Diaphragm

Introduction

In small animals, diaphragmatic injury may occur by direct or indirect trauma.^1,2 Indirect injury to the diaphragm is the most common cause of diaphragmatic hernia and originates from blunt trauma to the abdominal cavity.¹ Pleuroperitoneal pressure gradients vary from 7 to 20 cm H₂O during quiet inspiration and can increase to over 100 cm H₂O during maximal inspiration.³ Blunt trauma results in a sudden increase in abdominal pressure, and if it is concomitant with an open glottis, the resultant pleuroperitoneal pressure gradient increases dramatically and domes and tears the diaphragm.^1,2 Prolapse of abdominal viscera is expected to occur simultaneously with the tear. Direct injury to the diaphragm is rare, but it may be inflicted by gunshot, bite, or stab wounds.^4,5 latrogenic injury to the diaphragm may occur by inappropriate abdominal incision cranial to the xiphoid process or inappropriate placement of a chest drain.⁵

Loss of continuity of the diaphragm does not necessarily result in severe respiratory distress.⁶ The cause of respiratory impairment associated with diaphragmatic hernia is multifactorial.⁶ Hypovolemic shock, chest wall trauma, pleural fluid or air, pulmonary contusions, and cardiac dysfunction all contribute to hypoventilation.⁶ Rib fractures and an associated flail chest cause mechanical dysfunction. Pulmonary compliance is decreased by pleural fluid, by the presence of abdominal organs in the thorax, or by pneumothorax. Pulmonary hemorrhage, edema, and atelectasis reduce total lung capacity, vital capacity, and functional residual capacity. Myocardial contusion may decrease cardiac output and in conjunction with impaired ventilation, may result in tissue hypoxia. Pain resulting from chest and abdominal contusion and accompanying injuries causes voluntary restriction of motion (thoracic excursion).⁶

Diagnosis

Thoracic injury occurs in 39% of small animals with musculoskeletal trauma, and 2% have diaphragmatic hernia.⁷ Therefore, animals examined for blunt traumatic injury must be evaluated for diaphragmatic injury. The average length of time between traumatic injury and the diagnosis of diaphragmatic hernia is several weeks, but it ranges from hours to 6 years.^8,10 Young male dogs have the highest incidence of diaphragmatic hernia.^8,10 Clinical signs of diaphragmatic hernia vary from no overt signs to severe respiratory compromise and shock.^8,11,13 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.^8,11,13 Cardiac arrhythmias are present in 12% of small animals with diaphragmatic hernia.⁸ Other common clinical signs include muffled heart and lung sounds, thoracic borborygmi, a strong apex beat ausculted on one side of the chest because of shifting of the apex to one side, and an asymmetric decreased caudoventral resonance when the thoracic cavity is percussed.⁵ A “tucked up” abdomen is a rare finding.^5,14

Lateral radiographs of the thorax show an incomplete diaphragmatic silhouette in 97% of animals with a diaphragm tear.¹⁵ In 61% of these animals, airfilled small intestinal loops are identified on the thoracic side of the diaphragm.¹⁵ Hydrothorax, which may be pleural effusion or hemothorax depending on the chronicity of the hernia, may be identified and may obscure the diaphragm. Repeated radiography after thoracocentesis is advisable, but it may not show a diaphragmatic hernia definitively.¹⁵ 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.¹⁶ Ultrasound can show abdominal organs, can differentiate organs such as the spleen or liver from pleural fluid, and can sometimes demonstrate the defect in the diaphragm.¹⁶ Cytologic evaluation of pleural fluid in patients with acute hernias usually reveals hemorrhage, whereas in a chronic diaphragmatic hernia, a modified serosanguinous transudate is identified.⁵

Alternative techniques to attempt to confirm the presence or absence of a diaphragmatic hernia include barium administration (1.0 mL 1kg) to verify herniation of a portion of the gastrointestinal tract, pneumoperitoneography, and positive contrast peritoneography (using 1 to 2 mL/kg of an aqueous tri iodidinated contrast agent).^17,18 These techniques are done only if, in the clinician’s judgment, the patient can tolerate the stress of such a procedure and if plain radiographs and ultrasonography are nondiagnostic.¹⁵ Moreover, when viscera or omentum plugs the diaphragm defect, a false negative evaluation is made.^19,20

Ventilation can be evaluated by arterial blood gas analysis and noninvasive pulse oximetry.^21,22 These techniques may identify ventilation perfusion inequalities (alveolar arterial oxygen difference)¹⁴ and physiologic shunting (estimated shunt equation).¹⁴ Impaired ventilation (hemoglobin saturation) can be determined using pulse oximeter probes attached to the lip in the awake dog.²³ The ear, tail, and toe may also be used effectively in awake dogs if good contact is maintained across the vascular beds.²³

Timing of Surgical Intervention

The timing of anesthesia and surgical correction of diaphragmatic injury has a profound effect on the outcome of treatment.^5,14 Approximately 15% of small animals with diaphragmatic hernia die before surgery.⁵ Animals with diaphragmatic herniorrhaphy performed within the first 24 hours after injury have the highest mortality rate (33%).⁸ When surgery must be done depends on the extent of the initial cardiopulmonary dysfunction, the presence or absence of organ entrapment, and the degree of compromised pulmonary function.¹⁴ Diaphragmatic herniorrhaphy may become an emergency procedure if aggressive supportive care cannot stabilize respiratory function.⁹ Acute dilatation of a herniated stomach and strangulated bowel are situations in which emergency surgery may be indicated.⁹ Gastric outflow obstruction, metabolic alkalosis, and hypokalemia have been reported in a dog with diaphragmatic hernia.²⁴

A herniated stomach can rapidly distend from aerophagia, decreasing pulmonary compliance and can compress the caudal vena cava, decreasing venous return resulting in a vicious cycle that can be rapidly fatal.⁵

A herniated parenchymal organ such as the spleen may tear as it passes through the diaphragm; the result may be 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 because the mere presence of a diaphragmatic hernia is not an indication for emergency surgery.⁸ For example, thoracic injuries such as pulmonary contusion improve dramatically in 24 to 48 hours, and pneumothorax may be managed by thoracostomy tube insertion. The goal of initial management is to improve the cardiorespiratory status of the patient, thus improving the patient’s capability of tolerating the stress of anesthesia and surgery

Anesthesia

Anesthesia in the patient with diaphragmatic hernia is induced with as little stress as possible. Intravenous catheterization, appropriate intravenous fluid adminstration (crystalloid or colloid), and cardiorespiratory monitoring are important. Premedication with a phenothiazine or a narcoleptic combination may relieve apprehension, but care is taken not to use cardiorespiratory depressing drugs when possible if decompensation of the patient’s status is predictable.⁸ Mask induction of anesthesia is avoided because it’s stressful and does not allow control of respiration or provide the ability to assist ventilation.⁸ An ultra short acting barbiturate or propofol is used because it allows rapid induction of anesthesia, quick intubation and near immediate control of ventilation with assitance or by a mechanical ventilator.²⁵ Isoflurane is preferred for maintenance of anesthesia because a surgical plane of anesthesia is attained more quickly, it is associated with decreased recovery time, it subjects the patient to less cardiac depression, and it does not sensitize the myocardium to arrhythmias.⁸

Ventilation assistance is important as soon as anesthesia is induced because of decreased pulmonary compliance secondary to the presence of air, fluid, or abdominal viscera within the pleural space.^5,14 Assisted ventilation should not exceed 20 cm H₂O, to limit potential barotrauma from pulmonary hyperinflation.⁸ Overinflation of the lungs during surgery may result in rupture of pulmonary parenchyma, intrapulmonary hemorrhage, plumonary edema, and, rarely, pneumothorax.²⁶ Intraoperative elimination of atelectic areas subjects chronically atelectic lungs to mechanical and reperfusion injury.^8,26 In this situation, reperfusion of these collapsed vascular channels disrupts capillary integrity and causes fluid to leak into the interstitium; reexpansion pulmonary edema may result within several hours after surgery.^5,8,27 Atelectic areas that do not inflate with 20 cm H₂O gradually reexpand over several hours with a continual negative pleural pressure of 10 cm H₂O.²⁸ Preoperative treatment with glucocorticoids and antihistamines has been recommended (based on experimental evidence) to inhibit the effects of mediators of pulmonary vascular permeability that are activated by lung injury in patients with chronic diaphragmatic hernia, but care is advised because antihistamines may potentiate hypotension.^6,8

Surgical Approach

A ventral midline celiotomy extending from the xiphoid process to a point caudal to the umbilicus is used to provide initial exposure for diaphragmatic herniorrhaphy. The incision should be large enough to allow exploration of the abdominal cavity. This exposure allows access to all regions of the diaphragm. Most diaphragmatic tears are muscular and are located ventrally and may favor either the right¹² or left side.^10,29 The liver, small intestine, and pancreas are most commonly prolapsed 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.⁵ The surgeon must examine the entire diaphragm because more than one tear may occur.¹⁴ Exploration of the abdominal cavity is indicated because injury to other abdominal organs may be present and are potentially treated concomitantly. Should additional exposure be required to retrieve abdominal viscera adhered to structures within the thoracic cavity, surgical exposure can be improved by enlargement of the rent in the diaphragm, by paracostal extension of the celiotomy, or by caudal midline sternotomy (Figure 22-1). Lateral thoracotomy is not a practical or appropriate method to expose a diaphragmatic tear because it requires preoperative knowledge of the extent and side of the hernia, and the approach does not allow exploration of the abdomen.^8,14 Lateral thoracostomy also decreases thoracic compliance from pain and thus may contribute to hypoventilation.⁸
 

Strangulated viscera found within the thoracic cavity should be resected in situ without reestablishing circulation if possible.⁸ By doing so, prevention of toxemia from bacterial endotoxins and exotoxins and the by products of tissue autolysis is possible.⁸ Viscera may be incarcerated, strangulated, or obstructed after passing through a diaphragmatic hernia and the systemic effects such as gastrointestinal obstruction or extrahepatic bile duct obstruction may occur acutely or chronically.^5,14,30 Chronic strangulation of a liver lobe results in a modified serosanguinous transudate approximately 30% of the time.⁵ Before closing the diaphragm defect, a chest drain is placed from a paramedian stab incision, it is tunneled subcutaneously, and it is inserted intercostally into the pleural space (Figure 22-2). The advantages of placing the chest drain early are that the drain can be placed accurately with direct visualization and, after herniorrhaphy, control of the pleural space is obtained for the duration necessary. The diaphragm closure need not be airtight because the chest drain provides control. Should an inadvertent tear in the lung parenchyma occur during herniorrhaphy, the presence of the tube will detect it and allow simple management. The chest drain is managed for a short time, usually 8 to 12 hours, or until the volume of air or fluid is 2 to 3 mL/kg per day or less. Air can be aspirated from the pleural space as the last suture is tied, but if a parenchymal tear is leaking air or if the herniorrhaphy is not airtight, hypoventilation may result.
 

Assessment of the wound margin of the diaphragm is important after viscera have been replaced into the abdominal cavity. Debridement of the wound margins is usually not necessary, but sutures should be placed through portions of the torn edge of the diaphragm that has an intact fascial surface to afford good suture holding strength. Chronic hernias that have produced scar tissue and collagen at the wound margins have good suture holding strength, but the scar restricts the normal elasticity of the diaphragm. Paracostal incisions are usually sufficient to release the maturing scar tissue and to allow the elastic portions of the diaphragm to be advanced to close the defect.

The suture material and pattern used to appose the diaphragm depend largely on the surgeon’s preference. Radial tears are apposed with simple continuous patterns or a combination of a horizontal mattress pattern oversewn with a simple continuous pattern. A single layer simple continuous pattern is quickly completed, but it is susceptible to reherniation should the implant break. The surgeon should suture from the deepest portion of the tear toward the more superficial regions. Large tears or combined radial and paracostal tears may be apposed with several interrupted sutures to arrange apposition of the wound margins to minimize tension. Closure follows, using a simple continuous pattern (Figure 22-3). Polypropylene, monofilament nylon, poliglecaprone, (Monocryl, Ethicon, Inc., Somerville, NJ), polydioxanone, and polyglyconate are sutures materials acceptable for herniorrhaphy. Paracostal tears are sutured using simple continuous patterns by suturing the diaphragmatic wound edge to paracostal fascia or encircling the ribs. Mattress patterns that encircle the costal arch or paracostal muscle fascia may also be used. Preplacing sutures sometimes facilitates closure of chronic diaphragmatic defects. Use of 3-0 and 2 0 suture for small cats and dogs and 2 O and 1 0 for larger dogs is recommended. Larger sizes are appropriate for giant breeds.
 

Closure of large diaphragm defects sometimes requires mobilization of the diaphragm or other tissues.^5,9,14 Paracostal incisions may be made to release the diaphragm from restrictive scar tissue, and the diaphragm may be advanced cranially to allow apposition ventrally (Figure 22-4).^5,14 Muscle flaps originating from the transversus abdominis muscle can be used to close diaphragm defects.^31,32 In chronic hernias, the liver capsule may be thickened in response to incarceration, and if the liver lobe is viable and can be oriented to cover the defect in the diaphragm partially without tension, it can be used to close or partially dose the defect.³³ Autologous fascia and omentum has also been used to close large diaphragm defects or small defects that remain after mobilization of the diaphragm.^34,35 Synthetic materials, such as polypropylene mesh or silicone rubber may also be used.^32,36,37 If a rough material such as polypropylene mesh is used, it is advisable to mobilize omentum to create an “omental envelope” that provides angiogenesis to aid incorporation of the prosthetic material and to protect the adjacent soft tissues from the mesh surfaces (Figure 22-5). Sometimes, the time and trauma required to mobilize muscular pedicles, especially in small kittens and puppies, result in significant hemorrhage. and can jeopardize the life of the patient. Prosthetic materials may be a better option if the potential to use autologous tissue may injure the patient.

Abdominal closure is accomplished routinely in patients with acute hernias. In those with chronic hernias, accommodation of the viscera within the peritoneal cavity may be difficult because of the contracted abdominal musculature. The abdominal musculature relaxes over time.¹⁴ Increased intraperitoneal pressure may occur. If intra abdominal pressure increases over 13 cm H₂ O, hepatic and portal venous flow may decrease.³⁹ Intra abdominal pressure (30 cm H₂ O) in one dog necessitated surgical decompression.³⁹

Postoperative Care

Evacuation of air from the pleural space should be done carefully in patients with atelectasis that does not reinflate with inflation pressures of 20 cm H₂ O, such as may occur with chronic hernias. Air may be evacuated in these patients slowly over a 12 hour period by using periodic evacuations or by using a Pleurivac (water seal) with no greater than a negative pleural pressure of 10 cm H₂ O.

Oxygen supplementation can be administered during recovery by mask, nasal insufflation or by placing the patient in an oxygen cage (40% oxygen).⁸ Nasal insufflation allows the same degree of oxygen supplementation, but it offers the advantage of allowing frequent and close access to the patient should it be required. Heart rate, capillary refill time, mucous membrane color, pulse strength and character, and respiratory rate should be monitored. Direct or indirect blood pressure monitoring, blood gas analysis, and pulse oximetry may also be done.

Analgesics are administered to comfort the patient and to ease apprehension during recovery. Morphine, 0.1 to 0.2 mg/kg, may be used subcutaneously without significant respiratory depression.⁵ If a caudal median sternotomy is performed, intrapleural bupivicane may be administered for short term local analgesia.

Prognosis

Death from diaphragmatic hernia is usually attributed to hypoventilation resulting from lung compression, shock, cardiac dysrrhythmias, and multiorgan failure.⁵ The survival rate in dogs varies from 52 to 88%.^8,10,40,41 Approximately 1 in 3 dogs undergoing repair within the first 24 hours after trauma dies, as opposed to 1 in 10 dogs in which repair is delayed for 1 to 3 weeks.⁵ In dogs that had chronic diaphragmatic hernias repaired more than 1 year after trauma, 73% of the deaths were attributed to a problem unrelated to the hernia.⁵
 

References

1. Dronen SC. Disorders of the chest wall and diaphragm. Bmerg Med Clin North Am 1983;1:449.
2. Ticer JW, Brown SG. Thoracic trauma. In: Ettinger SJ, ed. Veter. mary internal medicine. Philadelphia: WB Saunders, 1975.
3. Marchand P. A study of the forces productive of gastro oesopha. geal regurgitation and hemiation through the diaphragmatic hiatus. Thorax 1957;12:189.
4. Bellenger CR, et al. Bile pleuritis in a dog. J Small Anint Pract 1975;l6:575.
5. Johnson KA. Diaphragmatic, pericardial, and hiatal hernia. In Slatter DH, ed. Textbook of small animal surgery. 2nd ed. Phila. deiphia: WB Saunders, 1985:485.
6. Altura BM, Lefer AM, Schumer W. Handbook of shock and trauma. New York: Raven Press, 1983.
7. Spackman CJA, et al. Thoracic wall and pulmonary trauma in dogs sustaining fractures as a result of motor vehicle accidents. J Am Vet Med Assoc 1984;185:975.
8. Boudrieau RJ, Muir WE. Pathophysiology of traumatic diaphragmatic hernia in dogs. Compend Contin Educ Pract Vet 1987;9:379 385. 
9. Bjorlirig DE. Management of thoracic trauma. In: Birchard S. Sherding S. eds. Saunders manual of small animal practice Philadelphia: WB Saunders, 1994:593 599.
10. Stokhof AA. Diagnosis and treatment of acquired diaphragmatic hernia by thoracotomy in 49 dogs and 72 cats. Vet Q 1986; 8:177.
11. Wilson GP, Muir WW. Diaphragmatic hernia, In: Bojrab MJ, ed. Current techniques in small animal surgery. 2nd ed. Philadelphia: Lea & Febiger, 1983.
12. Wilson GP, Hayes HM. Diaphragmatic hernia in the dog and cat: a 25 year overview. Semin Vet Med Surg (Small Anim) 1986;1:318 326.
13. Wilson GP, Newton CD, Burt JK. A review of 116 diaphragmatic hernias in dogs and cats. JAm Vet Med Assoc 1971;159:11421145.
14. Boudrieau RJ. Traumatic diaphragmatic hernia. In: Bojrab MJ ed. Current techniques in small animal surgery. 3rd ed. Philadelphia: Lea Er Febiger, 1990:309 314.
15. Sullivan M, Lee R. Radiological features of 80 cases of diaphrafmatic rupture. J Small Anim Pract 1989;30:561.
16. Stowater JL, Lamb CR. Ultrasonography of noncardiac thoracic diseases in small animals. J Am Vet Med Assoc 1989;1955 p. 14.
17. Myer W. Diagnostic imaging of the respiratory system. Birchard S, Sherding S. eds. Saunders manual of small anufla practice. Philadelphia: WB Saunders, 1994:534 535.
18. Punch Pt, Slatter DR. Diaphragmatic hernias. In: Slatter DII ed. Textbook of small animal surgery. Philadelphia: WB SaUfl ders, 1985.
19. Evans SM, Biery DN. Congenital peritoneopericardial diaphrmatic hernia in the dog and cat: a literature review and 17 additional case histories. Vet Radiol 1980;21:108.
20. Stickle RL. Positive contrast celiography (peritoneograPhY) for the diagnosis of diaphragmatic hernia in dogs and cats. J Vet Med Assoc 1984;185:295.
21. Kolata RJ, Kraut NH, Johnston DE. Patterns of trauma in urban dogs and cats: a study of 1000 cases. J Am Vet Med Assoc S01974;164:499 502.
22. Shapiro BA, Harrison RA, Walton JR. Clinical application of blood gases. 3rd ed. Chicago: New York Medical Publishers, 1982.

Introduction

About 5% to 10% of diaphragmatic hernias are congenital.^1-3 Congenital pleuroperitoneal hernia^4-8 and congenital peritoneopericardial diaphragmatic hernia^8-14 have been reported in puppies and kittens. Pleuroperitoneal hernias are thought to develop when the pleuroperitoneal membrane fails to fuse with the pleuroperitoneal canal during development of the diaphragm. This defect is proposed to be heritable by an autosomal recessive mechanism.^6,16,17 Congenital peritoneopericardial diaphragmatic hernias are thought to be the result of a uterine accident during embryogenesis and are not heritable.^12,18,19 The ventral diaphragmatic defect is believed to result from faulty development of the septum transversum.¹⁸ Because congenital peritoneopericardial diaphragmatic hernia may or may not be associated with cranioventral abdominal defects, some of these hernias are not easily identified at birth and some are obvious.¹²

Clinical Signs

Clinical signs of congenital diaphragmatic hernia may be identified at any age. Multiple breeds of dogs have been affected and in cats the domestic longhair and Himalayan breeds are over represented.²⁰ Overt structural defects such as cranioventral abdominal hernia result in an earlier diagnosis, often before 2 years of age. The diagnosis may be incidentally noted while radiographing the thorax for another reason, or it may be found at necropsy.^11,12,14 Respiratory signs including dyspnea, tachypnea, coughing, and wheezing are common, but many nonspecific signs such as vomiting and diarrhea may be identified.²¹ Respiratory signs may worsen after eating.¹⁷ Auscultation of the thorax may reveal muffled heart sounds, a heart murmur, and abnormal position of the apex beat.^12,21,20 An electrocardiogram may reveal electrical alternans or may be normal.²¹ Radiographs of the thorax usually reveal an ovoid cardiac silhouette that joins the ventral diaphragm ventrally. Gas-filled loops of bowel may be seen over the cardiac silhouette.^14,21 Congenital peritoneopericardial hernias are often symmetrical in appearance on radiographs whereas thoracic abnormalities in pleuroperitoneal hernias may be assymetrical.⁸ Pectus excavatum and sternal abnormalities may be seen with congenital diaphragmatic hernias in cats.²⁰ Other diagnostic procedures that may be used include administration of contrast material into the upper gastrointestinal tract, pneumoperitoneography or contrast peritoneography, and ultrasonography.¹⁰ Pneumoperitoneogrpahy may induce pneumothorax and therefore may risk decompensation so use of aqueous contrast is preferred.⁸ Ultrasonography from the right fifth intercostal space may reveal cardiac tamponade if liver lobes herniate into the pericardial sac and produce an effusion.^10,21 In general, ultrasonagraphic diagnosis of diaphragmatic hernia is difficult.²² Thoracoscopy can be used to directly observe the abdominal structure but careful inflation pressures are necessary to avoid compromising ventilation.²²

Congenital Diaphragmatic Hernia with Cranioventral Abdominal Defects

Congenital cranioventral abdominal wall defects in puppies occur cranial to the umbilicus, but they may extend caudally toward and to the umbilicus. (Figure 22-6). The cranial extent of the defect is often in the area of the commonly absent xiphoid process. Although cranioventral abdominal hernias are not frequently encountered in small animal practice, the clinician must recognize that the abnormality differs from the much more common umbilical hernia. Cranioventral abdominal hernias are commonly associated with four other defects, which are recognized as a syndrome in humans and which have been reported in dogs.^12,13 Cranioventral abdominal hernia, failure of caudal sternal fusion, intracardiac defects (most commonly ventricular septal defect) and caudoventral pericardial defect may commonly accompany a congenital diaphragmatic hernia.^12,13 These defects may occur in varying degrees, depending on the individual dog and they do not always appear together. Commonly, the heart has no apparent abnormality. This pentalogy of defects has been noted in several breeds, including cocker spaniels, Weimaraners dachshunds, and collies, and I have seen it in two kittens. This syndrome is similar in some respects to thoracoabdominal ectopia cordis in human infants and has been termed peritoneopericardial diaphragmatic hernia in small animals.^14,18 A recent report did not find abnormalities identical to the pentalogy found in puppies but skeletal and nonskeletal abnormalities did occur in 8 of 67 cats.²⁰ Peritoneopericardial diaphragmatic hernias are not always associated with cranioventral abdominal wall defects or intracardiac defects, and they are often difficult to detect unless clinical signs are obvious (usually exercise intolerance or a restrictive breathing pattern).

The sternum normally fuses from cranial to caudal in dogs, and the abdominal wall fuses from caudal to cranial. The ventral portion of the diaphragm is thought to originate from the septum transversum, which develops at the same time as cardiac septation; therefore, it seems reasonable that disruption of fetal development at this particular time could cause defects in both regions. Dogs do not have a communication between the pericardial cavity and the peritoneal cavity so if such a communication is present congenitally, it is due to a defect in development. The pericardium normally attaches to the ventral diaphragm by the sternopericardial ligament and visceral mediastinum. Communication of the peritoneal and pericardial cavities is not always obvious in this defect.

In human beings, these defects are attributed to a uterine accident and are not considered heritable. Parents with children affected with thoracoabdominal ectopia cordis have gone on to have anatomically normal children thereafter. No data support heritability of the pentalogy of defects in dogs or cats.

Surgical Correction

Surgical repair of the cranioventral abdominal defect and the diaphragmatic defect can be done early (I have performed such operations on animals as young as 7 weeks of age), usually between 8 and 12 weeks of age. The puppies are usually masked with isoflurane to induce and maintain general anesthesia unless they have significant respiratory restriction. In the latter example, anesthesia may be induced with propofol with prompt intubation, so ventilation may be carefully assisted. All puppies with these defects benefit from assisted ventilation because of the spaceoccupying abdominal viscera within their caudal mediastinum and/or pericardial sac.^13,23 Liver lobes, gall bladder, omentum and small intestine are commonly found in the caudal mediastinum or pericardial sac, and this appears to be similar in cats with congenital diaphragmatic hernias.²⁰

Surgical correction of the defects follows a midline abdominal incision that allows identification of the triangular diaphragmatic defect, the pericardial defect, and the flared, unfused caudal sternebrae (Figures 22-7 to 22-10). In most puppies, the diaphragm defect can be closed by using a simple continuous pattern from the dorsalmost aspect of the defect and continuing in a ventral direction (toward the sternal defect). When the diaphragm apposition becomes tense, the suture can be tied, and mattress sutures can be preplaced from the diaphragm to the costal arch to complete the separation of the thoracic and abdominal cavities. The pleural cavity does not have to be invaded or opened when this defect is closed. Accidental opening of the pleural cavity by dissection or by needle penetration is possible while suturing. After the mattress sutures are tied, the abdominal defect can usually be apposed with simple interrupted nonabsorbable suture, followed by routine subcutaneous and skin apposition. When closure of the defects as described is routine, young puppies and kittens recover quickly and often do not require specialized postoperative care, other than that appropriate for pediatric patients. Sometimes, the diaphragmatic defect is too wide to appose without excessive tension. Three methods can be used to alleviate this problem. First, the caudal sternal costal arch can be apposed by encircling with nonabsorbable suture. This can effectively decrease the distance between the right and left edges of the diaphragm and therefore can reduce the tension on the closure. The pliability of the unfused costal arch in the young puppies and kittens makes this maneuver possible. If caudal sternal apposition does not narrow the defect to a size that can be apposed without tension, the pericardium can be incised cranial to the diaphragm and flaps can be created to close the defect.²⁴ A free graft of pericardium may also be used to close the defect.²⁴ The third method is insertion of polypropylene mesh to separate the body cavities. Omentum can be mobilized and sutured to each side of the implant to cover its surface. Other synthetic implants, such as lyophilized collagen sheeting (derived from porcine submucosa) have been used successfully.¹⁷

Congenital diaphragmatic hernias that are not associated with ventral abdominal wall defects and that lack obvious clinical signs may not be diagnosed until much later in the pet’s life, often when the animal is radiographed for another reason. Correction of all congenital diaphragmatic hernias may not be necessary, especially hernias diagnosed in old animals with no clinical signs of abdominal viscera (usually omentum) in the caudal mediastinum or the pericardial sac. However, dogs or cats with clinical signs of congenital diaphragmatic hernia that are adults when the diagnosis is made are much more likely to have intrathoracic adhesions that prevent simple replacement of abdominal viscera into the abdominal cavity. These adhesions may require extension of the diaphragmatic defect or a caudal midline sternotomy to provide enough exposure for safe dissection within the caudal thorax. Closure of the diaphragmatic defect often requires releasing incisions from the paracostal arch using the inherent elasticity of the diaphragm to facilitate apposition. Entrance into the pleural space is inevitable in most situations and requires assisted ventilation during surgery, chest drain insertion, and intensive postoperative management for 24 to 48 hours.

Postoperative management of pain in dogs that have undergone diaphragmatic herniorrhaphy and especially those that have exposure extended by caudal midline sternotomy require analgesia.²⁵ Use of opioids in combination with non-steroidal antiinflammatory drugs will provide sufficient analgesia. Chest drains, when necessary, are usually removed 12 to 24 hours postoperatively.

References

1. Boudrieau SJ, Muir WW. Pathophysiology of traumatic diaphragmatic hernia in dogs. Compend Contin Educ Pract Vet 1987;9:379.
2. Wilson GP, Hayes JIM. Diaphragmatic hernia in the dog and cat: a 25-year overview. Semin Vet Med Surg (Small Anim) 1986;1:318-326.
3. Wilson GP, Newton CD, Burt JK. A review of 116 diaphragmatic hernias in dogs and cats. J Am Vet Med Assoc 1971;159:11421145.
4. Noden DM, De Lahunta A. The embryology of domestic animals: developmental mechanisms and malformations. Baltimore: Williams & Wilkins, 1985.
5. Pass MA. Small intestines. In: Slatter DH, ed. Textbook of small animal surgery. Philadelphia: WB Saunders, 1985.
6. Feldman DB, et al. Congenital diaphragmatic hernia in neonatal dogs. J Am Vet Med Assoc 1968;153:942.
7. Keep JM. Congenital diaphragmatic hernia in a cat. Aust VetJ 1950;26:193.
8. Mann FA, Aronson E. Surgical correction of a true congenital pleuroperitoneal diaphragmatic hernia in a cat. J Amer Anim Hosp Assoc 1991:27:501-507.
9. Frye FL, Taylor Don. Pericardial and diaphragmatic defects in a cat. J Am Vet Med Assoc 1968;152:1507. 
10. Hay WH, et al. Clinical, echocardiographic, and radiographic findings of peritoneopericardial diaphragmatic hernia in two dogs and a cat. J Am Vet Med Assoc 1989;195:1245.
11. Punch P1, Slatter DH. Diaphragmatic hernias. In Slatter DH, ed. Textbook of Small Animal Surgery. Philadelphia: WB Saunders, 1985.
12. Bellah JR, Spencer CP, Brown DJ, Whitton DL. Congenital cranioventral abdominal wall, caudal sternal, diaphragmatic, pericardial, and intracardiac defects in Cocker Spaniel littermates. J Am Vet Med Assoc 1989; 194:1741-1746.
13. Bellah JR, Whitton DL, Ellison GW, Phillips L. Surgical correction of concomitant cranial ventral abdominal wall, caudal sternal, diaphragmatic, and pericardial defects in young dogs. J Am Vet Med Assoc 1989; 195:1722-1726.
14. Evans SM, Beiry DN. Congenital peritoneopericardial diaphragmatic hernia in the dog and cat: a literature review and 17 additional case histories. Vet Radiol 1980;21:108.
15. Eyster GJ, et al. Congenital pericardial diaphragmiatic hernia and multiple cardiac defects in a litter of collies. J Am Vet Med Assoc 1977;170:516.
16. Valentine BA, et al. Canine congenital diaphragmatic hernia. J Vet Intern Med 1988;2:109.
17. Hunt GB, Johnson KA. Diaphragmatic, Pericardial, and Hiatal Hernia. In Slatter D (Ed.), 3rd Edition, Saunders, Philadelphia, 2003; 471-487.
18. Kaplan LC, et al. Ectopia Cordis and cleft sternum: evidence for mechanical teratogenesis following rupture of the choion or yolk sac. Am J Med Genet 1985;21:187.
19. Noden DM, De Lahunta A. The embryology of domestic animals: developmental mechanisms and malformations. Baltimore: Williams & Wilkins, 1985.
20. Reimer BS, Kyles AE, Filipowicz DE, Gregory, CR. Long-term outcome of cats treated conservatively or surgically for peritoneopericardial diaphragmatic hernia: 66 cases (1987-2002). J Amer Vet Med Assoc 2003;224: 728-732.
21. Thomas WP. Pericardial Disorders. In: Ettinger SJ, ed. Textbook of veterinary internal medicine: diseases of the dog and cat. 3rd ed. Philadelphia: WB Saudners, 1989.
22. Bellah JR. Diaphragmatic Hernias. Compendium’s Standard of Care in Emergency Medicine and Critical Care. June 2005;7.5:1-7.
23. Bednarski RM. Diaphragmatic hernia: anesthetic considerations. Semin Vet Med Surg (Small Anim) 1986;1:256-258.
24. Johnson KA. Diaphragmatic, pericardial, and hiatal hernia. In: Slatter DH, ed. Textbook of small animal surgery. 2nd ed. Philadelphia: WB Saunder, 1985:485.
25. Bellah JR. Traumatic Diaphragmatic Hernia. In Bojrab MJ (Ed), Current Techniques in Small Animal Surgery, 4th Edition, Williams and Wilkins, Baltimore, 1998: 315-321.