Diaphragmatic Injuries and Post-Traumatic Diaphragmatic Hernias

Current Problems in Surgery 54 (2017) 11–32
Contents lists available at ScienceDirect
Current Problems in Surgery
journal homepage: www.elsevier.com/locate/cpsurg
Diaphragmatic injuries and post-traumatic

diaphragmatic hernias
Patrizio Petrone, MD, MPH, MSHSA, FACSa,*,
Juan A. Asensio, MD, FACS, FCCM, FRCS (Engl)b,
Corrado P. Marini, MD, FACSa
Introduction
Establishing the clinical diagnosis of traumatic diaphragmatic injury (TDI) can be challenging
for the emergency department or the trauma surgeon or for both, as these injuries are often
clinically occult. Accurate diagnosis is critical, however, as a missed TDI may result in grave
sequelae due to herniation and strangulation of displaced intra-abdominal organs as well as
respiratory compromise. TDIs can result from blunt and penetrating trauma, and they less
commonly can be iatrogenic. The mechanism of injury (MOI) plays a significant role in the
probability of a patient having suffered a TDI; therefore, the physician taking care of the trauma
victim should inquire about the specifics of the MOI to minimize the chance of missing a
potential TDI.
The anatomophysiologic structure and function of the diaphragm is responsible for the
higher incidence of left-sided TDI. A congenital weakness along the embryonic fusion of the
costal and lumbar portions of the diaphragm predisposes the left hemidiaphragm to a greater
incidence of injury from blunt trauma. In contrast, the presence of the liver along with its
attachments underneath the right hemidiaphragm accounts for the lower incidence of
transdiaphragmatic herniation following small defects from either penetrating or blunt trauma.
In general, because of the significantly greater force required to cause right-sided TDI, patients
with injury to the right hemidiaphragm have a higher prehospital mortality rate when
compared to patients with left diaphragmatic injuries from associated severe hepatic and
vascular injuries. The diagnosis of TDI requires a multimodality diagnostic approach in view of
the fact that no single diagnostic study has been shown to be sensitive and specific enough to
From the a New York Medical College, Winthrop University Hospital, Mineola, NY; and b Division of Trauma Surgery,
Creighton University Medical Center, Omaha, NE
n
Address reprint requests to Patrizio Petrone, MD, MPH, MSHSA, FACS, Winthrop University Hospital, 222 Station
Plaza North, Suite 603, Mineola, NY 11501
E-mail address: patrizio.petrone@gmail.com (P. Petrone).
http://dx.doi.org/10.1067/j.cpsurg.2016.11.001
0011-3840/& 2017 Elsevier Inc. All rights reserved.
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12 P. Petrone et al. / Current Problems in Surgery 54 (2017) 11–32
diagnose accurately the presence of blunt or penetrating diaphragmatic injury. Minimally

invasive procedures such as diagnostic laparoscopy and thoracoscopy are more commonly used
to diagnose TDI in asymptomatic patients with penetrating trauma to the thoracoabdominal
region. The operative management of TDI depends on the clinical presentation of the patient and
on the timeliness of the diagnosis. Patients with acute TDI typically undergo immediate open or
laparoscopic operative management depending on the presence or absence of associated
injuries, whereas patients with missed TDI undergo repair via thoracotomy. The long-term
outcome of the different types of TDI has not been well documented in the literature. However, it
is clear that missed injuries or delayed diagnosis portend a poorer prognosis. The objectives of
this monograph include a review of the anatomy of the diaphragm as it relates to traumatic
injuries, to a discussion about the incidence of traumatic diaphragmatic injuries, and
development of a concise approach to their diagnosis, surgical management, and treatment.
Historical perspective
Sennertus1 was the first to describe a posttraumatic herniation of the stomach in 1541.
Similarly, in 1579 Paré2 described 2 patients who died of strangulated intra-abdominal organs
through diaphragmatic defects. The first patient was a French artillery captain who had
sustained a gunshot wound of the left chest 8 months earlier, and subsequently developed
colonic obstruction. The second patient suffered a blunt rupture of the diaphragm with gastric
incarceration.3
Petit4 was the first to identify and describe the differences between acquired and congenital
diaphragmatic hernias. In 1769, Morgagni5 described the different types of hernias occurring
through the natural diaphragmatic openings. Bowditch6 in 1853 was the first to diagnose an
antemortem traumatic diaphragmatic rupture. Then, in 1879 Bardenhewer7 performed a
proximal diverting colostomy in a patient who subsequently died and was proven later at
autopsy to have had herniation and strangulation of the colon. Riolfi in 18868 performed the first
successful diaphragmatic repair. Naumann9 successfully repaired in 1888 a traumatic
diaphragmatic hernia through which the stomach had herniated into the left chest. In 1899,
Walker10 was also successful in repairing a lacerated diaphragm in a patient who had been
struck by a falling tree. Hedblom11 in 1925 used a series of 378 patients who had undergone
surgical treatment to describe the etiology of diaphragmatic defects and the morbidity and
mortality associated with it.
Anatomy
The diaphragm is a domelike muscular and tendinous septum originating from the sternum,
the ribs, and the twelfth thoracic and first, second, and third lumbar vertebrae. It is the most
important inspiratory muscle and, unlike skeletal muscles, is constantly active. It separates the
thoracic from the abdominal cavity in a dynamic volumetric fashion because of its location in
inspiration as opposed to expiration (respectively, reduction as opposed to expansion of the
abdominal volume) (Fig 1). When relaxed and viewed from below, it forms a dome-shaped roof
for the abdomen. The undersurface of the diaphragm covers the liver, intra-abdominal portion of
the esophagus, stomach, spleen, adrenals, and kidneys, and to some extent the pancreas and
transverse colon. Clearly, the severity of injury and the consequent surgical challenges to the
management of diaphragmatic injury increase dramatically depending on the associated intra-
abdominal injuries.12
The diaphragm also provides a musculofibrous floor for the thorax. The peripheral muscular
portions of the diaphragm arise from the lower 6 ribs and costal cartilages, from the lumbar
vertebrae (right and left crus), and from the lumbocostal arches. The most anterior portion of the
diaphragm attaches to the lowermost aspect of the sternum at the posterior aspect of the
xiphisternal junction, whereas the most posterior portion inserts in the periosteal surfaces of the
P. Petrone et al. / Current Problems in Surgery 54 (2017) 11–32 13
Fig. 1. Side view of the diaphragm, showing its domelike shape and anterior and posterior areas of attachment: the
xiphisternal junction and the lumbar vertebral bodies. The level of the origin of each of the major apertures of the diaphragm
are shown. IVC, inferior vena cava. (Adapted and reproduced with permission from Asensio, Petrone and Demetriades.22)
first through the third lumbar vertebral bodies. The broadest portion of the diaphragmatic
muscle spans laterally and attaches to the internal surfaces of the lower ribs. This lateral
insertion extends from the sixth rib, anteriorly, to the twelfth rib, posteriorly. Additional fibers
arise from the xiphoid cartilages, and all the muscular elements converge into the central
tendon, roughly trifoliate in outline, which is the strongest and thinnest part. The central part
of the tendon underlies the pericardium, whereas the right and left divisions extend
posteriorly.12,13
Of the 3 major openings in the diaphragm, the aortic hiatus is the most posterior. It is situated
slightly to the left of the midline, immediately in front of the body of the first lumbar vertebra,
and is, therefore, behind the diaphragm, not in it. Precise knowledge of this anatomy allows the
trauma surgeon to locate the abdominal aorta to compress it, either digitally or with the help of
an aortic cross-clamp during episodes of hypotension and exsanguinating abdominal vascular
hemorrhage. The aorta, azygos vein, and thoracic duct pass through this opening. The
esophageal hiatus is limited to the transition of the esophagus and vagus nerves from the
thoracic to the abdominal cavity, and the inferior vena cava passes as a single structure through a
dedicated foramen, named the vena cava hiatus, also known as the quadrate hiatus, which lies
1.5-2 cm to the right of the midline. The splanchnic nerves and sympathetic chains pass through
2 small foramina in the crura. The internal mammary arteries with anterior lymphatic trunks
pass through a space between the sternal and costal portions of the diaphragmatic Morgagni
foramen, where hernias may develop.12,13
In relation to the diaphragm, there are 4 serous membranes—3 lining its upper or thoracic
surface and 1 lining its abdominal surface. The 3 serous membranes on its upper surface are the
pleura on each side and the serous layer of the pericardium, which covers the middle portion of
the tendinous center. The serous membrane covering the abdominal surface is a portion of the
general peritoneal membrane of the abdominal cavity.13,14
The diaphragm is innervated by the phrenic nerves. The right and left hemidiaphragm are
innervated separately by their respective ipsilateral phrenic nerves. The phrenic nerves arise
from the third through the fifth cervical roots, with the greatest contribution to diaphragmatic
innervation being consistently from the fourth cervical root. These nerves course anteriorly on
the medial border of the scalenus anticus muscle and traverse the thoracic cavity, traveling along
the posterolateral mediastinum on the pericardial surface. The phrenic nerves typically divide
into branches, either at the level of the diaphragm or 1-2 cm immediately above it. Some of the
lower intercostal nerves are thought to contribute to the sensory innervation of the diaphragm,
but motor innervation is supplied exclusively by the phrenic nerve on each side.12 Merendino
and colleagues15 provided an accurate description of the branching pattern of the phrenic
nerves. Each branch divides into 4 major rami—a sternal (anterior), an anterolateral, a
posterolateral, and a crural (posterior) ramus. The resulting pattern is best described as a double
“handcuff,” with the anterolateral and posterolateral branches being the main components
skirting circumferentially and laterally to the dome of the diaphragm.
Embryologic development
The diaphragm has a highly complex origin. The classic concept of formation16 stated that the
diaphragm originates from the septum transversum, the mesentery of the esophagus, the
pleuroperitoneal membranes, and the musculature of the chest wall. There are 2 paired
(pleuroperitoneal membranes and chest wall musculature) and 2 unpaired (septum transversum
and mesentery) components.
The septum transversum develops during the fourth week of gestation and initially appears
as a thick, incomplete partition between the pericardial and peritoneal cavities. Originally, the
septum is located opposite to the cervical vertebrae, but as it grows it becomes displaced
caudally to reach the level of the first lumbar vertebra. Eventually, it fuses dorsally with the
ventral mesentery to the esophagus and with the pleuroperitoneal membranes. In the adult, the
septum transversum forms the central tendon of the diaphragm. The dorsal mesentery of the
esophagus also appears during the fourth week of gestation and constitutes the median portion
of the diaphragm dorsal to the septum transversum. In the adult, this mesentery forms the crura
of the diaphragm, including the esophageal hiatus and aortic hiatus. During the fifth week of
gestation, the pleuroperitoneal membranes first appear along the lateral body wall and extend
medially, where they fuse with the dorsal mesentery of the esophagus and the dorsal portion of
the septum transversum, completing the partition between the thoracic and abdominal cavities
by the eighth week of gestation. Although the pleuroperitoneal membranes may form large
portions of the primitive diaphragm, they represent relatively small, intermediate portions of
the adult diaphragm. Finally, with further development of the lung, the pleural cavities enlarge
and burrow into the lateral body walls where chest wall musculature is split off, forming the
peripheral muscular portion of the diaphragm. Failure of any component to fuse with adjacent
structures may result in congenital continuity of the pleural and peritoneal cavities.14,17
Initially, the septum transversum lies opposite the cervical somites, and nerve components of
the third, fourth, and fifth cervical segments of the spinal cord into the septum. At first the
nerves, known as the phrenic nerves, pass to the septum through the pleuropericardial folds.
This explains why, with the further expansion of the lungs and descent of the septum, they are
located in the fibrous pericardium. Hence, in the adult the phrenic nerves reach the diaphragm
via the fibrous pericardium.17
Although the septum transversum lies opposite the cervical segments during the fourth
week, by the sixth week the developing diaphragm is located at the level of the thoracic somites.
This descent of the diaphragm is apparently caused by rapid growth of the dorsal part of the
embryo in comparison to the ventral part. By the beginning of the third month, some of the
dorsal bands of the diaphragm originate at the level of the first lumbar vertebra.17
The phrenic nerves supply the diaphragm with its motor and sensory innervation. As the
most peripheral part of the diaphragm is derived from mesenchyme of the thoracic wall, it is
generally accepted that some of the lower intercostal nerves contribute sensory fibers to the
peripheral part of the diaphragm.14,17
As the diaphragm is formed from the fusion of several components, a number of
developmental defects may occur, including complete absence of the diaphragm, diaphragmatic
hernias (posterolateral or Bochdalek, anterior or Morgagni, and paraesophageal), and
eventration. These abnormalities are not within the scope of this monograph, as the focus
here is diaphragmatic hernia because of trauma.
Physiology of the diaphragm
The diaphragm is the principal muscle of inspiration. When the muscle is at rest, it presents a
domed surface, concave toward the abdomen. When the muscular fibers contract, they become less
arched or nearly straight, causing the central tendon to descend. As a result, the level of the chest
wall is lowered and the vertical diameter of the chest is proportionally increased. During this
descent, the different parts of the tendon move unequally. The left leaflet descends to a greater
extent than the right leaflet, mainly because of the liver, and the central leaflet descends the least
because of its connection to the pericardium. While descending, the diaphragm compresses the
abdominal viscera and causes an outward projection of the abdominal wall. However, because the
central tendon becomes a fixed point, this enables the circumferential muscular fibers to contract
and elevate the lower ribs, thus expanding the lower part of the thoracic cavity. When at the end of
inspiration the diaphragm relaxes, the thoracic wall returns to its natural position as a consequence
of its elastic recoil and of the elasticity and weight of the displaced viscera.12,14
In all expulsive acts, the diaphragm is called into action to give an additional power to the
expulsive effort. Thus, before sneezing, coughing, laughing, and crying, and before vomiting,
defecation, urination, and delivery of a fetus from a gravid uterus, a deep inspiration takes place.12
The height of the diaphragm varies during respiration as the muscle is being carried upward
and downward from the average level. Its height also varies according to the distention of the
abdominal hollow viscera and the size of the liver. After a forced expiration, the right arch is on
the level of the fourth costal cartilage; at the side, with the fifth, sixth, and seventh ribs; and
behind, with the eighth rib, the left arch being usually 1-2 ribs’ breadth below the level of the
right one. In a forced inspiration, it descends between 1 and 2 in.12
Pathophysiology of diaphragmatic injury
The function of each hemidiaphragm revolves around the dynamic generation of a tidal
volume. The generation of a normal tidal volume produces a 3- to 5-cm bidirectional trajectory
of the diaphragm, with inferior displacement during inhalation and superior displacement
during exhalation. During exhalation, the right hemidiaphragm rises anteriorly to the level of
the fourth intercostal space whereas the left hemidiaphragm rises to the fifth intercostal space.
Posteriorly, both hemidiaphragms ascend to the eighth intercostal space. Constant diaphrag-
matic motion tends to preserve the negativity of the intrathoracic pressure, and during
inhalation increases to its maximum.
As the main respiratory muscle of the body, the diaphragm has both inspiratory and
expiratory functions. Changes in lung volume have a direct effect on diaphragmatic muscle fibers
and their function. It is known that the transdiaphragmatic pressure from stimulation of the
phrenic nerve decreases almost linearly with lung volume. This implies that the force-
generating capacity of the diaphragm is reduced.
A close relationship also exists between the diaphragm and the musculature of the
abdominal wall. These muscles also have both inspiratory and expiratory function. During
expiration they contract, forcing the diaphragm cephalad into the thoracic cavity. Physiological
factors such as sudden and abrupt increases in the pleuroperitoneal pressure gradient have been
identified as a pathogenetic mechanism of diaphragmatic injury. Marchand18 demonstrated that
there is a normal pattern of fluctuation in the intraperitoneal pressure during quiet respiration,
which ranges from þ 2 to þ 10 cm of H2O, whereas the corresponding intrapleural pressure
fluctuates from 5 to 10 cm of H2O. With the body in the supine position, the
pleuroperitoneal gradient fluctuates from þ7 to þ20 cm of H2O. With maximal inspiration,
this gradient may exceed þ100 cm of H2O. Sudden increases in intra-abdominal pressure of
þ 150 to 200 cm of H2O are associated with the acute transfer of large amount of kinetic energy
to the domes of the diaphragm, which in turn may cause diaphragmatic disruption. If a violation
of the anatomical integrity of the diaphragm occurs via laceration, perforation, or rupture, the
pleuroperitoneal gradient will favor transdiaphragmatic migration and, therefore, herniation of

intra-abdominal viscera.19
Diaphragmatic disruption is associated with immediate hemodynamic and respiratory
derangements. Transdiaphragmatic migration of herniating intra-abdominal viscera can restrict
ventricular filling, therefore, decreasing ventricular end-diastolic volumes and, thereby, reducing
cardiac output. The displaced intra-abdominal viscera that migrate into the ipsilateral chest
cavity can also compromise ventilation, and may eventually compromise ventilation in the
contralateral lung as the mediastinal shift increases.
Bark and colleagues20 studied the effect of hypoxemia on diaphragmatic function in a canine
model. He showed that the diaphragm is relatively resistant to hypoxemia, and that contractility
and oxygen consumption are maintained constant by compensatory increases in diaphragmatic
blood flow and oxygen extraction. Ali and Qi21 used a swine model of diaphragmatic injury with
herniated stomach to study the effect of increased intra-abdominal pressure produced by the
inflation of a military antishock trouser on cardiorespiratory function.
He showed that the increase in intra-abdominal pressure to 40 mm Hg produced by inflation
of the military antishock trouser was the major determinant of cardiorespiratory dysfunction in
diaphragmatic rupture.
Incidence and injury location
Diaphragmatic injuries occur infrequently in patients with both blunt and penetrating
trauma. In a large review of the literature22 that included 53,031 patients, a total of 592 patients
were identified to have suffered with TDI, accounting for an overall incidence of 3% of all
abdominal injuries. Data from other series suggest that TDI is present in 1%-7% of patients with
blunt trauma, and in 10%-15% of those with penetrating wounds, resulting in a penetrating vs
blunt trauma ratio of 2:1.22,23 Clearly, the incidence of the MOI depends on the reporting trauma
center. Penetrating injuries predominate as a MOI in the inner city urban trauma centers,
whereas blunt trauma is a much more common MOI of TDI in suburban and rural settings. 24,25
The more widespread use of computed tomography (CT) particularly for the evaluation of blunt
trauma patients has been associated with an overall relative increase in the incidence and
detection of blunt traumatic diaphragm injuries.26
Particularly in the setting of blunt trauma, left-sided hemidiaphragmatic injuries are
considerably more common than right-sided injuries. The incidence of left diaphragmatic was
reported to be 75% as opposed to 25% right TDI in a review of 32 series that included patients
with blunt TDI.27-29 Bilateral diaphragm injuries were uncommon, occurring in only in 2% of the
patients with TDI.
A congenital weakness existing along the embryonic fusion of the costal and lumbar parts of
the left hemidiaphragm predisposes this site to an increased likelihood of injury.30 Blunt left-
sided injuries are usually located at the posterolateral aspect of the hemidiaphragm between the
spleen and the abdominal aorta, and extend medially in a radial orientation toward the central
tendon. Left-sided defects may present with herniation of the stomach, small bowel, colon,
spleen, liver, or omentum into the thoracic cavity.31 While Hood32 reported an 87% incidence of
injuries to the left hemidiaphragm, Hardy33 in contrast, reported an almost equal distribution of
injury to each hemidiaphragm, with a slightly higher incidence of injury to the left
hemidiaphragm, at 54%.
Patients with right-sided hemidiaphragm rupture have higher prehospital mortality resulting
from the greater impacting force required to produce a right-sided TDI; with such greater force
is typically associated with significant vascular tears in the inferior vena cava or hepatic
veins.34,35 The apparent low incidence of right-sided TDI has been attributed to the cushioning
effect of the liver and to the greater force required to rupture the right hemidiaphragm as
opposed to the left, as demonstrated in experimental studies.36 The first case of traumatic
rupture of both leaves of the diaphragm was reported in 1955.34
It has been postulated that diaphragmatic injuries result from the transmission of force
through the abdominal viscera to the diaphragm, resulting in rupture. This would explain the
common involvement of the left hemidiaphragm, which is unprotected as compared to the right.
The energy from the force applied to the abdomen or flank should be distributed equally in all
directions throughout the abdominal visceral contents.
The left hemidiaphragm was also believed to be congenitally weaker than the right. To
elucidate the cause of the left-sided prevalence of diaphragmatic rupture, Bekassy and
colleagues37 harvested 10 diaphragms from cadavers within the first 24 hours of death. Both
the right and left hemidiaphragm were mounted separately in a pressure chamber, and
pressures were progressively increased until rupture of the hemidiaphragm occurred. Although
it appeared that the right hemidiaphragm required consistently higher pressures to rupture, the
data did not reach statistical significance. From these findings, the investigators concluded that
the right hemidiaphragm appears to be relatively resistant to applied pressures when compared
to the left, and these findings also suggested that the liver plays a protective role in preventing
injuries to the right hemidiaphragm.
Mechanisms of injury
A high index of suspicion for injuries to the diaphragm should arise from the prehospital
information regarding the MOI, and more specifically in the setting of blunt trauma, from the
velocity and direction of impact, the deformity to the surrounding vehicular structures, and from the
clinical presentation at the scene. When the MOI involves a fall, it is important to inquire about the
height of the fall and whether there has been a direct impact to the thoracoabdominal region.
A recent review of the National Trauma Data Bank revealed that patients with blunt
traumatic diaphragmatic injuries are older and have a higher injury severity score.38 Penetrating
injuries occur due to gunshot wounds, stab wounds, and shotgun wounds, whereas blunt
injuries result from motor vehicle collisions, falls from heights, or direct impacts to the
thoracoabdominal area from vehicles (as is in the case of pedestrians being struck by vehicles).
Blunt force trauma to the thoracoabdominal region or a history of crush injury should also alert
the trauma surgeon to the possibility of an underlying diaphragmatic injury.
Associated injuries
The diaphragm, because of its anatomical and its dynamic function, is rarely injured in
isolation; in fact, the presence of associated injuries is the rule rather than the exception. The
pattern of associated injuries generally depends on the mechanism of diaphragmatic injury (ie,
blunt vs penetrating and crush vs fall). Blunt trauma generally produces a significant number of
extra-abdominal or extrathoracic injuries or both, such as injuries to the central nervous system,
pelvis, and long bones. Rodriguez-Morales and colleagues39 reported a 55% incidence of
associated pelvic fractures in their series of 60 blunt diaphragmatic injuries. The energy required
to disrupt the pelvic ring is responsible for the sudden increase in intra-abdominal pressure,
which in turn is then transmitted to the dome of the diaphragm causing its rupture.
Meyers and McCabe40 cited a 40% incidence of associated pelvic fractures, a 25% incidence of
both hepatic and splenic injuries, and a 5% incidence of thoracic aortic tears in patients sustaining
blunt diaphragmatic injuries. Therefore, the presence of diaphragmatic injury in the setting of blunt
trauma should alert the physician to the high probability of associated solid-organ and pelvic injury.
Ilgenfritz and Stewart41 in a series of 52 patients with blunt diaphragmatic injuries reported a 90%
incidence of associated blunt thoracic injuries such as multiple rib fractures, 75% incidence of long-
bone fractures, and a 42% incidence of closed head injuries. Among the abdominal injuries, he
reported a 60% incidence of associated splenic injuries, a 35% incidence of liver injuries, and a 10%-
12% incidence of injuries to the kidney, pancreas, and small bowel. In a more recent review, Fair and
colleagues38 demonstrated that blunt diaphragmatic injury was associated with injuries to the
thoracic aorta, lung, bladder, and spleen.
Boulanger and colleagues42 compared the incidence of associated injuries stratified by right
and left blunt diaphragmatic rupture. He reported a 93% incidence of associated hepatic injuries
in patients with rupture of the right diaphragm, in comparison to a 24% incidence of associated
hepatic injuries in patients with injury to the left diaphragm. Kumar and colleagues43
corroborated the findings that right-sided diaphragmatic injury is associated with increased
mortality, again as a consequence of the other associated injuries owing to the amount of force
needed to generate such an injury.
Wiencek and colleagues44 in a series of 165 patients with diaphragmatic injuries, of which
154 were due to penetrating wounds, reported an average of 2 associated injuries in patients
sustaining stab wounds and 3 associated injuries in patients with gunshot wounds. This series
reported a 50% incidence of associated hepatic injuries, a 26% incidence of gastric injuries, and a
12%-18% incidence of pulmonary, colonic, splenic, and renal injuries.
Clinical presentation
Arriving to an early and accurate diagnosis of diaphragmatic injury in the setting of blunt and
penetrating trauma can be very difficult even with the help of sophisticated diagnostic
modalities. Information about the MOI from prehospital care personnel may help to generate a
higher index of suspicion regarding the possibility of diaphragmatic injury.
In patients involved in motor vehicle collision, information about the velocity of impact, the
severity of vehicular damage, where the patient was found within the vehicle, the direction of
impact, the presence or absence of passenger-compartment intrusion, the use and type of safety
restraints, deformity of the steering wheel, and the duration and type of extrication required to
retrieve the victim can be used by the treating physician to assess the severity of the accident
and to estimate the possible associated injuries.
Falls from great heights, direct impacts on the thoracoabdominal area from vehicles, or a history of
crush injury should also alert the trauma surgeon to the possibility of an underlying diaphragmatic
injury. In general, the severity of other associated injuries may distract the attention of the trauma
surgeon and compromise the ability to identify the presence of diaphragmatic injuries.
Although blunt trauma generally produces no external signs that are pathognomonic for TDI,
penetrating trauma in the thoracoabdominal area immediately alerts the trauma surgeon to the
possibility of diaphragmatic injury. The thoracoabdominal region consists of the lower chest and
upper abdomen, and it can be divided into the following: the anterior thoracoabdominal zone,
defined as the area between the nipples superiorly and the costal margin inferiorly; the lateral
component, defined superiorly by a line drawn from the anterior axillary line at the level of the
nipples posteriorly to the tip of the scapula and inferiorly to the costal margin; and the posterior
thoracoabdominal area, defined anteriorly by a line at the level of the tips of the scapula and
inferiorly by a line beginning at the posterior axillary line at the level of the inferior most ribs. In
general, the incidence of diaphragmatic injury is approximately the same for penetrating
injuries to the 3 thoracoabdominal areas.45
Presentation may range from hemodynamic stability with few or no physical findings to severe
hemodynamic compromise or presentation in extremis of patients with massive destruction of the
thoracoabdominal region from close-range shotgun injuries (less than 3 meters). In most patients,
there are no signs or symptoms directly attributable to the diaphragmatic defect. Symptoms and
signs attributable to TDI include shoulder or epigastric pain or both, respiratory distress, and the
presence of obvious bowel sounds in the involved hemithorax.22
In patients with delayed presentation and chronic herniation, symptoms of partial or
complete intestinal obstruction may be present. When this occurs because of an incarcerated
intrathoracic segment of bowel, the physical findings depend on the anatomical level of
obstruction. Gibson46 in 1929 stressed the importance of clinical signs in the diagnosis of
diaphragmatic hernia. He cited the following diagnostic symptoms: diminished expansion of the
chest, impairment of resonance, adventitious sounds, cardiac displacement, circulatory collapse,
cyanosis and dyspnea, and asymmetry of hypochondria.
Generally, symptoms attributable to the presence of a diaphragmatic hernia depend on the size
of the defect, the content of the hernia, the type of the herniated organ/s, and to whether the
herniated organ/s are incarcerated causing obstruction or conversely are acutely strangulated
leading to ischemic perforation. Thoracic symptomatology is related to the volume of the pleural
space occupied by the displaced abdominal viscera. Dyspnea, orthopnea, and chest pain are the
primary symptoms. The latter may be diaphragmatic and be referred to the scapular area, or may be
related to chest wall injury or pleural violation. In the instance of progressive gastric dilatation,
respiratory distress may become so extreme from lung collapse that it may mimic the presence of
tension pneumothorax. Physical findings include decreased breath sounds, multiple associated rib
fractures, and chest wall disruption in the form of a flail chest, which can be either central, with
sternal disarticulation, or peripheral, with floating rib segments. Abdominal symptoms tend to be
less pronounced, ranging from mild and localized to diffuse abdominal tenderness.
Diagnosis and imaging studies
The diagnosis of a diaphragmatic injury presents a challenge to the trauma surgeon, as

evidenced by the large number of investigative procedures employed to arrive to the diagnosis.
Injuries to the diaphragm can be diagnosed noninvasively with radiological studies or invasively
with interventional diagnostic procedures or can be diagnosed both noninvasively and
invasively. The initial test of choice is a chest radiograph, which can be diagnostic when hollow
abdominal viscera or a nasogastric tube is detected in the hemithorax. According to Miller and
colleagues,47 the initial chest radiograph is interpreted as normal in approximately 50% of
patients with TDI, whereas the radiographic findings in the remaining 50% are usually limited to
nonspecific findings such as a small pneumothorax or a hemithorax. The treating physician
must, therefore, be aware that on the initial films, diaphragmatic rupture may manifest as
atelectasis, hemothorax, pneumothorax, gastric dilatation, pulmonary contusion, intra-
abdominal fluid, traumatic pneumatocele, or congenital eventration.29 One particular radiologic
chest radiograph finding in blunt and penetrating trauma to the upper abdomen or to the lower
torso or to both is an abnormally elevated diaphragm in the absence of evidence of
transdiaphragmatic herniation. It is highly suggestive of an injury to the ipsilateral diaphragm;
therefore, it requires the necessary diagnostic evaluation to exclude a diaphragmatic injury.
Occasionally, in acute ruptures of the left hemidiaphragm, the nasogastric or orogastric tube
placed during the resuscitative phase can be found coiled in the left hemithoracic cavity (Fig 2).
Fig. 2. A coiled nasogastric tube within the left hemithoracic cavity is pathognomonic for a rupture of the left
hemidiaphragm. (Adapted with permission from Dr. Petrone's personal archives.)
Other findings occasionally identified radiographically are curvilinear shadows and air-fluid
levels consistent with hollow viscera, such as colon or small bowel in the intrathoracic space.
These findings are pathognomonic for rupture of the diaphragm.
Contrast studies are valuable in cases in which the initial chest radiograph is suspicious but
has failed to yield a definitive diagnosis of TDI. Clearly, the patient must be hemodynamically
stable to undergo these studies. In general, the vast majority of such studies are obtained to
investigate chronic, long-standing herniation of intra-abdominal viscera, although they have
also proven to be valuable in the acute settings. An upper gastrointestinal series and a barium
enema will often delineate the presence of the stomach or colon within the thoracic cavity.48
Although not generally considered helpful, real-time ultrasonography may occasionally reveal a
diaphragmatic rupture in expert hands, as reported by Somers and colleagues.49 Despite the
advent of the focused abdominal sonography for trauma as an accurate technique for the
diagnosis of intra-abdominal or pericardial fluid in trauma patients, no definitive reports have
emerged describing its usefulness for the diagnosis of TDI.
The use of magnetic resonance imaging to diagnose diaphragmatic rupture has been reported
by Mirvis and colleagues.50 These authors were the first to describe the use of magnetic
resonance imaging to assess the integrity of both hemidiaphragms in a patient who was found to
have herniation of the colon through a defect in the left hemidiaphragm. CT is much more
readily available in the acutely injured patient. Currently, reconstructed images are routinely
obtained in patients with chest radiographic findings suspicious of TDI (eg, an abnormally
elevated hemidiaphragm) and in patients with major injuries to the upper abdomen or lower
chest.51 The use of multidetector CT with coronal and sagittal multiplanar reformation has
improved the accuracy of CT for the diagnosis of TDI.52,53
The earliest invasive procedure used to diagnose traumatic diaphragmatic injuries was
diagnostic pneumoperitoneum. This technique was described by Clay and Hanlon54 in 1951 and
remains a technique of historical interest. Diagnostic peritoneal lavage (DPL) was introduced in
1965 by Root and colleagues55 and since then has been universally adopted for use in abdominal
trauma. Some studies56,57 have reported that DPL may not reveal diaphragmatic injury in the
absence of significant blood loss. Other authors58-60 have suggested that DPL has a low
sensitivity for the diagnosis of diaphragmatic injury from penetrating trauma when the red
blood cell (RBC) count of greater than 100,000 RBCs/mm3 is used as a threshold value. Therefore,
many authors have suggested lowering the threshold value to 5000 RBCs/mm3 for injuries to the
thoracoabdominal to increase the diagnostic sensitivity of the DPL.61,62
Minimally invasive techniques such as laparoscopy and thoracoscopy are now part of the trauma
surgeon’s diagnostic armamentarium. Ivatury and colleagues63,64 reported that the diagnostic
accuracy of laparoscopy was excellent for hemoperitoneum, solid-organ injuries, and diaphragmatic
lacerations, validating laparoscopy as an excellent tool for evaluating the diaphragm in
thoracoabdominal injuries. Murray and colleagues65 concluded in their study that the incidence
of diaphragmatic injuries from penetrating left thoracoabdominal trauma is high and states that
clinical and radiographic findings are unreliable at detecting occult diaphragmatic injuries.
Laparoscopy has been shown to be extremely useful to detect diaphragmatic injury in patients
who have no other indications for laparotomy.66 Hemodynamically stable patients without
abdominal symptoms with left thoracoabdominal penetrating trauma should undergo diagnostic
laparoscopy for the diagnosis and repair of diaphragmatic injury from penetrating trauma.67,68
Although thoracoscopy is used less frequently than laparoscopy, it has been shown to have a
high sensitivity and specificity with an accuracy rate of 98%-100% for the diagnosis of
diaphragmatic injury in stable patients.69 This technique has been used for diagnosis and repair
of diaphragmatic injuries for more than two decades. Freeman and colleagues70 in a
retrospective review of patients who underwent thoracoscopy after penetrating trauma
identified the following 5 risk factors as predictors of TDI: abnormal chest radiograph at
admission, associated intra-abdominal trauma, high-velocity injuries, entrance wound inferior
to the nipple or the scapula, and a right-sided entrance wound.
The main disadvantages of videothoracoscopy include the amount of time it takes to place the
patient in a thoracotomy position, the fact that it does not always allow repair of the diaphragm, and
the fact that it always requires chest tube insertion even if negative. These are the reported reasons
why thoracoscopy is used less frequently than laparoscopy.22 It is our opinion that the choice of
laparoscopy or thoracoscopy for the diagnosis and treatment of diaphragmatic injury in the setting
of penetrating trauma to the thoracoabdominal region depends on the familiarity and comfort level
of the individual trauma surgeon with each modality.67,71
Surgical management of diaphragmatic injuries
The surgical management of TDI is predicated on the timeliness of the diagnosis (ie, early vs
delayed diagnosis) and on its presentation.
Early diagnosis
The resuscitation of the patient is guided by the principles espoused by the Advanced Trauma
Life Support (ATLS) manual of the American College of Surgeons.72 O-negative blood must be
readily available for resuscitation,73,74 and broad-spectrum antibiotics should be administered
before laparotomy.75,76 In patients suspected of having TDI, special attention must be paid at
avoiding a low placement of thoracostomy tubes, particularly if the chest radiograph is
suggestive of the presence of herniated viscera into the chest.
Most TDIs can be approached through a standard laparotomy. The basic principles of a
trauma laparotomy include control of exsanguinating hemorrhage, control of spillage, assess-
ment of all injuries, and prioritization of repair, including early repair of TDIs. Full visualization
of the diaphragm is required; exposure of the right hemidiaphragm requires transection of the
falciform ligament, whereas visualization of the left hemidiaphragm requires gentle downward
retraction of the spleen and greater curvature of the stomach, along with the central tendon of
the diaphragm and the esophageal hiatus.22
All herniated viscera must be reduced, relocating organs in their original abdominal positions
(Fig 3). After careful reduction and relocation of all herniated viscera, debridement should be
Fig. 3. Abdominal approach used to reduce a gastric herniation. (Adapted and reproduced with permission from
Asensio, Petrone and Demetriades.22)
undertaken of any devitalized diaphragmatic tissue. The edges of the diaphragmatic defect can
be grasped with long Allis clamps and gently retracted exposing the hemithoracic cavity to
evaluate for the presence of any ongoing bleeding or contamination. The defect is repaired with
nonabsorbable suture, and an ipsilateral tube thoracostomy is usually performed under direct
visualization. The integrity of the diaphragmatic repair should be confirmed by having the
anesthesiologist inflate the lung with large tidal volumes (15 mL/kg) followed by a Valsalva
maneuver while the upper abdominal compartments are flooded with sterile saline.22
Diaphragmatic lacerations smaller than 5 cm should be repaired with nonabsorbable
material, in vertical mattress fashion placed at approximately 1 cm from the edges, everting
the diaphragmatic muscle. In the cases of lacerations larger than 5 cm, we favor repair with a
running interlocking suture with a nonabsorbable suture, such as polypropylene (Fig 4). A
diaphragmatic injury identified during laparoscopy or thoracoscopy may be repaired
laparoscopically or thoracoscopically.
Patients with TDIs associated with massive contamination of the pleural space from enteric
content should undergo anterolateral thoracotomy followed by copious lavage to evacuate the
contaminating material and placement of a 28-Fr right angle and 36-Fr straight chest tubes to
drain the chest cavity and to allow resorption of the pneumothorax, respectively. Penetration of
the pericardial cavity with contamination requires lavage, keeping the pericardium open and
with placement of a pericardial drain.
Although repair of acute TDIs can be accomplished through a thoracotomy, we believe that
the transabdominal approach offers advantages over the thoracotomy approach with respect to
Fig. 4. An alternative means of repairing diaphragmatic injuries involves a continuous running locked or unlocked
nonabsorbable material suture for reinforcement for more complex lacerations. (Adapted and reproduced with permission
from Asensio, Petrone and Demetriades.22)
the ease of reduction of herniated intra-abdominal viscera and with respect to the avoidance of
missed intra-abdominal injuries.
Massive destruction of the diaphragm and chest wall can be caused from close-range (less
than 3 meters) shotgun wounds. Patients who survive these devastating injuries present the
operating surgeon with technical challenges that require complex reconstruction of the
diaphragm and chest wall, sometimes with staged procedures. Immediate reconstruction of the
chest wall in patients with limited injury to the diaphragm that allows its use as a rotation flap
can be accomplished by detaching the affected hemidiaphragm from its anterior, lateral, and
posterior attachments and by translocating it to a position above the chest wall defect as shown
in Figure 5. Following the repositioning of the diaphragm, by suturing it to the muscles at a
higher level of intercostal space, the newly created abdominal wall defect can be repaired with a
latissimus myocutaneous flap (Fig 6).77
Fig. 5. After detaching the affected hemidiaphragm, it is then resutured to the muscle of a higher intercostal space,
translocating it to a position above the full-thickness chest wall defect. (Adapted and reproduced with permission from
Asensio, Petrone and Demetriades.22)
Fig. 6. Muscle flaps are used to cover thoracoabdominal wall defects. The figure shows a partial rotational flap of the
latissimus dorsi covering a thoracoabdominal wall defect. It may also be used to reconstruct complex injuries of the
chest wall and diaphragm. (Adapted and reproduced with permission from Asensio, Petrone and Demetriades.22)
Prosthetic nonabsorbable mesh material can also be used to reconstruct the diaphragm
(Fig 7), but its use is contraindicated in the presence of contamination in either or both cavities
because of the associated risks of infection.
We recommend using the American Association for the Surgery of Trauma-Organ Injury Scale
(AAST-OIS) to grade TDIs (Table 1),78 as it has value as both a descriptive and a research tool.
Treatment algorithms for both penetrating and blunt thoracoabdominal trauma are shown in
Figs 8 and 9.
Delayed diagnosis (missed TDI)

Patients with a missed diagnosis of TDI typically will have a clinical course over time (months
to years), characterized by progressive increase in visceral herniation, and the development of
symptoms and signs of cardiorespiratory compromise, obstruction, and occasionally strangu-
lation with perforation of the segment of the herniated gastrointestinal tract into the involved
hemithorax.
The diaphragm as a muscle tends to retract rapidly and it undergoes significant atrophy over
time. As a result, although its repair by reapproximating the edges of the defect can be
accomplished easily on the day of injury, the primary repair of a missed TDI is much more
Fig. 7. Patients in whom the initial diaphragmatic injury goes undiagnosed may present with large diaphragmatic defects at a
later date, becoming even larger over time. In cases in which the gap cannot be bridged, prosthetic materials will be necessary,
such as the mesh shown here. (Adapted and reproduced with permission from Asensio, Petrone and Demetriades.22)
difficult because of the presence of herniated viscera as well as from the retraction and atrophy
that have resulted from the delayed diagnosis. Owing to the changes that occur over time in the
diaphragm of patients with missed TDI, primary repair is associated with a high rate of suture
line failure; therefore, it is preferable to use alternate techniques to repair chronic TDIs,
including the use of prosthetic material to repair the defect. The algorithm for the treatment of
patients with delayed diagnosis of TDIs from blunt and penetrating trauma is shown in
Figure 10.
Miller and colleagues47 reported 2 missed injuries in a series of 102 patients, and Feliciano
and colleagues79 reported 16 patients who had a delay in diagnosis of diaphragmatic injuries
secondary to penetrating trauma; it is noteworthy that 3 of them had diaphragmatic injuries
missed at the time of laparotomy. Walschmidt and Laws80 reported a patient who underwent a
successful reduction of a TDI and repair 41 years after a blunt injury; this case report involves the
longest delay between time of the TDI and its treatment.
The repair of acute diaphragmatic injury is best accomplished through exploratory
laparotomy, whereas diaphragmatic injuries diagnosed on a delayed basis are more safely
treated and repaired through a thoracotomy. Asensio and colleagues,22 in a very extensive
review of the literature, have analyzed 27 series totaling 1530 patients with the diagnosis of TDI.
Of the 1530 reported TDIs, 1146 (75%) were repaired via laparotomy, 384 (25%) via thoracotomy,
Table 1
American Association for the Surgery of Trauma-Organ Injury Scale (AAST-OIS) for
diaphragmatic injuries.78
Grade Injury description
I Contusion
II Laceration r2 cm
III Laceration 2-10 cm
IV Laceration 410 cm with tissue loss r 25 cm2
V Laceration with tissue loss 4 25 cm2
Fig. 8. Algorithm for penetrating thoracoabdominal trauma. ATLS, Advanced Trauma Life Support; CT, computed
tomography; CXR, chest radiograph; OR, operating room; NGT, nasogastric tube. (Color version of figure is available
online.) (Adapted and reproduced with permission from Asensio, Petrone and Demetriades.22)
and 119 required a thoracoabdominal approach via either a single incision extended from the
abdomen to the chest or through two distinct incisions (Table 2).
Morbidity
The morbidity associated with traumatic diaphragmatic injuries can be subdivided into the
morbidity attributable to the injury itself and the morbidity resulting from the surgical
procedure required to repair the injury. The surgical morbidity includes suture line dehiscence,
and hemidiaphragmatic paralysis secondary to iatrogenic phrenic nerve injuries. The morbidity
directly attributable to the injury itself includes respiratory insufficiency, and the development
of empyema and subphrenic abscess. The morbidity associated with the missed diagnosis of TDIs
includes respiratory compromise, most often secondary to atelectasis of the ipsilateral lung,
pneumonia, bowel obstruction, strangulation, and occasionally, perforation of herniated intra-
abdominal viscera.
Rodriguez-Morales and colleagues39 reported a 65% incidence of atelectasis, a 28% incidence
of systemic sepsis, a 20% incidence of pneumonia and wound infection, an 18% incidence of
prolonged respiratory failure, and a 5% incidence of empyema. Chen and Wilson81 reported a
40% complication rate, with an 11% incidence of atelectasis and a 2%-6% incidence each of
pneumonia, multiple systems organ failure syndrome, empyema, lung abscess, and liver abscess.
Wiencek and colleagues44 reported a 31% incidence of complications in 146 of their 165 patients
who survived more than 48 hours; 18% of these patients developed atelectasis. Beal and
Fig. 9. Algorithm for blunt thoracoabdominal trauma. ATLS, Advanced Trauma Life Support; CT, computed tomography;
CXR, chest radiograph; LGT, lower gastrointestinal; MRI, magnetic resonance imaging; NGT, nasogastric tube; OR,
operating room; UGT, upper gastrointestinal. (Color version of figure is available online.) (Adapted and reproduced with
permission from Asensio, Petrone and Demetriades.22)
McKennan82 reported a 68% incidence of atelectasis and lobar collapse, a 23% incidence of
pleural effusion, an 18% incidence of pneumonia, and a 14% incidence of septic complications
from blunt diaphragmatic rupture. Meyers and McCabe40 reported that patients with blunt
trauma had a 60% incidence of complications as opposed to a 40% incidence of complications in
patients with penetrating trauma. Most morbidities reported in these series are the result of the
large number of associated injuries.
Mortality
Mortality from diaphragmatic injuries is generally due to the associated injuries. Wiencek
and colleagues44 in his series of 165 patients reported a mortality rate of 51% in patients with
4 or more associated injuries and shock lasting longer than 30 minutes. Hood32 reported a
mortality rate of 25%. In a collective review of mortality rates, Sharma83 reported an average
mortality rate of 17%.
In their review of 33 series that included 1799 patients with documented TDIs, Asensio and
colleagues22 reported that a mortality rate of 14% (246 deaths per 1799 patients with TDI).
The lowest mortality rate was reported by Mansour and colleagues,84 with no deaths a series
of 35 patients, whereas the highest mortality rate was reported by Boulanger and colleagues,42
with a mortality rate of 41% in a series of 80 patients. The mortality rates are higher in series
Fig. 10. Algorithm for diaphragmatic injury, chronic phase, after blunt and penetrating trauma. BE, barium enema; CT,
computed tomography; CXR, chest radiograph; MRI, magnetic resonance imaging; NGT, nasogastric tube; UGT, upper
gastrointestinal. (Color version of figure is available online.) (Adapted and reproduced with permission from Asensio,
Petrone and Demetriades.22)
reporting TDIs from blunt diaphragmatic injuries such as the series from Beal and McKennan,82
Holm and colleagues,27 and Rodriguez-Morales and colleagues39 reporting mortality rates of
40.5%, 33%, and 26.7%, respectively, as opposed to series of patients with TDIs from penetrating
trauma, such as those from Demetriades and colleagues85 and Aronoff and colleagues,86 which
report an average mortality rate of only 5%.
Strangulated diaphragmatic hernias
Gastrointestinal incarceration and strangulation are the most serious complications of

diaphragmatic hernias from the standpoint of accrued morbidity and mortality. Carter and
Giuseffi87 defined the strangulation of a diaphragmatic hernia as the arrest of the circulation of
the affected organ due to compression. In their study, history and physical findings included
(1) a history of previous thoracic injury; (2) dullness or tympany in the lower portion of the left
chest with aspiration of bloody fluid from the left pleural cavity; (3) radiographic findings
suggestive of a high left diaphragm with displacement of the heart to the right; and (4) signs of
acute gastrointestinal obstruction, particularly in the absence of abdominal distention. These
authors recommend the use of a combined thoracoabdominal incision for the definitive surgical
management of strangulated diaphragmatic hernias.
Table 2
Surgical approaches to repair diaphragmatic injuries.22
Surgical approach
Total number of patients Laparotomy Thoracotomy Thoracoabdominal*
1530 1146 (75%) 384 (25%) 119
n
Includes laparotomy and thoracotomy approaches from previous columns.
Sullivan88 reported 53 cases of obstruction and strangulation in diaphragmatic hernias caused

by penetrating injuries, and noted that the interval between the initial diaphragmatic insult and
the onset of symptoms averaged 4.6 years. The etiologic factor in most cases was a previous stab
wound, and the most common herniated organs were the colon and the stomach, followed by the
omentum in 40% of cases. Several authors have reported a 20% mortality rate from incarceration
and a 40%-57% mortality rate from strangulation of traumatic diaphragmatic hernias.29,87-92
Acute intrapericardial herniations
Rupture of the central tendon of the diaphragm involving the pericardium is rare. This can be
caused by isolated trauma to the chest and abdomen, but the most common mechanism causing
Fig. 11. In cases of lacerations through the central tendon, if the heart has herniated, it must be relocated after it has been
inspected to detect any associated cardiac injury. (Adapted and reproduced with permission from Asensio, Petrone and
Demetriades.22)
this type of injury is a combination of forces to both cavities (Fig 11). Lacerations of the central
tendon can be transverse, anteroposterior, and oblique based on the description by Hood.32
Jüttner and colleagues93 published the only case of herniation of intra-abdominal viscera into
the pericardium, causing pericardial tamponade, but the mortality rate in patients suffering this
type of TDI is usually because of the severity of the associated injuries such as blunt rupture of
the heart, aorta, or tracheobronchial tree or blunt rupture of all of these.
van Loenhout and colleagues94 reported 58 cases of traumatic intrapericardial diaphragmatic
hernia collected from the literature, with a high incidence of associated injuries. The organs
most commonly herniating into the pericardium were the transverse colon, stomach, omentum,
liver, and small bowel. Fulda and colleagues95 reported a series of 22 patients admitted with
blunt traumatic pericardial rupture over a 10-year period in 20,000 patients admitted to their
trauma center yielding an incidence rate of 0.1%. Five of the 22 patients (23%) died of the
associated cardiac injuries.
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Diaphragmatic Injuries and Post-Traumatic Diaphragmatic Hernias

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Current Problems in Surgery 54 (2017) 11–32

Contents lists available at ScienceDirect

Current Problems in Surgery

journal homepage: www.elsevier.com/locate/cpsurg

Diaphragmatic injuries and post-traumatic

diagnose accurately the presence of blunt or penetrating diaphragmatic injury. Minimally

Physiology of the diaphragm

Pathophysiology of diaphragmatic injury

pleuroperitoneal gradient will favor transdiaphragmatic migration and, therefore, herniation of

Incidence and injury location

Diagnosis and imaging studies

The diagnosis of a diaphragmatic injury presents a challenge to the trauma surgeon, as

Surgical management of diaphragmatic injuries

Delayed diagnosis (missed TDI)

Grade Injury description

Strangulated diaphragmatic hernias

Gastrointestinal incarceration and strangulation are the most serious complications of

Total number of patients Laparotomy Thoracotomy Thoracoabdominal*

1530 1146 (75%) 384 (25%) 119

Sullivan88 reported 53 cases of obstruction and strangulation in diaphragmatic hernias caused

Acute intrapericardial herniations

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