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in
Thoracic Surgery
FM Shamji
31-03-2011
Solitary Pulmonary Nodule - SPN
• Also called “coin lesion”
• Radiologic diagnosis
• Defined as: “Single nodular lesion within the lung
substance, 3 cm or less in diameter, well defined,
completely surrounded by normal-appearing lung tissue,
not cavitated but may be calcified, usually of clinically
undetermined etiology”
• Its importance lies in its diagnosis and a significant
number are malignant and resection is followed by good
survival rate
• Incidence of malignancy in mass survey varies from 3 to
6%
Classification of Solitary Pulmonary
Nodules
1. Neoplasms (45%)
Benign
•
•
•
•
•
Hamartoma (most common)
Fibroma
Leiomyoma
Localized fibrous tumor of visceral pleura
Bronchial adenoma
Malignant
•
•
•
•
Bronchial carcinoma
Carcinoid tumor
Metastases
Lymphoma
Classification of Solitary Pulmonary
Nodules
2. Granuloma (40%)
Histoplasmoma
Coccidiodomycoma
Cryptococcoma
Aspergilloma
Tuberculoma
3. Inflammatory (4%)
Lung abscess
Pneumonitis
Rheumatoid nodule
4. Miscellaneous (4%)
Fluid-filled cyst
Infarct
Arteriovenous
malformation
Amyloid
Management of Solitary Pulmonary
Nodules
Favour Benign Lesion
Favour Malignant Lesion
Well demarcated
Dense calcification
Unchanged in size over 2y
Absence of risk factors for
primary lung cancer
Absence of history of
previous malignancy
Size < 2cm (not absolute)
Young age < 40y (not
absolute)
Spiculated
Not calcified
Progressive growth over 2y
Presence of risk factors for
primary lung cancer
History of previous
malignancy
Size > 2cm (not absolute)
Older age >40y ( not
absolute)
Investigations for SPN
1.
2.
3.
4.
Attempt should be made to find any previous chest
films for comparison – present before, same size or
getting larger
CT scan chest is necessary to search for satellite
lesions, enlarged nodes in the mediastinum
Percutaneous Fine Needle Aspiration Biopsy is more
likely to establish diagnosis than by bronchoscopy
PET scan
Asymptomatic RLL Lesion found on
routine CXR in 39y man
Questions
• What is a solitary pulmonary nodule?
• What is the differential diagnosis of this
lesion?
• Is it necessary to investigate further and
how?
Primary Lung Cancer
• Lung cancer is a LETHAL disease
• Has profound effect on society
USA each year about 170,000 new cases
and 160,000 die
• Leading cause of cancer-related mortality worldwide
over 1.2 million people die of lung cancer each
year
Histological Cell Types
• WHO Committee (1999) pathologic classification
into two groups
1. Small cell lung cancer 15 to 20%
2. Non-small cell lung cancer 80 to 85%
– Squamous cell carcinoma 25 to 30%
– Adenocarcinoma 40 to 50%
– Large cell carcinoma 10 to 15%
Etiology and Risk Factors in Lung
Cancer
1. TOBACCO (in 85% of the cases)
:8 - to 12 - fold increased risk
:Former smokers remain at an elevated risk for
developing lung cancer even decades after they
stop smoking. 50% of newly diagnosed lung cancer
patients are former smokers
:Smoking cessation is vital to reducing rate of lung
cancer
:10 years after smoking cessation, risk of lung cancer
in former smokers is reduced to ½ of those who
continue to smoke
Etiology and Risk Factors in Lung
Cancer
2. Environmental Tobacco Smoke (ETS)
– Reports in 1981and 1986, non-smoking spouses of
active smokers are 30% more likely to develop lung
cancer than those married to non-smokers
3. Asbestos is the first occupational carcinogen
recognized to cause lung cancer 1955, as early
as 1939
– Insulating and fire-proofing
4. Radiation
5. Previous lung disease - pulmonary fibrosis
Etiology and Risk Factors in Lung
Cancer
• Radiation
– High linear energy transfer (LET) radiation is a risk
– Creates ionization in higher tissue density and more
tissue damage
– RADON is an inert gas with high LET
– Breakdown product in the decay of uranium emitting
alpha particles – affects DNA of respiratory epithelium
– Occupational risk factor in Uranium miners
– Concern is its presence in indoor air of buildings
– Prior treatment of thoracic malignancies (breast,
lymphoma, esophagus) with radiotherapy increases
risk for lung cancer
Scarring or fibrosis as a cause of
lung cancer
• Lung cancer can develop both in the vicinity of preexisting localized areas of pulmonary scarring and in
patients with more diffuse lung fibrosis
• Microscopic examination of lung scar tissue reveals
areas of epithelial hyperplasia  associated with
unexpected carcinomatous change
• ‘SCAR CANCERS’
• Personal smoking history and asbestos exposure in nonsmokers are highly relevant
• More adenocarcinoma cell type seen
Occupational causes of lung cancer
Cause
Occupation
Asbestos
Mining, processing, usage
Radioactivity (radon gas)
Metal ore mining, uranium mining,
Fluorspar mining
Nickel
Refining
Chromium salts
Extraction, production, usage
Arsenic
Metal refining, chemical industry,
insecticides
Chloro-ethers
Organic chemical industry
Mustard gas
Manufacture
Volatile coal products
Coke oven workers
Printing ink(?)
Printing industry
Clinical Presentation - Symptoms
GROUP I
Result of investigation of some
new respiratory symptom or
because their pre-existing
respiratory state has worsened
GROUP III
Non-specific symptoms such as
malaise, anorexia, weight loss,
loss of taste for food, fatigue,
depression or recurrent febrile
flu-like illness episodes
GROUP II
No respiratory symptoms at
diagnosis; chance finding of an
opacity on CXR ordered for some
other reason e.g. preoperative,
unrelated complaint – angina,
shoulder discomfort
GROUP IV
Specific Symptoms that are
1.LOCAL - bronchopulmonary
2.From DIRECT intrathoracic
spread OR
3.From SYSTEMIC metastatic
spread
Clinical Presentation: Group IV
Specific Symptoms that are directly caused by the lung
cancer
1.LOCAL – bronchopulmonary symptoms due to bronchial
obstruction – atelectasis - infection, irritation - cough,
ulceration - bleeding
2.From DIRECT intrathoracic spread
pleura, chest wall, ribs, thoracic spine, SVC, recurrent
laryngeal nerve, mediastinal lymph nodes, pericardium,
diaphragm, sympathetic chain at the apex
3.From SYSTEMIC spread – metastases to bone, brain,
liver, adrenal glands
Group 4: Symptoms from Systemic
Metastasis
• Lung cancer may already have spread to distant sites at
initial presentation – Stage IV
• Four most common sites of systemic spread are
– Brain, Bone, Liver, and Adrenal gland
• BRAIN metastasis – headaches, nausea, fatigue, motor
weakness, seizures, visual change, ataxia, or personality
change
• BONE metastasis – continuous pain, pathological
fracture, epidural spinal cord compression
• Liver metastasis – nausea, vomiting, cachexia
• Adrenals – often asymptomatic, lumbar pain
CLINICAL FINDING
INTERPRETATION
Marked dyspnea
Coexisting COPD
Hoarse voice with bovine
cough
Left RLN palsy from tumor
invasion
Clubbing, HPO
lung cancer NSCLC
Horner’s syndrome
Pancoast’s apical tumor
Supraclavicular LN
enlargement
Inoperable lung cancer
Stridorous respirations
Tumor extension into tracheal
carina or trachea
Unilateral wheezing and
delayed expansion of ipsilateral
hemithorax
Almost complete obstruction of
a main bronchus
New subcutaneous nodules
metastases
SVCO
SVC involved by mediastinal
LNs or direct invasion
Raised JVP
Pericardial effusion due to
tumor invasion
Five Types of Paraneoplastic
Syndromes
• Manifestations associated with malignancy but
not directly related to distant metastasis
• Very common in lung cancer occurring in
– 10% of patients with NSCLC
– 50% of patients with SCLC
1. ENDOCRINE manifestations (protein hormone)
Cushing’s syndrome (SCLC), Syndrome of Inappropriate
Antidiuretic hormone production (SCLC), hypercalcemia
(NSCLC – squamous cell), ß –HCG (NSCLC – large cell)
2. HEMATOLOGIC (SCLC and NSCLC)
Hypochromic anemia, Thrombocytosis,
Paraneoplastic Syndromes
3. NEUROLOGIC (SCLC)
–
–
–
–
due to autoimmune reaction to “onconeural” antigen shared by
the cancer and nervous system
Eaton-Lambert myasthenic syndrome
Subacute cerebellar degeneration – cerebellar ataxia
Peripheral neuropathies
Cancer-associated retinopathy
4. MUSCULOSKELETAL (NSCLC)
– Digital clubbing
– Hypertrophic pulmonary osteoarthropathy
5. DERMATOLOGIC (SCLC)
– Acquired tylosis, erythema gyratum repens, triple palm,
acanthosis nigricans
Local Symptoms: Cough and
Hemoptysis - cavitating lung cancer
Centrally located symptomatic lung cancer
Presenting Manifestation in Brain:
Hemiparesis – abnormal CT/ PET
Patient came to the ER with weakness in the leg and arm
and persistent headache
Brain metastases – vasogenic
edema
MRI done after PET scan
Abnormal radiologic finding in patient with CNS
symptoms: personality change and headache
Patient brought to the ER by spouse because of concern about his behaviour
RUL cancer and Brain Metastases
Fine Needle Aspiration Biopsy for peripheral lung cancer
Pancoast (Superior Sulcus) Tumour
• Lung cancer - mass at
the extreme apex of the
lung
• Pain - in the lower part of
shoulder and inner aspect
of the arm (C8 and T1)
• Horner’s syndrome –
stellate ganglion (T1)
• Hand – weakness and
muscle wasting
Pancoast Tumor: Persistent right
chest pain  right arm
Investigations needed are:
CT scan Chest, Abdomen, Head
MRI Thorax
PET scan
FNA biopsy
Mediastinal LN Biopsy
Investigations are performed for
Diagnosis and Staging
1.
2.
CHEST RADIOGRAPH is nearly always abnormal –
hilar mass, solitary pulmonary nodule, partial or total
atelectasis due to bronchial obstruction, pleural
effusion, raised paralysed diaphragm, rib destruction,
widening of mediastinum, cavitation in the lesion,
‘pneumonia-like’ changes
SPUTUM CYTOLOGY positive yield is increased
when tumor is centrally situated with increasing size
and when it is in lower lobe: positive cytology from
single specimen is 40% and increases to 80% with
four specimens
Investigations
3. BRONCHOSCOPY is very useful investigation
a. providing diagnostic material in centrally placed
tumors – main bronchus or lobar bronchus
b. providing information about inoperability –
paralysed vocal cord, definite tracheal
involvement, definite carinal involvement,
4. FINE NEEDLE ASPIRATION is very useful for diagnosis
in peripherally placed tumors that are beyond
bronchoscopic vision
5. Spiral CT scan Chest and Abdomen for diagnosis and
staging
5. Non-invasive preoperative staging by PET scan and
MRI or CT head
Treatment for NSCLC
Stage
Localized
Intention
Treatment
I + II
Cure
Surgery + CT;
add CT to
increase cure
by 10 – 15%
LocoRegional
IIIA + IIIB
Depends
Induction +
Surgery
Concurrent CT
+ RT
CT alone
Metastatic
IIIB Pleural +
IV
Palliative
BSC +/- CT
Treatment for Stage III NSCLC
IIIA
Minimal
Bulk
IIIA
Bulky
IIIB
IIIB
Induction
CT +
Surgery
RT + CT
Not
surgical
Pleural
Effusion
Not
surgical
30%
10 – 20 %
Small Cell Lung Cancer
• Highly malignant tumor
• Distinct cell type
• Most common lung cancer associated with
ectopic hormone production
• Strong relationship to cigarette smoking
– >98% found in smokers
– Only about 1% occur in non-smokers
• Most chemosensitive and radiosensitive
Investigating and Managing
Massive Hemoptysis
Causes of Hemoptysis
1.
Pulmonary Disease
a) Infection
Pneumonia, Lung abscess,
Bronchiectasis
TB
Mycosis
Aspergilloma
Mucormycosis
b) Neoplasm
Carcinoma, Carcinoid tumor,
Endobronchial Metastases –
sarcoma, renal cell ca, colon ca
c) COPD
d) Goodpasture’s syndrome
2. Cardiovascular Disease
a) Mitral stenosis
b) Pulmonary Infarction
c) Thoracic aortic Aneurysm
3. Bleeding Diathesis
a) Leukemia
b) Anticoagulation
–
Massive Hemoptysis
• Sudden expectoration of large amounts of blood
is an alarming development for patients and as
well physicians
• Patient is anxious and terrified at the sight of his
own blood, and imagines death to be imminent
• Hemoptysis, if copious, may cause SUDDEN
DEATH by ASPHYXIATION
Definition: > 600 mls blood
expectorated in 24 hours
• Patient may become drowned in his own blood,
which is partly coughed out and partly inhaled
into all parts of the tracheobronchial tree and
lungs Loss of Lung Function
• Respiratory gas exchange deteriorates,
sometimes too rapidly, causing death by
ASPHYXIATION
Impending Asphyxiation – Blood
Clots in the Airway Dead Space
Source of Bleeding
• Cause is almost always bleeding from a
ruptured abnormal BRONCHIAL ARTERY
• Susceptible lung parenchymal lesions are
– Cavity: usually of tuberculous origin
– Bronchiectasis
– Lung abscess
– Necrotizing pneumonia
– Aspergilloma
– Centrally located bronchogenic cancer
Common Errors of Clinical
Diagnosis and Treatment
• Airway hemorrhage misdiagnosed as SEVERE
HEMATEMESIS: patient arrived in the ER c/o of
“throwing up” large amounts of blood and was found to
be hypotensive. A bleeding peptic ulcer was suspected
even though gastroscopy did not confirm the diagnosis.
Readmitted after discharge from ER with same
symptom.
• Airway hemorrhage misdiagnosed as SEVERE
EPISTAXIS and was referred by the ER physician to
ENT specialist who performed nasopharyngeal
endoscopy and discharged patient home when source of
bleeding could not be seen. Severe bleeding recurred
within 24 hours.
Common Errors of Clinical
Diagnosis and Treatment
• Severe airway hemorrhage correctly diagnosed but NOT
managed properly. Respirologist consulted by ER
physician. Flexible bronchoscopy performed was
unsatisfactory because of active bleeding – it appeared
to be coming from right lung from an area of “extrinsic
compression” – missing information was previous right
thoracoplasty for chronic pulmonary tuberculosis
• Severe airway hemorrhage correctly diagnosed in the
ER. Patient was advised by the ER physician to return to
home town 400 km away. Hemoptysis continued enroute
and arrived in the ER very requiring urgent operation
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
• Any hemoptysis should be considered massive
when it ceases to be a sign of underlying lung
disease and becomes a threat to life in its own
right
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. Acute Bronchial Obstruction: 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
We are addicted to Oxygen
Impending Asphyxiation - Airway
Dead Space Blood Clots
We are addicted to Oxygen
Etiology of Massive Hemoptysis
•
•
•
•
•
•
Lung abscess
Bronchiectasis
Necrotizing pneumonia
Aspergilloma
Tuberculosis
Lung Cancer
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
• Rupture of a bronchial artery
– most common source
– Tuberculous cavity, aspergilloma, lung abscess,
bronchiectasis, lung cancer, necrotizing pneumonia
• 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
• Risk of Asphyxiation from proximal airway
obstruction
• You have a potential life threatening situation
• Admission to hospital is mandatory
• Resuscitation in the operating room
• Inform interventional radiology after life-saving
measures in the OR
• Inform ICU for transfer after angiogram and
bronchial artery embolization
Five Phases of Treatment
1st phase: Emergency Room
Second phase: Operating Room
Third phase: Interventional Radiology
Fourth phase: Intensive Care Unit
Fifth phase: Interval Definitive Operation
Management in the ER: 1st phase
1. See patient immediately
2. Evaluate patient quickly – administer supplemental
oxygen, secure intravenous access, rapid clinical
assessment with patient sitting upright
3. Ask for CXR quickly – 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. Organize urgent OR and inform interventional radiology
for urgent angiogram and possible embolization
Management in the OR: 2nd phase
• Secure patency of proximal airway and protect
against threat of asphyxiation by rigid
bronchoscopy
• Implement endobronchial measures – cold
saline or dilute epinephrine solution irrigation to
arrest bleeding temporarily
• Separate two lungs with double lumen tube to
protect the good lung from aspiration of blood
• Interventional radiology for bronchial artery
angiogram for embolization of abnormal artery;
may need to look for non-bronchial collaterals to
embolize as well
Remove threat of asphyxiation
quickly
Only by Rigid Bronchoscopy
Rigid Bronchoscopy is necessary
to restore patency of the airway
Advantages of Rigid Bronchoscopy
• Visualize - good optics
• Suction - large channel
• Ventilate - resembles endotracheal tube
“ A situation where the margin between life and
death is narrow, it will save the patient’s life
Bronchoscopy is the key to successful
management
• Rigid bronchoscopy performed first
– Ventilate patient easily
– Suction effectively to remove obstructing blood clots
and restore oxygenation
– Good optics to visualize and determine SIDE of
bleeding “Lateralization”
– Implement endobronchial control measures to protect
good lung and to arrest bleeding: cold saline and
dilute epinephrine solution irrigation
• Flexible bronchoscopy after rigid bronchoscopy to
determine SITE of bleeding and possible cause “Localization”
• Lung separation with double lumen tube to protect good
lung and then come out of the OR
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 – 4ºC
Bronchial Blocker and
Double Lumen Tube
• Dilute epinephrine
solution – 200mcg in
500mls N/S
• Oxygen saturation
monitor
Lung Separation Single Tube and
Bronchial Blocker
Blocker in the Left Lung
Lung Separation
Double Lumen Tube
Lung Separation
Uncut Single ETT
Interventional Radiology: 3rd phase
• Important component of optimal medical treatment
• Safe after patient has been stabilized in OR and the two
lungs have been separated
• Thoracic aortogram and subclavian arteriogram
• Search and embolize abnormal bronchial (aorta) and
non-bronchial collateral arteries (intercostal, branches of
subclavian artery)
• Embolization stops bleeding and permits safe semiurgent pulmonary resection with low operative mortality
• Resect diseased portion of lung - after bleeding has
stopped and patient has made functional recovery
• 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 and becomes definitive
treatment
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
Management in the ICU: 4th phase
• Patient is transferred to the ICU from the
Radiology Department or the OR for close
monitoring and assisted ventilation
• Plan for extubation after bleeding has subsided
for 24 hours
Interval definitive treatment:
5th phase
• Time is required for full recovery of lung function
and thorough assessment of cardiopulmonary
reserve
• Plan for definitive elective or semi-urgent
operation for pulmonary resection in surgical
patients with lung lesion with acceptable low
operative mortality <3% when risk for rebleeding is high
Spontaneous Pneumothorax
Spontaneous Pneumothorax
Definition: Any pneumothorax occurring in the absence of
trauma (needle aspiration biopsy, needle thoracentesis,
rib fractures, ruptured esophagus) may be described as
spontaneous
Classification of Spontaneous Pneumothorax:
1. Primary
2. Secondary
Sub-classification into:
• Simple
• Complicated
• Tension or valvular pneumothorax
• Associated bleeding – hemopneumothorax
Spontaneous Pneumothorax
Simple
Tension
Complicated Spontaneous
Hemopneumothorax
Spontaneous Pneumothorax
1. PRIMARY TYPE
Absence of clinical
evidence of pre-existing
respiratory disease
• Rupture of a Local
Defect usually near the
lung apex
– small bulla >1cm
– bleb <1cm (a
localized collection of
air within the visceral
pleura from ruptured
distended alveolus)
2. SECONDARY TYPE
Indicates presence of a
clinically recognizable
coexisting structural or
functional parenchymal
abnormality in the lung
• Rupture from an
underlying diffuse lung
parenchymal disease
• Most common is
emphysema
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)
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
Diagnosis
• 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
Simple Spontaneous pneumothorax
• SIMPLE,
UNCOMPLICATED
1. Observation depends on the degree of
lung collapse and
assuming that the air leak
from the lung surface has
sealed immediately, and
it is small in size < 20%
 the rate of reexpansion 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 if large in size
>30% for about 72 hrs
• COMPLICATED
Treatment is different
1. Tension type: urgent
needle decompression
and chest tube insertion
in 2nd intercostal space in
midclavicular line
2. Recurrence affecting
the same lung is 20% to
30% after 1st episode;
50% after 2nd episode;
80% after 3rd episode
(surgical)
3. Sepsis (empyema),
trapped lung (surgical)
4. Associated
hemothorax (surgical)
Management of Spontaneous Pneumothorax
Treat by Observation only
• FIRST EPISODE
• Without associated complications of Tension Quality,
Bleeding – Hemothorax, or Infection – Empyema
• Patient is stable and reliable
• Degree of lung collapse is small <20%
• 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
 be aware: Small unpredictable risk of becoming
tension type
Complicated Spontaneous
Pneumothorax
1. Tension or valvular type in any closed
pneumothorax
life-threatening situation demanding urgent
care
2. Bleeding – hemothorax
 demands drainage and chest operation
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
1. Life-threatening situations in Spontaneous
Pneumothorax – Tension or Valvular Type
• 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
Diagnosis, Treatment
• SIMPLE SPONTANEOUS PNEUMOTHORAX
– 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
• TENSION PNEUMOTHORAX
– Do not waste time
– Do not do CXR or CT scan
– Clinical diagnosis and immediate treatment – needle
decompression in 2nd ICS and then chest tube
insertion
Spontaneous Hemopneumothorax
• Due to rupture of systemic blood vessels
between 2 and 3 mm size in the vascularized
intrapleural adhesions which tear as the lung
collapses
• Blood loss can be substantial
2. Life-threatening situations in Spontaneous
Pneumothorax – Associated Hemothorax
• Clinical pointers
1. sudden onset
2. severe unilateral chest pain worse on breathing
3. increasing respiratory distress, hypoxia and
tachycardia are early signs
4. Pallor and low Hb
5. postural hypotension, collapsed neck veins
6. dullness to percussion in the lower chest and
absent or diminished breath sounds on affected
side of chest
Treatment for Spontaneous
Hemopneumothorax
• FIRST EPISODE
• Operation is necessary
– Resuscitate
– Intercostal chest tube drainage
– Surgical chest exploration for evacuation of
blood clots, surgical hemostasis, and apical
bullectomy, pleural symphysis by abrasion
(not pleurectomy) of parietal pleura
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 - air pilot, scuba diver, work at high
altitude
• Synchronous bilateral
• Life-threatening episode of tension pneumothorax - if
access to immediate care is unavailable
• Patient living in remote areas
Therapeutic Options
• Apical bullectomy and parietal
pleurectomy in all young adults
– Video-assisted thoracoscopic approach
– Limited thoracotomy
• Chemical pleurodesis in elderly patients
with serious co-morbid illnesses or severe
COPD
– Talc
– Tetracycline
Dysphagia
Clinical Presentation
•
•
•
•
•
•
•
•
An elderly 75y old man
Intermittent cervical dysphagia for 3y
Gurgling noises in the neck on drinking liquids
Occasional regurgitation of undigested food
eaten hours earlier
Foul breath
Intermittent left neck swelling
Spells of choking on swallowing
One episode of pneumonia due to choking
What is the diagnosis on barium swallow?
•
•
•
What are the
complications of this
condition?
Is treatment
necessary?
What treatment is
possible ?
Zenker’s Diverticulum
• Most common
esophageal diverticulum
• “Pulsion” diverticulum
containing mucosa and
submucosa
• Develops at the
Pharyngo-esophageal
junction in the neck
• Just above the UES
(cricopharyngeus muscle)
through Killian’s triangle
Develops on posterior wall of pharynx between
upper and lower divisions of inferior constrictor
muscle
UES
Zenker’s Diverticulum
• Acquired – 80% occur in
age >50 yrs
• Pathophysiology:
– Develops because the
UES does not relax in
coordination with
pharyngeal contraction
Treatment is necessary
and it requires an
operation
• To prevent lifethreatening complications
due to recurrent acute
aspiration pneumonia,
lung abscess and
empyema
• For symptomatic relief
Treatment for Zenker’s Diverticulum
• OPERATION IS NECESSARY
• There is no medical treatment
• Surgical treatment is curative
 Always perform Cricopharyngeal Myotomy
 For the diverticulum
– Small < 3cm size  leave it alone
– Large > 3 cm size  add diverticulectomy
Clinical Presentation
• A 35y old man
• With a Triad - slowly worsening difficulty
swallowing, regurgitation, and some weight loss
over 18 months
• Past medical history is unremarkable
– No caustic ingestion
– No GERD, Ulcer dyspepsia
– No previous esophageal or stomach operation
What is the diagnosis on barium study?
1. What is necessary to
confirm diagnosis?
2. What treatment would
you recommend?
Esophageal Manometry confirms
Diagnosis of Achalasia
LES does not relax during swallow
Absence of peristalsis
Achalasia is a neurogenic
esophageal motility disorder
• Characterized by 3
manometric findings
1. Absence of
peristalsis in the body
of the esophagus
2. Failure of LES to
relax during
swallowing relaxation is absent or
incomplete
3. Higher than normal
resting LES pressure
Achalasia
What is the Cause?
• North America
– cause is unknown, viral
infection, autoimmune
• South America
– Chagas’ disease due to
parasite Trypanosoma
Cruzi
• Finding: degeneration of
ganglion cells in
Auerbach’s plexus
Clinical Presentation
– 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
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
Treatment for Achalasia – chronic
condition, no cure for it
• Aim of Treatment: relieve distal esophageal functional
obstruction (LES does not relax during swallowing)
• Choices of treatment:
1.Pneumatic “Balloon” dilatation of LES, success
rate of 80% decreases to 50% at 10 years;
esophageal perforation risk of 5%
2.Intra-sphincteric injection of Botox, symptomatic
relief of 60% decreases to 30% at 2.5 years
3.Treatment of choice is Distal esophagomyotomy
and partial fundoplication effective in 90%, late
problem of Postop GERD is about 15% over time
Distal Esophago-Myotomy and
Partial Fundoplication
Distal Esophageal Spasm (DES)
•
•
Clinical: severe, intermittent anterior chest pain
(confused with angina), dysphagia, and presence of
esophageal diverticulae
Defined by Esophageal Manometry
1. Simultaneous contraction waves in the body of
esophagus in >20% of the swallows
2. Prolonged contractions in the distal esophagus
(>6 sec)
3. Frequently presence of high pressure amplitudes
in the distal esophagus
4. LES abnormal – incomplete relaxation
DES
• “The lower part of the esophagus (smooth muscle
portion) of patients with diffuse esophageal spasm is
simultaneously and firmly contracted for an abnormally
long time”
• Clinical Presentation
 Severe spontaneous chest pain, intermittent
dysphagia, and presence of esophageal diverticulae on
barium swallow
• Differential Diagnosis
 Angina pectoris
 Psychoneurosis
Distal Esophageal Spasm
Corkscrew Esophagus
Treatment of DES
• Reassurance in most cases
– heart disease ruled out by cardiologist
– Not dealing with life-threatening condition
– Medical Therapy with nitrates, calcium channel
blockers, antireflux measures
• Surgical treatment cannot correct the functional disorder
 Long Esophagomyotomy to lower amplitude of waves
and resting pressure; add Partial Fundoplication
– Performed in selected refractory cases
– Successful symptomatic relief in 50% to 65%
Nutcracker Esophagus
• Manometric Findings
• 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
Pathologic Gastroesophageal
Reflux Disorder
Definition
• Frequent retrograde flow
of gastric contents across
the GE junction into the
esophagus
Pathophysiology
• Incompetent LES
• Loss of barrier function of
the LES, either
continuous or intermittent
REFLUXATE
– Acid or Alkaline reflux
HCL
Pepsin
Bile acids
 Bile salts
What are the normal properties of
LES?
•
•
•
•
•
•
Major barrier to reflux – HIGH PRESSURE ZONE
Physiological sphincter
Located in the distal 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
Incompetent Lower Esophageal
Sphincter causes GERD
• WHAT ARE THE
CAUSES OF
PATHOLOGIC GERD?
• Idiopathic - majority
• After pneumatic dilatation
or esophagomyotomy for
Achalasia
• Scleroderma
• Large fixed 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
1. ESOPHAGUS
reflux esophagitis:
inflammation, erosion,
ulceration, fibrosis and
peptic stricture
 chronic blood loss
and iron deficiency
anemia,
Barrett’s epithelium
and risk of
adenocarcinoma
2. UES SPASM  Zenker’s
diverticulum
3. MOUTH teeth decay
and loss of enamel
4. PROXIMAL AIRWAY 
laryngitis, wheezing,
cough
5. 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
• 24-hour impedance pH study detects number of reflux
episodes and whether acid or alkaline reflux
What is the treatment for GERD?
1. Always consider medical
treatment first
• 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
2. Surgical therapy requires
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 – recurrent
aspiration, asthma like
symptoms, laryngitis
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. Would you have sent
her home on first visit to
the ER with chest pain
and MI was ruled out?
2. What condition is
shown?
3. How does it affect the
patient?
4. 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
Combination of GERD
and Incarceration
Type III
Associated GERD
Risk of Incarceration/strangulation
Type IV hiatus hernia - volvulus
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 45y old patient
whose complaint for difficulty swallowing was
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,UK,
Europe, Australia – 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
Symptomatic GERD  Barrett’s Esophagus Adenocarcinoma
Barrett’s Esophagus
Esophageal Cancer
Clinical Presentation
1. Progressive dysphagia,
initially for solids and later
for liquids
2. Progressive weight
loss
3. Other symptoms –
chest pain, back pain,
hoarseness, choking and
aspiration, symptoms of
metastasis
Diagnostic Tests
• Barium UGI series
• Esophagoscopy and
mucosal biopsies
Tests for Staging
• CT scan chest and
abdomen
• Esophageal U/S and LN
biopsy
• PET scan
Treatment for Esophageal Cancer
1. Surgical: esophagectomy and reconstruction with
stomach or colon interposition
2. Induction chemotherapy and radiotherapy before
surgery
3. Definitive Radiotherapy only: local treatment
• Intent: palliation – symptom control
• Intent: cure – disease control
4. Definitive chemotherapy combined with radiation
5. 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
Chest Trauma
Acute Cardiac Tamponade
• Immediately life-threatening chest injury
• Disturbed physiology occurs because of combination of
two factors:
1. inability of the fibrous parietal pericardium to stretch in
acute situation
2. rapid intrapericardial accumulation of blood
 In acute situation even as little as 120 to 150 ml blood
in the pericardial space can lead to acute cardiac
tamponade
Acute Cardiac Tamponade
• Pathophysiology: is due to Poor Cardiac Filling
– Rapid bleeding into the pericardial sac  pressure on
right side of the heart  impaired venous return to the
heart  decreased stroke volume and cardiac output
(the pericardium does not stretch!)
• Clinical Features
– Suggestive wound – blunt or penetrating chest injury
– Pulse↑, BP↓, JVP↑ Pulsus paradoxus, Kussmaul’s
sign (Jugular venous distension with inspiration)
• Define Beck’s Triad
– Hypotension, Raised JVP, Muffled heart sounds
Acute Cardiac Tamponade
Intrapericardial Pressure
parameters
Hempericardium120 -150 mls
Acute Cardiac Tamponade
Diagnosis of Acute
Cardiac Tamponade in
Chest Trauma
1. Echocardiogram is
diagnostic test
2. Nature of the chest
injury
3. Not from CXR – don’t
expect to see
cardiomegaly
Treatment is Urgent
• Trauma Resuscitation
Protocol for ABC
• Immediate IV fluid bolus
• Perform needle
pericardiocentesis and
follow with mandatory
surgical exploration
• Pericardiocentesis is a
temporizing procedure
Pericardiocentesis
Sub-xiphoid approach
Massive Hemothorax
• Immediate threat to life
• How is it diagnosed?
– Pulse↑, BP↓, JVP↓, O2 ↓
– Abnormal clinical chest
findings - decreased
breath sounds and
dullness to percussion
– Abnormal CXR, CT
– Large blood loss from
chest tube: initial
1500mls  300mls/hr
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
Massive Hemothorax
What is the source of significant bleeding into the
pleural space?
1. Low pressure bleeding from lung laceration
caused by jagged, sharp ends of a fractured
rib  often self-limiting
2. High pressure bleeding from Intercostal artery,
Internal mammary artery, Aorta, Major arch
arteries, Vena Cava, Azygous vein 
continuous bleeding and not-self limiting
Treatment of Massive Hemothorax
URGENT TREATMENT
1.Replace blood volume
lost
2.Insert chest tube and
monitor for blood loss
3.Aim to evacuate blood
and blood clots as
much as possible
4.Use cell saver, if
available
5.Consider urgent
operation
When do you decide that
urgent operation is
indicated in Massive
Hemothorax?
• Initial chest tube drainage
of >1500 mls of blood
• Persistent bleeding after
initial drainage: >300mls
of blood loss/hr for 3 hrs
• Unevacuated residual
blood and blood clots on
CXR
Open Pneumothorax
• Immediately lifethreatening chest injury
• Serious because it
causes Acute Ventilatory
Failure
• What is the medical term
for a “sucking chest
wound”?
– Open pneumothorax
Penetrating chest injury – gun shot
Open Pneumothorax
• Diagnosis of Open
Pneumothorax is obvious
• Clinical Features are:
1. open chest wound
2. with air movement
through the chest wall
defect
3. lung is not expanded
on CXR
1. If the chest wall defect is large – 2/3rd size of tracheal
lumen
 the effect is very serious and immediate
 air preferentially passes through the defect (least
resistance) during inspiration
 immediate respiratory distress  ACUTE
VENTILATORY FAILURE  death occurs rapidly
from hypoxia
2. If the chest wall defect is small
 the effect is less serious
and outcome will depend on vital capacity
Pathophysiology
Treatment in the ER should be
Immediate
• How is open
pneumothorax treated?
1. Cover the chest wall
defect with sterile threesided occlusive airtight
dressing
2. Insert intercostal chest
tube as soon as feasible
3. Alternate treatment is
endotracheal intubation
and assisted positive
pressure ventilation
4. Surgical closure in OR
20y 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. What is the
management?
Pulmonary Contusion is very Serious
• Interstitial & parenchymal
hemorrhage  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%
Seen immediately on CXR
Segmental, Lobar, Whole lung
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 severe hypoxia is
a.
b.
c.
d.
e.
fluid restriction
intravenous albumin
assisted ventilation with pressure support
diuresis
methylprednisone
Treatment of Pulmonary Contusion
1. Restrict IV Fluids giving <1500mls/day (important)
2. Antibiotic seldom indicated and only for sepsis
complicating contusion
3. IV serum albumin and IV Lasix to reduce alveolar edema
(helps)
4. 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
– Uncomplicated lung contusion will heal in 5 to 10
days
Flail Chest Injury
Immediately life-threatening
chest injury
• Indicates that blunt chest
trauma is severe
• Clinically obvious by
paradoxical chest wall
movement if it is anterior
or lateral but not if
posterior in location
• Occurs because of two
separate fractures in
more than 3 adjacent ribs
A. Anterior Flail
B. Lateral Flail
Diagnosis of Flail Chest Injury
– Blunt chest injury with
multiple rib fractures
seen on CXR
– Paradoxical chest wall
movement  Flail
Segment of chest wall
sucks in with inspiration
and pushes out with
expiration opposite to
the movement of rest of
the chest wall
– Respiratory
compromise (hypoxia)
is not due to
paradoxical respiration
TRAUMA VICTIM
CHEST INJURY
BRUISING ON CHEST WALL
SURGICAL EMPHYSEMA
ACUTE CHEST PAIN
BREATHING DIFFICULTY
In Flail Chest Injury  Hypoxia is
caused by combination of 4 factors
1. Damaged painful unstable chest wall (multiple rib
fractures  cannot breathe well and cough well 
retention of bronchial secretions, blood clots  retention
atelectasis  V/Q mismatch  hypoxia)
2. Underlying lung contusion (always present  intraparenchymal and alveolar bleeding plus increased
capillary permeability  V/Q mismatch  hypoxia
3. Pleural space problems ( always hemopneumothorax 
compressive atelectasis  V/Q mismatch  hypoxia)
4. Chest wall muscle damage and spasm  expansion↓
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 
Acute chest wall pain
Lung contusion is always present
 Impairs gas exchange
Management of Flail Chest Injury
ISOLATED FLAIL CHEST 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
FLAIL CHEST INJURY combined
with MULTIPLE INJURIES
– Admit to ICU after lifethreatening injuries have
been looked after
– Assisted ventilation to
maximize oxygenation
– Optimal pain control
– Chest tube inserted on
injured side to prevent
tension pneumothorax (risk
of positive pressure
ventilation)
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
hyper-resonant to percussion. Contralateral tracheal
deviation is present. 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
Tension Pneumothorax
• Immediate treat to life is due to
combination of
HYPOXIA and
HYPOTENSION
• HYPOXIA due to V/Q
Mismatch
– Ipsilateral lung collapse
– Mediastinal shift
contralateral lung
compression
• HYPOTENSION due to
positive intra-thoracic pressure
– Impaired venous return
– Reduced stroke volume 
reduced cardiac output 
hypotension
This is a Clinical Diagnosis
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*
Pneumothorax
TENSION
SIMPLE
Pathogenesis of Tension
Pneumothorax
• Any closed pneumothorax (spontaneous or traumatic)
has the potential to become tension (valvular) type under
the right circumstances
• One-way air leak from lung surface (ruptured bulla,
lacerated lung) is always present
• Progressive accumulation of air in the pleural space
under positive airway pressure (right circumstance!) until
intra-thoracic pressure becomes positive
– Severe coughing and straining
– Endotracheal intubation and assisted ventilation
Problem
Finding
Tension
Bulging
pneumothorax is a hemithorax,
clinical diagnosis
unilateral
diminished breath
sounds, severe
May occur in
dyspnea, pleuritic
simple closed
pneumothorax or chest pain,
tachypnea
closed traumatic
subcutaneous
pneumothorax
emphysema,
contralateral
tracheal deviation
shock, cyanosis,
distended neck
veins
Emergency
Treatment
Immediate
decompression of
pleural space by
angiocath needle
inserted in the 2nd
intercostal space
in midclavicular
line
Followed by chest
tube insertion and
under 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
Thoracic Aortic Injury
Rib Fracture
• A single rib fracture in patient with preexisting compromised lung function may
precipitate respiratory failure
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
Management of Traumatic Closed
Pneumothorax
• Indications for chest tube insertion
– When large pneumothorax present is compromising
lung function
– When small pneumothorax and/or surgical
emphysema present in patient requiring general
anesthesia – to prevent tension pneumothorax
– When hemo pneumothorax present
– Patient placed on assisted ventilation in the OR or in
ICU
• Size of chest tube needed in trauma
– Large bore 28F or 32F
Single or Multiple Rib Fractures in
Blunt Chest Injury
• Expect damage to extra-thoracic soft tissue and
muscles, laceration of intercostal vessels and nerves
• Suspect associated underlying lung injury – contusion or
laceration
• Acute chest wall pain prevents deep breathing and
effective coughing  resulting in retention of bronchial
secretions  with consequent atelectasis  and finally
Hypoxia due to V/Q mismatch  worsening respiratory
distress and infected atelectasis
• Beware of associated complications of rib fractures
• Pneumothorax
• Hemothorax
• Associated injuries in the chest and abdomen
Optimal Management of Fractured Ribs
Out-patient Treatment
– Reliable patient without
pre-existing lung disease
with 1 to 3 fractured ribs
without pneumothorax,
hemothorax and hypoxia
– Able to breathe well and
cough well
– Effective relief of acute
chest wall pain for 3 weeks
is necessary – NSAIDS,
Oral Narcotics, intercostal
Nerve Blocks
In-patient Treatment
– > 3 fractured ribs with or
without associated
complications of
pneumothorax or
hemothorax, requiring
supplemental oxygen
– Need effective control of
pain with IV narcotics or
epidural analgesia,
physiotherapy, tracheal
suctioning and
bronchodilators
– May need intercostal chest
tube drainage
Rib Fracture
• A single rib fracture in patient with pre-existing
compromised lung function may precipitate
respiratory failure
• Multiple rib fractures >3 # admit to hospital for
minimum of 72 hours – adequate pain control,
monitor for complications in the chest –
hemothorax, pneumothorax
• Effective pain control for minimum of 3 weeks
clinical assessment and repeat CXRs
Chest Injury and Acute Chest Wall Pain
• Demands immediate and optimal pain relief
• Must restore ability to breathe well and cough well to
protect the lungs against retention atelectasis  V/Q
mismatch and hypoxia
• Use
– Oral opiods and NSAIDS
– Intercostal nerve blocks
– Epidural analgesia – most effective
• Watch out for respiratory depression
– if opiods used in hypoxic patient