MANAGEMENT OF DIAPHRAGMATIC HERNIAS

MANAGEMENT OF DIAPHRAGMATIC HERNIAS Theresa W. Fossum DVM, MS, PhD, Diplomate ACVS Professor of Veterinary Surgery; Vice President for Research and Strategic Initiatives, Midwestern University, Glendale, AZ 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. DIAGNOSIS 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. Diagnostic Imaging 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 Page 1 of 6

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 the abdomen, and incomplete visualization of the abdominal surface of the diaphragm. Positivecontrast celiograms should be interpreted cautiously, because omental and fibrous adhesions may seal the defect, resulting in false negative studies. MEDICAL MANAGEMENT If the animal is dyspneic, oxygen should be provided by face mask, nasal insufflation, or an oxygen cage. Positioning the animal in sternal recumbency with the forelimbs elevated may help ventilation. If moderate or severe pleural effusion is present, thoracentesis should be performed. Fluid therapy and antibiotics should be given if the animal is in shock. SURGICAL TREATMENT Chronic diaphragmatic hernias may have a higher mortality than acute diaphragmatic hernias; 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. Preoperative Management 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. Anesthesia Chamber or mask induction should be avoided in animals with diaphragmatic hernia. Supplementing oxygen before induction improves myocardial oxygenation. Because of the animal s already compromised ventilation, drugs with minimal respiratory depressant effects should be used. Injectable anesthetics allowing rapid intubation are preferred. Inhalation anesthetics should be used for maintenance of anesthesia. Intermittent positive pressure ventilation should be performed, and high inspiratory pressures should be avoided to help prevent reexpansion pulmonary edema. The lungs should be allowed to expand slowly after surgery. Nitrous oxide is contraindicated in patients with diaphragmatic hernia. Drugs such as methylprednisolone may be beneficial for preventing reexpansion pulmonary edema in animals with chronic diaphragmatic hernia. Positioning The animal is placed in dorsal recumbency for a midline abdominal incision. The entire abdomen and caudal one half to two thirds of the thoracic cavity should be prepared for aseptic surgery. Because acute ventilatory compromise may occur during positioning, these animals should be carefully monitored during this period. Page 2 of 6

SURGICAL TECHNIQUE Make a ventral midline abdominal incision; if greater exposure is needed, extend the incision cranially through the sternum. Replace the abdominal organs in the abdominal cavity (if necessary, enlarge the diaphragmatic defect). If adhesions are present, dissect the tissues gently from the thoracic structures to prevent pneumothorax or bleeding. With chronic hernias, debride the edge of the defect before closure. Close the 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 the 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 the peritoneum and transverse abdominal muscle caudal to the diaphragm. The graft is elevated, placed over the defect, and sutured to the diaphragm. Figure 1 From: Fossum, TW: Small Animal Surgery, Mosby Publishing Co., St. Louis, Mo, POSTOPERATIVE CARE AND ASSESSMENT Patients should be monitored postoperatively for hypoventilation, and oxygen should be provided if necessary. Reexpansion pulmonary edema (RPE) is a possible complication associated with rapid lung reexpansion after repair of a diaphragmatic hernia. Postoperative analgesics should be provided. COMPLICATIONS The most common complication after surgical repair of diaphragmatic hernias is pneumothorax, especially if the hernia is chronic and adhesions are present. Reexpansion pulmonary edema may occur in lungs that have been chronically collapsed (see above). PROGNOSIS If the animal survives the early postoperative period (i.e., 12 to 24 hours) the prognosis is excellent, and recurrence is uncommon with proper technique. Reported mortality rates for animals with traumatic DH have varied from 12% to 48%. Reported survival rates for animals with traumatic DH who are treated surgically are close to 75%. PERITONEOPERICARDIAL DIAPHRAGMATIC HERNIA Peritoneopericardial diaphragmatic hernias are less commonly recognized by small animal clinicians than traumatic diaphragmatic hernias. Although PPDH often are associated with respiratory embarrassment, asymptomatic PPDH is common. PPDH may occur as a result of trauma in human beings (in whom the diaphragm forms one wall of the pericardial sac); however, these hernias are always congenital in dogs and cats, in which no direct communication exists between the pericardial and peritoneal cavities after birth. The most widely accepted theory regarding the embryogenesis of this defect is that the hernia occurs because of faulty development or prenatal injury of the septum transversum. This could be a result of a teratogen, genetic defect, or prenatal injury. Cardiac abnormalities and sternal deformities often occur concomitantly with PPDH. The combination of congenital cranial abdominal wall, caudal sternal, diaphragmatic, and pericardial defects has been reported in dogs, often associated with ventricular septal defects or other intracardiac defects. It is not known if this condition is heritable; however, several breed predispositions have been recognized (see below). Polycystic kidneys have been reported in association with PPDH in cats. Page 3 of 6

DIAGNOSIS Signalment. Although PPDH is congenital, it is not uncommon for the diagnosis to be made when the animal is middle-aged or older because clinical signs vary and may be intermittent. Weimaraners and cocker spaniels may be at increased risk. Domestic longhair and Himalayan cats may be predisposed. History. The clinical signs may be referable to the gastrointestinal, cardiac, or respiratory systems and include anorexia, depression, vomiting, diarrhea, weight loss, wheezing, dyspnea, exercise intolerance, and/or pain after eating. Neurologic signs may occur as a result of hepatoencephalopathy. Physical Examination Findings Physical examination findings in animals with PPDH may include ascites, muffled heart sounds, murmurs caused either by displacement of the heart by visceral organs or by intracardiac defects, and concurrent ventral abdominal wall defects. The most commonly herniated organ is the liver, and associated pericardial effusion is common. Diagnostic Imaging A tentative diagnosis of PPDH may be made based on the history, clinical signs, and physical examination, but radiography or ultrasonography (or both) is essential for a definitive presurgical diagnosis. Table 1 lists the radiographic signs of PPDH. Contrast studies (i.e., nonselective angiogram, barium contrast study) should be undertaken only if a definitive diagnosis cannot be made on survey films or with ultrasound. A distinct curvilinear radiopacity has been identified between the cardiac silhouette and the diaphragm on a lateral thoracic radiograph in cats with PPDH. This radiographic finding has been called the dorsal peritoneopericardial mesothelial remnant; however, it is not always apparent on radiographs of affected cats. Ultrasonography is useful because there often is discontinuity of the diaphragmatic outline and more importantly, abdominal organs may be visualized in the pericardial sac. Hepatic herniation usually is evident. Echocardiography should be performed in animals with murmurs. SURGICAL TREATMENT Surgical repair should be performed as early as possible (generally when the animal is between 8 and 16 weeks of age), when it is unlikely that adhesions will be present and the pliable nature of the skin, muscles, sternum, and rib cage facilitates closure of large defects. Early correction of PPDH may prevent acute decompensation and the possible development of acute postoperative pulmonary edema. If the hernia is not diagnosed until the animal is older, conservative or surgical management may be used; however, owner satisfaction was higher in operated animals than in animals managed conservatively in a recent study. Some animals that are initially managed medically may have progression of clinical signs necessitating surgical intervention or resulting in death. Preoperative Management Prophylactic antibiotics should be given before induction of anesthesia in animals with hepatic herniation. In animals with hepatic strangulation or vascular compromise, repositioning of the liver into the abdominal cavity may cause a massive release of toxins into the bloodstream; premedicating such patients with steroids may be beneficial. Positioning The animal is placed in dorsal recumbency for a midline abdominal incision. The entire abdomen and caudal two thirds of the thoracic cavity should be prepared for aseptic surgery. SURGICAL TECHNIQUE Make a ventral midline abdominal incision. If greater exposure is needed, extend the incision cranially through the sternum. Enlarge the diaphragmatic defect if necessary and replace the abdominal organs in the abdominal cavity. If adhesions are present, gently dissect the tissues from the thoracic structures, resecting or debriding necrotic tissue as necessary. Debride the edges of the defect and close in a simple continuous suture pattern. Do not close the pericardial sac. Remove air from the pericardial sac or pleural cavity or both after closing the defect. If continued pneumothorax or effusion is likely, place a chest tube. Repair concomitant sternal or abdominal wall defects. Page 4 of 6

POSTOPERATIVE CARE AND ASSESSMENT These patients should be monitored postoperatively for hypoventilation, and oxygen should be provided if necessary. Reexpansion pulmonary edema (RPE) is a possible complication associated with rapid lung reexpansion after diaphragmatic hernia repair. Patients with PPDH may also have pulmonary hypoplasia, which contributes to the development of high intrapleural pressures and RPE. Postoperative analgesics should be provided. HIATAL HERNIAS General Considerations and Clinically Relevant Pathophysiology Hiatal hernias are usually caused by congenital abnormalities of the hiatus that allow cranial movement of the abdominal esophagus and stomach. The phrenicoesophageal ligament is lax or stretched and allows the gastroesophageal junction to be displaced through the hiatus into the caudal mediastinum. Malpositioning or lack of support of the gastroesophageal sphincter reduces gastroesophageal sphincter pressure and leads to gastroesophageal reflux. Gastroesophageal reflux and subsequent esophagitis and megaesophagus are responsible for most of the clinical signs. Hiatal hernia is occasionally secondary to trauma and has occurred concurrently with respiratory distress. Trauma may damage diaphragmatic nerves and muscles, resulting in hiatal laxity and subsequent herniation. In patients with upper respiratory obstruction, reduced intrathoracic pressure during inspiration has been theorized to contribute to esophageal reflux and visceral herniation. Hiatal hernia has been reported with tetanus. With hiatal hernias, the stomach commonly slides in and out of the thorax. If the hernia is large enough, other abdominal viscera may also be cranially displaced into the thorax. Various types of hiatal abnormalities have been described. In patients with sliding or axial hiatal hernias, the gastroesophageal junction is located within the thoracic cavity. In patients with paraesophageal or rolling hiatal hernias, the gastroesophageal junction is usually located in a normal position and the gastric fundus or other abdominal viscera are displaced through the hiatus and located within the thorax. Some hiatal hernias are a combination of sliding and paraesophageal hernias with the gastroesophageal junction and gastric fundus both displaced. Diagnosis Signalment. Hiatal hernias may occur in a variety of dog and cat breeds; however, males and Chinese Shar-pei dogs appear to be predisposed to this condition. Most symptomatic animals have signs relating to congenital hiatal hernia before reaching 1 year of age, although diagnosis may occur later. Patients with acquired hernias may develop signs at any age. History. Regurgitation is the primary clinical sign in symptomatic individuals, but many patients are asymptomatic. Other signs may include vomiting, hypersalivation, dysphagia, respiratory distress, hematemesis, anorexia, and weight loss. Radiography/Ultrasonography Hiatal hernias usually appear as a mass near the esophageal hiatus in the caudodorsal thoracic region on survey radiographs. However, with sliding hernias, several radiographs may be necessary to identify the herniation because herniation may be intermittent. The presence of gas in the herniated portion aids in identification of the mass as herniated stomach. Varying degrees of megaesophagus and pneumonia may be noted. A positive contrast esophagram should show the gastroesophageal junction, rugal folds, or both cranial to the hiatus. Occasionally, strictures may be identified. Fluoroscopy may demonstrate hypomotility, delayed clearing of the distal esophagus, or gastroesophageal reflux. Compressing the abdomen while observing fluoroscopy may help identify hernias. Esophagoscopy can confirm mild to severe esophagitis (inflammation, mucosal erosion), gastric reflux, or strictures. Gastric mucosa that has entered the thoracic cavity can sometimes be identified. Some hiatal hernias are intermittent (sliding) and require multiple radiographs and/or fluoroscopy to diagnose. Do not confuse hiatal hernias with peritoneopericardial or traumatic diaphragmatic hernias, despite their sometimes having a similar radiographic appearance. Page 5 of 6

Surgical Treatment Affected patients may benefit from medical treatment for gastroesophageal reflux or esophagitis; however, surgery is generally recommended in symptomatic animals with congenital disease. A number of surgical techniques have been described for correction of this condition. Diaphragmatic hiatal reduction and plication, esophagopexy, and left-sided fundic gastropexy are described here. Gastropexy is probably the most important step in the repair. If esophagitis is severe and oral intake is to be prohibited for several days, a tube gastropexy allows early alimentation without further esophageal irritation. Sphincter enhancing procedures such as a Nissen fundoplication (antireflux procedure) are performed by some surgeons instead of the aforementioned techniques. However, fundoplication or other antireflux procedures are only indicated in patients with evidence of gastroesophageal reflux. In dogs and cats, primary incompetence of the caudal esophageal sphincter has not been documented in association with hiatal hernia, and therefore antireflux procedures are not routinely recommended. Preoperative Management Reflux esophagitis and aspiration pneumonia should be treated before anesthetic induction. Feeding frequent, small meals of high-protein/low-fat foods may be beneficial. If megaesophagus is present, feeding affected animals in a standing, upright position may decrease regurgitation. Surgical Technique Make a cranial ventral midline incision extending caudal to the umbilicus to expose the diaphragm and stomach. Retract the left lobes of the liver medially to expose the esophageal hiatus. Pass a stomach tube (28-32 French) to help identify and manipulate the esophagus. Grasp the stomach and reduce the hernia with gentle traction. Examine the hiatus. Dissect the phrenicoesophageal membrane, freeing the esophagus from the diaphragm ventrally. Preserve the vagal trunks and esophageal vessels during dissection. Place an umbilical tape sling around the abdominal esophagus to displace it caudally and facilitate manipulations. Perform a diaphragmatic hiatal plication/reduction, esophagopexy, and leftsided fundic gastropexy. Accomplish diaphragmatic hiatal plication/reduction by excoriating or debriding the margins of the hiatus and then place three to five sutures (2-0 polydioxanone or polypropylene) to appose the edges and narrow the hiatus. Plication should occur around a large stomach tube (28-32 French). The hiatus is reduced to 1 or 2 cm, a size that allows passage of one finger. Esophagopexy is accomplished by placing sutures (3-0 or 2-0 polydioxanone or polypropylene) from the remaining margin of the hiatus through the adventitia and muscular layers of the abdominal esophagus. Either a left-sided tube gastropexy or incisional gastropexy completes the repair. The fundus is fixed with slight to moderate caudal traction to prevent cranial movement of the gastroesophageal junction into the thorax. Evacuate air from the chest via thoracentesis or tube thoracostomy and lavage and close the abdomen. Postoperative Care and Assessment Patients should be postoperatively monitored for dyspnea resulting from pneumothorax and air should be evacuated from the thorax as necessary. Nasal oxygen may benefit dyspneic animals. Analgesics should be provided as necessary to control pain. Affected animals may continue to regurgitate after surgery because of persistent esophagitis. Treatment of esophagitis and aspiration pneumonia should be continued postoperatively. Feeding from an elevated platform may be beneficial in animals with concurrent megaesophagus. Postoperative radiographic studies may be beneficial in patients with persistent clinical signs to identify persistent herniation, obstruction, or ulceration. Prognosis Objective data comparing medical and surgical treatment in animals with hiatal hernias is not available. The prognosis without surgery is good in asymptomatic patients; however, symptomatic patients who are not surgically repaired may develop severe esophagitis and stricture. The prognosis is good with the described surgical repair; however, aspiration pneumonia must be controlled for a favorable outcome. Patients with gastroesophageal sphincter incompetence may benefit from additional antireflux procedures. Page 6 of 6