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Diaphragmatic Hernias
191
pulmonary hypoplasia in CDH; therefore, it was not possible to determine which neonates
would otherwise not survive. Although there are no randomized controlled studies that have
demonstrated the efficacy of ECMO in infants with CDH, ECMO, if available, should be
considered for almost all infants that cannot be managed with conventional therapy.
In early experience of patients with CDH, ECMO was used when instability developed
after an early repair. With the advent of delayed repair in the mid-1980s, stabilization of the
severely hypoxic infant became possible [Hazebroek et al., 1988; Langer et al., 1988; Goh et
al., 1992; Nio et al., 1994]. ECMO is now performed before, during, or after repair of CDH.
In particular, the use of ECMO preoperatively is advocated as a means to support the patient
until the reactive component of pulmonary hypertension resolves, which may take weeks.
The prime indication for ECMO is failure of conventional therapy [Frenckner et al.,
1997; Wilson et al., 1997; Downard et al., 2003]. We use the following criteria:
Inability to maintain preductal saturations >85% or postductal PaO
2
>30 mm Hg
Peak inspiratory pressure >28 cm H
2
O or mean airway pressure >15 cm H
2
O
Hypotension that is resistant to fluid and inotropic support
Inadequate oxygen delivery with persistent metabolic acidosis
Traditional inclusion criteria also include all of the following [Lally, 1996]:
Birth weight >2 kg
Gestational age >34 weeks
Absence of intracranial hemorrhage >grade I
Absence of other congenital or chromosomal anomalies
Exclusionary criteria for ECMO vary between institutions. Most ECMO centers exclude
patients with lethal chromosomal abnormalities, severe prematurity, pre-existing sepsis or
severe intracranial hemorrhage. However, there have been reports of patients with cardiac
disease, low-grade intracranial hemorrhage, and prematurity who have been placed on ECMO
and survived [Van Meurs et al., 1990; Breaux et al., 1992; Ryan et al., 1994]. Complications
of ECMO include intracranial bleeding (primarily seen in premature infants), bleeding from
the surgical site, sepsis and neurological impairment. Bleeding complications may be
minimized by the use of aminocaproid acid or tranexamic acid and by minimized dissection
during repair.
It is difficult to accurately assess the benefit of ECMO given the absence of clinical trials.
Survival data on 3100 patients from the CDH Study Group demonstrated a 49% survival rate
for patients managed with ECMO compared to the overall survival rate of 67%
[Seetharamaiah et al., 2009]. Of the patients who underwent ECMO and surgical repair, the
survival rate increased to 61%, which most likely excluded the most severely ill patients who
were too ill for surgical intervention. The highest survival rate (75%) occurred in those
patients who did not require ECMO, who presumably had less severe illness.
Surgical Repair
Surgical repair consists of reduction of the abdominal viscera and primary closure of the
diaphragmatic defect. Most surgeons use a subcostal incision for repair of the diaphragmatic
Ivan Martinez Serna and Antonio Pablo Gamez Garcia
192
hernia. Usually there exists a small posterior lip or rim of diaphragm, which must be
mobilized by dividing the overlying peritoneum. The edges of the diaphragm are then
approximated with a nonabsorbable suture material.
The diaphragmatic defect may be repaired with suture alone, but if the defect is too large
or if the suture is under great tension, a prosthetic patch can be used to repair the defect.
[Lally et al., 1993; Tsai et al., 2012]. If the abdominal wall is difficult to close following
hernia reduction, the use of a temporary abdominal wall silo or patch may be helpful
[Schnitzer et al., 1995].
Timing of Surgery
The classic standard approach to surgical repair of the critically ill infant with CDH was
surgery immediately following diagnosis. This was based on the belief that the intrathoracic
viscera were causing acute decompensation since pressure, and surgical reduction of the
hernia would permit lung expansion. It has now become clear, however, that the major cause
of early death in these children is pulmonary hypoplasia, not acute pressure from the
intrathoracic viscera. Emergency repair of the hernia is associated with worsening pulmonary
compliance which can be avoided by a period of preoperative stabilization [Nakayama et al.,
1991]. Clinical studies have demonstrated that survival rates are as high or higher with
preoperative stabilization than with emergency repair [Hazebroek et al., 1988; Langer et al.,
1988; Roberts et al., 1994; de la Hunt et al., 1996] and many centers have now moved toward
initial stabilization with surgery delayed for at least 24 hours and even several weeks in some
cases [Reickert et al., 1996]. Survival rates in newborns with CDH managed with pre-
operative stabilization and selective use of ECMO followed by delayed surgical correction are
reported to be 79 to 92% [Reickert et al., 1996; Frenckner et al., 1997; Kays et al., 1999;
Boloker et al., 2002; Downard et al., 2003; Logan et al., 2007].
The timing of the surgery is dependent on the severity of the respiratory distress:
In patients with only mild symptoms and on minimal support, there may be no
pulmonary hypertension or vascular lability; therefore, repair can be undertaken after
48 to 72 hours. In patients with no or mild pulmonary hypoplasia and reversible
pulmonary hypertension, the timing of repair is delayed until maximum benefit is
achieved from short-term, time-related resolution of pulmonary hypertension and
improvement in pulmonary compliance [Greenholz, 1996]. In this regard, the time
course is variable. The most common group of patients will demonstrate initial
lability, but then stabilize, allowing repair after 5 to 10 days. In a few patients having
severe pulmonary hypoplasia and/or pulmonary hypertension, there will be no
response to therapy of any kind, including ECMO. In this group, support is often
withdrawn.
In patients who require ECMO therapy, there is some controversy about timing of the
operative repair. One approach is to repair the defect while the infant is on ECMO
[Dassinger et al., 2010]. However, early studies reported a high rate of hemorrhagic
complications and high mortality once bleeding developed [Lally et al., 1992;
Vazquez and Cheu, 1994]. The repair may also be postponed until the point when the
patient is ready to wean off ECMO or after resolution of pulmonary hypertension
[Sigalet et al., 1995].
Diaphragmatic Hernias
193
Finally, some advocate a return to conventional ventilation and decannulation before
repair of CDH [Lally, 1996].
Intrautero Therapy
It is possible to repair CDH intrautero with a prosthetic patch or by means of fetal
tracheal occlusion. Fetal tracheal occlusion is based on the effect of raising the
intrapulmonary pressure to restrict the flow of amniotic fluid in the lungs. Early studies in
humans showed a 13% survival when done via hysterotomy compared to 33% when done via
the open approach. There are some controversies regarding the timing and duration of the
occlusion with respect to adverse effect on type II pneumocytes. Although randomized
studies are needed to establish indications for fetal tracheal occlusion, some results in cases
with CDH characterized by poor prognostic factors have shown encouraging results [Jani et
al., 2006].
Lung Transplantation
Infants with critical pulmonary hypoplasia associated with CDH are faced with virtually
100% mortality. Lung transplantation, using ECMO as a bridge, could theoretically provide
an opportunity for survival. Barriers to the use of this modality for infants with CDH include
a shortage of neonatal organs, a time limit of several weeks that a child can be maintained on
ECMO, and the associated left ventricular dysfunction that may be present in many of these
infants [Allan et al., 1996]. To deal with the shortage of donors, some authors have suggested
the use of living-related or cadaveric lobar transplantation. Further experience with pediatric
lung transplantation is needed before this approach can be adequately evaluated.
CDH in Adulthood
Approximately 5% of CDH cases are diagnosed in adulthood [Richardson and Bolton,
2002]. According to Horton et al. [2008], 72% of adults affected by Morgagni hernia have
predominantly respiratory symptoms. Bochdalek hernias are more often associated with
gastrointestinal symptoms (intestinal obstruction) due to its posterolateral location. Imaging
methods are typically diagnostic. Surgical correction is required, even in asymptomatic
patients, in order to avoid future complications. The abdominal approach is recommended in
the case of associated abdominal complications (strangulated, incarcerated, or perforated
hernia) and provides an easier hernia reduction as well as the ability to directly explore both
sides of the diaphragm. A thoracotomy is recommended in cases where there are adhesions
between the hernia sac or herniated viscera and the pleural space. Minimally invasive surgery
is gaining popularity in recent years but long-term studies are needed to confirm overall
utility of that approach.
Long-term Outcome
In previous decades, infants with CDH who survived were thought to have an excellent
long-term prognosis, Mild subclinical abnormalities in pulmonary function were documented
Ivan Martinez Serna and Antonio Pablo Gamez Garcia
194
and there was a small incidence of developmental delay that was thought to be due to
neonatal hypoxia [Reid and Hutcherson, 1976; Freyschuss et al., 1984]. With improvements
in neonatal care and improved rates of survival, increasing morbidity has been documented
[Lund et al., 1994; Nobuhara et al., 1996]. In the short term, some severely affected children
develop bronchopulmonary dysplasia, but interestingly most children have only minor
residual lung dysfunction on long-term follow up [Falconer et al., 1990; Ijsseltstijn et al.,
1997]. Instead, some studies have documented significant morbidity due to gastroesophageal
reflux, neurologic and developmental disorders, and musculoskeletal problems.
Gastroesophageal reflux is present in over 50% of patients with neonatal CDH [Koot et al.,
1993]. This may lead to a number of sequelae, including recurrent aspiration, exacerbation of
pre-existing reactive airway disease, and failure to thrive. Although most patients can be
managed medically, approximately 10% to 20% of children ultimately require a
fundoplication procedure.
A significant number of infants with CDH have concomitant neurological and
developmental abnormalities. For example, disabilities such as motor dysfunction, seizures,
hydrocephalus, hearing loss, visual problems and developmental delay may all occur [Lund et
al., 1994]. A number of etiologic mechanisms may play a role, including neonatal hypoxia,
intraventricular hemorrhage, hyperventilation and alkalinization therapy, ototoxic
medications, and microthrombi as a result of ECMO [Nobuhara et al., 1996]. Further, ECMO
may play an important role in neurodevelopmental morbidity [Schumacher et al., 1991;
D´Agostino et al., 1995]; and infants with CDH who undergo ECMO seem to fare worse
those undergoing ECMO for other causes [Stolar et al., 1995]. Musculosketal problems such
scoliosis, chest wall hypoplasia, and pectus deformities occur in 10 to 20% of infants with
CDH [Vanamo et al., 1996].
For many CDH patients, subsequent surgery may be required to correct gastroesophageal
reflux recurrence of the diaphragmatic hernia or adhesive small bowel obstruction.
TRAUMATIC DIAPHRAGMATIC HERNIAS
In traumatic diaphragmatic hernias (TDH), the diaphragmatic defect occurs as a result of
blunt or penetrating thoracic or abdominal trauma that results in herniation of the abdominal
viscera into the chest. The presence of abdominal viscera in the chest can be the origin of
cardiorespiratory or digestive disorders.
The earliest description of a TDH is attributed to Sennertus in the 14th century but the
first detailed anatomic description was made in the 16
th
century by Ambrosio Paré in post-
mortem studies. The first surgical repair of a traumatic diaphragmatic hernia was made by
Walter in the 19th century.
Incidence
Diagnosed traumatic injuries of the diaphragm are generally rare but there is a relative
increase in recent years due to improved diagnostic methods and increased accidents related
to traffic and workplace. The overall incidence is estimated between 1-6% [Mansour, 1997;
Diaphragmatic Hernias
195
Rosati, 1998]. TDH can result from either penetrating or blunt injury. In direct mechanism
injuries, stab attacks and gunshot wounds are the most common causes with a 10-15%
incidence of rupture [Rosati, 1998; Reber et al., 1998; Cerón et al., 2008; Hanna et al., 2008].
Indirect mechanism injuries, mainly by high increase of abdominal pressure, occur in between
1 and 7% of such cases.
In virtually all cases, traumatic rupture of the diaphragm is associated with multisystem
injuries which more directly determine survival in the acute setting [Cristophi, 1983], and
there are no reliable clinical signs or symptoms. Associated injuries in multiple trauma
patients are responsible for the severe clinical condition of patients with TDH, with acute-
stage mortality between 15-42% for blunt trauma, 1-10% for penetrating stab wounds, and
15-20% for gunshot wounds [Bergeron et al., 2002]. In chronic stage TDH, complications and
mortality can be up to 40%, thus early diagnosis and treatment are critical in the prognosis of
these patients.
Etiology
As already mentioned, TDH occur as a result of a blunt thoracoabdominal trauma that
generates a high increase in abdominal pressure; or less frequently, TDH occurs as the result
of laceration associated with rib fractures, or penetrating trauma, usually secondary to stab or
gunshot injuries. The lesion size can be variable and depends on the mechanism of injury, the
body position at the time of trauma, diaphragm mobility and the dynamic phase of respiration.
Penetrating injuries usually have a smaller size (1-4cm) than blunt injuries [Hanna et al.,
2008]. Defects caused by blunt force are almost always larger than 2cm and are sometimes
more than 10cm in length [Voeller et al., 1990]. Penetrating wounds are usually less than 2cm
in length [Wise et al., 1973]. There is considerable evidence that injuries are more frequent on
the left side [Bergeron et al., 2002; Gomez et al., 2002; Hanna et al., 2008; Cerón et al., 2008]
with an incidence of around 75% on the left compared to 20% on the right side and 5%
bilateral [Cerón et al., 2008]. This is likely because of the protection of the right side given by
the liver and greater strength on that side due to embryological development and inherently
greater weakness of the left hemidiaphragm [Boulanger et al., 1993]. Blunt traumatic tears
can involve any portion of the diaphragm, although they usually involve the posterior central
aspect of a hemidiaphragm and extend radially, or result in disruption of the posterolateral
attachments. Cupular injuries are more frequent than peripheral ones. Bilateral ruptures are
rare [Reber et al., 1998].
The healing of diaphragmatic injuries is often difficult due to the pressure gradient and
the continued mobility of the diaphragm, encouraging subsequent migration of abdominal
organs. On the right side, the lesion is usually occluded by the liver but occasionally colon or
omentum can be herniated, or involve a rotation of the gallbladder or gastric volvulus. On the
left side, herniation most frequently involves the stomach but can also involve the large or
small bowel, omentum or spleen [Rodriguez-Morales et al., 1986; Voeller et al., 1990].
Thoracic or abdominal injuries sustained in the context of multiple trauma patients are usually
fairly constant and depend on the magnitude of the trauma [Gomez et al. 2002; Cerón et al.,
2008; Hanna et al., 2008]. Rib fractures, pleural occupation (i.e., pneumothorax, hemothorax),
and pulmonary contusion are the most frequent associated injuries. In the abdomen, solid
Ivan Martinez Serna and Antonio Pablo Gamez Garcia
196
abdominal viscera are the most frequently affected although perforation of hollow viscera is
estimated to occur in 8% of cases [Boulanger et al., 1993]. Further, associated head injuries or
severe pelvic injuries may influence prognosis [Cerón et al., 2008; Hanna et al., 2008].
Clínical Features
The clinical features of TDH depend on the clinical stage, the magnitude of
diaphragmatic injury, and the organs herniated into the chest. Thus, in the acute stage the
patient can range from asymptomatic to symptoms typical of severe hemodynamic
compromise. In penetrating injuries, a diaphragmatic injury should be considered with any
lesion below the 4th anterior rib and below the 8th in the posterior arch. With diaphragmatic
rupture due to blunt trauma, respiratory symptoms are predominant, with the magnitude of
symptoms dependent upon pain, diaphragmatic contractile inefficiency, and occupation of
affected hemithorax. After initial resuscitative measures and with stabilization the patient may
present with nonspecific symptoms. Both an acute period with obvious symptoms and a later
paucisymptomatic period, in which diaphragmatic rupture may go undetected can be
differentiated. In the chronic state, the patient may remain asymptomatic or have nonspecific
dyspepsia or pleuritic pain. In general, the diagnosis in chronic stage is low, ranging around
8% [Pagiarello and Carter, 1992]
Diagnostic Imaging
The diagnosis of diaphragmatic rupture may be difficult particularly in the context of the
multiple trauma patient and in patients presenting with few symptoms. The percentage of
initially undiagnosed injuries are between 12% and 60% and may be an intraoperative finding
in 25-50% of the operated cases [Gomez et al., 2002]. In any case, the possibility of
diaphragmatic rupture should be considered in multiple trauma patients [Cerón et al., 2008].
Early diagnosis is important since the pleuroperitoneal pressure gradient can cause defects to
enlarge over time, with eventual bowel incarceration, strangulation and obstruction
[Boulanger et al., 1993].
Numerous studies have found the chest radiograph to be the most valuable tool in the
preoperative diagnosis of diaphragmatic rupture. However, the range of reported diagnostic
accuracy of chest radiograph is wide, ranging from 20 to 71% [Ward et al., 1981; Rodriguez-
Morales et al., 1986; Voeller et al., 1990; Gelman et al., 1991]. The chest radiograph is
abnormal in 77% of patients evaluated for TDH, although diagnosis can be confirmed in only
25-50% of patients due to the absence of herniated organs being noted in the chest
radiograph; however, when herniated organs are noted, the diagnostic accuracy is much
higher. Diaphragmatic rupture should be suspected whenever radiographs reveal apparent
elevation of a hemidiaphragm, although elevation also may be due to atelectasis, eventration,
posttraumatic paralysis, or subpulmonic pleural effusion. Since nonspecific apparent
elevation of the hemidiaphragm is usually the only sign of right hemidiaphragm rupture,
right-sided rupture is more difficult to detect. Evidence of rupture may not be present on the
initial radiograph, but may develop on subsequent films, thus serial radiographs can be
helpful in diagnosis [Rodriguez-Morales et al., 1986; Voeller et al., 1990; Gelman et al.,
Diaphragmatic Hernias
197
1991]. Other radiographic findings consistent with a diagnosis of diaphragmatic injury
include hemothorax, basal lung opacity, and abnormal contour of a hemidiaphragm. Rarely,
herniated omental fat can simulate pleural fluid on chest radiographs, falsely suggesting
strangulation. Because radiographic findings are absent or nonspecific in most penetrating
injuries, early diagnosis typically requires direct inspection. On the left side of the chest,
diaphragmatic silhouette, diaphragmatic elevation, mediastinal shift, and the presence of
intrathoracic gas may all suggest diaphragmatic hernia. Herniation of hollow viscera into the
chest and identification of a nasogastric tube in the intrathoracic stomach are the most specific
radiographic signs. On the right side, basal diffuse or nodular condensations, and
diaphragmatic elevation, sometimes with gallbladder rotation, are suggestive of
diaphragmatic hernia.
The chest CT scan is ideal for diagnosis of diaphragmatic hernia because of its high
sensitivity and specificity (71-100%) [Gomez et al., 2002]. The utility of CT is greater in left-
side lesions, achieving a sensitivity of 92% [Van Hise et al., 1998]. Diaphragmatic tears are
often documented on CT scans, with several findings indicative of traumatic disruption
[Worthy et al., 1995]. Abrupt discontinuity of the diaphragm may be visible, with or without
visceral herniation. Inability to identify the diaphragm (absent diaphragm sign) in an area
where it does not contact another organ, and should normally be seen, may be noted.
Identification of abdominal structures external to the diaphragm indicates intrathoracic
herniation. Finally, focal constriction of the stomach (collar or hourglass sign) at the site of
herniation is occasionally observed by CT with barium radiography studies. However,
although retrospective analysis indicates that most diaphragmatic hernias are detectable by
CT [Worthy et al., 1995], several studies have found CT to be limited of value in diagnosis
[Voeller et al., 1990; Chen and Wilson, 1991]. In problematic cases, direct coronal or sagittal
MR imaging or spiral CT with coronal or sagittal reformatting can be definitive [Mirvis et al.,
1988; Dosios et al., 1993; Shanmuganathan et al., 1996]. These imaging planes can be of
particular value in depicting the secondary sign of a focal bulge in the diaphragmatic contour,
especially on the right where diagnosis can be difficult.
Other imaging studies are sometimes useful when results of radiographic or CT
examinations are equivocal. Ultrasound may be of particular value in assessing the right
hemidiaphragm by depicting the free edge of the hemidiaphragm as a flap within pleural
fluid, or demonstrating liver herniated into the chest [Somers et al., 1990]. Barium contrast
radiography may be useful in suspected herniation of hollow viscera. MRI provides excellent
assessment of diaphragmatic pathology, but its indications in acute trauma patients are very
restricted. The use of diagnostic laparoscopy or thoracoscopy to confirm the injury, assess
associated injuries, and provide treatment are the main advantages of these techniques.
Treatment
The diagnosis of diaphragmatic injury is an absolute indication for surgery, and it should
be performed in the acute phase after effective resuscitation. However, the surgery may be
delayed temporarily in multiple trauma patients who require urgent stabilization or prior
treatment for other wounds. The surgical approach depends on the type and location of the
lesion. For left side hernias, laparotomy is the preferred surgical approach in acute phase, due
to the high incidence of associated abdominal injuries that may require surgical treatment.
Ivan Martinez Serna and Antonio Pablo Gamez Garcia
198
Viscera reduction from the thorax to the abdomen and diaphragmatic suture is easily
performed. For right side hernias, or those repaired in the chronic phase, approach via
thoracotomy allows greater flexibility for suturing of the diaphragm and minimizes adhesion
formation between abdominal viscera and parietal pleura. In some cases, combined
approaches are useful. It can be useful to conduct a full assessment of the diaphragm using
thoracotomy to assess the posterior region and laparotomy to assess both domes, because
some of these lesions can be diagnosed only after thorough surgical exploration.
The need for prosthetic material in repair of TDH is rare except in chronic phase hernias
with large defects or atrophic diaphragms. The treatment of these lesions by minimally
invasive surgery has produced satisfactory [Koehler and Smith, 1994; Smith et al., 1995]. The
minimally invasive approach can be useful for stable patients with diaphragmatic injuries that
do not require open approaches for the treatment of other lesions.
Postoperative morbidity may range between 10 and 53%, with respiratory complications
being the most frequent and severe [Gomez et al., 2002]. Postoperative morbidity together
with the frequent occurrence of severe associated injuries are the main risk factors for
mortality with TDH [Hanna et al., 2008; Gomez et al., 2002].
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