lmcc review in thoracic surgery april 2010 dysphagia gerd and hiatus hernia chest trauma massive...
Post on 11-Jan-2016
216 Views
Preview:
TRANSCRIPT
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
top related