Abdominal Wall Reconstruction and Hernias

Chapter 84

Abdominal Wall Reconstruction and Hernias

An abdominal hernia is any full-thickness defect or weakness in the wall of the abdomen that may allow protrusion of abdominal contents. Organ herniation through a ring of tissue confined within the abdominal cavity, such as a diaphragmatic hernia or organ displacement through a mesenteric rent, is considered an internal abdominal hernia. This chapter discusses external wall defects only.

Definitions and Hernia Components

A hernia is composed of a ring (the anatomic limits of the wall defect), sometimes a sac, and the protruding contents (Figure 84-1). The ring may be confined within a normal aperture in the abdominal wall (considered a true hernia) or may occur in other areas (false hernias) as a result of trauma or through a disrupted surgical approach (an acquired hernia). Very large hernial rings or small defects rarely cause clinical problems; however, hernias just large enough to entrap viscera and obstruct blood supply to the contents (strangulation) are most dangerous to the patient. Contraction of scar tissue at the hernial ring during the healing process may cause a delay in onset of clinical signs as the organs become entrapped (incarcerated) or obstructed. Whereas in developmental (congenital) hernias, the hernial sac is a mesothelial membrane (peritoneum) covering the contents, in acute traumatic or incisional hernias, no sac is present. Over time, a peritoneal sac may form over the contents of chronic traumatic or incisional hernias; this process is termed peritonealization. Hernial contents without a mesothelial covering are at risk for developing adhesions that restrict movement of the contents (irreducible hernias); this may lead to obstruction or torsion of the protruding tissue. Traumatic hernias most often occur from blunt trauma with avulsion of muscle fascia or penetrating injury. When a traumatic abdominal hernia caused by a fractured rib penetrating through the paracostal musculature results in organ herniation, it is termed an auto-penetrating hernia.41,106 Contents of a hernia may be predicted based on the site of the defect (e.g., inguinal hernias often have the uterus involved because of the tethering effect of the round ligament) or more mobile structures such as the omentum or intestine can travel longer distances into nearly any abdominal hernia site.

Anatomy of the Abdominal Wall

The tough abdominal wall confines the abdominal organs within the largest cavity in the body, extending from the diaphragm to the pelvic canal (Figure 84-2). The arrangement of the aponeuroses of abdominal muscles, their attachments, and fiber direction are important to understand when attempting hernia reconstruction. Fibers of the tendinous aponeuroses of the external abdominal oblique, internal abdominal oblique, and transverse abdominal muscles converge and join on midline to form a thick white band, termed the linea alba, which is located between the rectus abdominis muscles. The linea alba is widest in the cranial abdomen, and it narrows considerably before it attaches to the pubis by the prepubic tendon (sometimes termed the cranial pubic ligament). Fibers of the flat tendinous aponeuroses of abdominal wall muscles pass either superficially or deep to the rectus abdominis muscles that extend in a cranial and caudal direction from the first costal cartilage to the pecten of the pubis. The external abdominal oblique aponeurosis always runs superficial to the rectus abdominis muscle. The location of the aponeurosis of the internal abdominal oblique varies along the length of the abdomen. In the cranial third of the abdominal wall, fibers pass both deep and superficial to the rectus abdominis muscle. From the umbilicus caudally, all of the internal abdominal oblique fibers run superficial to the rectus abdominis muscle. Fibers of the transverse abdominal muscle pass deep to the rectus abdominis muscle in the cranial two thirds of the abdominal wall, but in the caudal third, fibers run superficial to the rectus abdominis muscle. Whereas the external rectus sheath contains tendinous aponeuroses of the abdominal muscles that run superficial to the rectus abdominis muscle, the internal rectus sheath is composed of sheets of fascia that are deep to this muscle. The external rectus sheath has been shown to be the primary strength-holding layer throughout ventral midline closures.101

On the lateral aspect of the abdomen, fibers of the external abdominal oblique muscles originate from the fourth or fifth to the twelfth rib and from the last rib and thoracodorsal fascia and extend in a caudoventral direction before giving rise to their broad aponeurosis. Fibers of the internal abdominal oblique muscle, which lie immediately deep to the external abdominal oblique muscle, arise from the thoracolumbar fascia caudal to the last rib and from the tuber coxae. These fibers extend cranioventrally, crossing the more superficial fibers of the external abdominal oblique muscles at nearly right angles. The deeper transverse abdominal muscle comes from two parts: the lumbar portion arises from the transverse processes of the lumbar vertebrae and the thoracolumbar fascia and the costal portion arises from the medial sides of the twelfth and thirteenth ribs and from the eighth to eleventh costal cartilages. Fibers from this muscle extend in a dorsoventral direction. The transverse fascia and peritoneum line the inner surface of this muscle. The anatomy of the inguinal and femoral triangle areas are discussed separately under the inguinal and scrotal hernia and femoral hernia sections of this chapter.

Location of Abdominal Hernias

Although hernias can occur virtually anywhere in the abdominal wall, most defects are found in select areas (Figure 84-3). Cranial ventral midline hernias are most often congenital in origin and include umbilical hernias and substernal (or ventral) hernias. Defects in the more lateral areas of the abdominal wall most often result from trauma and include the paracostal defects just off the caudal rib margin or dorsal lateral hernias found just ventral to the lumbar transverse processes. Caudal abdominal hernias include congenital scrotal and inguinal hernias and those most often caused by trauma—the prepubic and femoral hernias.

Pathophysiology of Abdominal Hernias

The overall success of a hernia repair (and often the prognosis for the patient) rarely depends on the repair itself but more on management of the sequelae to organ herniation or internal damage from trauma that impair normal body function. The severity of functional alteration depends on the cause, location, and content of the hernia. Important, often life-threatening, sequelae associated with abdominal hernias can be attributed to space-occupying effects (known as loss of domain), incarceration or obstruction, or strangulation. The clinical condition of the animal at presentation, whether the hernia is open to the outside or not, concurrent injuries to distant structures, and organ compromise from the trauma must also be factored when attempting to predict patient outcome.106

Space-Occupying Effects

“Loss of domain” occurs when the abdominal wall has become accustomed to a relatively small intraabdominal volume because of organ displacement outside the cavity (usually through a large defect). Manual reduction of the hernia contents and primary closure of the defect is difficult or impossible in this situation. Repair of the restricted abdominal wall by forcing the herniated contents back into the abdomen results in excessive tension on the repair, increasing the risk of recurrence. Even more deleterious are acute pulmonary complications, secondary to restriction of diaphragm function, and poor organ perfusion (abdominal compartment syndrome).57,59 High intraabdominal pressure has been documented in a series of client-owned dogs undergoing abdominal surgery, necessitating surgical decompression; one case occurred after hernia repair.21

Several techniques have been used in humans to reduce complications from loss of domain by using a tissue expansion principle.15,17 Progressive pneumoperitoneum and tissue expansion with inflatable Silastic expanders gradually stretch the abdominal wall in much the same way as pregnancy. Staged reduction of open congenital abdominal defects with a Silastic sac has achieved excellent results with little mortality in infants. Most adult human patients with loss of domain are repaired using prosthetic materials (e.g., mesh) to help span the defect; this avoids tension and reduces hernia recurrence and postoperative complications related to loss of domain.17,60


Incarceration of organs such as the intestine, uterus, or bladder most often alters normal function because of luminal obstruction. Acutely incarcerated organs are irreducible and can become lethal strangulated obstructions within hours; therefore, urgent repair should be considered in this situation. The severity and onset of the clinical signs related to the incarcerated obstruction often depends on the contents of the hernia and size of the defect. Abdominal defects with small, inelastic hernial rings, such as scrotal or femoral hernias, are at high risk for incarceration and strangulation.120

Incarceration of the uterus may be associated with inguinal hernias or large umbilical hernias. An irreducible, viable, nongravid uterus within a hernia rarely causes clinical problems; however, incarceration of a pyometra or gravid uterus may lead to severe systemic alterations and dystocia. Small intestine may become incarcerated within any hernia; it is the author’s clinical impression that the risk is greatest when the hernial ring approximates the size of the bowel. Larger hernias rarely trap or obstruct bowel unless they are caused by acute trauma or the entrapped intestines undergo torsion. Intermittent intestinal dysfunction may occur, however, even if intestines are reducible within the hernia. After signs of intestinal obstruction (acute abdominal pain, vomiting, depression, anorexia) occur, early intestinal decompression via exploratory laparotomy is warranted after patient stabilization. The urinary bladder may become obstructed in incarcerated perineal, ventral, inguinal, and traumatic pubic hernias. As urine flow becomes partially obstructed within the hernia, the bladder progressively distends, further obstructing outflow. Immediate bladder decompression and diversion of urine flow can be provided via needle cystocentesis and catheterization; tube cystostomy is considered if the previous methods are unsuccessful. Surgical reduction of the bladder and hernia repair is attempted after the patient has been adequately stabilized.


A strangulated hernia implies that the hernial contents are incarcerated and undergoing devitalization from arrested circulation. Arrested circulation may be from venous or arterial occlusion or a combination of the two. Early venous obstruction results in reversible organ engorgement, but eventually arterial stagnation occurs from back pressure at the capillary beds. Arterial stagnation or obstruction causes rapid organ necrosis if the collateral blood supply is insufficient, resulting in organ rupture. Generally, venous obstruction occurs early in most strangulated hernias, but by the time surgical decompression is attempted, irreversible arterial stagnation has occurred.

Strangulation occurs from several mechanisms, including constriction of the blood supply at the hernial ring or torsion of the vascular pedicle with increased organ mobility. Organs with long, freely movable vascular pedicles (e.g., uterus, omentum, spleen, intestine, testicles) are more prone to torsion. Incarceration of a hollow viscus favors strangulation because increasing intraluminal pressure further obstructs venous outflow from the organ and opposes circulatory pressure. Traumatic hernias are at risk for delayed incarceration and strangulation because adhesions trap organs within the hernia, and contraction during wound healing eventually narrows the hernia ring.

The threat of complication and death is 50% higher in humans with incarcerated or strangulated hernias than in hernias containing reducible viable tissue; therefore, early diagnosis and surgical correction of incarcerated hernias is critical to prevent life-threatening sequelae relating to organ devitalization. Sequelae to hernia strangulation vary depending on chronicity and the organ involved. Strangulated umbilical, inguinal, femoral, and prepubic hernias most often contain falciform ligament or omentum, uterus, prostatic fat, and urinary bladder, respectively.108,120 The clinical course of affected patients depends on the degree of vascular compromise, volume of body fluids lost from obstruction or sequestration, and absorption of bacteria and toxins. The presence of strangulated, contaminated hollow viscus may result in significant blood, protein, and fluid loss and often rupture, causing rapid toxemia and septicemia. Bacteria migrate transmurally through devitalized intestine even before evidence of gross spillage occurs.10 Before overt signs of infection or contamination occur, vasoactive substances such as arachidonic acid metabolites, cytokines, leukotrienes, and kinins from tissue and blood cell autolysis cause redistribution of body fluids and severe cardiopulmonary effects.16 Strangulated viscera within external abdominal hernias may be more isolated from the vascular system than those strangulated within the peritoneal cavity. Liberated vasoactive substances are not absorbed as quickly through the subcutaneous tissue as the permeable abdominal cavity; thus, patients with external strangulated hernias may have a more delayed onset of clinical signs and shock. Severely compromised patients often decompensate and die under anesthesia during attempts at surgical reduction and repair of strangulated hernias; this is thought to be caused by rapid release of vasoactive substances into the circulation from necrotic strangulated organs during surgical reduction. En bloc resection of the devitalized herniated tissue, with release of the constricting ring only after the vascular supply is occluded, may help reduce this fatal complication.108

Principles of Abdominal Hernia Repair

The main goals of hernia repair are to (1) ensure the viability of entrapped hernia contents; (2) release and return viable hernia contents into their normal location within abdominal cavity; (3) obliterate redundant hernia sac tissue; and (4) provide a tension-free and secure primary closure of the defect using strong, healthy surrounding tissue. Adequate surgical exposure and access to the hernia are important to assess hernia contents and isolate strong tissue for defect repair. If abdominal trauma is the suspected cause of a hernia, a midline celiotomy approach is preferred to allow the surgeon access to the entire abdominal cavity to assess for concurrent injuries. Likewise, when strangulation of hernia contents is expected, a midline approach is recommended to isolate the abdominal cavity from the necrotic, often highly contaminated, local hernia environment. In uncomplicated hernias without evidence of obstruction or strangulation, an approach over the hernia rings is considered. Making an incision in a safe region of the ring can facilitate release of the hernia contents. If the defect cannot be repaired primarily using direct approximation of local tissue, the skin and subcutaneous incision may be extended to provide access for muscular or fascial flap development and defect reconstruction. Use of muscular or vascular fascial flaps is particularly important if the surgical site has gross contamination. When autogenous tissue cannot be used to close a large defect without undue tension, prosthetic implants may be considered, especially if the wound is considered clean. Polypropylene sheets are readily available and are often placed preperitoneally (inside the abdominal wall) for a permanent abdominal wall substitute (see Reconstruction of Large Abdominal Hernias later in this chapter).

Surgical Conditions

Ventral Abdominal Hernias

Anatomy, Etiology, and Pathogenesis

In an embryo, the abdominal wall is formed by migration of cephalic, caudal, and lateral folds. The umbilical aperture, which serves as a passageway for the contents of the cord (umbilical blood vessels, small vitelline duct, and stalk of the allantois), remains after normal migration and fusion of these folds.62 The umbilicus is a cicatrix identifying the previous attachment site of the umbilical cord in a fetus. In mature animals, the falciform ligament (the remnant of the umbilical vein) and middle umbilical ligament of the bladder (the remnant of the urachus) are attached to the internal aspect of the umbilicus.35 Congenital umbilical hernias result from failure of fusion or delayed fusion of the lateral folds (principally, the rectus abdominis muscle and fascia) at the umbilicus after normal return of the midgut from the umbilical cord in the canine fetus, which normally occurs at the sixth week of gestation.62 Most umbilical hernias are inherited and are probably the result of a polygenic threshold character, involving a major gene whose expression is mediated by the breed background.51,99 Until more is known about the inheritance and expression, affected dogs or cats should not be bred.

Umbilical hernias have been associated with fucosidosis, an inherited, autosomal recessive, neurovisceral lysosomal storage disease.115 Of 31 English Springer spaniels with fucosidosis, 10 had umbilical hernias, and one had a scrotal hernia. This hernia has also been associated with a congenital, sex-linked, recessive disorder in dogs called ectodermal dysplasia.79

Cryptorchidism frequently coexists in dogs with umbilical hernias or other congenital defects.9,90 Congenital cranioventral abdominal hernias, incomplete caudal sternal fusion, and umbilical defects with concomitant diaphragmatic hernias of various types occur in dogs.81 Successive breedings of a Labrador retriever and an American foxhound with these defects created ratios of affected offspring suggestive of an autosomal recessive mechanism.36 Developmental causes were also suspected in a litter of cocker spaniels with diaphragmatic, cardiac, and abdominal wall defects similar to thoracoabdominal ectopic cordis syndrome.8 In humans, cardiac malposition may result in a mesodermal defect characterized by partial or complete failure of transverse septum development and supraumbilical fusion failure.25,28,62 Defects associated with infraumbilical midline hernias in humans include exstrophy (abdominal wall protrusion) of the bladder, hypospadias, and imperforate anus.62,103 Findings such as these suggest that a thorough search for other congenital defects is important when examining patients with umbilical hernias.

Omphaloceles are large midline umbilical and skin defects that permit abdominal organs to protrude from the body. Herniated contents are initially covered by a transparent membrane (amniotic tissue) attached to the edges of the umbilical defect until minor trauma ruptures the membrane, exposing the prolapsed contents to contamination (Figure 84-4).25,56,62 The incidence of these defects is difficult to determine because most affected animals either die or are destroyed without veterinary attention. Attempted surgical repair in one litter of 5-day-old kittens was unsuccessful because tension sutures pulled through the thin abdominal wall.56 Gastroschisis grossly appears like an omphalocele, but the defect is paramedian. This anomaly has been reported in cats and often results in early neonatal death.25

Acquired causes of umbilical hernia are uncommon. Umbilical hernias may form from excessive traction on the umbilical cord at parturition. Severance or ligation of the umbilical cord too close to the abdominal wall may also create such a defect. Occult congenital umbilical hernias may suddenly become clinically evident in adult animals because of increased intraabdominal pressure from obesity or trauma or with protracted straining.

Umbilical hernias are the most common abdominal hernias in small animals. In an epidemiologic study involving congenital abnormalities found in pet store dogs over a 2-year period, umbilical hernias were found in 0.6% (10 of 1679) of animals.102 Airedale terriers, basenjis, Pekingese, pointers, and Weimaraners are at greater risk.51 The incidence of umbilical hernia is about the same in cats and dogs when the aforementioned dog breeds at risk are excluded.99 A high incidence of umbilical hernia was noted in one family of Cornish rex cats.99 There is no sex predilection for umbilical hernia in the general population; however, females of predisposed dog breeds have a greater incidence of umbilical hernia for unknown reasons.51,99

Diagnosis: Owners usually identify animals with obvious, large umbilical hernias soon after birth. A patient’s history and location of the lesion usually leave little doubt about the diagnosis, although smaller hernias require careful inspection and palpation. Examination of the animal in dorsal recumbency facilitates reduction of the contents of the hernia and hernial ring palpation. Be aware that other masses located in the region of the umbilicus in the puppy or kitten may appear like an umbilical hernia.22

Once an umbilical hernia is found, a careful search for other related congenital defects is undertaken. Abdominal radiography is generally not indicated for patients with small, uncomplicated, reducible umbilical hernias. Animals with large umbilical or supraumbilical abdominal wall defects, especially when incomplete caudal sternal fusion is present, are specifically examined for other congenital diaphragmatic or cardiac defects before correction. Animals with multiple congenital defects, incarcerated hernias, or signs suggesting possible strangulation or obstruction are further examined by radiography, ultrasonography, or both. Dilated, displaced organs outside the abdominal wall; an obstructive intestinal pattern; or free abdominal fluid may indicate strangulation. Early surgical exploration should be considered in these patients. Fine needle aspiration of an incarcerated umbilical mass is rarely indicated because cytologic findings are unlikely to change surgical decision making.

Treatment: Most small, reducible umbilical hernias in dogs and cats contain only falciform fat and are of little clinical significance. Initially, healthy puppies with small (<2 to 3 mm) hernias are treated conservatively because spontaneous closure has been reported as late as 6 months of age.97 Affected animals are neutered because of genetic predisposition to this disease.

The decision to repair or to conservatively treat an umbilical hernia depends on the risk of potential complications. Hernias with inelastic rings that approximate the size of intestine (one finger size in a small to medium-size dog) may be at greater risk for strangulation; the author recommends surgical correction in this instance. Smaller defects or those that are much larger generally do not represent significant risk to an animal and are dealt with during other elective surgical procedures or treated conservatively and observed carefully. If surgery is elected in an animal with omphalocele, it is attempted immediately after birth to help prevent further organ damage or contamination.

When umbilical hernias are corrected at ovariohysterectomy, the hernia repair is completed during routine abdominal wall closure. The initial skin incision is extended cranially over the hernial sac. Alternatively, an elliptical incision is made around the base of a large sac to remove redundant tissue. Skin margins are retracted, and the sac is dissected free. If fat alone is present in the sac, the neck of the hernia is ligated, and the sac and remaining contents are excised. Small sacs with no internal adhesions can be inverted into the abdomen. Usually, no debridement of wound edges or rectus sheath is required, and closure is routine. Recurrence after repair is uncommon.

Umbilical hernias containing abdominal organs may require more extensive surgery. The skin incision is made around the base of the hernia, leaving enough skin to close the defect without tension. In incarcerated hernias without strangulation, the hernial sac is dissected free without damaging the contents. The hernial ring is enlarged along the linea alba to release the contents into the abdomen. The released contents are inspected for viability. Any adhesions to the hernial sac or ring are meticulously broken down. Irreversibly damaged organs or tissues are resected or repaired. The sac is excised, and the hernial ring is debrided if adhesions or scar tissue obscure the edges of the linea alba during closure.

Most umbilical hernias can be primarily closed with tension-relieving suture patterns. If the edges of the hernia cannot be apposed easily with thumb forceps, reliance on sutures alone to relieve wound tension is not recommended. Use of a Mayo mattress (“vest over pants”) suture pattern for herniorrhaphy is controversial.37,80,109 This pattern permits more contact with apposing wound edges but, in doing so, increases unwanted tension on the repair. Primary side-to-side repairs in humans are superior if wound edges can be apposed without tension.37

In rare situations, absence of a region of the abdominal wall accompanies large umbilical hernias. Releasing incisions can be made to reduce tension on the primary suture line, provided that the rectus muscles and underlying fascia have adequate strength (Figure 84-6). Incisions are made at least 2 cm away from the defect through the external rectus fascia only. The fascia is elevated or dissected off the rectus abdominis muscle and shifted toward the midline, thereby reducing tension on the primary repair. Alternately, a component separation technique can be utilized to allow a tension-free midline closure.95 The author prefers to use prosthetic materials for reconstruction of very large, clean defects rather than rely on shifting local tissues such as fascia (see Reconstruction of Large Abdominal Hernias later in this chapter).

Animals with supraumbilical hernias and diaphragmatic defects generally have enough tissue for routine primary closure. The diaphragmatic hernia is repaired with primary closure first so that normal pulmonary function is resumed. Incomplete sternal bones and midline defects are apposed with interrupted sutures of heavy-gauge monofilament nylon or polypropylene.

Caudal Abdominal Hernias

Hernia Categorization

Caudal abdominal hernias include defects in the inguinal, scrotal, and femoral regions. True hernias in the inguinal region are categorized as direct or indirect. With indirect hernias, the abdominal viscera enter the cavity of the vaginal process (Figure 84-7). With direct hernias, the less common form in humans and small animals, organs pass through the inguinal rings adjacent to the normal evagination of the vaginal process.47,125 Direct hernias are usually large, and most do not cause incarceration or strangulation.120 In contrast, indirect inguinal hernias in male dogs (scrotal hernias) more often cause organ dysfunction because the vaginal process narrows considerably at the relatively inelastic inguinal ring.

Inguinal Hernias

Inguinal hernias are less common than umbilical hernias. They result from a defect in the inguinal ring through which abdominal contents protrude.85,125 Inguinal hernia generally denotes direct and indirect hernias in females and direct hernias in males. Indirect hernias in males are considered separately as scrotal hernias.

Congenital inguinal hernias in dogs and cats are rare and often coexist with umbilical hemias.9,51,93 Basenji, Pekingese, poodle, basset hound, Cairn terrier, Cavalier King Charles spaniel, Chihuahua, cocker spaniel, dachshund, Pomeranian, Maltese, and West Highland white terrier breeds are predisposed.9,51 Congenital inguinal hernias develop more often in male dogs than in females, possibly because of delayed inguinal ring narrowing from late testicular descent.38,54,120

Acquired inguinal hernias are relatively common in dogs and most often involve middle-aged, intact bitches.83,85,98,120 No breed predilection has been documented,125 although toy-breed dogs and Shar-Peis may be overrepresented. In one case series, female dogs with inguinal herniation were older and significantly lighter than affected male dogs. These female dogs belonged to breeds that were overrepresented compared with the general hospital population.9 Sporadic cases of acquired inguinal hernias in cats have been described, with equal occurrence in the sexes and breeds examined.51

Anatomy and Pathogenesis: The vaginal process, which contains the spermatic cord in males or the round ligament in females, passes through openings in the caudoventral abdominal wall known as inguinal rings (Figure 84-8). In both sexes, the genital branch of the genitofemoral nerve, artery, and vein and the external pudendal vessels pass through the caudomedial aspect of the canal. The sagittal slit between the abdominal muscles that connects the external and internal inguinal rings is termed the inguinal canal. The internal inguinal ring is bounded medially by the rectus abdominis muscle, cranially by the caudal edge of the internal abdominal oblique muscle, and laterally and caudally by the inguinal ligament. The external inguinal ring is a longitudinal slit in the aponeurosis of the external abdominal oblique muscle. Close superimposition of the external and internal inguinal rings in small animals does not form a true “canal,” as its name implies, but a potential gap through which hernial disruption may occur. An “interstitial hernia” forms when a structure passes through the internal ring alone without continuing past outer wall layers. This condition is described in humans but has not been reported in small animals because of differences in anatomy of the inguinal canal (see Figure 84-8).

The pathogenesis of inguinal hernias is uncertain. Few studies have proven a significant heritable influence, except in golden retrievers, cocker spaniels, and dachshunds.66 Inheritance in the last two breeds may be polygenic.98 Affected small animals should be neutered until evidence excluding heritability as a cause of this disease process is conclusive.38

Factors potentially involved in inguinal hernia formation can be grouped into three major areas: anatomic, hormonal, and metabolic. Enlargement of the entrance to the vaginal process, which, unlike that in humans, remains open, is the most important cause of inguinal hernias in domestic animals.51,125 In humans, a congenital persistent vaginal orifice is essential for development of indirect inguinal hernias.6,94 The internal abdominal oblique muscle in humans acts as a shutter to help prevent herniation of abdominal contents with abdominal contraction.125 Prevention of inguinal hernias in small animals may depend on a similar neuromuscular reflex in addition to a normal anatomic barrier at the inguinal rings.72 Bitches may be predisposed because the inguinal canal is shorter and of larger diameter than in males.33 Congenital inguinal hernias may disappear spontaneously at 12 weeks of age because of a decrease in the relative size of the inguinal rings.38 Traumatic inguinal hernias in dogs may result from a preexisting anatomic weakness in the area.83

Evidence indicates that sex hormones play an important role in the cause of inguinal hernias. In females, most inguinal hernias appear during estrus or in pregnant bitches. Acquired inguinal hernias are much less frequent in neutered females.120 Therefore, estrogen production is considered to have a close relationship to the development of inguinal hernia.98 Sex hormones may change the strength and character of the connective tissue, weakening or enlarging the inguinal rings.88 Experimentally, a sex hormone imbalance has been directly linked to formation of inguinal hernia in male and female mice.53

A multiinstitutional investigation was undertaken to examine the association between inguinal and perineal hernias in male dogs.104 Among male dogs older than 4 years with acquired, nontraumatic inguinal hernias, four of the nine dogs described in the literature and all five dogs at one institution had concurrent unilateral or bilateral perineal hernias. Most dogs did not show marked clinical problems from the perineal hernias, nor were hernias apparent to the owners. In two other studies, three of 11 and two of 16 males with nontraumatic inguinal hernias had concurrent perineal hemias.9,120 These observations may suggest a similar cause of these concurrent hernias.

Weakening of the abdominal wall may result from altered nutritional or metabolic status.85 Obesity increases intraabdominal pressure, forcing abdominal fat through the inguinal canals.83 Furthermore, accumulation of fat around the round ligament may dilate the vaginal process and inguinal canal, allowing hemiation.6

Signalment and Clinical Signs: In general, inguinal hernias are more common in female dogs. In two case series, males accounted for only 8% to 11% of dogs with inguinal hernias.84,113 Of dogs with nontraumatic inguinal hernias, 37% were male.120 Males with inguinal hernias were younger than females and accounted for five of eight dogs younger than 2 years.120

Affected animals usually present with a painless, unilateral or bilateral mass with a soft, doughy consistency.9,35,58,83,112 In dogs, more unilateral inguinal hernias occur on the left side than on the right.9,29,120 The external appearance may vary, depending on the amount of vascular occlusion and the nature of the contents. Inguinal hernias may be undetectably small. Large hernias may contain a gravid uterus (hysterocele), bladder, or jejunum (Figure 84-9). Large inguinal hernias in bitches that extend caudally following the round ligament to the vulva may resemble a pendulous perineal hemia.38,83 Direct inguinal hernias in male dogs may be confused with scrotal hernias because of venous or lymphatic obstruction at the inguinal ring and subsequent swelling and edema of the testicle and spermatic cord.

Diagnosis: Diagnosis is usually based on historic findings and physical examination. Vomiting, abdominal pain, and depression suggest obstructed intestine. In one report of dogs with inguinal hernias, vomiting for 2 to 6 days predicted a strangulated small intestine. In that study, all dogs with entrapped, nonviable small intestines vomited, but none of the dogs with inguinal hernias containing viable small intestine vomited.120 History of an inguinal mass and previous vaginal bleeding or discharge may indicate uterine involvement. History is usually not helpful for diagnosis of hernias when omentum or fat alone protrudes through the inguinal canals. The risk of strangulated intestine in dogs with long-standing inguinal hernia is less than 5%.120

Diagnosis is confirmed by manual reduction of hernia contents and palpation of the hernial ring. Hernia reduction can be facilitated by elevating the hindquarters with the animal in dorsal recumbency to reduce caudal intraabdominal pressure. Careful palpation of both inguinal canals is recommended because inguinal hernias can be bilateral, and small hernias may remain undetected until complications arise.

Incarcerated hernias present more of a diagnostic challenge because palpation may not yield a diagnosis. All inguinal masses, including mammary tumors and cysts, lipomas, enlarged lymph nodes, abscesses, and hematomas, must be considered as differential diagnoses. Although immediate surgical exploration facilitates diagnosis of an inguinal mass or hernia, surgical correction of such disorders should proceed with greater precision if the anatomic aspects are delineated first. The nature of herniated contents can be confirmed with plain or contrast radiography or computed tomography (CT). During image evaluation, particular attention is paid to the caudal abdominal wall structure (“abdominal strip”) and the fascial detail of the flank musculature; loss of definition in these areas suggests herniation.7 Contents of inguinal hernias may include omentum, fat, ovary, uterus, small intestine, colon, bladder, or spleen.4,7,9 A herniated gravid uterus is easily detected on plain radiographs by the appearance of the fetal skeleton after 43 days of gestation or, before skeletal ossification, as a lobulated fluid density.7 The bladder can be identified by taking plain radiographs before and after emptying the bladder by catheterization or with positive or negative contrast cystography. In children with inguinal hernias, pneumoperitoneography has been used to detect occult hernias on the contralateral side.48 Fine needle aspiration may help differentiate an inguinal mass from an incarcerated hernia but is rarely used because accidental puncture of a loop of intestine or pyometra could cause leakage and gross contamination.

Surgical Repair: Inguinal hernias are generally best repaired at the time of diagnosis; delay may result in more difficulty in performing the operation and may increase the risk of complications. Successful surgical repair of inguinal hernias depends on knowledge of regional anatomy and appropriate surgical technique, which includes apposition of strong tissues without tension and high hernial sac ligation. Uncomplicated unilateral inguinal hernias are approached over the inguinal rings. In more complicated hernias (incarcerated or strangulated contents, concurrent serious intraabdominal trauma), the approach is first through the ventral midline for exploration; hernia repair is subsequently performed extraabdominally.

Some surgeons repair inguinal hernia through the abdominal cavity.9 With this approach, sutures are placed through the parietal peritoneum, the aponeurosis of the transversalis muscle, and the rectus abdominis and internal abdominal oblique muscles.9 Laparoscopic repair of inguinal hernia in affected beagle dogs by direct sac ligation or prosthesis onlay has been described in an endosurgery text.116

The conventional surgical approach to inguinal hernias begins with an incision over the lateral aspect of the swelling parallel to the flank fold.58,61,83,112 The hernial sac is exposed through blunt dissection, and the sac and contents are milked or grasped and twisted to gently push the contents through the canal. If the hernia is not easily reducible, the sac is opened (Figure 84-10), and the canal is enlarged by incising through the inguinal ring in a craniomedial direction. The neck of the hernial sac is ligated as close to the internal inguinal ring as possible, and the sac is amputated. The enlarged external inguinal ring and any incisions in the abdominal wall are closed with prolonged absorbable or nonabsorbable sutures. In traumatic inguinal hernias or when the external inguinal ring is weak, sutures can be placed between the inguinal ligament, external rectus fascia, and internal oblique abdominal muscle to aid in hernia closure.

A midline approach may be preferred over the conventional approach for several reasons (Figure 84-11).83,89,124,125 This approach avoids incising through mammary tissue, an advantage especially in a lactating animal. It also permits exploration of both inguinal rings, which is recommended by the author because small hernias are frequently missed on palpation.83,89,125 In some animals, mammary tissue must be dissected directly off the external rectus fascia bilaterally to adequately expose the inguinal regions through a midline approach. A single midline incision permits simultaneous hernia repair of uncomplicated bilateral hernias and access to the abdominal cavity for complicated hernias. Additionally, it is necessary for ovariohysterectomy, which is the simplest option for treatment of a herniated gravid uterus. Successful primary repair of the hernia and replacement of the incarcerated uterus can be performed up to the seventh week of gestation if a valuable litter is expected. After 7 weeks, an ovariohysterectomy or hysterotomy may be recommended before primary hernia repair, depending on the health of the bitch and its value.98

In most animals, inguinal hernias can be repaired with the patient’s own tissues. Patients with large traumatic defects or recurrent inguinal hernias may require reinforcement of the primary hernia repair with prosthetic materials. Inguinal hernias in three intact, small female dogs were successfully repaired by an onlay polyethylene mesh technique.20 A cranial sartorius muscle flap (see Reconstruction of Large Abdominal Hernia section) has been suggested for reconstruction of large inguinal hernias when primary repair is not possible.121 A sartorius muscle flap was used in conjunction with synthetic implants to repair large chronic caudal abdominal hernias in two young cats.114

Complications, Aftercare, and Prognosis: The most common complication after inguinal hernia repair is hematoma or seroma formation from inadequate hemostasis, extensive tissue dissection during herniorrhaphy, or excessive activity after surgery. Patients are frequently reluctant to walk for several days after surgery, presumably because stretching and motion on the repair cause inflammation and pain. Swelling and tenderness in the inguinal area may also be associated with incorporation of nerves and vessels in the hernia repair or ensuing infection. If suppuration occurs, the skin and subcutaneous layers are opened, and local treatment measures are undertaken. Early recognition and treatment of infection reduce the risk of hernia dehiscence.109

In a large series of inguinal hernia repairs in dogs, the overall prevalence of postoperative complications was 17%, and the mortality rate was 3%. Incisional infection, peritonitis and sepsis, and hernia recurrence were responsible for most postoperative complications. One dog died of intestinal dehiscence after resection of an entrapped, nonviable intestinal segment within the hernia.120

Perioperative antibiotics and postoperative bandages are generally not necessary in uncomplicated hernias. If excessive dead space is anticipated, especially after trauma, dressings with or without placement of a closed drain may help prevent seroma formation. Exercise is strictly limited until suture removal. Controlled leash walking soon after surgery is encouraged to decrease postoperative edema. The incision is monitored for swelling or discharge, and skin sutures are removed in 10 to 14 days. Prognosis for uncomplicated repair of inguinal hernia is good to excellent. In one study, all but one of 61 dogs with inguinal hernias survived.9

Scrotal Hernia

Anatomy and Pathogenesis

Scrotal hernias are indirect hernias that result from a defect in the vaginal ring, allowing abdominal contents to protrude into the vaginal process alongside spermatic cord contents (see Figure 84-7).78 Herniated organs within the vaginal process do not necessarily have to extend as far distally as the scrotum for the condition to be considered a scrotal hernia. These hernias are rare, particularly in cats.35,67,76 Most case reports involve young male dogs.* Dog breeds with scrotal hernias are generally larger than breeds of female dogs with inguinal hemias.9 Strangulation of contents occurs more frequently in male dogs with scrotal hernias than in females with indirect inguinal hernias.98,120 In a study of 35 dogs with inguinal hernias, five had strangulated bowel, and four were young male dogs.120

Literature regarding the pathogenesis of scrotal hernias is limited. Unlike the situation in humans, heritability of this disorder in dogs and cats remains unknown. A congenital anatomic defect or weakness may be present in the vaginal orifice in dogs with scrotal hemias.125 Occasionally, scrotal hernia formation is associated with trauma.25 Ectopic testes have been reported in 19% to 33% of male dogs with inguinal hemias.113,120 An increased risk for inguinal hernias was found in dogs with cryptorchidism.90

The anatomic boundaries of the inguinal rings are described earlier (see Inguinal Hernia section). The relative size of the inguinal canal and the structures found within the inguinal rings differ between the sexes. The cremaster muscle in males is a continuation of the free caudal border of the internal oblique abdominal muscle. Normal contents of the spermatic cord (ductus deferens and associated artery and vein and testicular artery, vein, and nerves) pass through the inguinal rings within the vaginal process.

Clinical Signs

Presenting signs of scrotal herniation result from protrusion of abdominal contents through the vaginal process, causing pain, swelling, and frequently organ dysfunction. Scrotal hernia is predominantly unilateral, with equal occurrence on both sides, although several bilateral cases have been reported.9,25,33,47 In humans, 15% of patients with unilateral scrotal hernia eventually developed a contralateral hernia; therefore, it would seem prudent to consider inspecting the contralateral inguinal ring in animals with unilateral scrotal hernia.96

The reported contents of scrotal hernias include periprostatic fat, omentum, and intestine.47,58 The external appearance of scrotal hernia depends on the sac contents and amount of vascular obstruction at the hernial ring. Swelling is generally cordlike, extending from the inguinal ring to the caudal aspect of the scrotum (Figure 84-12).67 Strangulated hernias have a dark discoloration of the tissues within the hernia, which is often visible externally. Signs of sharp pain are commonly exhibited during palpation of the hernia.

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Jul 18, 2016 | Posted by in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Abdominal Wall Reconstruction and Hernias
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