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Thymoma

Thymoma is an uncommon canine and feline neoplasm of thymic epithelial cells. It is seen in various breeds but may occur more frequently in Labrador Retriever and German Shepherd Dogs. Middle-aged or older dogs (average age of 11 years) can be affected and no sex predilection exists. Affected cats are usually older than 9 years of age. A paraneoplastic syndrome of myasthenia gravis, nonthymic malignant tumors, and/or polymyositis occurs in a significant number of dogs with thymoma. Clinical signs are variable and are related to a space-occupying cranial mediastinal mass and/or manifestations of the paraneoplastic syndrome. Dyspnea is the most common presenting clinical sign. Thoracic radiographs usually show a cranial mediastinal mass. Lymphoma is the main differential diagnosis. A definitive diagnosis may be made by fine needle aspiration of the mass under ultrasound guidance or closed biopsy, but is more likely to be confirmed by thoracotomy. Thymomas may be completely contained within the thymic capsule or may spread by local invasion or metastasis. A staging system allows for an accurate prognosis and a therapeutic plan. Surgical removal of encapsulated thymomas may result in long-term survival or cure. Invasive or metastatic thymomas carry a guarded prognosis. Manifestations of the paraneoplastic syndrome complicate treatment. Adjuvant radiation and chemotherapy may be of value for advanced cases; however, adequate clinical trials have not been done in the dog or cat.

Most dogs and cats with a cranial mediastinal mass will present with signs of dyspnea, coughing, and/or exercise intolerance. Other signs may include regurgitation, vomiting, or gagging secondary to esophageal compression or paraneoplastic myasthenia gravis. Generalized myasthenia gravis may also occur with a primary complaint by the owner of recurrent weakness or collapse. Precaval syndrome (swelling of the head, neck, and/or thoracic limbs) is possible if the mediastinal mass causes compression of or invades the cranial vena cava. On physical examination, if the cranial mediastinal mass is extremely large, muffled lung sounds will be noted. While most cranial mediastinal masses are usually thymoma or lymphosarcoma, other causes may include ectopic thyroid tissue, branchial cyst, chemodectoma, or thoracic wall tumor. Lymphadenopathy due to infectious or inflammatory causes can also be found in the cranial mediastinum. Fluid within the cranial mediastinum (transudate, exudate, hemorrhage) can occasionally mimic a mediastinal mass. Hypercalcemia may occur in both thymoma and lymphoma. Non-specific azotemia secondary to pre-renal and renal causes may be found. Animals with lymphoma and liver involvement may have variable increases in serum ALP, ALT, and total bilirubin. Hyperphosphatemia can be seen with renal failure, and hypophosphatemia is usually associated with hypercalcemia of malignancy. Two or three thoracic view radiographs (ventrodorsal or dorsoventral and one or two lateral views) are the preferred way to diagnose an intrathoracic mass versus pulmonary, airway, or pleural diseases causing respiratory signs. Tracheal elevation is a consistent sign of a mediastinal mass on the lateral image. Differentiating a pulmonary or thoracic wall mass from a mediastinal mass may be done with the ventrodorsal view. The mediastinum should be twice the width of the spine in the dog. Fat in obese dogs can widen the mediastinum in the absence of a true mass. Pulmonary masses will usually be positioned lateral to the mediastinum, and thoracic wall masses will be peripheral and often cause rib lysis or spreading and cats with a cranial mediastinal mass will present with signs of dyspnea, coughing, and/or exercise intolerance. Other signs may include regurgitation, vomiting, or gagging secondary to esophageal compression or paraneoplastic myasthenia gravis.

Dogs and cats with thymoma and paraneoplastic myasthenia gravis may also exhibit signs of megaesophagus. Myasthenia gravis is an immune-mediated disorder where autoantibodies directed against nicotinic acetylcholine receptors (ACHRs) on the postsynaptic membrane of the neuromuscular junction cause abnormal neuromuscular transmission. Antibody binding to the ACHRs leads to the loss of functional receptors by complement lysis, accelerated internalization, and degradation of ACHRs; blockage of acetylcholine from the receptors; and decreased synthesis of new receptors. The lack of functional receptors impedes the transfer of the action potential from the neuron to the muscle. There are many presenting clinical signs and 3 clinical syndromes may be present:

  1. Focal MG with muscle weakness restricted to specific groups of the pharyngeal, esophageal, laryngeal, or facial muscles
  2. Generalized MG with exercise induced appendicular muscle weakness and megaesophagus
  3. Acute fulminating MG that involves a rapid onset of appendicular muscle weakness, megaesophagus, and collapse

Due to the striated musculature in the canine esophagus, megaesophagus is present in 85% of canine cases of MG. Thymoma combined with MG and megaesophagus has a poor prognosis. Aspiration pneumonia is a common complication. Dogs with acquired MG have a 1-year mortality rate of 60%, and 48% of affected dogs may die within 2 wk of being diagnosed, due to severe respiratory compromise. In a review of thymoma in dogs, 30% to 50% of dogs had MG. The link between thymic disease and MG is complex and may involve the following: general immune dysfunction and loss of self-tolerance, antigenic similarity between the proteins of the neurofilaments of the thymic myoid cells and ACHRs, expression of an ACHR by thymic myoid cells when challenged by a virus or bacterium. Myasthenia gravis associated with thymic disease in dogs is usually generalized and acute.

The definitive diagnostic test for MG is an ACHR antibody titer obtained with an immunoprecipitation radioimmunoassay. The sensitivity of this test is more than 90% and false positives have not been documented. Electromyographic (EMG) findings and the results of a tensilon response test can support a diagnosis of MG. The initial EMG is normal, but it is followed by a decremental muscular response to a sustained electric nerve stimulus. The tensilon test uses edrophonium chloride, which temporarily prevents the hydrolysis of acetylcholine at the neuromuscular junction by competing with acetylcholine. This increases the acetylcholine concentration and the probability of an action potential at the neuromuscular junction and decreased muscle weakness.

In cats, a generalized, erythematous, dermatitis with marked, multifocal crusting, and skin thickening is a not uncommon thymoma associated paraneoplastic cutaneous syndrome. This exfoliative dermatosis is characterized by multifocal plaques of inflammatory alopecia, ulceration, easily epilated coat, target lesions, and painful, contracted skin. Histopathology of these lesions is suggestive of erythema multiforme, an immune mediated disease in which lymphocyte mediated attack is directed at epidermal and follicular keratinocytes. Drug reaction, infection, and occult neoplasia are important triggers for EM. Apparently, the abnormal population of mast cells and lymphocytes associated with thymoma is the responsible mechanism by which these characteristic skin changes occur in cats.

Ultrasound of the cranial mediastinum can be useful in differentiating a cranial mediastinal mass from pleural fluid and may be helpful in determining an aspiration or biopsy site. Ultrasound of the abdomen is indicated in staging of lymphoma, to determine intra-abdominal organ involvement. Because thymomas are rarely metastatic, abdominal ultrasound is not routinely performed in these dogs, except when attempting to differentiate thymoma from lymphoma or in the case of potential intra-abdominal organ dysfunction, based on hematologic or serum chemistry profile abnormalities.

Aspiration cytology can differentiate thymoma from lymphoma in many instances. Thymomas contain mature lymphocytes, neoplastic epithelial cells, and often mast cells. Lymphomas are usually lymphoblastic with large, immature lymphocytes. A lymphocytic lymphoma or a cystic thymoma may cause cytology to be misleading, and tissue samples may be required. Cytology of pleural effusion can also be diagnostic for lymphoma if there are exfoliated lymphoblasts present.

Thymomas are invasive or non-invasive. Staging should include thoracic radiography to rule out obvious metastatic disease and further testing based on clinical signs, physical examination, or hematologic and serologic findings.

Imaging of the thoracic cavity may not indicate the invasiveness of disease, and the presence of effusions should not rule out exploratory surgery. Exploratory surgery is still the best staging procedure to determine resectability.

The treatment options for thymoma in dogs and cats include thymectomy, chemotherapy, and radiation. Thymectomy is the treatment of choice for noninvasive thymoma without megaesophagus. Dogs undergoing a thymectomy with megaesophagus have poor survival because of aspiration pneumonia, mass recurrence, and worsening of signs. A combination of chemotherapy and radiation therapy may be the most effective treatment for invasive thymoma with megaesophagus. Dogs without signs of megaesophagus that have their mass completely resected usually have prolonged survival times. Animals with megaesophagus often have very short survival times, and surgery may be contraindicated due to the morbidity and mortality associated with the procedure, usually related to aspiration pneumonia. Paraneoplastic syndromes associated with thymoma may or may not resolve with therapy and may occur later in life despite successful therapy. There have been reports of prolonged survivals in some animals with no therapy for their thymomas, which may indicate the slow-growing nature of some tumors.

As previously mentioned, surgical excision is the treatment of choice. While thymoma tends to be more invasive and difficult to resect in dogs, it is usually less invasive and easier to remove in cats. An intercostal or rib pivot approach is utilized for small masses while median sternotomy is required for removal of large masses. Non-invasive thymomas do not adhere to intrathoracic structures and are removed using a combination of careful blunt-sharp dissection. The cranial vena cava and phrenic nerves are located along the craniodorsal aspect of most cranial mediastinal masses necessitating careful dissection in this area. Invasive thymomas usually invade vital structures and therefore these animals are difficult surgical candidates, with incomplete removal being much more likely.

In a recent study involving patients where complete excision was possible (and without the utilization of adjunctive chemo or radiation therapy), the median overall survival time for the cats was 1,825 days with a 1-year survival rate of 89% and a 3-year survival rate of 74%. The median overall survival time for the dogs was 790 days with a 1-year survival rate of 64% and a 3-year survival rate of 42%. Recurrence of thymoma was observed in 2 cats and 1 dog, and a second surgery was performed in each with subsequent survival times of 5, 3, and 4 years following the first surgery. The percentage lymphocyte composition of the mass was the only factor that was significantly correlated with survival time; animals with a high percentage of lymphocytes lived significantly longer. The results of this study indicated that most cats and dogs with thymomas did well after complete excision. Even cats and dogs with invasive masses that survived the surgery and the few cats and dogs with recurrent thymomas or paraneoplastic syndromes had a good long-term outcome. For these reasons, excision should be considered an effective treatment option for dogs and cats with thymomas. Once again, as mentioned previously, radiation and/or chemotherapy may play a role in management of thymoma in dogs and cats, especially in those cases in which complete removal cannot be obtained at surgery. The lymphoid component of the thymoma may determine the completeness of the response to chemo and/or radiation therapy.


Pyometra

Pyometra is an infection of the uterus in dogs and cats. It is relatively common, affecting approximately 25% of unspayed female dogs and cats. It is a serious condition which results in a variety of clinical and pathological signs requiring emergency surgery to remove the infected uterus. While medical treatment is sometimes attempted for this condition, it is often ineffective, and can be dangerous. Although the disease has been recognized for decades, the true pathogenesis has still not been completely understood. It is generally recognized that progesterone and estrogen and their receptors have a role in the development of pyometra; however, the infection is triggered by bacterial involvement. The cyclical hormonal influences of the female allow the uterus to go through changes that will be acceptable for fertilization of an embryo. If bacteria are introduced into the uterus at a certain time during the cycle, hormonal regulation of the uterus allows the infection to start and become fulminate. If bacteria enter the uterus at the times when the protective physical barriers are breached, such as estrus, parturition, or immediately after parturition, the normal uterine defense mechanisms are likely to eliminate these bacteria. However, the hormonal influences may not allow the body to clear the bacteria. The bacteria typically cultured from the pyometra are bacteria that would be found in the areas of the intestines and vagina (E coli is the most common). Therefore, many of the infections are considered either from an ascending infection from the vagina, a concurrent urinary tract infection or fecal contamination. Certain bacteria are more virulent than others and therefore allow a bacterium that is normally found on the dog to develop into an infection. Pyometra is most commonly seen in intact dogs 4-8 weeks after estrus (mean time of 5.4 weeks); however, it can be seen 4 months post estrus as well. Although seen less commonly, cats generally develop pyometra between 1-4 weeks after estrous. Pyometra generally occurs in older (7 to 8 years) intact bitches and queens; however, it may occur in younger animals that have been given estrogen (mis-mating shots) or progestins for estrus suppression.

If pyometra is allowed to continue untreated for a significant period of time, it can affect the entire body, leading to critical disease, shock and death. Because the infection can be so overwhelming, the reasons for presentation are not limited to the genital tract. The animal can become so overwhelmed by the inflammation associated with the infection that the animal may die from its own uncontrolled inflammatory process. A dog with an open pyometra (the cervix is open) will often have vaginal discharge, which can look like blood, pus or mucus. Many dogs and cats will have a closed cervix and therefore the obvious sign of a bloody to mucopurulent, hemorrhagic vaginal discharge may not be present. Furthermore, many dogs will clean themselves, removing any trace of vaginal discharge before it is visible to an owner which makes detection more difficult. The most common clinical signs that are present in greater than 50% of cases include lethargy, depression, anorexia, fever, excessive water intake and excessive urination. Pale mucous membranes, vomiting, diarrhea, weight loss, abdominal distension, and inflamed eyes have been reported although much less frequently. Up to 16% of patients may have no clinical signs other than purulent vaginal discharge. It is the bacterial infection of the uterus which causes increasing inflammation within the organ and leads to the systemic effects observed in the majority of patients. The severity of the resulting illness is greatly influenced by the degree of drainage from the uterus. If the cervix is closed, then fluids and toxins accumulate, with potential for toxic effects. Rupture or slow leakage from one of the uterine horns can release inflammatory products into the abdominal cavity, causing peritonitis. If the cervix is patent, or open, then drainage limits the accumulation of inflammatory products and bacterial toxins, and increases the likelihood of early recognition of the problem. The clinical signs of increased thirst and urination have been linked to the direct influence of bacterial toxins on the kidneys’ urine concentrating mechanisms. Bacterial infection and toxins may cause secondary damage to the liver as well. Endotoxic shock alters blood supply to all tissues and can disrupt normal blood clotting mechanisms. Microscopic blood clots or clumps of circulating bacteria can further impact upon the blood supply to vital organs such as the heart and brain, permitting seizures, cardiac rhythm disturbances and other grave consequences. The most life threatening complications associated with pyometra are sepsis and systemic inflammatory response syndrome (SIRS) /multiple organ dysfunction syndrome (MODS). If an unspayed female dog or cat is exhibiting any of these symptoms, they should be evaluated immediately.

Diagnosis is based in part on the history, reproductive status, and clinical signs. Physical examination of the pyometra patient reveals abdominal distention, an enlarged, palpable uterus, vaginal discharge if the cervix is open, and lethargy. A closed-cervix pyometra more likely will result in the animal showing signs of septicemia, including shock, hypothermia, dehydration, vomiting, and collapse. Laboratory testing and imaging are frequently used to aid in the diagnosis. A complete general chemistry profile, complete blood count, urinalysis, abdominal radiographs, abdominal ultrasound and perhaps vaginal cytology analysis are performed in suspected pyometra cases. The dog’s complete blood count, or CBC, is influenced by the degree of drainage from the uterus. Patients with a closed cervix and limited uterine drainage are more likely to show significant elevations of or reductions in, the white blood cell count. The white blood cells are also more likely to appear immature or unhealthy in those patients. Red blood cell counts are often reduced; patients with chronic disease frequently have low-grade anemia. Dehydration can mask this feature by reducing the amount of water in the bloodstream; consequently, the red blood count appears higher than it really is. Blood urea nitrogen, or BUN, and creatinine reflect blood flow to the kidneys. The level of these nitrogenous waste products in the blood will frequently rise with dehydration and kidney dysfunction, which are common in patients with pyometra. Elevated blood protein levels and disturbed electrolytes will often reflect the state of dehydration. The urine may be very dilute, reflecting toxic influences on the kidneys, or well concentrated as an appropriate response to dehydration. The urine may contain bacteria or inflammatory cells, if collected after voiding, due to contamination by the vaginal discharge. If pyometra is suspected, urine samples are rarely collected directly from the urinary bladder, via needle aspiration, because of worries about perforation of the distended, fluid-filled uterus. Urinary protein levels may be elevated if the kidneys have been damaged by the presence of chronic infection The vaginal discharge can be examined microscopically for the presence of white blood cells and bacteria. Diagnostic x-rays of the abdominal cavity may demonstrate a fluid-dense tubular structure. A ground-glass appearance on the x-ray may suggest fluid accumulation around the diseased uterus if leakage has contributed to peritonitis. Ultrasound imaging will help to detect or verify the uterine enlargement and to define uterine size and wall thickness.

Pyometra necessitates immediate medical and surgical therapy. Those patients with a closed cervix may be more ill at the time of diagnosis. Intravenous fluids and antibiotics are routinely administered to patients that are severely ill, irrespective of the patency of the cervix. Potent antibiotics are given by injection, in combinations to target the most common bacterial pathogens. Supportive measures are customized for individual patient needs, according to the levels of shock, dehydration, electrolyte imbalance, organ dysfunction or cardiac arrhythmia. The patient is stabilized medically, if possible, to prepare for emergency ovariohysterectomy, or spay, to remove the infected uterus and the ovaries from the abdominal cavity. The prognosis with ovariohysterectomy can be as high as 90-100% if abdominal contamination is avoided during surgical intervention and shock/sepsis is managed appropriately perioperatively. It should be mentioned that a pyometra spay is considerably more challenging than a routine spay. Special care has to be taken so that the infected, dilated, friable and easily breakable uterus does not rupture and spill its toxic contents into the sterile abdomen. If severe sepsis and organ failure develops, the prognosis can be grave. Some patients may remain PU/PD (increased urination and water intake) and in a state of permanent kidney damage. Although surgery is considered the therapy of choice, very special case selection meeting certain criteria may allow valuable breeding bitches to be treated medically. Stable patients may be given prostaglandin f2-alpha by injection for several consecutive days to dilate the cervix, stimulate uterine contractions and to decrease the blood progesterone level. The dog must remain hospitalized for observation, monitoring for side effects of the prostaglandin or for worsening condition, and for continued antibiotic administration. Clinical improvement may be expected within the first 48-96 hours of medical treatment. Surgery should be considered for patients that deteriorate. If purulent vaginal discharge persists seven days after conclusion of treatment, or if other parameters indicate ongoing infection or uterine enlargement, then repeating the treatment may be advised, provided that the patient remains physiologically stable. Dogs are susceptible to developing pyometra again after medical treatment; the recurrence rate is as high as 80%. In addition, the chance of successful subsequent breeding after medical management of pyometra is approximately 50:50. Because of the high rate of recurrence and diminished breeding capacity, even those dogs that have been successfully managed medically should receive an ovariohysterectomy when their breeding purposes are finished.

The majority of patients are released two to three days following an uncomplicated surgical procedure. Antibiotic therapy and pain management are continued for seven to 10 days after most procedures. It should be emphasized that pyometra is extremely easy to prevent. An appropriately performed spay procedure between 6 months and one year of age will prevent the development of pyometra. However, an inappropriately performed spay in which a portion of the ovarian tissue, uterine body or horn is not removed may result in what is called uterine stump pyometra. Ultrasound imaging is especially helpful in detecting stump pyometra. Surgical removal of the infected remnant is usually curative. In conclusion, an elective spay procedure of the young dog or cat will virtually eliminate the possibility of pyometra from ever developing in the overwhelming majority of pets. Clearly, hormone administration for mismating events and estrus suppression should be avoided except for the absolute necessities, as avoidance of estrogen or progesterone administration will decrease the risk of pyometra in both young and mature pets. When pyometra does occur, the combination of aggressive and prompt medical and surgical intervention is successful in almost all cases.


Medical and Surgical Treatment of Diaphragmatic Hernia in Dog and Cat

The diaphragm is the muscular separation between the chest and abdominal cavities that functions as a barrier and aids in respiration. Diaphragmatic hernia is a disruption of the diaphragm which allows abdominal organs to migrate into the chest cavity. Almost exclusively the result of blunt trauma to the abdomen, acquired or traumatic diaphragmatic hernia is a common injury in companion animals, with motor vehicle accidents being responsible for 85% of cases documented in one study. A rapid rise in intra-abdominal pressure following a forceful blow and failure of the epiglottis to remain closed, allowing the stabilizing effect of the air filled lungs to be lost acutely, is the classic explanation for diaphragmatic rupture. While diaphragmatic hernia can occur in any dog or cat, as most dogs and cats that suffer diaphragmatic hernias have been hit by a car or have experienced some other type of trauma, most dogs are young intact males, and most affected cats spend time outdoors. In most cases, acute diaphragmatic hernia results in significant respiratory difficulty. The trauma which caused the hernia may also result in rib fractures, lung lacerations, and lung bruising. These injuries may lead to pneumothorax, or hemothorax. If abdominal contents have entered the chest cavity, this can further compromise the ability to expand the lungs. If the initial insult is tolerated, a diaphragmatic hernia may be diagnosed later as an incidental finding in a relatively asymptomatic animal. For these reasons, the clinical signs of diaphragmatic hernia vary from none to severe respiratory compromise and shock. As mentioned previously, 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. Cardiac arrhythmias are present in approximately 12% of small animals with diaphragmatic hernia. Other common clinical signs include muffled heart and lung sounds, thoracic borborygmi, and evidence of trauma, such as abrasions. Chronically, abdominal organs, such as the liver or intestines can become adhered in the chest cavity and the animal may exhibit signs associated with liver or gastrointestinal disease such as vomiting or anorexia.

It is important to remember that loss of continuity of the diaphragm does not necessarily result in severe respiratory distress. The cause of respiratory impairment associated with diaphragmatic hernia is multifactorial. Hypovolemic shock, chest wall trauma, pleural fluid or air, pulmonary contusions, and cardiac dysfunction are factors that contribute to hypoventilation. Other injuries such as rib fractures or flail chest may compound mechanical dysfunction. Pulmonary compliance is decreased by pleural fluid, the presence of abdominal organs in the thorax, or pneumothorax. Pulmonary hemorrhage, edema, and atelectasis reduce total lung capacity and functional residual capacity. Myocardial contusion often accompanies other traumatic injuries and may decrease cardiac output. When myocardial injury is concomitant with impaired ventilation tissue hypoxia can result. Pain resulting from chest and abdominal contusion and accompanying injuries causes voluntary restriction of motion (thoracic excursion) and may therefore further compromise ventilatory capability.

Chest radiographs must be taken to diagnose the disease, and to look for any other abnormalities. In the normal animal, a diaphragmatic line, a cardiac silhouette, and air-filled lung fields are appreciated on chest radiographs. In the case of diaphragmatic hernia, loss of the diaphragmatic line, loss of the cardiac silhouette, displacement of lung fields, and presence of abdominal contents within the chest cavity may be noted on chest radiographs. Most cases of diaphragmatic hernia can be diagnosed from radiographs. However, fluid in the chest cavity can obscure the diaphragmatic line in the absence of a hernia. Repeating chest radiographs after thoracocentesis is advisable but may not definitively show a diaphragmatic hernia. In this case, ultrasound may be helpful to differentiate abdominal organs from pleural fluid. 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. Ultrasound may identify abdominal organs, differentiate organs such as the spleen or liver from pleural fluid, and will sometimes identify the defect in the diaphragm. Contrast radiography, performed by injecting contrast material into the abdominal cavity, and MRI or CT evaluation may also be helpful.

Initial stabilization of diaphragmatic hernia patients consists of medical therapy for shock and respiratory distress, possible antimicrobial utilization and close observation. Adequate volume replacement is the best therapy for hypovolemic shock. However, volume overload can be as detrimental as hypovolemia, particularly in patients with traumatic diaphragmatic hernias because concurrent pathology such as atelectasis, pulmonary contusions, and physical compression of the lungs by fluid or organ entrapment predisposes patients to pulmonary edema. The resuscitation fluid of choice is the subject of much debate. Isotonic crystalloids have long been the mainstay of volume replacement in treating hypovolemic shock and probably remain the recommended fluid for initiating therapy; however, hypertonic saline, colloids, and combinations of these fluids offer many potential advantages in trauma patients, including effective low-volume resuscitation and less expansion of the interstitial space compared with traditional isotonic fluid therapy. Volume and speed of fluid replacement are dictated by cardiovascular parameters such as capillary refill time, pulse quality, mucous membrane color, and central venous pressure, as well as respiratory parameters such as ventilatory rate, auscultatory findings, and pulse oximetry.

Signs such as dyspnea, cyanosis, tachypnea, tachycardia, reduced mentation, and postural changes such as an “oxygen hungry” stance (i.e., abducted elbows, extended head and neck, and open-mouthed breathing) are suggestive of hypoxia and should be treated quickly. Various modes of oxygen delivery are available . The actual method chosen depends on a number of factors, including patient size and temperament, available equipment and desired level of oxygen to be delivered. In patients with marked shunting, delivery of even 100% oxygen does little to correct arterial hypoxemia because shunted blood is never exposed to the higher alveolar oxygen tensions and therefore continues to depress PaO2 while the blood perfusing ventilated alveoli is already almost fully saturated and improves only minimally with exposure to 100% oxygen. However, some elevation of arterial oxygen content occurs (mainly in the form of increased dissolved oxygen), making oxygen therapy a useful aid in immediately treating dyspneic patients with traumatic diaphragmatic hernias.

Removal of pleural effusion may also improve ventilation in selected cases. Antimicrobials may be used during the preoperative period to prevent infection-related pulmonary problems. Every patient with traumatic diaphragmatic hernia needs close observation, since rapid changes in ventilatory function may occur. Patients failing to respond adequately to pre-surgical management or rapidly deteriorate despite appropriate management should be taken to surgery as soon as possible.

The timing of anesthesia and surgical correction of diaphragmatic injury may have an important effect on the outcome of treatment. Approximately 15% of small animals with diaphragmatic hernia will die prior to surgery, and animals with diaphragmatic herniorrhaphy performed within the first 24 hours after injury have the highest mortality rate (33%). The timing of surgical repair depends upon the extent of the initial cardiopulmonary dysfunction, the presence or absence of organ entrapment, the degree of compromised pulmonary function, and whether or not the animal’s condition is improving, stable, or deteriorating. Diaphragmatic herniorrhaphy may require immediate surgery if aggressive supportive care cannot stabilize respiratory function. Acute dilatation of a herniated stomach or strangulated bowel are examples of situations where emergency surgery may be indicated. A herniated stomach can rapidly distend from aerophagia, decreasing pulmonary compliance and compress the caudal vena cava decreasing venous return resulting in a vicious cycle that can be rapidly fatal. A herniated parenchymal organ such as the spleen may tear as it passes through the diaphragm causing 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, therefore the presence of a diaphragmatic hernia, on its own, is not indication for emergency surgery. Accompanying thoracic injuries such as pulmonary contusion will improve dramatically in 24 to 48 hours. The goal of initial management is to improve the cardiorespiratory status of the patient to improve their capability of tolerating the stress of anesthesia and surgery.

Induction of anesthesia in the diaphragmatic hernia patient is done with as little stress as possible and with the goal of quick control of ventilation. Intravenous catheterization, appropriate intravenous fluid administration (crystalloid or colloid) and cardiorespiratory monitoring are important. Propofol is preferred because it allows rapid induction of anesthesia, quick intubation, and near immediate control of ventilation with assistance or by a mechanical ventilator. Isoflurane is preferred for maintenance of anesthesia because a surgical plane of anesthesia is attained more quickly, it is associated with decreased recovery time, subjects the patient to less cardiac depression, and does not sensitize the myocardium to arrhythmias. Assisted ventilation is required soon after induction because the patient usually has decreased pulmonary compliance secondary to the presence of air, fluid, or abdominal viscera within the pleural space. Inspiratory pressure should not exceed 20 cmH2O to limit potential barotrauma from pulmonary hyperinflation which may result in over-inflation of the lungs during surgery. Rupture of pulmonary parenchyma, intrapulmonary hemorrhage, plumonary edema, and rarely pneumothorax may result. Resolution of atelectic areas in chronically atelectic lungs during surgery may subject the lung to mechanical and reperfusion injury. Damage from reperfusion in the collapsed vascular channels may disrupt capillary integrity causing fluid to leak into the interstitium resulting in reexpansion pulmonary edema within several hours after surgery. Reexpansion of atelectic areas that will not inflate with 20 cm H2O will gradually re-expand over several hours with a continual negative pleural pressure of 10 cm H2O.

The preferred surgical approach is a ventral midline celiotomy, extending from the xiphoid process to a point caudal to the umbilicus. This exposure allows access to all regions of the diaphragm. The incision should be large enough to allow exploration of the abdominal cavity because injury to other abdominal organs may be present and treatable concomitantly. Most diaphragmatic tears are muscular and are located ventrally and may favor either the right or left side. The liver, small intestine and pancreas are most commonly prolopsed 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. It is essential to examine the entire diaphragm because more than one tear may occur. Should additional exposure be required to retrieve abdominal viscera adhered to structures within the thoracic cavity, surgical exposure can be improved by enlarging the rent in the diaphragm, paracostal extension of the celiotomy, and by caudal midline sternotomy. Visibility of the diaphragmatic defect is enhanced by placing a pediatric Balfour retractor over the towel-protected abdominal incision. Abdominal or pleural fluid is removed by suction. The abdominal viscera are carefully retracted from the thorax using gentle traction. Final, definitive positioning of the viscera is delayed until the diaphragmatic defect is closed. Inspection of the lungs and pleural cavity is usually performed after the herniated contents have been retrieved from the pleural cavity. Closure of the diaphragm is achieved with either absorbable or nonabsorbable suture material, in a simple-interrupted or simple-continuous pattern. The least accessible part of the defect is closed first, taking care to avoid traumatizing the aorta, caudal vena cava, hepatic veins or esophagus. On closure of the diaphragmatic defect, residual air is removed from the pleural cavity either by thoracentesis performed through the diaphragm using a 20 gauge catheter, three-way stop-cock, and 35 ml syringe or by placing a thoracostomy tube. Exploration of the abdomen, with particular attention given to the previously displaced tissues, is performed. Any lesions requiring attention are repaired. Closure of the abdomen is achieved after definitive replacement of the abdominal viscera.

Postoperative considerations for the patient with a repaired diaphragmatic hernia include ventilatory support, analgesic administration, and close observation. Ventilatory support is continued until the patient is adequately ventilating spontaneously. Particular care is necessary when administering positive pressure ventilation during and after surgery, since trauma to the lungs from overzealous ventilation is a definite possibility. Re-expansion pulmonary edema following re-oxygenation of chronically collapsed lungs is a major cause of perioperative death, particularly in animals with long-standing diaphragmatic hernias. Reperfusion injury, with release of superoxide radicals which cannot be effectively scavenged, is thought to result in increased pulmonary capillary permeability and pulmonary edema. Spontaneous ventilation in the postoperative patient is assisted by maintaining the patient in a forequarters-elevated position and the appropriate use of analgesics. Analgesic administration is done to comfort the patient and to ease apprehension during recovery.

The prognosis for animals presenting with a traumatic diaphragmatic hernia is variable depending on other injuries incurred. Of the patients that survive to presentation, the timing of surgery will significantly affect prognosis. Animals that have surgery greater than 24 hours after trauma have a lower mortality rate than those having surgery within the first 24 hours owing to resolution of shock after appropriate medical stabilization. The proper utilization of medical stabilization followed by surgical intervention results in an overall success rate of over 90%. The most common complication following surgical intervention is the development or persistence of pneumothorax. While complications can occur in the immediate postoperative period, most are transient and self limiting and will resolve with conservative therapy.


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