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Chapter 17 · Surgery of the diaphragm



                  the diameter of the hiatus is reduced too much, or if a fund -   cranial displacement of the liver or caudal displacement of
                  oplication procedure is performed. Iatrogenic pneumo -   the  developing  lung  bud  into  the  canal  may  prevent  its
        VetBooks.ir  ligament and adequate measures for controlled ventilation   may fail to guide the posthepatic mesenchymal plate to
                                                                       closure. Alternatively, atrophy of the developing lung bud
                  thorax may follow disruption of the phrenico-oesophageal
                                                                       fusion (Mann et al., 1991). The facts that the left lung bud
                  and pleural drainage should be available.
                     Continued regurgitation or vomiting may be due to
                                                                       that pleuroperitoneal hernias develop predominantly on
                  unresolved oesophageal motility disorders, continuing   develops more slowly than the right in many species and
                  gastro-oesophageal reflux, unresolved oesophagitis, mega -   the left side appear to support the latter hypothesis (Mann
                  oesophagus and gastric hypomotility. Gastric hypomo tility   et al., 1991).
                  may be caused by iatrogenic trauma to the ventral vagus
                  trunk or may be part of generalized gastrointestinal  tract   Pathophysiology:  The pathophysiological events in
                  hypomotility (Prymak et al., 1989; Callan et al., 1993).  animals with sufficiently large defects are similar to those
                                                                       in animals with traumatic diaphragmatic rupture, with dis-
                  Prognosis: Surgical management of hiatal hernia using   placement and compression of the thoracic viscera by
                  sphincter-enhancing techniques has a high rate of failure   abdominal organs and, less commonly, incarceration of
                  and frequent complications (Merdan Dhein  et al., 1980;   abdominal viscera in the thorax. Animals may be dead at
                  Ellison et al., 1987). Operative mortality can be high, up to   birth or die soon after with cyanosis and dyspnoea
                  64% (Ellison et al., 1987), and success rates are not con-  because of an inability to expand the lungs. Organs that
                  sistently high; for example, in one study only 25% of    commonly herniate include the stomach, liver, spleen,
                  animals were relieved of all clinical signs (Ellison  et al.,   duodenum and pancreas (Feldman et al., 1968). Hernias
                  1987). However, if surgical closure of the hiatus and fixa-  formed by incomplete muscular invasion of the pleuro-
                  tion of abdominal organs is performed, and if care is taken   peritoneal folds have a hernial sac that limits the extent of
                  to identify and correct predisposing conditions, then the   herniated organs, compared with hernias formed by
                  prognosis is good (Burnie et al., 1989; Prymak et al., 1989;   incomplete closure of the pleuroperitoneal canals.
                  Bright  et al., 1990; White, 1993; Hardie  et al., 1998;
                  Lorinson and Bright, 1998).                          Diagnosis: Puppies or kittens may be born dead or may
                                                                       exhibit severe dyspnoea and cyanosis. Less severely
                                                                       affected animals may show mild dyspnoea and abdominal
                  Pleuroperitoneal hernia
                                                                       breathing  (Feldman  et  al.,  1968; Mann  et  al.,  1991) or  no
                  Anatomy and incidence: This is the least common of the   clinical signs (Voges et al., 1997).
                  congenital diaphragmatic hernias. A  defect is  present  in   Radiography reveals a soft tissue opacity at the cranial
                  the dorsolateral diaphragm, which may range from a lack   extent of the diaphragm (Figure 17.10), which may mimic a
                  of the intermediate part of the left lumbar muscle of the   mass lesion affecting the diaphragm, lung lobes or pleura.
                  crus to absence of both crura and a portion of the central   Ultrasonographic examination may reveal an abnormally
                  tendon (Feldman et al., 1968; Valentine et al., 1988). These   thin diaphragm with a hernial defect and abdominal organs
                  defects do not involve the pericardial sac.          passing cranial to the diaphragm (Mann et al., 1991).
                                                                          Differentiating a pleuroperitoneal hernia from a rup-
                  Aetiology:  Two aetiologies for these hernias are sug-  tured diaphragm may be difficult if there is no history of
                  gested, which explain their dorsolateral location:   trauma. This differentiation is relatively simple for com-
                                                                       plete tears of the diaphragm. However, this may be diffi-
                  •  Incomplete closure of the pleuroperitoneal canals: the   cult in the case of a subtotal diaphragmatic tear, in which
                     pleuroperitoneal folds and posthepatic mesenchymal   there is a traumatically induced rent in the musculotendi-
                     plate fail to fuse with the septum transversum and   nous portion of the diaphragm, but the parietal pleura on
                     dorsal mesentery of the oesophagus, and an opening   the thoracic surface of the diaphragm remains intact
                     (foramen of Bochdalek) persists between the thoracic   (Voges et al., 1997). This is sometimes referred to as even-
                     and abdominal cavities (Feldman et al., 1968; Valentine   tration of the diaphragm. In this situation, the abdominal
                     et al., 1988)                                     organs are bounded by a membrane that mimics the
                  •  Failure of the pleuroperitoneal folds to incorporate   hernial sac of the true pleuroperitoneal hernia, although
                     muscular components of the body wall: the         this membrane may be difficult to recognize.
                     pleuroperitoneal canals are closed, but myoblasts from   Criteria used to help differentiate a congenital pleuro-
                     the posthepatic mesenchymal plate and abdominal   peritoneal hernia from a ruptured diaphragm are shown in
                     wall fail to invade this tissue and the lumbar portion of   Figure 17.11.
                     the diaphragm remains membranous rather than
                     muscular, and acts as a hernial sac. This type is   Treatment:  Surgical closure of the hernia may be pos-
                     referred to as a true pleuroperitoneal hernia (Mann et   sible, depending on the size of the defect. However, in
                     al., 1991; Voges et al., 1997).                   those animals that survive beyond birth, the  hernia is
                                                                       likely to be relatively small and bounded by a hernial sac.
                     On the basis of finding the defect in litters from   Herniorrhaphy is performed in a similar manner to that
                  repeated matings, an autosomal recessive mode of inherit-  for a ruptured diaphragm (see below), although the pres-
                  ance has been proposed in the dog (Feldman et al., 1968;   ence of the intact pleuroperitoneal membrane in most
                  Valentine et al., 1988). In humans, the left side of the dia-  cases means that there is no direct continuity between
                  phragm is also more commonly affected and an autosomal   the thoracic and abdominal cavities and intraoperative
                  mode of inheritance is also suspected. These hernias have   pneumothorax will not occur unless this membrane is
                  also been induced by exposure to various teratogens,   incised or is absent.
                  such as thalidomide and polybrominated biphenyls, as
                  well as by vitamin A deficiency (Mann et al., 1991).  Postoperative care and complications: Postoperative
                     Failure of the pleuroperitoneal membranes to close   recovery is usually uncomplicated. Complications have not
                  may be caused by interference by viscera. For instance,   been reported.


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