Abdominal Hernias

An abdominal hernia is a defect or opening in the wall of the abdominal cavity (external abdominal hernia) or within a compartment of the peritoneal space (internal abdominal hernia). Under certain clinical conditions, the defect allows protrusion (herniation) of an abdominal structure. Organs or tissue located in the immediate vicinity are usually found within the defect. However, predicting the organ involved may be difficult because freely movable organs with long vascular pedicles may travel considerable distances to occupy the hernia. It is important to understand that the defect itself may not be the most important clinical problem presenting to the veterinarian for treatment. Instead, it is the cause and effect of vital structure entrapment within the confines of the defect (hernial ring) or concurrent organ damage from trauma, which often dictates whether prompt and aggressive medical or surgical treatment is needed. Frequency and types of complications, success of surgical repair, and ultimately, final outcome are often dependent on the initial condition of the patient and the organ involvement [1-3]. Whether an uncomplicated hernia defect requires surgery depends on the surgeon's estimate of the risk of future organ displacement. The causes of an abdominal hernia should also be determined so proper decisions can be made to help prevent perpetuation of the defect in offspring and to reduce the risk of incisional breakdown (dehiscence) or recurrence.

Hernia Classification and Terminology

Abdominal hernias are described in many ways depending on the nature of the herniation or defect, the location or anatomy of the hernia, the etiology, and most importantly, the condition of the structures protruding through the hernia and the functional alterations resulting from this protrusion.

The abdominal wall is composed of multilaminar arrangements of muscles, their aponeuroses, strong fascia, fat, and either skin or peritoneum. Generally speaking, the abdominal wall functions as a barrier to contain (limit movement) and offer protection for vital abdominal organs. Several normal anatomic openings lined with peritoneum penetrate the external abdominal wall, providing nourishment to the fetus (umbilical aperture), passageway and neurovascular supply for the testicles (inguinal canal), and neurovascular supply to the rear limbs (femoral canal) [4].

"True" hernias are generally formed from a congenital (present at birth) weakness or absence of tissues surrounding the normal abdominal apertures. More rarely, true hernias include midline abdominal wall fusion defects. This weakness or lack of a barrier leads to enlargement of the opening (hernial ring) and eventual organ protrusion. True hernias have a complete lining or sac of peritoneum (hernial sac) surrounding the contents. Congenital defects in the ventral midline of the abdominal wall, so called "ventral hernias or substernal hernias", often associated with internal hernias (diaphragmatic), are also considered true hernias because peritoneum usually covers the hernia contents. This slippery peritoneal lining helps reduce adhesion formation of herniated organs or tissue to periabdominal tissue so these hernias are frequently reducible (contents freely move from within the hernial sac to the abdomen) and often pose no immediate threat to the patient.

"False" hernias allow protrusion of organs outside the normal apertures of the abdominal wall. False hernias initially do not contain a complete peritoneal sac. Generally, these hernias are acquired, caused either by accidental trauma to the abdomen (traumatic hernias) or following breakdown of a surgical approach to the abdomen (incisional hernia). One recent report described a dog with a traumatic abdominal hernia caused by a fractured 12th rib penetrating through the paracostal musculature, resulting in liver herniation; this was termed an "auto-penetrating hernia" [5]. Owing to the lack of a peritoneal covering, false hernias often lead to development of organ adhesion to surrounding periabdominal tissues causing complications such as incarceration (hernial contents become trapped or irreducible). In contrast to true hernias, contents of false hernias are exposed to local tissue inflammation and may sustain constriction of blood supply as the hernial rings contract during healing. When vascular supply to the contents within a true or false hernia is compromised it is said to be strangulated, and this is a surgical emergency.

Causes and Pathophysiology

The etiology of a hernia may be from a single obvious defect, such as trauma, or, more commonly, from multiple predisposing factors. Hernias may be the result of either congenital or acquired factors. Congenital defects result when injury or altered development of the fetus occurs as a result of various factors (developmental) or from genetic mechanisms that are transmissible from generation to generation (hereditary). Developmental hernias may be caused by lack or excess of some necessary substance (vitamin, protein) or by a toxin, resulting in abnormal fetal development. As investigation continues into causes of congenital hernias, more and more "developmental" hernias may be found, in some way to be caused by as yet unknown genetic influences. Therefore, until genetic causal factors have been eliminated for specific congenital abdominal hernias, it is prudent for the veterinarian to advise sterilization of affected patients.

Developmental Hernias

Congenital inguinal and umbilical hernias have well explained developmental causes. Male dogs develop congenital inguinal hernias more often than do females [1]. This is believed to be a result of delayed inguinal ring narrowing because of late testicular descent in dogs [1,6,7]. Congenital umbilical hernias result from failure or delayed fusion of the lateral folds (principally tissues forming the rectus abdominis muscle and fascia) at the umbilicus after normal return of the midgut (6th week of gestation) from the umbilical cord in the fetus [8]. Omphalocele congenitalis is a congenital defect formed when loops of intestine are delayed in their transit from the umbilical cord into the abdominal cavity. Gastroschisis is another congenital abnormality appearing similar to omphaloceles, except that the abdominal wall defect is paramedian [9]. Spontaneously occurring femoral and scrotal hernias seen in adult dogs are thought to be caused by an underlying congenital weakness of the musculofascial tissues surrounding the respective abdominal apertures. Factors such as trauma and increased intraabdominal pressure, from obesity or chronic straining from constipation for example, may then trigger hernia occurrence later in life [3].

Hernias are often found in patients with other congenital defects. Cranioventral abdominal hernias, incomplete caudal sternal fusion, and umbilical defects with concomitant diaphragmatic hernias of various types have been described in puppies [10]. Successive breedings of a Labrador retriever and American foxhound with these defects created ratios of affected offspring suggesting an autosomal recessive mechanism [11]. Another investigation describing diaphragmatic, cardiac, and abdominal wall defects in a litter of cocker spaniel dogs, similar to thoracoabdominal ectopic cordis syndrome, however, suggested a developmental cause [12]. Cardiac malposition in humans may cause a mesodermal defect resulting in partial or complete failure of septum transversum development and subsequent supraumbilical fusion failure [8,13]. Congenital heart defects and portosystemic shunts may be associated with supraumbilical defects [14]. Defects associated with caudal ventral midline (infraumbilical) hernias include exstrophy of the bladder, hypospadius, and imperforate anus [8,15]. In addition, dogs with umbilical hernias often have cryptorchidism as well as other congenital defects [16,17]. These findings confirm the need to examine patients with congenital hernias closely for other important developmental problems before attempting surgical repair [2].

Heritable Hernias

Many congenital umbilical and inguinal hernias are thought to be caused by hereditary influences. Heritable inguinal hernias have only been documented, however, in the golden retriever, cocker spaniel, and dachshund [18]. In man, persistence of the process vaginalis (opening into the evaginated peritoneum surrounding the testicle) and enlarged inguinal rings have a similar familial tendency. Although most umbilical hernias appear to be inherited, no definitive information has been presented regarding the mode or pattern of inheritance affecting the fibrosis and union of the abdominal aponeuroses. Results of one study indicated that this defect is probably the result of a polygenic threshold character, possibly involving a major gene whose expression is mediated by the breed background [19,20]. Umbilical hernias have also been associated with fucosidiosis, an inherited neurovisceral lysosomal storage disease. Of 31 English springer spaniels diagnosed with fucosidiosis, 10 had umbilical hernias and 1 had a scrotal hernia. This disease is believed to be inherited in an autosomal recessive manner [21]. Neutering should be recommended for all small animals with congenital inguinal or umbilical hernias until conclusive evidence is demonstrated regarding the heritable nature of this disease process [6].

Hernias Caused by Metabolic and Hormonal Imbalance

Certain pathophysiologic conditions predispose to acquired abdominal herniation. Inguinal hernias are most commonly seen in older intact female dogs [1]. These hernias occur as a result of multiple factors including obesity, decreased connective tissue strength, and increased intraabdominal pressure. Obesity causes increased intraabdominal pressure, forcing fat through abdominal wall apertures and further dilating the hernial rings [22]. Onset of hernia occurrence is often associated with estrus or pregnancy, suggesting hormonal imbalance as a contributing cause [23]. Estrogen production is considered to have a close relationship with development of inguinal hernias. Sex hormones may change the strength or character of the connective tissue, weakening or enlarging the inguinal rings [24]. Experimentally, sex hormone imbalance has been directly linked to formation of inguinal hernia in male and female mice [25]. Ovariohysterectomy, therefore, is recommended to reduce the incidence of acquired inguinal hernias; this procedure may help to prevent recurrence following repair. Supporting structures of the abdominal wall may also become weak or stretch owing to nutritional or metabolic problems (for example, hyperadrenocorticism or diabetes mellitus). Accumulation of fat around the round ligament may dilate the vaginal processes and inguinal canal, allowing herniation [26]. Maintenance of normal body weight and eliminating hormonal or metabolic disturbances should help reduce the incidence of acquired nontraumatic abdominal hernias.

Traumatic Hernias

It has been proposed that the contents of acute traumatic hernias may be more prone to adhesion formation to extra abdominal structures and to incarceration because such hernias lack a complete serosa lined hernial sac. Traumatic hernias may undergo organ strangulation owing to swelling caused by acute inflammation or from hernial ring contraction during healing [22]. However, adhesion formation, incarceration, and strangulation have not been found to be common sequelae of traumatic hernias in retrospective studies. The important cause of organ damage may be from the trauma itself, rather than from the hernia. None of the contents of 21 traumatic hernias in one retrospective study demonstrated any evidence of vascular obstruction from incarceration during abdominal exploration; although 2 dogs had evidence of traumatic intestinal devitalization [27]. One dog developed organ compromise as a result of mesenteric avulsion in a recent report of 36 traumatic body wall hernias in dogs and cats [5].

Most abdominal hernias are caused by blunt trauma (automobile accidents, kicks, falls). Of 21 consecutively studied traumatic abdominal hernias, 17 were caused by blunt trauma (automobile accident) and 4 by penetrating trauma (dog fight) [27]. Hernias can occur in a variety of locations, often dictated by the mode of trauma [22,28]. The most common areas of herniation caused by blunt trauma in one study were in the ventrolateral caudal abdominal (inguinal or prepubic areas) and paracostal regions [27]. In a more recent study, 28 of 36 dogs and cats with abdominal hernias were caused by bite wounds [5]. The lateral paralumbar site was the most common hernia location in dogs in Shaw's study [5], whereas the ventral body wall and femoral sites were more common in cats. All pubic ligament ruptures in this study were caused by vehicular trauma.

Hernia location depends on various factors, including the local direction of the traumatic force and intra-abdominal pressure changes. Blunt trauma, applied while abdominal muscles are contracted but the glottis is open, thus limiting increase in intra-abdominal pressure, may result in traction or avulsion type injury to tissues with minimal elasticity (muscle attachments to bone) [22,27]. Common hernias resulting from avulsion forces are the prepubic (ruptured cranial pubic ligament), inguinal, and dorsolateral hernias (muscle avulsion from transverse processes of lumbar vertebrae termed paralumbar or lateral hernias) [27,29]. Rupture of the cranial pubic ligament is often associated with concurrent inguinal ligament damage (a traumatic femoral or inguinal hernia may result). A sudden increase in intra-abdominal pressure may cause rupture in the weakest area of the abdominal wall. Paracostal hernias occur when the origin of the external oblique abdominal and transverse abdominal muscles avulse from their rib or costal cartilage origin, or they are caused by a broken rib lacerating adjacent musculature (autopenetrating hernia) [5]. Abdominal viscera herniate laterally into the subcutaneous tissues in paracostal and paralumbar hernias. Paracostal hernias frequently occur with diaphragmatic rupture, presumably as a result of similar initiating forces. Direct local trauma caused by a blunt object (shoe, fence post) results in separation (tearing) of the wall at the location of impact [30].

Blunt trauma may cause widespread crush, rupture, or avulsion damage to intra-abdominal organs. Up to 75%of traumatized small animal patients with abdominal hernias have other significant injuries; most are orthopedic and usually involve the pelvis. In decreasing order of frequency, the respiratory, gastrointestinal, and genitourinary systems are also injured [27]. In a recent study, over 50% of patients with traumatic hernias suffered injury to other structures. One quarter had more than one associated injury. One third of the hernias had associated body cavity injuries including diaphragmatic hernia, kidney avulsion, bladder rupture, and mesenteric avulsion. In addition, 9 of 36 animals had concurrent orthopedic injuries [5]. A thorough examination of patients with traumatic hernias is imperative to assess for significant associated injuries.

Abdominal hernias may rarely occur through a fracture defect (sacroiliac luxation, pubic or symphyseal fracture) [31,32]. In addition to the fracture, severe damage to underlying soft tissue structures, such as ligaments and mesenteric attachments, is required to allow organ herniation [28]. Traumatic body wall hernias may also result from shearing forces that are distributed over boney projections of the pelvis or caudal thorax rib cage. These forces result in the tearing of muscles or tendons from their boney attachments [33].

Sharp trauma (bite wounds, gunshot, knife stabs) may cause herniation anywhere in the abdominal wall. Animal fight wounds are more apt to cause multiple hernias located in the dorsal or lateral abdominal wall [5,27]. Tears, perforation, and laceration of intra-abdominal structures occur frequently with sharp trauma. Shaw reported that nearly 25% of animals with perforating abdominal wall trauma had evidence of intestinal damage requiring resection and anastomosis [5]. Therefore, patients with penetrating abdominal trauma and herniation should undergo emergency abdominal exploration after stabilization [34,35].

Incisional Hernias

Incisional hernia incidence is reported to be between 1% and 11% in humans, and is as great as 16% in large animals, depending on the surgical approach to the abdomen, predisposing factors, and overall status of the patient [36,37,38]. Incisional hernia in small animals is less common. Sequelae to incisional hernia often are extremely serious and costly (e.g., total abdominal wound dehiscence in humans is associated with a 15 to 20% mortality rate) [24,39].

Predisposing causes of acute and chronic incisional hernia vary, appear interrelated, and occur at different times after surgery. Acute incisional hernias generally occur within the first 7 days after surgery, whereas chronic hernias are noted weeks to years postoperatively. Reported risk factors for acute incisional hernia include increased intraabdominal pressure because of pain, entrapped fat between hernia edges, inappropriate suture material use, infection, chronic steroid treatment, and poor postoperative care [40]. Technical error in surgery is the most common cause of acute wound disruption [3,39]. Factors associated with chronic incisional hernia in humans include obesity, hypoproteinemia, cardiopulmonary complications, abdominal distention, skin wound dehiscence, and deep fascial infection. Local wound complications, especially deep infection, are considered the most important predisposing causes of chronic incisional hernias [37,41].

Incisional hernias result from either excessive forces acting on the abdominal incision or poor holding strength of the sutured wound.

Excessive Forces on the Incision

Forces disrupting the abdominal incision are mainly derived from excessive intraabdominal pressure or muscle tension. Experimentally created abdominal wounds healing under increased tension were less resistant to rupturing compared with wounds under normal tension, at 15 days [42]. Vigorous uncontrolled activity or violent coughing or straining postoperatively certainly predispose to wound breakdown. Increased intraabdominal pressure is observed in such conditions as obesity, abdominal effusions, pregnancy, or organ distention because of ileus or obstruction; all these problems increase incisional hernia risk [39,42].

The gravity dependent ventral midline and paramedian approaches pose a greater risk for incisional herniation. Experimentally created transverse abdominal incisions in rabbits offer better security against dehiscence than ventral midline incisions because the suture/tissue interface is stronger in this area [42]. "Grid incisions" or those that involve muscle splitting, such as the flank approach, may be less susceptible to incisional hernia because wound edges are drawn together with muscle contraction.

Poor Holding Strength of the Wound

The choice of suture material for abdominal closure is rarely the sole cause of incisional hernia, provided the appropriate size is used [39,42]. Choice of suture type may be critical in patients that have prolonged wound healing or are severely catabolic and when wound infection is present, particularly when an unpredictable, rapidly absorbable suture such as chromic gut is used [39].

A tied suture is only as strong as its knot. The nature of disruptive forces produced by normal physical activity applied to sutures and their knots remains unknown. An in vitro knot testing study found that suture materials placed in an interrupted pattern, except polydioxanone and monofilament nylon, were secure with three square throws. Square knots used to begin or end a continuous pattern require an additional one or two square throws, respectively, to be secure. Granny knots, loose asymmetrical square knots, and loosely tied square knots were not as secure as snug square knots for most suture materials tested [43].

Whether suture is placed in an interrupted or continuous pattern or the abdomen is closed in a single or double layer has little significance in incisional hernia formation, provided the strength holding layer is incorporated [42,43,44]. Of 52 human patients with acute incisional hernia, 88% of the disruptions contained intact sutures that had pulled through tissue, whereas only 12% had broken sutures. The problem with most of the closures was inclusion of too little rather than too much tissue [39]. The holding power of abdominal wounds closed in a single layer was stronger than that of double layer closures in one experimental study involving rabbits [42]. Interrupted suture patterns are the more secure choice in situations where wound edges have questionable viability or strength or if other predisposing incisional hernia factors are present.

Successful, lasting abdominal wall closures must include the external rectus fascia. Identifying this layer before attempting closure is critical. Sutures should incorporate at least 5 mm of healthy fascia to ensure adequate anchorage.

Prevention of incisional dehiscence is best afforded by preventing excessive continual intraabdominal pressure (reducing coughing, straining) or abdominal distention, and preventing local wound complications (infection, seroma). Necrosis within a suture loop caused by excessive tightening should be prevented. Meticulous surgical technique placing sutures in strong tissue with adequate tissue bites using proper knot tying will reduce the incidence/occurrence/development of most acute wound dehiscences.

Causes of Hernia Recurrence

Overall, abdominal hernia recurrence appears to be much less frequent in small animals compared with humans. Abdominal hernia repair breakdown in humans ranges from less than 1% to 20%, depending on the cause and type of hernia and patient variables. Most hernia recurrences stem from infection, extreme tension on the repair, incorporating tissues with poor strength in the repair, poor anatomic reconstruction, or more obvious technical failure such as inappropriate suture type or size. Overall, it appears that the choice of suture material is less important than the technique and placement of sutures for prevention of hernia recurrence. The prime etiologic factor in late hernia recurrence is tension on the suture line, which is the cause of suture or tissue disruption. Increased intraabdominal pressure from vomiting, coughing, or straining to urinate or defecate greatly increases the risk of dehiscence. Severe obesity triples the risk of hernia recurrence in humans owing to increased intraabdominal pressure [3].

High sac ligation to help reduce hernia recurrence, popularized by Marcy in some of the earliest reports of successful hernia repair, was until recently a universally accepted goal of hernia repair technique [45]. It is now known that the peritoneum lining the hernia sac is relatively weak and regenerates rapidly. Healing of large serosal defects is usually complete in less than one week [46]. Clinical and experimental studies have shown that the risk of incisional disruption is no greater if the peritoneum is not sutured at laparotomy or herniorrhaphy. Because of these findings, many surgeons now believe that high hernial sac ligation does not prevent recurrence, provided the other aspects of the repair are properly performed [47]. Suturing the peritoneum may cause deleterious effects such as local ischemia, delayed healing, increased postoperative pain, and adhesion formation [48].

When a hernia recurs many times, it is unwise to always assume that the prior surgeon and surgical procedure were inadequate. Underlying tissue weakness may be responsible for the failure. In one recent experimental study, progressive fascial wound failure decreased the fidelity of subsequent incisional hernia repair, compared with identically sized acute abdominal wall defect repairs. The mechanism appears to include decreased fascial wound strength and decreased tissue compliance after herniorrhapy [49]. Mesh reconstruction of these complicated recurrent hernias is now routinely recommended in humans because defects of any size can be repaired without tension. In addition, polypropylene mesh sets up a scaffolding that, in turn, induces the synthesis of collagen [50]. A biologic approach to combat acute wound failure is gaining more attention in human surgery. Treatment of experimentally created abdominal fascial incisions with growth factors in one study prevented development of incisional hernias in the rat model. TGF-beta stimulated fascial macrophage and fibroblast chemotaxis as well as collagen production [51].

Sequelae to Organ Herniation and Trauma

Most abdominal wall defects can be reconstructed easily and successfully if the previously described surgical principles are observed. The overall success of a hernial repair (and often the prognosis for the patient), however, relies heavily on how the surgeon manages the sequelae to organ herniation or internal damage from trauma, which tend to impair normal body function. The severity of the functional alteration depends on the cause, location, and content of the hernia. Important, often life-threatening sequelae can be attributed to space-occupying effects or the condition termed "loss of domain," incarceration, or strangulation. The condition of the animal at presentation, concurrent injuries to distant structures, as well as organ compromise owing to the trauma must also be factored when attempting to predict patient outcome [5].

Space-Occupying Effects

“Loss of domain" occurs when the abdominal cavity has become accustomed to a small intra-abdominal volume so reduction of the hernia contents and primary closure of the defect are impossible. This is most commonly associated with closure of large chronic hernias. Repair of the abdominal wall and forcing the herniated contents back into the abdomen often result in excessive tension on the repair (increasing recurrence risk). Even more deleterious are acute pulmonary complications (caused by restriction of diaphragm function) and poor organ perfusion. High intra-abdominal pressure has been documented in a series of client-owned dogs undergoing abdominal surgery, necessitating surgical decompression; one case was following hernia repair [52].

Several techniques have been employed in human patients to reduce this "loss of domain" complication, using a tissue expansion principle [53,54]. Progressive pneumoperitoneum and tissue expansion using inflatable silastic expanders function to gradually expand the abdominal wall in much the same way that pregnancy does. 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 to help span the defect to avoid tension and hernia recurrence, as well as postoperative complications [54,55].

Other examples of space-occupying effects occur when organs herniate into the pleural or pericardial spaces. The negative pressure in the pleural space tends to draw abdominal organs into the chest. Organs herniating into the chest or pericardial sac reduce lung expansion and cardiac function, respectively, creating problems with patient management particularly at anesthetic induction. Severity of compromise depends on the volume and rate of expansion of the space-occupying herniated tissue. For example, a herniated liver lobe, spleen, or omentum rarely causes major problems for the patient unless strangulation occurs, so most are surgically repaired on an elective basis. A rapidly expanding herniated stomach, on the other hand, causes severe progressive respiratory distress and is a surgical emergency.

Incarceration

Incarceration of organs such as the intestine, uterus, or bladder most often alters normal function because of luminal obstruction. Incarcerated organs are irreducible and can become (within hours) lethal strangulated obstructions. 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-sized, rather inelastic hernial rings, such as scrotal or femoral hernias, are at high risk for incarceration and strangulation [1].

Incarceration of the uterus is often 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. Toxemia, resulting from obstructed drainage of an infected uterus or from uterine rupture, and dystocia are sequelae of uterine incarceration. Emergency surgical resection of the diseased uterus or caesarian section is given first priority following aggressive patient stabilization with appropriate fluid and antibiotic therapy. Surgical repair of the hernia is attempted only if the patient's vital parameters are stable following uterine surgery; otherwise repair is performed under more controlled conditions.

Small intestine may become incarcerated within any hernia, but it is my clinical impression that the risk is greatest when the hernial ring approximates the size of the bowel. Smaller hernias rarely allow intestinal protrusion. 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. Once signs of intestinal obstruction occur (acute abdominal pain, vomiting, depression, anorexia) early intestinal decompression is warranted. Electrolyte, acid-base, and body fluid imbalances associated with the particular level of intestinal obstruction are corrected without delay before surgery. Adhesions, if present, are broken down and an incision is made in the hernial ring to help reduce the intestines and relieve the obstruction.

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. Complete obstruction causes severe metabolic consequences such as azotemia, hyperkalemia, and metabolic acidosis, and eventually causes bladder-wall necrosis. Death results within 2 to 3 days if the obstruction is not relieved. Immediate bladder decompression and diversion of urine flow via needle cystocentesis, catheterization, or tube cystostomy are imperative. Diuresis is established with appropriate intravenous fluids following bladder decompression. If kidney function is not impaired, azotemia and electrolyte abnormalities usually normalize within 24 hours, after which surgical reduction of the bladder and hernia repair are attempted.

Strangulation

A strangulated hernia implies that the hernial contents are incarcerated and undergoing devitalization from arrested circulation. The arrested circulation may be from venous or arterial occlusion, or from 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 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 such as constriction of the blood supply at the hernial rings or from allowing organs more freedom of movement, resulting in torsion of a vascular pedicle. Organs with long, freely movable vascular pedicles (e.g., uterus, omentum, spleen, intestine, testicle) are more prone to torsion. Incarceration of a hollow viscus organ favors strangulation because increasing intraluminal pressure further obstructs venous outflow from the organ and opposes circulatory pressure. Traumatic hernias are more prone to incarceration and strangulation because organs are held within the hernia by adhesions, and the hernia ring eventually narrows from contraction during wound healing. Pleural effusions resulting from entrapped, compromised liver lobes in chronic diaphragmatic hernias are an example of this process. Decompression of ascites in humans with reducible umbilical hernias may result in rapid incarceration and strangulation. Decompression apparently reduces tension on the hernial margins, acutely narrowing the defect.

The threat of complication and death is 50% higher in human patients with incarcerated or strangulated hernias versus hernias containing reducible viable tissue. Early diagnosis and surgical correction of incarcerated hernias, therefore, is critical to prevent life-threatening sequelae relating to organ devitalization. Sequelae of hernia strangulation vary, depending on the organ involved and chronicity. Strangulated umbilical, inguinal, femoral, and prepubic hernia most often contain falciform ligament or omentum, uterus, prostatic fat, and urinary bladder, respectively [12]. The clinical course is affected by the degree of vascular compromise, volume of body fluids lost from obstruction or sequestration, and absorption of bacteria and toxins. Strangulated contaminated hollow viscus organs may result in significant blood, protein, and fluid loss, and often rupture, causing toxemia and septicemia. Bacteria migrate transmurally through devitalized intestine even before evidence of gross spillage occurs [56]. Before overt signs of infection or contamination occur, vasoactive substances such as arachidonic acid metabolites (cytokines, leukotrienes, kinins) from tissue and blood cell autolysis cause redistribution of body fluids and severe cardiopulmonary effects [57].

Strangulated viscera within external abdominal hernias (when compared with intra-abdominal strangulated viscera) are more isolated from the vascular system. Liberated vasoactive substances are not absorbed as quickly through the subcutanous tissue as the permeable peritoneal lining, and thus, external strangulated hernias may have a more delayed onset of clinical signs and shock. Initial management of patients with strangulated hernias include aggressive restoration of tissue perfusion, pain management, acid-base, and electrolyte balance, appropriate antimicrobial and shock therapy if infection and toxemia are present, and lastly, emergency surgical correction. Ventral midline celiotomy is the preferred approach to most strangulated hernias because it allows complete abdominal exploration, and the affected organ can be isolated with surgical towels to avoid further soilage of the peritoneum. Manual reduction of strangulated organs should not be attempted. 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 herniated devitalized tissue, releasing the constricting ring only after the vascular supply is occluded, may help reduce this fatal complication [2].

Conclusion

Successful management of an abdominal hernia not only requires observation of sound surgical principles (anatomic closure of the defect without tension, incorporating strong tissue with meticulous technique) but a solid understanding of the disease mechanisms reviewed in this chapter. Attempts at hernia repair without searching and correcting for the underlying cause or the pathophysiologic consequences or effects associated with organ herniation often lead to hernia recurrence, severe postoperative complications, or death [58].