LMCC Review in Thoracic Surgery
April 2010
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Dysphagia
GERD and Hiatus hernia
Chest trauma
Massive hemoptysis
Pneumothorax
Empyema
A barium swallow was performed on an ELDERLY
patient who had difficulty in swallowing
1. What is the diagnosis?
2. What are the
complications of this
condition?
3. Is treatment
necessary?
4. What treatment is
possible ?
Dysphagia – Zenker’s Diverticulum
WHAT IS IT?
• Pharyngo-esophageal
diverticulum
• False “pulsion”
diverticulum containing
mucosa and submucosa
• Occurs in the neck just
above the UES at the
pharyngoesophageal
junction through Killian’s
triangle
Develops on posterior wall of pharynx between
upper and lower divisions of inferior constrictor
muscle
UES
Zenker’s Diverticulum
• In most cases the
initiating cause is
unknown
• In some cases the cause
is GERD related UES
spasm
• ACQUIRED – 80% occur
in age >50 yrs
• Most common
esophageal
diverticulum
• WHAT ARE THE
SYMPTOMS AND
SIGNS?
• Intermittent cervical
dysphagia
• Gurgling noises in the
neck on drinking liquids
• Food regurgitation
• Foul breath
• Left neck swelling
• Spells of choking
Zenker’s Diverticulum
• HOW IS THE
DIAGNOSIS MADE?
Barium Swallow
• IS IT SERIOUS?
• Life-threatening due to
acute aspiration
pneumonia, lung abscess
and empyema
• Disability due to recurrent
aspiration pneumonia,
fibrosis, bronchiectasis
• Total dysphagia can
occur with large
diverticulum distending
with retained food
causing extrinsic
compression
What is the treatment?
• NEED AN OPERATION
1. Cricopharyngeal
myotomy in all the cases
2. Management of
diverticulum depends on
size
• Small < 3 cm: no
need for excision
• Large > 3 cm: add
diverticulectomy
• Concomitant
Symptomatic GERD
– Should be managed
first - otherwise risk
free aspiration after
operation for
diverticulum
– Reason: Reflux is due
to incompetent LES.
Operation for Zenker’s
diverticulum will make
UES hypotensive
A 35-year-old man with slowly worsening difficulty
swallowing had barium study performed
1. What is
demonstrated in this
barium swallow?
2. What are the
essential clinical
features?
3. What is necessary to
confirm diagnosis?
4. What treatment
would you suggest?
Dysphagia - Achalasia
WHAT IS IT?
• Esophageal motility
disorder characterized by
1.Absence of peristalsis in
the body of the
esophagus
2.Failure of or incomplete
relaxation of LES is
response to swallowing,
3. Higher than normal
resting LES pressure
Achalasia
WHAT IS THE CAUSE?
• NA – cause is unknown,
viral infection,
autoimmune
• SA – Chagas’ disease
due to parasite
Trypanosoma Cruzi
• Finding: degeneration of
ganglion cells in
Auerbach’s plexus
• WHAT ARE THE
SYMPTOMS?
• Dysphagia for both solids
and liquids; worse with
liquids
• Retrosternal burning
discomfort due to food
stasis and retention
esophagitis
• Nocturnal regurgitation of
food and choking
episodes  aspiration
Esophageal Manometry confirms
the diagnosis
LES does not relax during swallow
Absence of peristalsis
Achalasia: Investigations and
Results
BARIUM SWALLOW
APPEARANCE IS
CHARACTERISTIC
Esophageal dilatation
Spastic non-peristaltic contractions
Retention of contrast above poorly
relaxing LES at G-E junction
‘bird’s beak’ with obstruction
UGI ENDOSCOPY IS
NECESSARY TO RULE OUT
CANCER (PSEUDOACHALASIA)
AND PEPTIC STRICTURE
Evidence of stasis
Dilated esophagus with retained
food, liquid, saliva
Mucosal inflammation ‘retention
esophagitis’
ESOPHAGEAL MANOMETRY IS
NECESSARY TO CONFIRM THE
DIAGNOSIS
Incomplete or absent relaxation of
LES
Absence of normal peristalsis in
body of esophagus
Diagnosis of Achalasia
• Suspect diagnosis:
from symptoms
• Support diagnosis:
from esophagogram
see “Birds Beak”
deformity
• Confirm diagnosis:
from UGI Endoscopy
and Manometry
Achalasia and Epiphrenic
Diverticulum
Always suspect underlying cause for epiphrenic diverticulum
The cause must be treated as well
Complications of Achalasia
• ESOPHAGUS
– Malnutrition
– Progressive dilatation
– Retention esophagitis
– Epiphrenic
diverticulum
– Esophageal cancer:
squamous (due to
retention esophagitis)
adenocarcinoma ( due
to post treatment
reflux – Barrett’s
epithelium)
• RESPIRATORY
– Aspiration pneumonia,
empyema, lung
abscess, fibrosis,
bronchiectasis
– Dyspnea due to
extrinsic tracheal
compression
• PSYCHOSOCIAL
– Unable to eat in public
– withdrawn
What is the treatment for
Achalasia?
• Chronic condition, no cure for it
• Aim of Treatment: relieve distal
esophageal functional obstruction
• Choices of treatment:
• Pneumatic “Balloon” dilatation, initial success rate
of 80% decreases to 50% at 10 years; esophageal
perforation risk of 5%
• Intra-sphincteric injection of Botox, symptomatic
relief of 60% decreases to 30% at 2.5 years
• Distal esophagomyotomy and partial
fundoplication gives the best sustained result of
90%, postoperative reflux is about 15% over time
Distal Esophago-Myotomy and
Partial Fundoplication
Distal Esophageal Spasm
Abnormality
LES
May be abnormal
Incomplete relaxation
Esophageal Body Contractions
20% or more simultaneous*
Repetitive >2 peaks
Prolonged duration > 6 sec
Spontaneous contractions
Intermittent normal peristalsis*
High amplitude not common
Distal Esophageal Spasm
• “The lower part of the
esophagus (smooth
muscle) of patients with
diffuse esophageal
spasm is simultaneously
and firmly contracted for
an abnormally long time”
• Severe pain, dysphagia,
and presence of
esophageal diverticulae
Treatment
• Reassurance in most
cases
• Surgical treatment cannot
correct the functional
disorder
• Long Esophagomyotomy
to lower amplitude of
waves and resting
pressure; add Partial
Fundoplication
Distal Esophageal Spasm
Nutcracker esophagus
• High Amplitude,
Peristaltic Esophageal
Contractions
• > 180 mmHg amplitude
• Long duration
contractions > 6 sec
• LES is normal
Treatment
• Reassurance in most
cases
• Must exclude myocardial
ischemia
• Long Esophagomyotomy
in selected cases; add
Partial Fundoplication
Nutcracker Esophagus
Abnormality
LES
May be hypertensive
Esophageal Body
High amplitude
mean DEA>220 mm Hg
May be long duration
Mean > 6 sec
Normal peristalsis
Gastroesophageal Reflux Disorder
WHAT IS IT?
• Frequent retrograde flow
of gastric contents across
the GE junction into the
esophagus
• WHAT ARE THE TWO
TYPES OF REFLUX?
– Physiological
– Pathological – GERD
WHAT IS THE REASON?
• Loss of barrier function
of the LES, either
continuous or intermittent
• REFLUXATE
– Acid or Alkaline reflux
– HCL, Pepsin, Bile, Bile
salts
What are the properties of LES?
•
•
•
•
•
•
Major barrier to reflux – HIGH PRESSURE ZONE
Physiological sphincter
Located in the last 2 to 4 cm of esophagus
Normal resting tone 15 to 30 mm. Hg
Relaxation is coordinated with primary peristalsis
LES pressure is decreased by estrogen, progesterone,
nitroglycerine, calcium channel blocker, cigarette
smoking, alcohol, fat rich meals, gastric distension,
coffee, chocolates, vagotomy, distal esophagomyotomy
Lower esophageal sphincter has
become incompetent in GERD
• WHAT ARE THE
CAUSES OF
PATHOLOGIC GERD?
• Idiopathic - majority
• After pneumatic dilatation
or esophagomyotomy for
Achalasia
• Scleroderma
• Fixed large hiatus hernia
• Gastric outlet obstruction
• Prolonged nasogastric
tube insertion
• WHAT ARE THE
TYPICAL SYMPTOMS?
• Unpleasant and intense
substernal burning
sensation
• Substernal chest pain
• Postural and/or
postprandial regurgitation
• Water brash
• Flatulence
• Intermittent difficulty with
swallowing
Complications of Pathologic
Gastroesophageal Reflux Disorder
• ESOPHAGUS - reflux
esophagitis:
inflammation, erosion and
ulceration
 chronic blood loss
and iron deficiency
anemia, fibrosis and
peptic stricture,
Barrett’s epithelium 
dysplasia 
adenocarcinoma
• UES SPASM  Zenker’s
diverticulum
• MOUTH - teeth decay
and loss of enamel
• PROXIMAL AIRWAY laryngitis, wheezing,
cough
• LUNGS - aspiration
pneumonia  lung
abscess, pulmonary
fibrosis, bronchiectasis,
empyema
Reflux and Esophageal Damage
How is the diagnosis of GERD
made?
• Barium swallow and UGI series
– radiologic reflux, hiatus hernia, esophageal stricture,
aspiration, spasm in UES
• Upper GI endoscopy
– esophagitis (erythema, erosions, ulcerations,
stricture formation), columnar-lined esophagus
• Esophageal manometry
– decreased LES, ineffective esophageal peristalsis
• 24-hour esophageal pH monitoring
• Most sensitive test for acid reflux: number of
reflux episodes, duration of reflux, upright vs.
supine
What is the treatment for GERD?
• FIRST MEDICAL
THERAPY
• Dietary modification
– Small meals, avoid
eating for 2 hrs before
going to bed
• Elevate head of the bed
• Abstain from coffee,
alcohol, trigger foods
• Drugs: Antacids, PPI, H2blockers
• SURGICAL THERAPY IS
BY FUNDOPLICATION
• When GERD is
refractory to optimal
medical therapy given for
a minimum of 6 months
• When GERD is
associated with
complications of hiatus
hernia, complications in
the airway
An elderly patient in the ER complaining of central
chest pain radiating into left shoulder, retching, and
coffee ground emesis. Barium study from 12
months ago for similar complaint is shown
1. What condition is
shown?
2. How does it affect
the patient?
3. What serious
problem can occur?
Complications of Hiatus Hernia
1. Incarceration  strangulation  ischemic
perforation  death
2. Anemia – chronic blood loss due to mucosal
congestion
3. Dyspnea – large hernia
4. Cardiac Arrhythmias – extrinsic pressure
5. Volvulus obstruction
6. Perforation
7. Massive Bleeding
Type I
Type II
Type III
Type IV hiatus hernia
Intrathoracic stomach with risk of volvulus, associated herniation
of transverse colon, small bowel
Management of Hiatus Hernia
Classification
Type I – most
common
Type II – very
rare
Type III –
mixed Type I
and II
Type IV
INCIDENCE
85% to 90%
Pure is rare <
1%
About 6%
Least
common
SYMPTOMS
May be
asymptomatic
or have
GERD
Asymptomatic Symptoms of
or come to ER incarceration
with
and reflux
incarceration/
strangulation
Nearly whole
stomach in
the chest; risk
of volvulus,
obstruction,
bleeding
INDICATION
FOR
OPERATION
GERD
refractory to
medical
therapy
To prevent
strangulation
and ischemic
perforation
Anatomical
correction is
indicated
Medical
therapy is not
that effective
A barium study is finally given to a patient whose
complaint for difficulty swallowing was for ignored
for 5 months
• What are the clinical
features of this
condition?
• What is the
differential diagnosis?
• What investigations
should be
undertaken?
• What treatments are
available?
Esophageal Cancer
• WHAT ARE THE TWO
MAIN CELL TYPES?
• Adenocarcinoma
• Squamous cell carcinoma
• WHAT IS THE MOST
COMMON HISTOLOGY?
• Worldwide: squamous
cell carcinoma 95%
• Western world:
adenocarcinoma
Squamous Cell Cancer – what are
the etiological factors?
• Strong association with excess cigarette smoking and
alcohol consumption
• Three dietary factors are high intake of nitrosamines
(food preservatives), low intake of both vitamin A and
nicotinic acid, and chronic iron deficiency
• Long standing achalasia, accidental caustic ingestion
• Tylosis palmaris et plantaris
• Celiac disease
• Silica in wheat
• Previous radiation therapy to the mediastinum
Adenocarcinoma – what is the
cause?
• Incidence of adenocarcinoma is rising in
NA – an explosion
• Due to Chronic GERD – not necessarily
acid reflux
• Refluxate: acid, pepsin, bile salts, bile
• Develops in acquired metaplastic Barrett’s
epithelium
Chronic GERD: Adenocarcinoma
Mucosal Squamous Epithelium
Metaplasia
Mucosal Columnar Epithelium
“Barrett’s Esophagus” specialized intestinal
Dysplasia
Low grade
High Grade
Adenocarcinoma
In situ
Invasive
Barrett’s Esophagus
Esophageal Cancer
• WHAT ARE THE
SYMPTOMS?
• Progressive dysphagia,
initially for solids and later
for liquids
• Progressive weight loss
• Means only one
diagnosis – Cancer
• Other symptoms – chest
pain, back pain,
hoarseness, choking and
aspiration, symptoms of
metastasis
• HOW IS THE
DIAGNOSIS MADE?
• Barium UGI series
• Esophagoscopy and
mucosal biopsies
• HOW IS STAGING
DONE?
• Staging requires CT scan
chest and abdomen,
Esophageal U/S, PET
scan
Treatment for Esophageal Cancer
• Surgical: esophagectomy and reconstruction
with stomach or colon interposition
• Induction chemotherapy and radiotherapy before
surgery
• Definitive Radiotherapy only: local treatment
• Intent: palliation – symptom control
• Intent: cure – disease control
• Definitive chemotherapy combined with radiation
• Esophageal stent: palliation
Esophagectomy
Benign Tumors of Esophagus
• Leiomyoma is the most common
• 90% occur in the lower 2/3rd of the
esophagus
• Grow slowly and cause dysphagia when
size becomes >5 cm
• Treatment is surgical by enucleation
Esophageal Leiomyoma
Immediately life-threatening chest
injury - Cardiac Tamponade
• WHAT IS IT?
Bleeding into the pericardial
sac, resulting in constriction of
right side of the heart, impaired
venous return to the heart
resulting in decreased stroke
volume and cardiac output
• In acute situation – the
pericardium does not stretch
and rapid intrapericardial
accumulation of even 150mls
blood can lead to cardiac
tamponade
• WHAT ARE THE SYMPTOMS
AND SIGNS?
– Suggestive wound
– Pulse↑, BP↓, JVP↑ Pulsus
paradoxus, Kussmaul’s
sign
• DEFINE BECK’S TRIAD
– Hypotension, Raised JVP,
Muffled heart sounds
• WHAT IS KUSSMAUL’S
SIGN?
– Jugular venous distension
with inspiration
Cardiac Tamponade in Chest
Trauma
• HOW IS CARDIAC
TAMPONADE
DEFINITELY
DIAGNOSED IN CHEST
TRAUMA?
• By Echocardiogram
• Nature of the chest
injury
• Not from CXR – don’t
expect to see
cardiomegaly
• WHAT IS THE
TREATMENT?
• Resuscitation protocol for
Airway – Breathing –
Circulation
• Immediate IV fluid bolus
• After pericardiocentesis
follow with mandatory
surgical exploration
• Pericardiocentesis is a
temporizing procedure
Chest Trauma: Cardiac Tamponade
Intrapericardial Pressure
(mm Hg)
Immediately life-threatening chest
injury - Massive Hemothorax
• WHAT IS IT?
– Bleeding into the pleural
space
• HOW IS IT DIAGNOSED?
– Hypotension
– Decreased or absent
breath sounds on one or
both sides
– Dullness to percussion
– CXR, CT scan
– Chest tube output
Immediately life-threatening chest
injury - Massive Hemothorax
• WHAT IS THE SOURCE
OF BLEEDING?
– LOW pressure
bleeding from lung
laceration; often
SELF-LIMITING
– HIGH pressure
bleeding from ICA,
IMA, Aorta, Major arch
arteries, Vena Cava,
Azygous vein;
PERSISTENT
BLEEDING
Massive Hemothorax
• WHAT IS THE TREATMENT?
– Replace blood volume
lost
– Insert chest tube and
monitor for blood loss
– Aim to evacuate blood
and blood clots as
much as possible
– Use cell saver, if
available
– Consider urgent
operation
• WHAT ARE THE
INDICATIONS FOR
EMERGENY
THORACOTOMY FOR
HEMOTHORAX?
• Initial chest tube drainage
of >1500 mls of blood
• Persistent bleeding after
initial drainage: >200mls
of blood loss/hr for 3 hrs
• Unevacuated residual
blood and blood clots on
CXR
Massive Hemothorax
• Pleural space can accommodate large amount
of free and clotted blood >1.5L
• Hypotension from loss of circulating volume and
tension effect
• Hypoxia from compressive atelectasis
• Bleeding into pleural space is of two types
– High pressure bleeding from systemic arteries and
veins; continuous and not self-limiting
– Low pressure bleeding from torn lung parenchyma;
self-limiting and stops with lung re-expansion
Hemothorax
• Insert a large bore chest tube # 28F or 32F
• Measure initial blood loss
• CXR is lung expanded? Unevacuated clotted
blood/blood clots?
• Monitor for on-going bleeding and recognize lifethreatening situation
• > 500 ml in 1 hr
• > 400 ml/hr for 2 hrs
• > 300 ml/hr for 3 hrs
• Action: Urgent Thoracotomy to stop bleeding
Immediately life-threatening chest
injury – Open Pneumothorax
• What is the medical term
for a “sucking chest
wound”?
– Open pneumothorax
Penetrating chest injury – gun shot
Open Pneumothorax
• HOW IS AN OPEN
PNEUMOTHORAX
DIAGNOSED?
• Diagnosis is usually
obvious, with air
movement through a
chest wall defect and
pneumothorax seen on
CXR
Pathophysiology of
Open Pneumothorax
1. If the chest wall defect is large
 the effect is very serious
 immediate respiratory distress  ACUTE
VENTILATORY FAILURE  death occurs rapidly
2. If the chest wall defect is small
 the effect is less serious
and outcome will depend on vital capacity
Treatment of Open Pneumothorax
• How is open
pneumothorax treated?
– Treatment in the ER
should be immediate
– Cover the chest wall
defect with sterile
occlusive airtight
dressing
– Insert intercostal chest
tube as soon as feasible
– Alternate treatment is
endotracheal intubation
and assisted positive
pressure ventilation
Patient involved in MVA is found to be markedly
hypoxic in the ER. CXR was performed.
1. What is illustrated on
CXR?
2. Why is there a
change in oxygen
saturation?
3. What is the reason
for NGT insertion?
4. How should he be
managed?
Pulmonary Contusion
• Interstitial & parenchymal
hemorrhage with alveolar
collapse
• Extravasation of blood and
plasma into alveoli.
• V-Q Mismatch
• Hypoxemia that is refractory
to increase in FiO2
• Decrease in pulmonary
compliance and increase in
work of breathing.
• Occurs in 70% of severe
blunt trauma
• Mortality overall 20 – 30%
Chest Trauma
• The most common physiologically significant injury
resulting from blunt chest trauma is
a.
b.
c.
d.
e.
flail chest
pulmonary hematoma
subcutaneous emphysema
pulmonary contusion
diaphragm rupture
Chest Trauma
• The most effective single modality in treating severe
pulmonary contusion associated with post-traumatic
respiratory distress and hypoxia is
a.
b.
c.
d.
e.
fluid restriction
intravenous albumin
assisted ventilation with pressure support
diuresis
methylprednisone
discussion
• Fluid restriction is certainly indicated giving
<1500mls/day
• Antibiotics only for sepsis complicating contusion
• Serum albumin to reduce alveolar edema
• The single most effective modality for treatment
of pulmonary contusion is mechanical ventilation
with addition of PEEP
– Improves FRC
– Improves oxygenation by keeping alveoli open
– Insert chest tube to prevent tension pneumothorax
Immediately life-threatening chest
injury – Flail Chest
• WHAT IS FLAIL CHEST
INJURY?
– Due to two separate
fractures in three or
more rib
– Anterior, Lateral, or
Posterior location
– Indicative of severe
blunt chest trauma
Immediately life-threatening chest
injury – Flail Chest
• HOW IS IT DIAGNOSED?
– PARADOXICAL
RESPIRATION
– Flail segment of chest
wall sucks in with
inspiration and pushes
out with expiration
opposite the rest of the
chest wall
– Respiratory
compromise is not due
to paradoxical
respiration
TRAUMA VICTIM
CHEST INJURY
BRUISING ON CHEST WALL
SURGICAL EMPHYSEMA
ACUTE CHEST PAIN
BREATHING DIFFICULTY
Flail Chest Injury  Hypoxia
1. Damaged painful unstable chest wall
2. Underlying lung contusion
3. Pleural space problems
4. Chest wall muscle damage and spasm
Paradoxical respiration is not the cause of deranged physiology
What is the cause of respiratory
compromise in Flail Chest Injury?
1.Damaged painful unstable chest wall
– Normal ventilatory force is lost  lung expansion
decreases  FRC falls
– Cough is impaired  retention of secretions 
retention atelectasis  V/Q mismatch  hypoxia
2. Underlying lung contusion
– Hemorrhagic, edematous, non-compliant lung 
impaired diffusion  hypoxia
3. Pleural space problems
– Hemothorax and/or pneumothorax  compressive
atelectasis  V/Q mismatch  hypoxia
4. Chest wall muscle damage and spasm, increased
work of breathing and oxygen demand, hypoxia 
muscle fatigue and oxygen debt
Flail Chest Injury
Multiple rib fractures
Lung contusion is always present
Management of Flail Chest Injury
• ISOLATED INJURY
– Admit to ICU, supplemental
oxygen, optimal pain
control (best is by thoracic
epidural analgesia),
physiotherapy, insert chest
tube if needed,
bronchodilators, restrict IV
fluids (worsens edema
from lung contusion)
– Refractory hypoxia admit to
ICU, assisted ventilation,
insert chest tube (must do
this, otherwise risk tension
pneumothorax
• MULTIPLE INJURIES
– Admit to ICU after lifethreatening injuries have
been looked after
– Assisted ventilation to
maximize oxygenation
– Optimal pain control
– Chest tube inserted
Chest Trauma
• A 24-year-old man is brought into the ER after a fall from
a ladder. His breathing is laboured, and he is cyanotic.
He is complaining of right chest pain. There is
subcutaneous emphysema on the right side. No breath
sounds can be heard in the right lung field, which is
resonant to percussion. Among the following choices, the
most appropriate next step in his management is:
a. obtaining a stat chest X-ray
b.
c.
d.
e.
insertion of an endotracheal tube
cricothyroidotomy
stat arterial blood gas analysis
Immediate needle decompression and chest tube insertion
Pathophysiology of Tension Pneumothorax
1. Progressive
accumulation of
air in pleural
space under
pressure
2. Ipsilateral lung collapse
V/Q mismatch  hypoxia
6. Rapid cardio-respiratory
collapse
Tension
Pneumothorax is life-threatening
5. Impaired venous
return ↓CO*
3. Contralateral mediastinal
shift and lung compression
V/Q mismatch  hypoxia
4. Severe impairment
of ventilation*
Tension Pneumothorax
• Death may occur relatively
rapidly due to combination of
HYPOXIA and
HYPOTENSION
• HYPOXIA due to V/Q
Mismatch
– Ipsilateral lung collapse
– Mediastinal shift
contralateral lung
collapse
• HYPOTENSION due to
positive intra-thoracic pressure
– Impaired venous return
– Reduced stroke volume 
reduced cardiac output 
hypotension
This is a Clinical Diagnosis
Problem
Tension
pneumothorax is
a clinical
diagnosis
Finding
Bulging
hemithorax,
unilateral
diminished breath
sounds, severe
dyspnea, pleuritic
May occur in
chest pain,
simple closed
pneumothorax or tachypnea
closed traumatic subcutaneous
emphysema,
pneumothorax
contralateral
tracheal shift,
shock, distended
neck veins
Emergency
Treatment
Immediate
decompression of
pleural space by
needle aspiration
Followed by chest
tube insertion
and water seal
drainage
19-year-old man has presented to the ER
complaining of severe difficulty breathing and left
acute chest pain after a fall off a roof.
1. What are the clinical
features of this
condition?
2. What is the reason for
P140/min,R40/min,
BP80/60, O2 sat 87%?
3. Was CXR absolutely
necessary for
diagnosis?
4. What is the immediate
treatment?
Immediately life-threatening chest
injury: Tracheal-bronchial Injuries
• Penetrating 3-8%
– Usually cervical
• Blunt 0.5 – 2%
– 80% occur < 2 cm. from
carina
– Mechanisms:
– Blunt: “dashboard” injury
in neck
– Thoracic: Traction –
Rupture - Shearing
• Associated injuries are
common and often the
determinant of prognosis
Extensive subcutaneous emphysema due to
ruptured right main bronchus
SUSPECT diagnosis and confirm by BRONCHOSCOPY
Chest Injury
• High speed MVA
• Blunt chest injury on
left side with lower rib
fractures
• Bleeding in the
peritoneal cavity
• Pelvic fracture
• What is the injury in
the chest on CXR?
Ruptured left hemidiaphragm and hemothorax
with contralateral mediastinal shift
Ruptured Diaphragm L:R = 10:1
Thoracic Aortic Injury
Deleterious effects of hypoventilation and
acute blood loss following thoracic injury
Flail chest
Lung contusion
Pneumothorax
Hypoxia
Respiratory Acidosis
Decreased
Alveolar
Ventilation
Hemothorax
Shock
Shunting
V/Q mismatch
Decreased
Cardiac Output
Heart & vessel injury
Associated injury
Metabolic
Acidosis
Death
Factors producing pulmonary
insufficiency after thoracic injury
Reduced cardiac output
Increased work
of breathing
Fractured ribs
Aspiration
Hypoxia
and
Respiratory
Acidosis
Lung contusion
Atelectasis
CNS injury
Restrictive Pulmonary Insufficiency
Pneumothorax
Diaphragm Rupture
Pleural effusion & Hemothorax
Single Rib Fracture
• Beware of complications
• Pneumothorax
• Hemothorax
• Associated injuries in the chest and abdomen
• 1st rib fracture – worry about
– Neural-vascular injury at the thoracic inlet
– Thoracic aorta
• 10th,11th,and 12th ribs
– Fracture on right side  Liver laceration
– Fracture on left side  Spleen rupture
– Either side  diaphragm
Rib Fracture
• A single rib fracture in patient with preexisting compromised lung function may
precipitate respiratory failure
Chest Injury
• Patients with fractured ribs even when
uncomplicated should have a chest tube
inserted if undergoing general anesthesia
for other injuries
• Risk for tension pneumothorax
Management of Fractured Ribs
• Uncomplicated:
– 1 to 3 ribs: relieve pain – nsaids, opiods, intercostal
nerve blocks and follow-up as out-patient
– > 3ribs: require in-patient management and
monitoring
• Complicated:
– Treat the fractures
– Treat the complications
• Pneumothorax: simple, tension
• Hemothorax
Chest Trauma
• A 55 year old man involved in a car accident has been placed on
assisted ventilation because of severe head injury. He was noted to
have bruising and surgical emphysema on the right lateral chest wall
but no pneumothorax. The ventilator setting is rate 16/min, tidal
volume 500 mls, FIO2 of 40%, and PEEP of 10 cm of water
pressure. He develops sudden tachycardia, hypotension, increase in
airway pressure, and hypoxia. The most likely cause is
a.
b.
c.
d.
e.
open pneumothorax
systemic air embolism
cardiac tamponade
tension pneumothorax
myocardial contusion
Traumatic Pneumothorax
• Insert 28F or 32F chest tube and expect lung to expand
immediately
• Find massive air leak from chest tube
• What is the reason?
– Fault with chest tube insertion
– Fault with connections or drainage system
– Large lung laceration
– Rupture of tracheal-bronchial tree or esophagus
– Unrecognized penetrating chest wound
• Action: stop suction, examine chest tube insertion site,
examine all connections and drainage bottle, immediate
CXR, urgent bronchoscopy for airway injury and if
present, urgent operation
Management of Traumatic
Pneumothorax
• Indications for chest tube insertion
– When large pneumothorax present
compromising lung function
– When small pneumothorax and/or surgical
emphysema present in patient requiring
general anesthesia – to prevent tension
pneumothorax
– When hemo pneumothorax present
• Size of chest tube needed in trauma
– Large bore 28F or 32F
Traumatic Pneumothorax
• Large size: immediately insert large bore chest tube 28F or 32F and expect lung to expand immediately
• Find massive air leak from chest tube
– Fault with chest tube insertion
– Fault with connections or drainage system
– Large lung laceration
– Rupture of tracheal-bronchial tree or esophagus
– Unrecognized penetrating chest wound
• Action: stop suction, examine chest tube insertion site,
examine all connections and drainage bottle, immediate
CXR, urgent bronchoscopy for airway injury and if
present, urgent operation
Pneumothorax
TENSION
SIMPLE
Investigating
and
Managing
Life-threatening Hemoptysis
Life-threatening Airway Hemorrhage
Definition
MASSIVE HEMOPTYSIS
Cause of Death
Asphyxiation
> 600 mls blood loss in 24 hours
EXSANGUINATING HEMOPTYSIS
> 1000 mls blood loss in 24
hours
> 150 mls blood loss per hour
Both Hypotension and
Asphyxiation
Definition
Volume > 600 ml/24 hr
or
Volume > 300 ml/expectoration
or
Impending airway obstruction
or
Need for transfusion
Serious problem that carries a high
mortality rate
Authors
Medical
Treatment
Surgical
Treatment
Conlan
1983
31.8%
17.6%
Crocco
1968
75%
23%
Garzon
1974
75%
18%
Massive Hemoptysis and threat of
Asphyxiation
Gas exchange is impaired by 2 mechanisms
1. Bronchial obstruction by blood clots: as little as
150 mls of blood clot can fill the anatomical
dead space causing proximal airway
obstruction  asphyxiation
2. A large volume of blood can flood the entire
lobe or lung  asphyxiation
Impending Asphyxiation - Anatomical dead
space filled with Blood Clot
Causes of Massive Hemoptysis
•
•
•
•
•
•
Lung abscess
Bronchiectasis
Necrotizing pneumonia
Lung cancer
Aspergilloma
Tuberculosis
Literature review of Causes
N=123 patients
TB
Bronchiectasis
Necrotizing pneumonia
Lung abscess
Lung cancer
Bronchovascular fistula
Lung fungal infection
Miscellaneous
Number of cases
47
37
11
6
6
5
4
7
Sources of Bleeding
• BRONCHIAL ARTERY EROSION
– most common
– Pulmonary infections, lung cancer
• Pulmonary artery erosion occasionally
– Behcet’s syndrome, Rasmussen’s aneurysm in
tuberculous cavity, sleeve lobectomy
• Major systemic artery
– Thoracic aortic aneurysm or graft eroding into lung
– Tracheal-innominate artery fistula complicating
tracheostomy, tracheal resection
Management is urgent
•
•
•
•
Potential life threatening situation
Remove threat of ASPHYXIATION
Admission to hospital is mandatory
Inform ICU for transfer after resuscitation
in the operating room
• Plan urgent operation and inform
interventional radiology
What should be done in the ER
1. Immediate clinical assessment – with patient upright
2. Urgent resuscitation – administer supplemental oxygen,
secure intravenous access, IV antibiotic
3. Obtain CXR now – may give clue to side of bleeding,
and then turn patient with bleeding lung side down to
protect uninvolved lung from aspiration of blood
4. Obtain immediately: CBC, serum electrolytes, arterial
blood gas analysis, PTT and INR, EKG, type and xcross match blood, and consent for OR
5. PRIORITY 1 in the OR
6. Inform interventional radiology for urgent angiogram
and possible embolization of bleeding vessel
Key to the management is
Bronchoscopy
• Remove obstructing blood clots in the airways
• Restore oxygenation
• Temporarily arrest bleeding with endobronchial
control measures: with cold saline (4°C) or dilute
epinephrine solution irrigation (200mcg of
1:1000 epinephrine in 500 mls N/S)
• SEPARATE TWO LUNGS with double lumen tube to
protect the good lung from aspiration of blood
Bronchoscopy should be done in the
OR
• RIGID BRONCHOSCOPY FIRST
– Ventilate patient easily
– Suction effectively to remove obstructing blood clots and
restore oxygenation
– Good optics to visualize and determine SIDE of bleeding
• Flexible bronchoscopy after rigid bronchoscopy to
determine SITE of bleeding and possible cause
• Implement endobronchial control measures to protect
good lung and to arrest bleeding: cold saline and dilute
epinephrine solution irrigation
• Lung separation with double lumen tube to protect good
lung and then come out of the OR
• Don’t leave the OR until patient is completely stable
General Principles of Treatment
Early Bronchoscopy
• Clear the Airway
• Secure the Airway
• Separate the Two Lungs
• Handle the Cause
Endobronchial Control Measures
Emergency Bronchoscopy Tray
•
•
•
•
Rigid bronchoscope
Flexible bronchoscope
Cold N/S – 4 Celsius
Bronchial Blocker and
Double Lumen Tube
• Dilute epinephrine
solution
• Oxygen saturation
monitor
Rigid Bronchoscopy
• Optics - excellent for Visualization
• Channel - excellent for Suctioning
• ETT – excellent for Ventilation
“ A situation where the margin between life
and death is narrow, it will save the patient’s
life”
Lung Separation Single Tube and
Bronchial Blocker
Blocker in the Left Lung
Lung Separation
Double Lumen Tube
Interventional Radiology for
Angiogram and Embolization
• Safe after patient has been completely stabilized in OR
• Look for abnormal bronchial artery and non-bronchial
collaterals
• Arrest bleeding - important component of medical
treatment
• Thoracic aortogram (bronchial and intercostal arteries)
and subclavian arteriogram (non-bronchial collateral
arteries from intercostal, internal mammary,
acromiothoracic and lateral thoracic arteries)
• Permits elective definitive operation under more safe
conditions and with low mortality – resect diseased
portion of lung in operable patients
• Complication of embolization: spinal cord ischemia
Bronchial artery angiogram and
embolization
• Important component of medical treatment
• Safe after patient has been stabilized in OR and the
healthy lung has been separated from bleeding lung
• Thoracic aortogram and subclavian arteriogram
• Need to look for abnormal bronchial (aorta) and nonbronchial collateral arteries (intercostal, branches of
subclavian artery)
• Embolization done first will facilitate planning of safe and
precise pulmonary resection with low operative mortality
• Permits definitive operation under more safe conditions
and with low mortality – resect diseased portion of lung after bleeding has stopped and patient has recovered
• Complication of embolization: spinal cord ischemia
Result of Embolization
• Remy in France
• Recanalization leads to recurrent
hemorrhage in < 4months
• Bleeding stopped immediately in 41/49
patients
• Recurrence of bleeding in 6/41patients
within 2 to 7 months
• In poor surgical risk patient – embolization
is the only real solution
Bronchial A-V malformation and
abnormal internal elastic lamina
Aspergilloma in an old tuberculous
cavity
Segmental Pulmonary Artery
Aneurysm
Bronchiectasis LLL and RML
Aortic graft
Pulmonary Fistula
Pneumothorax
• Because of the subatmospheric pressure
in the pleural space, whenever the pleural
membrane is breached so as to allow
communication with the atmosphere, air will
enter the space and a pneumothorax will
result
• Classification according to the cause
Spontaneous Pneumothorax
• Due to spontaneous rupture of the visceral
pleura either because of some local defect or
because of underlying diffuse lung disease
• Local defect usually near the lung apices
– either a small bulla due to tractional emphysema
associated with small scar
– or a bleb which is a localized collection of air
within visceral pleura due to ruptured distended
alveoli beneath the visceral pleura
– commonest cause in young
• Diffuse lung disease usually emphysema
– Older patient, chronic smoker
Simple Closed Secondary Spontaneous
Pneumothorax
•
•
Commonest cause is pulmonary emphysema
Others are
1. asthma
2. interstitial lung disease
3. cystic fibrosis
4. active tuberculosis
5. histiocytosis X
6. pulmonary metastases from sarcoma
7. lymphangioleiomyomatosis (LAM)
8. Birt-Hogg-Dube syndrome
9. catamenial (related to menstruation)
Spontaneous Pneumothorax
• PRIMARY spontaneous
pneumothorax
• Local defect usually near
the lung apices
– small bulla >1cm (due to
scar and tractional
emphysema)
– bleb <1cm (a localized
collection of air within the
visceral pleura from
ruptured distended
alveolus)
• SECONDARY
spontaneous
pneumothorax
• Underlying lung disease
is present
• Most common is
emphysema
Spontaneous Pneumothorax – 3 types
1. Simple closed: primary and secondary
2. Tension or valvular in any closed pneumothorax
3. Complicated - associated with
1. infection – chronic, trapped lung, empyema
2. bleeding - hemothorax
3. open: broncho-pleural fistula between the bronchial
tree and pleural cavity
esophago-pleural fistula complicating
post-emetic ruptured esophagus
Spontaneous Pneumothorax
• Simple pneumothorax
– tear in the pleural surface is small, resulting
retraction of lung allows hole to close and prevent
further egress of air while the intrapleural
pressure is still below atmospheric
• Complicated pneumothorax
– Tear is larger and persists, mean intrapleural
pressure becomes atmospheric, and risk of
secondary infection, causing entrapment of lung
and empyema; associated bleeding from the
chest wall
Simple Closed Primary Spontaneous
Pneumothorax
• CAUSE: an emphysematous bulla or a bleb ruptures and
air leaks into the pleural cavity
• AGE incidence: young adults are especially liable
• CLINICAL POINTERS:
1. sudden onset
2. unilateral pleuritic chest pain; mild dyspnea
3. diminished breath sounds over the affected
lung
4. dry cough is usually but not always present
• INVESTIGATIONS: Chest x-ray on inspiration and
expiration confirms diagnosis; sometimes CT scan
needed
Management of Simple Closed
Spontaneous Pneumothorax
• Duration of pneumothorax depends on treatment:
1. Expectant observation - depends on the degree of
lung collapse and assuming that the air leak has
sealed immediately  the rate of re-expansion of
the lung is 1.25% per day: 10% lung collapse will
resolve in 8 days and 20% in 16 days
2. Intercostal chest tube drainage: about 72 hrs
• Complications: 1. small risk of becoming tension type
2. recurrence affecting the same lung is
20% to 30% after 1st episode; 50%
after 2nd episode; 80% after 3rd episode
3. sepsis (empyema), trapped lung
4. associated hemothorax
Tension or Valvular Pneumothorax
• Cause
1. any simple closed pneumothorax has the potential
to become tension under the right circumstances
2. communication between the lungs and the pleural
cavity allows unidirectional passage of air and
transmission of positive airway pressure into pleural
cavity but not out of it  allows considerable
tension to be built up inside the pleural cavity
• Precipitating factors
1. valve action at the site of air leak persists
2. severe coughing generates positive airway pressure
3. assisted ventilation with positive airway pressure
Tension or Valvular Pneumothorax
• Clinical pointers
1. sudden onset
2. severe unilateral chest pain worse on breathing
3. increasing respiratory distress, hypoxia and
tachycardia are early signs
4. cyanosis (not always present), hypotension,
distended neck veins, and tracheal deviation are
late signs of a tension pneumothorax
5. increased resonance and absent or diminished
breath sounds on affected side of chest
(hyperinflated)
6. evidence of contralateral mediastinal shift
Life-threatening situations in
Spontaneous Pneumothorax
• Tension Pneumothorax
– Clinical diagnosis
– Respiratory distress,
tachycardia, cyanosis
– Hypotension and hypoxia
– Mediastinal displacement
to opposite side
– Hyper-inflated chest and
absent air entry
• Associated intrathoracic bleeding
• Hemopneumothorax
– Rupture of systemic blood
vessels in the vascularized
intrapleural adhesions
which tear as the lung
collapses
– Blood loss can be
substantial
– Pleuritic chest pain, low
hemoglobin, tachycardia,
postural hypotension,
dullness to percussion at
the base
Simple Spontaneous pneumothorax
Complicated Spontaneous
Hemopneumothorax
Spontaneous pneumothorax
Simple
Tension
Diagnosis, Treatment
• CXR taken in full inspiration and expiration
• EKG and serum cardiac enzymes to rule out
acute coronary syndrome in age >40 years
• Chest CT scan if in doubt
• First episode of small pneumothorax usually
requires no treatment, consider surgical
intervention for recurrence
• Tension pneumothorax is an acute emergency
demanding decompression of the pleural cavity
without delay and without initial CXR
Management
• Conservative treatment is based on natural tendency for
gases in pneumothorax to be reabsorbed and lung reexpands at rate of 1.25% per day provided the hole in
the lung has closed
• Preferred treatment
• 1st episode and large > 20% or small but symptomatic
with acute pain and/or severe dyspnea, insert intercostal
chest tube # 24F or 28F, or pigtail catheter 8F
• Tension pneumothorax needs immediate needle
decompression followed by chest tube insertion
Initial Treatment
• Tension pneumothorax
– Immediate decompression with 2nd interspace
needle insertion followed by chest tube
placement
• Simple pneumothorax
– If small, observe and monitor with CXR q 3
days  insert chest tube for ↑size, air fluid
level, ↑symptoms
– If large, insert chest tube
Indications for Operation – bullectomy
and, pleurectomy
• 2nd or 3rd recurrent pneumothorax on same side
– 1st episode  20 to 30% ipsilateral recurrence
– 2nd episode  50% ipsilateral recurrence
– 3rd episode  80% ipsilateral recurrence
•
•
•
•
1st episode on the opposite side
Intrathoracic bleeding, Hemopneumothorax
Associated infection in pleural space, empyema
High risk group – air pilot, scuba diver, work at high
altitude
• Tension pneumothorax – if access to immediate care is
unavailable
Indications for chest tube
insertion in Pneumothorax
•
•
•
•
•
•
•
•
Large size at initial presentation
Increasing size
Symptomatic
Associated hemothorax
Undergoing general anesthesia
Bilateral
Tension quality
Contralateral
Indication for Surgery
•
•
•
•
•
•
•
•
•
•
First episode with prolonged air leak > 3 days
2nd or 3rd recurrence on same side
1st occurrence on contra-lateral side
Associated hemothorax >1000mls
Associated pleural sepsis
Incomplete re-expansion
Occupational risks
Synchronous bilateral
Life-threatening episode
Patient living in remote areas
Therapeutic Options
• Apical bullectomy and parietal
pleurectomy
– Video-assisted thoracoscopic approach
– Limited thoracotomy
• Chemical pleurodesis
– Talc
– Tetracycline
Empyema
• An empyema is a localized collection of pus in
the pleura; it is a mature abscess, the end result
of an acute suppurative process initiated by
pyogenic bacteria gaining access to the pleural
cavity
• Complicate pneumonia, esophageal tear,
descending necrotizing mediastinitis, rupture of
lung abscess, penetrating chest wound,
extension of subphrenic abscess
Infection in Pleural Space
Bacteria introduced into pleural cavity by:
1. Local spread (from infected lung) – pneumonia,
lung abscess
2. Implantation – at operation (pulmonary resection,
esophagectomy, chest wall resection,
mediastinal operation, hiatus hernia repair)
3. Lymphatic trans-diaphragmatic spread (from
subphrenic abscess)
4. Blood-borne spread (pleural effusion becoming
secondarily infected – pneumonectomy space)
Pathogenesis – Three Phases
Stage or Phase
of empyema
Early Acute
“Exudative”
Intermediate
Subacute
“Fibrinopurulent”
Third 4-6 wks
Chronic
True Empyema
“Purulent”
I – 1ST week
II – 2ND week
III – 4TH week
acute septic pleurisy,
free, seropurulent
pleural effusion
Fluid is thin and watery
subacute suppurative
effusion gradually
thickens and becomes
more and more purulent;
limiting adhesions
develop causing multiple
loculations (unless
empyema is total)
localized abscess is
formed with its walls
lined by a deposit of
fibrin.
Symptoms and Signs
Stage
Early – Stage I
Acute pleurisy,
Exudative
Intermediate –
Stage II,
Fibrinopurulent
Late – Stage III
Empyema,
Pyothorax
Clinical
Findings
• Sharp stabbing
chest pain
aggravated by chest
movements
• Pleural rub
• Chest movements
and breath sounds
are reduced by
conscious effort to
avoid the pain
• Moderate fever
and dry cough
usually accompany
the pain
• General – toxemia,
dyspnea, fever,
malaise, fatigue,
sweating episodes
• General –
• Local – chest pain,
worsened by
breathing
• Local- chest pain
toxemia, fever,
malaise, loss of
appetite and weight
Diagnosis and Treatment
• Chest x-ray and CT scan
• Avoid delay in thoracentesis, specimens for C/S,
drainage tube insertion (may need intervention radiology
to insert if loculated) to re-expand the lung
• IV antibiotic for 6 weeks
• Monitor with daily CXR and weekly CT scan
• Avoid premature removal of drainage catheter
• Must assure complete re-expansion of the lung
• Consider drainage alone, drainage with intrapleural
instillation of fibrinolytic agent, decortication - all aiming
to re-expand the lung
Pathogenesis – Three Phases
• Exudative – Acute, develops over 1 week
– Outpouring of sterile pleural fluid
• Fibrinopurulent – Transitional, develops over 2 to 3
weeks
– PMN/turbidity
– Fibrin deposition
– Biochemical changes
• Organizing – Chronic, develops after 4 weeks from onset
– Organization of pleural “peel”
– Viscous fluid – 75% sediment
Etiology
•
•
•
•
Pneumonia
Post – surgical
Extension from subphrenic
Other
50%
25%
10%
5%
– Esophageal perforation
– Descending necrotizing mediastinitis
– Anastomotic leak post-esophagectomy
Right Empyema
Use of intrapleural fibrinolytic agent
30-09-2009
27-10-2009
Clinical Presentation
• Acute versus Chronic Phase
• Complications by extension, by secondary
infection, by fibrosis
–
–
–
–
–
–
–
–
Empyema necessitans
Septic chondritis
Osteomyelitis
Broncho-pleural fistula
Pericarditis
Mediastinal abscess
Septicemia
fibrothorax
Diagnosis of Empyema
• Radiology
• CXR, U/S, CT scan
• Thoracentesis
–
–
–
–
–
Cultures 50% positive
pH<7
Glucose<2
WBC>15,000
Protein>2.5
• Bronchoscopy
• Barium swallow/esophagoscopy
Treatment of Pleural Infection
1. Treat the Infection
• Antibacterial drugs
• Look for primary site of infection and treat
2. General Supportive Treatment
• Rest, treat toxemia, supplement oxygen, relieve pain
3. Remove the Pleural Effusion to allow Lung to expand
completely to eliminate infection and restore lung
function
• Insert intercostal (closed) catheter, intrapleural fibrinolytic agent –
streptokinase, TPase
• Open drainage once pus is too thick, multiple loculations present,
and lung is trapped – decortication, rib resection