Download Report

Trauma 2001; 3: 235–247
Management of flail chest
Aaron M Ranasinghe, Jonathan AJ Hyde and Timothy R Graham
Thoracic injuries are directly responsible for 25% of trauma deaths in the United
Kingdom, and a significant contributory factor to another 25%. The majority of
these injuries are due to blunt thoracic trauma and flail chest can be a significant
component in these injuries. Flail chest is a condition that is managed by a range of
specialties, including cardiothoracic and orthopaedic surgeons, as well as anaesthetists and intensivists. Simple cases can be easily managed by analgesia and
supplemental oxygen therapy. However, the literature available supports a number
of practices including elective ventilation and possibly surgical fixation for more
complex cases. This article sets out to review the literature on the pathophysiology, investigation, and management of this potentially life-threatening condition
with particular regard to the additional management of underlying pulmonary
contusion.
Key words: flail chest; pulmonary contusion; thoracic trauma
Introduction
Thoracic injuries are responsible for 25% of trauma
deaths in the United Kingdom and are a signiﬁcant
contributory factor to another 25% (Mansour, 1997;
Rooney et al., 1999; Stellin, 1991). Within the UK the
most common cause of thoracic injury is blunt trauma.
Blunt thoracic trauma is almost exclusively caused by
rapid deceleration or crush injuries sustained in
road trafﬁc accidents (Richardson et al., 1982; Roux
and Fisher, 1992). The majority of these injuries occur
to the drivers or front seat passengers of cars. Within
this group 30–40% of victims sustain rib fractures, of
which 20–30% also sustain a ﬂail chest (Westaby and
Odell, 1999).
A ﬂail chest occurs when an isolated segment of the
chest wall loses bony continuity with the rest of the
thoracic cage. This is usually as a result of multiple rib
fractures. In other words, the ﬂail chest can be deﬁned
Department of Cardiothoracic Surgery, University Hospital
NHS Trust, Birmingham B15 2TH, UK.
Address for correspondence: TR Graham, Department of
Cardiothoracic Surgery, University Hospital NHS Trust,
Edgbaston, Birmingham, B15 2TH, UK.
# Arnold 2001
as two or more ribs fractured in two or more places
(Figure 1). The ﬂail segment therefore consists of
several ribs, but may also involve the vertebral column
or sternum (American College of Surgeons, 1997).
Flail chest is an area of thoracic trauma that often
presents a difﬁcult management problem. Before we
consider the available strategies for this relatively
common condition, it is important to have an understanding of both thoracic anatomy and the basic
principles of the pathophysiology of thoracic trauma.
Anatomy
The thoracic cage consists of the sternum, 12 thoracic
vertebrae and 12 pairs of ribs plus their accompanying
costal cartilages. These structures form a complete
bony ring with the sternum to the anterior and the
vertebral column to the posterior. All are attached
posteriorly to the vertebral column. The ﬁrst rib
and costal cartilage articulate with the manubrium
via a primary cartilaginous joint. Thus the ﬁrst
rib and manubrium are ﬁxed to each other and
move as one. The ﬁrst rib is short and relatively
well protected by the overlying clavicle. Hence,
fracture of this rib generally indicate a considerable
application of force to the thoracic wall and is therefore
1460-4086(01)TA216OA
236
AM Ranasinghe et al.
The two main contributing factors associated with the
morbidity of ﬂail chest are:
1) Underlying pulmonary contusion.
2) Paradoxical movement of the chest wall.
Of these, pulmonary contusion is by far the most
important, and is present in the majority of cases.
Paradoxical motion disrupts the mechanics of ventilation leading to a decrease in total lung capacity (TLC)
and functional residual capacity (FRC).
Hypoxia is a serious consequence of ﬂail chest and
can be caused by a number of factors including ventilation=perfusion mismatch secondary to contusion,
haematoma or alveolar collapse, and inadequate tissue
oxygen delivery (often due to pneumothorax). Hypercarbia may also result, due to inadequate ventilation
and decreased conscious levels. Metabolic acidosis is
also a common ﬁnding that must not be overlooked,
and occurs secondary to tissue hypoperfusion.
Investigations
Figure 1 A plain chest radiograph showing right-sided rib
fractures, and a left-sided flail segment with rib fractures
from 3 to 9 with surgical emphysema
a marker of severe potential underlying organ damage.
The second to seventh ribs are attached to the body of
the sternum by their own costal cartilages via a synovial joint. The eighth, ninth and tenth pairs of ribs are
all attached anteriorly to each other and also to the
seventh rib by means of their costal cartilages and
synovial joints. Ribs eleven and twelve have no anterior attachment and are referred to as ﬂoating ribs
(Basmajian and Slonecker, 1989; Sinnatamby, 1999).
Pathophysiology of thoracic trauma
There are two main processes that may lead to serious
physiological derangement in thoracic trauma.
1) Respiratory insufﬁciency with subsequent hypoxia.
2) Circulatory shock with subsequent hypoperfusion.
Trauma 2001; 3: 235–247
Once the initial primary survey has been carried
out and any immediately life-threatening conditions
(Table 1) have been identiﬁed or excluded, it is important to assess the patient rigorously to identify any
potentially life-threatening conditions (Table 2). A
detailed history of the accident should be obtained
from the best available source, with particular emphasis on the mechanism of injury. Special note should be
taken of the previous cardiac, respiratory and vascular
status of the patient. At this stage it is also useful to
carry out a detailed physical examination of the patient
if clinically stable. The following investigations are
mandatory.
Routine blood tests
Routine blood tests should be carried out for full blood
count, electrolytes and cross match.
Table 1 Immediate threats to life in thoracic trauma
Airway problems
Tension pneumothorax
Open pneumothorax
Massive haemothorax
Flail chest
Cardiac tamponade
Management of ﬂail chest
Table 2 Potential threats to life following thoracic trauma
Pulmonary contusion
Myocardial contusion
Aortic disruption
Diaphragmatic rupture
Tracheobronchial rupture
Oesophageal rupture
Arterial blood gases
Arterial blood gases should be assessed for hypoxaemia, hypercarbia and acid–base balance.
Electrocardiograph monitoring
Electrocardiograph monitoring should be carried out
for cardiac arrhythmias or ischaemia.
The plain chest radiograph
This is the single most important investigation for
patients sustaining thoracic trauma. Ideally it should
be performed within ten minutes of the patient’s arrival
237
at hospital, but should not be performed at the expense
of treating life-threatening conditions (Rooney et al.,
1999). An erect ﬁlm is best, with a posteroanterior
view, if possible, to allow for optimal assessment of
lung expansion and assessment of free air or blood
within the thoracic cavity. A lateral chest ﬁlm may also
be useful at a later stage of management. The plain
chest radiograph is an excellent diagnostic tool, allowing the diagnosis of rib fractures (either single or
multiple), pulmonary contusion, haemothorax, pneumothorax, sternal fracture, widened mediastinum and
many other associated injuries. Great care needs to
be taken in the interpretation of the chest ﬁlm as it
has been reported that only 50% of rib fractures
are evident on the initial chest radiograph (Hyde et al.,
1998). Fractures involving the ﬁrst three ribs or scapula
should arouse suspicion of a high-energy injury and
the possibility of damage to intrathoracic organs
(Richardson et al., 1975). Fractures of the lower four
ribs may be associated with intra-abdominal injuries,
Figure 2 A CT scan (soft tissue window settings) of the upper chest=root of neck showing soft tissue trauma and
surgical emphysema
Trauma 2001; 3: 235–247
238
AM Ranasinghe et al.
particularly those of the liver, kidneys and spleen, as
well as diaphragmatic injuries.
Pneumothorax or haemothorax are usually quite
apparent if present, but less obvious features such as
pulmonary contusion may be more signiﬁcant. Pulmonary contusion may appear radiographically in a
variety of ways, ranging from diffuse inﬁltrate within
the involved segment of lung to complete whiteout of
the affected side.
It is important that serial chest radiographs are
obtained during the ongoing management of the
patient sustaining thoracic trauma. The timing of
these radiographs is dictated by the nature of the initial
injury to the patient and their subsequent progress.
They are a necessity after the placement of intercostal
drains, central monitoring lines and endotracheal
intubation. They are particularly important in the
patient with pulmonary contusion to evaluate the
development and extent of injury, as changes may
develop in an insidious manner.
Computed tomography (CT) scans
CT has become increasingly popular as an imaging
modality in thoracic trauma as it provides much more
sensitive information (Wagner et al., 1989 and Tocini
and Miller, 1987). In a previous study by Wagner and
colleagues, CT ﬁndings were compared with those of
chest radiographs in patients sustaining thoracic
trauma (Wagner and Jamieson, 1982). Excluding rib
fractures, CT was a much more sensitive indicator
of underlying pathology than the chest radiograph,
identifying 423 abnormalities compared with 151,
respectively. The use of CT is mainly limited by the
fact that the patient must be transferred to the scanner.
This is often inappropriate in the haemodynamically
unstable trauma patient. When applied, however, it is
particularly useful in assessing areas of consolidation
with regard to parenchymal damage and viability of
lung tissue, and for this reason it is one of the mainstays
of management and monitoring of suspected pulmonary contusion (Figures 2, 3 and 4).
Figure 3 A CT scan (soft tissue window settings) of the chest showing haematoma within the anterior mediastinum,
extensive soft tissue trauma and surgical emphysema
Trauma 2001; 3: 235–247
Management of ﬂail chest
239
Figure 4 CT scans (soft tissue (a) and lung window (b) settings) of the chest showing soft tissue trauma and left-sided
pulmonary contusion. A chest drain is also visible on the left side
Trauma 2001; 3: 235–247
240
AM Ranasinghe et al.
Other imaging modalities
These include ultrasound scanning (USS) and magnetic resonance imaging (MRI), which is limited by
expense and availability and the fact that there are
long periods of patient isolation, as well as the local
radiological expertise.
Rib fractures and the flail chest
syndrome
Rib fractures in isolation are not usually fatal. The
point at which they become part of a major source of
morbidity and mortality to patients is when they are
associated with other underlying problems such as
pulmonary contusion or laceration, pneumothorax
haemothorax. A single, uncomplicated rib fracture
may typically lead to a blood volume loss of up to
150 ml (Greaves et al., 1995).
Analgesia
It is of paramount importance to administer appropriate analgesia, even with simple rib fractures. If
opioid analgesia is necessary then caution should be
observed as it may cause centrally mediated respiratory depression. Intercostal nerve blocks are another
important adjunct to treatment, and are recommended
for multiple rib fractures. They may be performed by
inﬁltrating the affected area with 0.25–0.5% bupivicaine (beneath the inferior borders of all the fractured
ribs plus the rib above and below to allow for overlap
of innervated ﬁelds). Epidural analgesia is also an
excellent way of achieving pain relief and should be
encouraged if the clinical situation permits. Not only is
administration of analgesia humane, it allows for
improved chest wall excursion and alveolar ventilation, helping to correct the frequently encountered
hypoxia. Supplemental high ﬂow oxygen should also
be administered in all cases.
Fixation
There is no place for surgical ﬁxation of simple rib
fractures in current practice. If the patient requires
thoracotomy for another reason then it may be possible to stabilise rib fractures by the use of wires or plates,
although this is rarely performed.
Trauma 2001; 3: 235–247
Mechanism of injury
Any blunt injury of the chest wall can lead to the ﬂail
chest syndrome, with associated mechanical inefﬁciency due to the wide distribution of the applied
force. This is usually supplied in the form of gravity
(i.e., a fall from a height) or a motor vehicle accident.
As the incidence of road trafﬁc accidents has
increased so has the number of major chest and
intrathoracic injuries, including ﬂail chest (Goldstraw, 1998).
The bony ring of the thorax is compressed when an
external force is applied to it. The degree of damage
sustained by both the bony ring and underlying structures depends on both the energy applied to it and the
area over which the force is distributed (Figure 5). As
the force increases, the bony elements are more likely to
fracture. The pliable nature of the chest wall in children
means that these forces, unless particularly violent,
commonly cause underlying pulmonary contusion
without associated rib fractures (Morgan et al., 1990).
If the applied force causes a fracture of the bony ring in
at least two points on the circumference, then a ﬂail
segment may occur.
The ﬂail chest syndrome produces an isolated segment of thoracic cage, completely separate from the
rest of the chest wall. This results from a combination
of several fractures causing paradoxical movement of
the chest wall during respiration. On inspiration, the
ﬂail segment of the chest wall becomes indrawn by the
negative intrathoracic pressure, as it is no longer in
continuity with the bony ring. Similarly during expiration the ﬂail portion is pushed out while the rest of the
bony ring is ‘contracted’. A ﬂail chest may not always
be immediately apparent, clinically, due to splinting of
the chest wall, but a high index of suspicion is of
paramount importance. Palpation of abnormal
respiratory movements or crepitus of rib fractures
should act as a warning as to the possibility of a ﬂail
segment.
The real signiﬁcance of the detection of paradoxical
movement lies in the fact that the severity of trauma
necessary to produce a ﬂail segment has implications
with respect to damage of underlying intrathoracic
structures (Trinkle et al., 1975). The early mortality
attributable to the ﬂail chest syndrome is due to
massive haemothorax and pulmonary contusion,
whereas late mortality is largely due to adult respiratory distress syndrome (ARDS) (Tsai et al., 1999) and
associated infection.
Management of ﬂail chest
241
Table 3 Principles of the initial management of simple
rib fractures with flail segments
Minimise further lung injury
Analgesia
Ventilation and re-expansion of the lung if appropriate
Administration of high flow humidified oxygen and
cautious fluid resuscitation
further injury to the underlying lung, provide adequate
analgesia, and maintain oxygenation.
Table 3 represents an appropriate schematic method
of treatment for simple rib fractures with ﬂail segments. The greatest difﬁculties in management arise
in the polytrauma patient and in those who have
sustained extensive thoracic wall injury with large
ﬂail segments and pulmonary contusion. Stabilisation
of the ﬂail segment by the application of a sandbag or
by extensive strapping is contraindicated in the hospital environment as this leads to restriction of thoracic
wall movement (Myllynen et al., 1983).
In severe cases, conservative management will not
sufﬁce. More intensive management with ventilation
and surgical intervention will be required.
Mechanical ventilation
Figure 5 (a) The dynamics of a lateral flail chest injury.
Initially the ribs deform leading to contusion of the underlying lung. If the force is great enough the ribs fracture at
anterior and posterior angles. This segment of chest wall
can now move medially causing further damage to mediastinal structures and even the contralateral lung. After
the force stops acting, the flail segment returns to lie
within the arc of the chest wall. If intrapleural pressure
becomes positive (coughing) or less negative (pneumothorax) the flail segment resumes a normal anatomical
position or bulges outwards. (b) Application of force to the
anterior chest wall may lead to rib fracture at the anterior
and posterior angles on one or both sides. Reprinted from
New Aird’s Companion to Surgical Studies, Goldstraw,
1998, p. 555. By permission of the publisher Churchill
Livingstone
Management
The treatment of ﬂail chest remains controversial.
There are strong arguments in favour of all treatment
modalities (conservative, elective ventilation and surgery). The initial management of any patient with ﬂail
chest must be based on simple principles—minimise
Mechanical ventilation as a means of treating ﬂail chest
has been reported since 1952 (Jensen, 1952). Severe
respiratory distress is a deﬁnite indication for ventilation in ﬂail chest. Bertelsen and colleagues (1981)
suggested that patients with ﬂail chests should be
ventilated immediately if one or more of the conditions
listed in Table 4 were also present.
Patients requiring ventilation tend to need support
for periods of between 7 and 14 days. Christensson and
colleagues (1979) published a study in which they
carried out intermittent positive pressure ventilation
(IPPV) on a consecutive series of 35 patients with ﬂail
Table 4 Potential indications for ventilation in patients
with flail chest
Shock
Several associated injuries
Severe head injuries
Previous pulmonary disease
Fracture of eight or more ribs
Age >65 years
Trauma 2001; 3: 235–247
242
AM Ranasinghe et al.
chest. From this group one patient died due to haematological complications, and the remainder were safely
discharged. Late follow-up was possible on 18 of these
cases and spirometry studies performed at follow-up
showed minimal impairment of total pulmonary function. Radioisotope studies showed a signiﬁcant reduction of regional perfusion in only ﬁve patients, which
has limited signiﬁcance (Christensson et al., 1979).
However, the overwhelming evidence remains that
surgical ﬁxation is only indicated in a minority of cases
(Carbognari et al., 2000). The indications, approach
and techniques for stabilisation remain uncertain and a
number of different methods have been described
(Carbognari et al., 2000, Menard et al., 1983).
Pulmonary contusion
Surgical intervention
Ahmed and Mohyuddin (1995) studied a group of
patients with ﬂail chest at two major hospitals over a
10-year period. In over 400 patients who presented to
them during this period, ﬂail chest was the predominant pathology in 64 of them. Of these, 25 were treated
by surgical intervention and ventilatory support. The
remainder were treated by elective endotracheal intubation and IPPV. The average duration of ventilation
for the group treated by surgical intervention was four
days compared with 15 days for the non-surgically
managed group, with an average intensive care unit
stay of 9 and 21 days respectively. They noted that
there were a greater number of complications including
septicaemia, chest infection and insertion of tracheostomy in the non-operative group. The mortality rate
was also higher; 29% compared with 8%. All deaths in
both groups were attributed to ARDS. The aim of surgical intervention in these patients was to decrease the
amount of time spent on the ventilator and therefore
avoid the many complications associated with both
long-term ventilation and intensive care unit stay.
Voggenreiter and colleagues, performed a retrospective study on the outcomes of patients who underwent
surgical ﬁxation of ﬂail chest (Voggenreiter et al.,
1998). Two distinct groups were identiﬁed; those with
ﬂail chest and pulmonary contusion and those without
pulmonary contusion. The diagnosis of pulmonary
contusion was made by a combination of plain chest
radiography and ﬂexible bronchoscopy. A further two
groups with the same criteria as the original groups
were also identiﬁed. These patients were treated without surgical ﬁxation. They found that surgical ﬁxation
conferred a beneﬁt on early extubation only in patients
without pulmonary contusion. The conclusion was
that the patients suffering from pulmonary contusion
should only be considered for surgical intervention in
the case of progressive thoracic cage collapse during
weaning from the ventilator after resolution of the
pulmonary contusion.
Trauma 2001; 3: 235–247
The management of pulmonary contusion is the most
important aspect of management in the patient with
ﬂail chest. As already described, blunt thoracic trauma
and ﬂail chest often lead to pulmonary contusion. Both
thoracic wall injury and pulmonary contusion are
serious conditions, but contusion is the single most
important in terms of its contribution to respiratory
failure (Taylor et al., 1982 and Clark et al., 1986).
In younger patients, severe pulmonary contusion
can occur without fractures of the bony thorax due to
the compliant nature of the thoracic cage. Conversely
in elderly patients severe rib fractures and ﬂail segments
can be present with minimal underlying pulmonary
contusion due to the brittleness of the bones. It is
important therefore to recognise pulmonary contusion
as a serious but potentially isolated complication
following blunt thoracic trauma.
Pulmonary contusion is essentially haemorrhage
within the lung parenchyma secondary to direct
damage from an external source. This haemorrhage is
often localised to areas that are adjacent rib fractures,
but this is not always the case. Contusion of the
underlying lung leads to an accumulation of interstitial
ﬂuid with the consequence of ventilation=perfusion
mismatch, which may lead to respiratory embarrassment. Arterio-venous shunting often occurs. Failure of
adequate expansion due to mechanical insufﬁciency
leads to further respiratory compromise and the work
of breathing increases. Pain, restricted chest wall
movement and paradoxical motion further compound
these problems. These all lead to further deterioration
in respiratory function and decline in arterial blood
gases, potentially leading to a type I respiratory failure.
In animal studies, Fulton and Edward (1970) have
shown that pulmonary contusion is a progressive condition, at least within the ﬁrst 24 hours following
injury. The initial injury is mainly parenchymal haemorrhage. However, following the injury oedema
accumulates within the lung interstitium and alveoli.
The normal cellular responses following injury are
particularly harmful in the lung. This is due to the
Management of ﬂail chest
formation of a barrier between the alveolar air space
and capillary blood vessels, increasing the diffusion distance for both oxygen and carbon dioxide. An increase
in pulmonary vascular resistance is also noted to
occur. The oxygen diffusion barrier is frequently not
improved by IPPV.
Trinkle and colleagues (1975) realised the importance of treating the underlying pulmonary contusion
in cases of ﬂail chest. They studied two comparable
groups of patients who had experienced thoracic
trauma. The ﬁrst group was treated with early intubation and mechanical ventilation. The second group was
treated aggressively by ignoring the paradox associated with the ﬂail chest and concentrating on the
underlying lung injury. The essentials of management
of this group were ﬂuid restriction, diuretics, vigorous
pulmonary toilet, steroids and albumin (Table 5)
(Mulder, 1980). This treatment regimen produced
excellent results with signiﬁcant reductions in mortality and complication rates as well as a decrease in
average hospital stay from 31 to 9 days.
The management of patients with pulmonary contusion with respect to ﬂuid resuscitation presents
difﬁcult management issues, particularly in the
patient who has sustained multiple injuries. The
underlying damaged lung is particularly sensitive to
ﬂuid overload (Fulton and Peter, 1973). Aggressive
administration of ﬂuids without careful monitoring
leads to increased lung water, consolidation and
increased intrapulmonary shunting. There is strong
evidence for the application of hypotensive resuscitation in these cases (Hyde et al., 1997). The type of
ﬂuid administered needs to be considered carefully in
pulmonary contusion and most would advocate the
use of colloid or blood products as the resuscitative
ﬂuid of choice whilst restricting crystalloids. Loop
diuretics such as frusemide have a role in the treat-
Table 5 Trinkle’s regimen for treating underlying lung
injury in thoracic trauma
Intravenous fluid restriction
Frusemide 40 mg on admission and then 40 mg daily
for the next 3 days
Methylprednisolone 500 mg i.v. on admission then
qds for 3 days
Salt-poor albumin
Replace intravascular volume with plasma or whole blood
Vigorous tracheobronchial toilet
Morphine and intercostal nerve blocks for analgesia
Supplemental oxygen to maintain pO > 80 mmHg
2
243
ment of those patients who have been overloaded
with crystalloid. For these reasons, such patients
should be monitored in a critical care setting where
ﬂuid administration can be carefully monitored by
central venous and if necessary pulmonary artery
catheters with an aim to keeping the patient in at
least an even and preferably a negative ﬂuid balance
depending on their parameters of tissue perfusion and
organ function.
Case study 1
A 21-year-old male was admitted to our Trauma Unit
as an air ambulance trauma alert. He had been the
driver of a car with no other passengers when he lost
control at speed on the motorway and hit a lamppost.
On arrival he was maintaining his own airway. He had
reduced breath sounds bilaterally. Bilateral chest
drains were inserted. Chest radiograph demonstrated
right posterior fractures of ribs 3 to 8 with a ﬂail
segment, a basal pleural effusion and pulmonary contusion. The left side revealed posterior rib fractures.
Due to low systolic blood pressure and a distending
abdomen the patient was taken forward to laparotomy
where haemostasis of two liver lacerations was
achieved by packing. He was transferred to the intensive care unit.
A cardiothoracic surgical opinion was sought. The
patient had impaired gas exchange on IPPV. Judicious
ﬂuid input was advised, aiming to limit crystalloid
infusion to 1500 ml in 24 hours and maintain ﬂuid
balance with either colloid or blood products. A
prolonged period of IPPV for 10 to 14 days was
suggested. A CT scan of the chest and transthoracic
echocardiography were requested. CT scan conﬁrmed
the right-sided ﬂail segment and pulmonary contusions. Six days after admission the sequence of chest
radiographs was consistent with developing ARDS
and pneumonic changes, and the patient was still
ventilated with high oxygen requirements. Eight days
after admission, the patient was seen by the cardiothoracic surgeons, who were concerned with his general
lack of progress. Daily chest radiographs were
requested and a CT chest as soon as the patient was
stable enough to travel to the scanner.
Ventilatory requirements increased and at this
stage the patient’s chest radiograph was consistent
with ARDS. Concerns were raised regarding a possible loculated pleural effusion or developing lung
abscess. Intercostal drainage was now minimal. CT
Trauma 2001; 3: 235–247
244
AM Ranasinghe et al.
scan of the chest was reported as showing extensive
widespread pulmonary consolidation most marked
posteriorly with small bilateral pleural effusions and
no signiﬁcant pneumothorax. The overall appearances were in keeping with ARDS and no convincing
intrapleural abscess could be seen. One week later a
repeat CT scan of the chest showed little change,
with bilateral pulmonary consolidation with air
bronchograms.
Slow improvement was noted over the next few
days with a decrease in oxygen requirements and
several periods of spontaneous ventilation. The
patient continued to make slow improvement. A
tracheostomy was inserted in order to aid weaning
from the ventilator. Excellent progress ensued, culminating in conversion to a CPAP (Continuous Positive
Airway Pressure) circuit. Weaning continued and
eventually after 33 days patient was managing to self
ventilate without any need for pressure support.
The patient was eventually transferred out to a
trauma ward. After 51 days the patient was transferred
to his local hospital for a period of rehabilitation. He
was seen three months after his accident in the orthopaedic outpatient clinic and noted to be making an
excellent recovery.
Figure 6
Case study 2
A 47-year-old male was admitted to our Trauma Unit
as a helicopter trauma alert. The patient was involved
in a sidecar race and made impact with a brick wall at
approximately 100 mph with the left side of his chest.
The immediate care team on site noted that he had
surgical emphysema and clinical evidence of a left ﬂail
chest with decreased air entry on the right. Therefore,
bilateral chest drains were inserted. The patient was
electively intubated for transfer. A total of two litres of
intravenous crystalloid was given at the scene.
On arrival, the patient was haemodynamically
stable, with good air entry bilaterally. A chest radiograph showed right-sided rib fractures, and a leftsided ﬂail segment with rib fractures from 3 to 9
(Figure 1). In addition, there were bilateral haemopneumothoraces and an increased cardiothoracic
ratio with a pneumomediastinum. A cardiothoracic
opinion was sought and a CT scan of thorax
and abdomen and a transthoracic echocardiogram
were requested. Advice was also given with regard to
ﬂuid balance to limit intravenous crystalloid administration to less than 1.5 litres per day. The plan
was to give a period of intermittent positive pressure
A plain chest radiograph taken in the outpatient clinic 10 weeks after the initial flail chest injury
Trauma 2001; 3: 235–247
Management of ﬂail chest
ventilation and aim to wean from ventilatory support in 10–14 days with a thoracic epidural for
adequate pain relief. CT scan of the chest demonstrated underlying pulmonary contusion and a left
ﬂail segment. Oxygen requirements decreased over
the next few days and excellent progress was made in
terms of weaning from the ventilator. A thoracic
epidural was inserted four days after the initial
injury. The patient was extubated without any problems eight days after the initial injury. Both chest
drains were also removed at this point. The patient
was then transferred to the cardiothoracic high
dependency unit where he made excellent progress
and was discharged after 16 days. He was reviewed
in the outpatient clinic six weeks after discharge and
had returned to a normal life with no limitations
(Figure 6).
Case study 3
A 39-year-old male motorcyclist was admitted to a
peripheral district general hospital following a collision with a tree. On arrival he had a Glasgow coma
245
score of 15, and pain on the left side of his chest. He
had clinical evidence of surgical emphysema with a
left-sided ﬂail segment. Chest radiography conﬁrmed
the left-sided ﬂail segment and an associated haemopneuthorax. An intercostal drain was inserted, which
drained 1.5 litres of blood. He was then cautiously
ﬂuid resuscitated with crystalloid and six units of
blood.
The patient was transferred to the ITU. He had been
intubated prophylactically for ambulance transfer. On
arrival he had good gas exchange. Chest radiography
revealed the ﬂail segment with underlying pulmonary
contusion of the left mid and upper zones. The left
intercostal drain was in a satisfactory position, but an
air leak was noted. CT scan of the chest and transthoracic echocardiogram were requested. The
CT chest demonstrated a persistent left-sided pneumothorax (approximately 40%). The management
was discussed with the cardiothoracic surgeons and
suction on the chest drain was increased to 10 kPa. The
pneumothorax persisted and a second intercostal drain
was inserted (Figure 7). A repeat CT demonstrated a
large anterior left-sided pneumothorax with a normal
aerated left lung. Flexible bronchoscopy demonstrated
Figure 7 A plain chest radiograph showing the use of multiple intercostal drains in the management of a persistent
pneumothorax following a left-sided flail segment
Trauma 2001; 3: 235–247
246
AM Ranasinghe et al.
a crushed lingular bronchus. A third intercostal drain
was inserted and all drains were placed on separate
suction systems. In view of the crushed lingular
bronchus and probability of a bronchopleural ﬁstula
a decision was made to take the patient to theatre for
thoracotomy.
In theatre rigid bronchoscopy revealed normal airway anatomy on the right. A left posterolateral
thoracotomy was performed through the 5th intercostal space. Both upper and lower lobes were contused and solid. There were a number of parenchymal
lacerations involving the apical segment of the lower
lobe and the inferior surface of the lingular. A major
air leak was identiﬁed emanating from the lower lobe.
It was not possible to identify the site of the bronchial
tear and a decision was made to proceed to an
anatomical left lower lobectomy. The procedure was
carried out uneventfully and the bronchial stump was
tested and airtight. Apical and basal drains were
placed. The ﬂail segment was not treated by surgical
ﬁxation. Sedation and ventilatory support were
weaned and he was extubated four days postoperatively. Serial chest radiographs demonstrated a
left-sided whiteout and an ultrasound of the chest
performed demonstrated consolidation with no ﬂuid
collection.
On transfer to the cardiothoracic high dependency
unit, sputum culture grew MRSA and a course of
vancomycin was started. Chest radiography at this
stage demonstrated a collection at the left base. Rigid
bronchoscopy was performed and this showed tracheitis, the left upper lobe bronchus was full of pus and
bronchial toilet was performed. The left lower lobe
staple line was noted to be healthy and no bronchopleural ﬁstula was demonstrated. CT-guided aspiration of this collection was performed with a pigtail
catheter. This was exchanged for a larger intercostal
drain one week later. Minimal drainage was obtained
from this. An air leak subsequently developed and
again concerns about a bronchopleural ﬁstula were
raised. Repeat CT scan demonstrated a ﬂuid-containing space with the intercostal drain in situ. Repeat
bronchoscopy showed normal left main stem bronchus, the left lower lobe stump showed no evidence of
ﬁstula. The patient’s antibiotics were eventually
stopped and he was discharged home. He was reviewed
in the outpatient clinic one month after discharge. The
patient remained clinically well and the chest radiograph showed progressive obliteration of the cavity on
left side. He is under outpatient review, and remains
clinically well.
Trauma 2001; 3: 235–247
Summary
Flail chest with associated pulmonary contusion is a
potentially lethal condition. The bony injury itself
usually only requires conservative treatment, which
is effective analgesia. The underlying pulmonary
contusion may develop insidiously over days, and it
is vital that this fact is suspected and recognised early.
Treatment with oxygenation, and early intubation and
ventilation in appropriate patients should be standard
management. If basic principles are adhered to, and all
suspected patients are closely monitored, excessive
morbidity and mortality may be avoided.
References
Ahmed Z, Mohyuddin Z. 1995. Management of ﬂail chest injury:
internal ﬁxation versus endotracheal intubation and ventilation. J Thor and Cardiovasc Surg 110: 1676–80.
American College of Surgeons, Committee on Trauma. 1997.
Thoracic trauma. In: Advanced trauma life support for doctors: student course manual, 6th edition. ACS.
Basmajian JV, Slonecker CE. 1989. In: Grant’s method of anatomy: A clinical problem-solving approach. 11th edition.
Bertelsen S, Bugge-Asperheim B, Geiran O, Siebke H. 1981.
Thoracic injuries. Ann Chir et Gynae 70: 237–50.
Carbognani P, Cattelani L, Michele R, Bellini G. 2000. A technical
proposal for the complex ﬂail chest. Ann Thor Surg 70:
342–43.
Christensson P, Gisselson L, Lecerof H, Malm AJ, Ohlsson MM.
1979. Early and late results of controlled ventilation in ﬂail
chest. Chest 75: 456–60.
Clark GC, William PS, Trunkey DD. 1986. Variables affecting
outcome in blunt chest trauma: ﬂail chest vs. pulmonary
contusion. J Trauma 28(3): 298–304.
Fulton RL, Edward ET. 1970. The progressive nature of pulmonary contusion. Surgery 67(3): 499–506.
Fulton RL, Peter ET. 1973. Physiologic effects of ﬂuid therapy
after pulmonary contusion. Am J Surg 126: 773–77.
Goldstraw P. 1998. In: Burnand KG, Young AE eds. The new
Aird’s companion in surgical studies. 2nd edition. Churchill
Livingstone.
Greaves I, Dyer P, Porter KM. 1995. In: Handbook of immediate
care. WB Saunders.
Hyde JAJ, Rooney SJ, Graham TR. 1997. Hypotensive resuscitation. In: Greaves, Porter, Ryan eds. Trauma. London:
Edward Arnold.
Hyde JAJ, Shetty A, Kishen R, Graham TR. 1998. In: Driscoll PA,
Skinner DV eds. Trauma care: beyond the resuscitation room.
1st edition. London: BMJ Publications.
Jensen NK. 1952. Recovery of pulmonary function after crushing
injuries of the chest. Dis Chest 22: 319.
Mansour KA. 1997. Trauma of the chest. Philadelphia: WB
Saunders.
Menard A, Testart J, Philippe JM, Grise P. 1983. Treatment of
ﬂail chest with Judet’s struts. J Thor and Cardiovasc Surg 86:
300–5.
Management of ﬂail chest
Morgan WE, Salama FD, Beggs FD, Firmin RK, Rowles JM.
1990. Thoracic injuries sustained by the survivors of the M1
(Kegworth) aircraft accident. The Nottingham, Leicester,
Derby, Belfast Study Group. Eur J Cardiothoracic Surg 4:
417–20.
Mulder DS. 1980. Chest trauma: current concepts. Can J Surg
23(4): 340–42.
Myllynen P, Kivoja A, Wilppula E, Rokkanen P, Mattila S,
Laakso E. 1983. Flail chest—pathophysiology, treatment
and prognosis. Ann Chir et Gynae 72: 43–46.
Richardson JD, Adams L, Flint LM. 1982. Selective management
of ﬂail chest and pulmonary contusion. Ann Surg 196(4):
481–87.
Richardson JD, McElvein RB, Trinkle JK. 1975. First rib fracture: a hallmark of severe trauma. Ann Surg 181(3): 251–54.
Rooney SJ, Hyde JAJ, Graham TR. 1999. In: Skinner D,
Driscoll P, Earlham R eds. ABC of major trauma. 3rd edition.
London: BMJ Publications.
Roux P, Fisher RM. 1992. Chest injuries in children: an analysis
of 100 cases of blunt chest trauma from motor vehicle
accidents. J Paed Surg 27(5): 551–55.
Sinnatamby CS. 1998. In: Last’s anatomy: Regional and applied.
10th edition. Churchill Livingstone.
Stellin G. 1991. Survival in trauma victims with pulmonary
contusion. Am Surg 57(12): 780–84.
247
Taylor GA, Hensley A, Miller MB, Shulman HS, DeLacey JL,
Maggisano R. 1982. Symposium on trauma. Controversies in
the management of pulmonary contusion. Can J Surg 25(2):
167–70.
Tocini I, Miller MH. 1987. Computed tomography in blunt chest
trauma. J Thor Imaging 2(3): 45–59.
Trinkle JK, Richardson JD, Franz JL. 1975. Management of ﬂail
chest without mechanical ventilation. Ann Thor Surg 19: 355.
Tsai FC, Chang YS, Lin PJ, Chang CH. 1999. Blunt trauma with
ﬂail chest and penetrating aortic injury. Eur J Cardiothorac
Surg 16: 374–77.
Voggenreiter G, Neudeck F, Aufmkolk M, Obertacke U, SchmitNeuberg KP. 1998. Operative chest wall stabilization in ﬂail
chest—outcomes of patients with or without pulmonary
contusion. J Am Coll Surg 187(2): 130–38.
Wagner RB, Crawford WO, Schimpf PP. 1982. Classiﬁcation of
parenchymal injuries of the lung. Radiology 167: 77–82.
Wagner RB, Jamieson PM. 1989. Pulmonary contusion: evaluation and classiﬁcation by computed tomography. Surg Clin
North Am 69(1): 31–40.
Westaby S, Odell JA eds. 1999. Cardiothoracic trauma. 1st
edition. London: Arnold.
Trauma 2001; 3: 235–247