneous pneumothorax usually occurs in large and "deep-chested"; however, it may occur in small dogs. Dogs of any age may develop spontaneous pneumothorax; in one study the average age was 6.3 years (range 1 to 13 years). Male and female dogs appear to be equally affected.
History. Pneumothorax secondary to trauma usually results in acute dyspnea. The history of trauma is often vague or unknown, complicating the differentiation of traumatic from spontaneous pneumothorax. Although the history of dogs with spontaneous pneumothorax varies depending on underlying etiology, most animals present with an acute history of dyspnea. Occasionally a chronic cough or fever may be noted. Recurrence of dyspnea in an animal previously treated for pneumothorax suggests spontaneous rather than traumatic pneumothorax.
Physical Examination Findings
Most animals with pneumothorax have bilateral disease and present with an acute onset of severe dyspnea. Dogs are able to tolerate massive pneumothorax by increasing their chest expansion. Respiration becomes ineffectual in animals with tension pneumothorax as the chest becomes barrel-shaped and fixed in maximal extension. This condition is life-threatening. Occasionally, subcutaneous emphysema will be noted in animals with pneumomediastinum and pneumothorax. The air may migrate from the mediastinal space to the thoracic inlet and be noticeable under the skin over the neck and trunk.
Thoracic radiographs should be delayed until after thoracentesis in dyspneic animals. Pneumothorax usually occurs bilaterally in animals because air easily diffuses across the thin mediastinum. Pneumothorax results in an increased width of air-filled space in the pleural cavity. The most sensitive view is a horizontal-beam, laterally recumbent thoracic radiograph. On a recumbent lateral thoracic radiograph the lungs collapse and retract from the chest wall and the heart usually appears to be elevated from the sternum. This apparent elevation of the heart is not noticeable on a standing lateral radiograph. Partially collapsed or atelectic lung lobes appear radiopaque when compared to the air-filled pleural space. As the lungs collapse, the vascular pattern will not extend to the chest wall; this may be particularly noticeable in the caudal thorax on a ventrodorsal view. Radiographs should be carefully evaluated for underlying pulmonary disease (i.e., abscess, neoplasia) or associated trauma (i.e., rib fractures, pulmonary contusion). Pulmonary blebs found in some animals with spontaneous pneumothorax are seldom visible radiographically.
Medical management of an animal with pneumothorax consists of initially relieving dyspnea by thoracentesis. If the pleural air accumulates quickly or cannot be effectively managed with needle thoracentesis, a chest tube should be placed. Providing an enriched oxygen environment may be beneficial, particularly in animals with concurrent pulmonary trauma (e.g., pulmonary contusion/hemorrhage). Providing analgesics to animals with fractured ribs or severe soft tissue damage may improve ventilation. Surgical intervention is seldom required in animals with traumatic pneumothorax.
Surgical therapy of animals with traumatic pneumothorax is seldom necessary. However, non-surgical management of spontaneous pneumothorax usually results in a less than satisfactory outcome. Mechanical pleurodesis of the lungs may decrease the recurrence of pneumothorax in animals operated for spontaneous pneumothorax. Mechanical pleurodesis damages the pleura such that healing results in adherence of the visceral and parietal pleural. Postoperative pneumothorax or pleural effusion must then be prevented as they will result in separation of the parietal and visceral pleura, precluding adhesion formation. If an underlying pulmonary lesion is readily identified (i.e., pulmonary abscess or neoplasia) and can be localized to one hemithorax, an intercostal thoracotomy allows lobectomy to be performed more readily than from a median sternotomy approach. However, diffuse, bilateral pulmonary disease with multiple bullae is usually present in dogs with spontaneous pneumothorax. A median sternotomy allows visualization of all lung lobes, plus partial resection of any diseased lobes. Mechanical pleurodesis should be performed in dogs with spontaneous pneumothorax to decrease recurrence.
Identify and remove diseased lung. If the source of the pleural air is not evident, fill the chest with warmed, sterile saline or water and look for air bubbles when the anesthetist ventilates the animal. If multiple, partial lobectomies are necessary, use an automatic stapling device to decrease operative time. Perform pleural abrasion using a dry gauze sponge. Gently abrade the entire surface of the lung and parietal pleura. Prior to closure, fill the chest cavity with warmed fluid and look for air bubbles when the animal is ventilated to ensure that there are no further air leaks. Place a chest tube and remove residual air before recovering the animal. Postoperatively, if continuous air leakage is present, or pleural effusion develops, place the animal on a continuous suction device. In animals with an open pneumothorax, definitive closure of large thoracic wall defects may require mobilization of adjacent muscle in order to provide an air-tight closure.