LMCC Review in Thoracic Surgery April 2010

• 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 diverticulumThe 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

LESMay be abnormal

Incomplete relaxation

Esophageal Body Contractions20% or more simultaneous*

Repetitive >2 peaksProlonged duration > 6 secSpontaneous 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

LESMay be hypertensive

Esophageal BodyHigh amplitude

mean DEA>220 mm HgMay be long duration

Mean > 6 secNormal peristalsis

Gastroesophageal Reflux Disorder

WHAT IS IT?• Frequent retrograde flow

of gastric contents across the GE junction into the esophagus

WHAT IS THE REASON?• Loss of barrier function

of the LES, either continuous or intermittent

• WHAT ARE THE TWO TYPES OF REFLUX?– Physiological– Pathological – GERD

• 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, H2-

blockers

• 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 herniationof 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 or come to ER with incarceration/strangulation

Symptoms of incarceration and reflux

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

Medical therapy is not that effective

Anatomical correction is indicated

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 life-

threatening 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 ofOpen 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. flail chestb. pulmonary hematomac. subcutaneous emphysemad. pulmonary contusione. diaphragm rupture

Chest Trauma

• The most effective single modality in treating severe pulmonary contusion associated with post-traumatic respiratory distress and hypoxia is

a. fluid restrictionb. intravenous albuminc. assisted ventilation with pressure supportd. diuresise. 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 VICTIMCHEST INJURY

BRUISING ON CHEST WALLSURGICAL EMPHYSEMA

ACUTE CHEST PAINBREATHING 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 hypoxia4. 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 life-

threatening 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-rayb. insertion of an endotracheal tubec. cricothyroidotomyd. stat arterial blood gas analysise. Immediate needle decompression and chest tube insertion

TensionPneumothorax is life-threatening

1. Progressive accumulation of air in pleural space under pressure

2. Ipsilateral lung collapse V/Q mismatch hypoxia

3. Contralateral mediastinal shift and lung compression V/Q mismatch hypoxia

4. Severe impairment of ventilation*

5. Impaired venous return ↓CO*

6. Rapid cardio-respiratory collapse

Pathophysiology of Tension Pneumothorax

Tension Pneumothorax

• Death may occur relatively rapidly due to combination ofHYPOXIA 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 Finding Emergency Treatment

Tension pneumothorax is a clinical diagnosis

May occur in simple closed pneumothorax or closed traumatic pneumothorax

Bulging hemithorax, unilateral diminished breath sounds, severe dyspnea, pleuritic chest pain, tachypnea subcutaneous emphysema, contralateral tracheal shift, shock, distended neck veins

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 Hypoxia Lung contusion Respiratory AcidosisPneumothorax

Decreased Alveolar Shunting

Ventilation V/Q mismatch

Hemothorax Shock Decreased Cardiac Output

Heart & vessel injury

Associated injury Metabolic Acidosis

Death

Factors producing pulmonary insufficiency after thoracic injury

Reduced cardiac output

Increased work Aspiration

of breathing

Fractured ribs Atelectasis

Lung contusion CNS injury

Restrictive Pulmonary Insufficiency Pneumothorax Diaphragm Rupture Pleural effusion & Hemothorax

Hypoxiaand

RespiratoryAcidosis

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 pre-existing 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. open pneumothoraxb. systemic air embolismc. cardiac tamponaded. tension pneumothoraxe. 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 Cause of Death

MASSIVE HEMOPTYSIS Asphyxiation

> 600 mls blood loss in 24 hours

EXSANGUINATING HEMOPTYSIS Both Hypotension and Asphyxiation

> 1000 mls blood loss in 24 hours

> 150 mls blood loss per hour

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 Number of cases

TB 47

Bronchiectasis 37

Necrotizing pneumonia 11

Lung abscess 6

Lung cancer 6

Bronchovascular fistula 5

Lung fungal infection 4

Miscellaneous 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 upright2. 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 x-cross match blood, and consent for OR

5. PRIORITY 1 in the OR6. 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 TreatmentEarly Bronchoscopy

• Clear the Airway

• Secure the Airway

• Separate the Two Lungs

• Handle the Cause

Endobronchial Control MeasuresEmergency 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 SeparationDouble 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 non-

bronchial 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 graftPulmonary 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. asthma2. interstitial lung disease3. cystic fibrosis4. active tuberculosis5. histiocytosis X6. pulmonary metastases from sarcoma7. lymphangioleiomyomatosis (LAM)8. Birt-Hogg-Dube syndrome9. 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

• Cause1. 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 pointers1. sudden onset2. severe unilateral chest pain worse on breathing3. increasing respiratory distress, hypoxia and tachycardia are early signs4. cyanosis (not always present), hypotension, distended neck veins, and tracheal deviation

are late signs of a tension pneumothorax5. 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 intra-thoracic 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 re-expands 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 I – 1ST week II – 2ND week III – 4TH week

Early Acute

“Exudative”

acute septic pleurisy, free, seropurulent pleural effusion

Fluid is thin and watery

Intermediate Subacute

“Fibrinopurulent”

subacute suppurative

effusion gradually thickens and becomes more and more purulent; limiting adhesions develop causing multiple loculations (unless empyema is total)

Third 4-6 wks

Chronic

True Empyema

“Purulent”

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

• Local – chest pain, worsened by breathing

• General – toxemia, fever, malaise, loss of appetite and weight

• Local- chest pain

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 50%

• Post – surgical 25%

• Extension from subphrenic 10%

• Other 5% – Esophageal perforation– Descending necrotizing mediastinitis– Anastomotic leak post-esophagectomy

Right Empyema

Use of intrapleural fibrinolytic agent

27-10-200930-09-2009

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