Page 230 - BSAVA Manual of Canine and Feline Head, Neck and Thoracic Surgery, 2nd Edition

Chapter 17 · Surgery of the diaphragm

Pathophysiology: Which abdominal organs become dis- • Filling of the pleural space with air, fluid or abdominal
viscera
placed into the thoracic cavity is dependent upon their • Pulmonary contusions
VetBooks.ir Therefore, one or more lobes of the liver are most com- • Pain associated with normal respiratory movements,
proximity to the diaphragmatic defect and their mobility.
e.g. in animals with fractured ribs.
monly displaced, being found in the thoracic cavity in
approximately 88% of patients with a ruptured diaphragm
(Wilson and Hayes, 1986; Boudrieau and Muir, 1987). Systemic pathophysiological changes: The inciting trauma
Other organs that can be displaced into the thoracic cavity may also result in circulatory shock, which may be:
following a diaghramatic rupture, in approximate descend-
ing order of frequency, include the small intestine, • Hypovolaemic, e.g. from bleeding externally or
stomach, spleen, omentum, pancreas, colon, caecum internally into the pleural or peritoneal space
and uterus (Garson et al., 1980; Stokhof, 1986; Wilson and • Cardiogenic, e.g. from myocardial contusions, or
Hayes, 1986). When the right side of the diaphragm tears, release of depressant factors from the hypoxic
the liver, small intestine and pancreas herniate, whereas in pancreas if herniated
left-sided tears, herniation of the stomach, spleen and • Obstructive, e.g. from obstruction of the hepatic veins
small intestine is more common (Garson et al., 1980). following herniation of the liver
Gastric tympany may occur following herniation of • Endotoxic, e.g. from liberation of toxins from bacteria
the stomach; as the stomach expands it compresses the proliferating in devitalized herniated organs (e.g.
lungs, the heart and venae cavae, reducing alveolar venti- intestine, liver).
lation and cardiac output. These events can be rapidly
fatal, and emergency gastric decompression by orogastric Cardiac arrhythmias are present in approximately 12%
intubation or transthoracic needle gastrocentesis should of patients with a ruptured diaphragm, which may reduce
be performed. Obstruction of the small intestine may be tissue perfusion and exacerbate the shock caused by other
partial or complete and may affect the proximal or distal pathophysiological changes (Boudrieau and Muir, 1987).
small intestine. Strangulating obstruction may lead to Shock may continue as multiple organ system failure. In
ischaemic necrosis, intestinal perforation and abscess- particular, pulmonary function, which is already compro-
ation, peritonitis and pleuritis. Although these complica- mised, may deteriorate further, with an increase in pulmo-
tions are not as immediately life-threatening as gastric nary vascular permeability and pulmonary oedema.
dilatation, corrective surgical therapy should not be Patients with diaphragmatic rupture are often on the
delayed once the animal is stable. Treatment of such edge of fatal cardiopulmonary decompensation and a great
patients is very demanding. deal of care is required in their management. Fre quently,
Displacement of the liver lobes may result in intra- these patients benefit from 24–48 hours of stabilization prior
hepatic venous hypertension and cause effusion from the to surgical therapy of the diaphragmatic injury. Exceptions
liver surface. Hydrothorax and ascites develop in approxi- to this rule include those with intra thoracic gastric tympany
mately 30% of animals with herniation of the liver (Wilson and intestinal entrapment causing obstruction of the bowel.
et al., 1971; Boudrieau and Muir, 1987).
Pleural effusion is generally from entrapped liver lobes, Diagnosis: The time interval between trauma and diag-
but may also derive from other organs (e.g. lung lobe nosis of diaphragmatic rupture ranges from several hours
torsion). Effusion is typically, therefore, a modified transu- to several years, with a mean of several weeks in published
date, but haemothorax, chylothorax or bile pleuritis are studies (Garson et al., 1980; Stokhof, 1986; Boudrieau and
also occasionally seen. Muir, 1987). In one report, 20% of cases were diagnosed
Proliferation of bacteria normally resident in the liver, more than 4 weeks after the injury (Boudrieau and Muir,
such as clostridia, may occur in areas of liver with a poor 1987). The time interval from the traumatic incident to
vascular supply. These organisms may release toxins diagnosis may depend on whether or not the trauma was
whilst the lobe is malpositioned or once the lobe has been observed, the size and nature of the hernia, the clinical
surgically repositioned. A potential long-term sequelae is signs shown and the degree of investigation performed.
abscessation of the liver. Any animal with a known history of trauma, or with
Effects on thoracic viscera are caused by compres- injuries consistent with a traumatic aetiology, should be
sion or displacement resulting from the presence of considered at risk for diaphragmatic rupture. It is prudent,
abdominal organs, fluid or air in the pleural space. Effects therefore, to evaluate these animals carefully for the pres-
i
on abdom nal viscera include obstruction or stran gu- ence of thoracic (and abdominal) disease. These investiga-
lation, Incarceration or strangulation may be caused by tions should include thoracic and abdominal imaging,
pressure applied by the edge of the diaphragmatic tear when the patient is stable. This approach will facilitate
as the organs pass over it, or may be the result of fibrous early diagnosis and treatment of diaphragmatic rupture in
adhesions. particular. Failure to evaluate the patient for the results of
Filling of the pleural space with air, fluid or abdominal thoracic and abdominal trauma often results in a delayed
organs will prevent normal coupling between movements diagnosis and makes surgical therapy more complicated.
of the chest wall and the lungs, resulting in inefficient It is hypothesized that some individuals may be
breathing movements. Furthermore, compression of the presented with a diaphragmatic tear and either subtle or
lung lobes may lead to atelectasis with resulting hypoventi- no herniation of viscera. Diaphragmatic rupture in these
lation, ventilation/perfusion mismatching and hypoxia. animals may go unnoticed during initial radiographic evalu-
Dyspnoea is the most common clinical sign following ation. Herniation subsequently develops or worsens over
acute traumatic rupture of the diaphragm and may be the next few days, particularly if the animal is subjected to
due to: sedation, anaesthesia or manipulation for other injuries
sustained at the time of trauma. The clinician should there-
• Lack of a functioning diaphragm fore remain open to the diagnosis of diaphragmatic
• Trauma to other accessory components of respiration, rupture, even in a patient that apparently had normal
e.g. intercostal muscles and ribs thoracic radiographs shortly after trauma.

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