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 What is the diagnosis? What are the complications of this condition? Is treatment necessary? 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? Concomitant Symptomatic GERD NEED AN OPERATION 1. Cricopharyngeal myotomy in all the cases 2. Management of diverticulum depends on size Small < 3 cm: no need for excision Large > 3 cm: add diverticulectomy Concomitant Symptomatic GERD Should be managed first - otherwise risk free aspiration after operation for diverticulum Reason: Reflux is due to incompetent LES. Operation for Zenker’s diverticulum will make UES hypotensive

A 35-year-old man with slowly worsening difficulty swallowing had barium study performed 1. What is demonstrated in this barium swallow? 2. What are the essential clinical features? 3. What is necessary to confirm diagnosis? 4. What treatment would you suggest?

Dysphagia - Achalasia WHAT IS IT? Esophageal motility disorder characterized by 1.Absence of peristalsis in the body of the esophagus 2.Failure of or incomplete relaxation of LES is response to swallowing, 3. Higher than normal resting LES pressure

Achalasia WHAT IS THE CAUSE? NA – cause is unknown, viral infection, autoimmune SA – Chagas’ disease due to parasite Trypanosoma Cruzi Finding: degeneration of ganglion cells in Auerbach’s plexus WHAT ARE THE SYMPTOMS? Dysphagia for both solids and liquids; worse with liquids Retrosternal burning discomfort due to food stasis and retention esophagitis Nocturnal regurgitation of food and choking episodes  aspiration

Esophageal Manometry confirms the diagnosis LES does not relax during swallow Absence of peristalsis

Achalasia: Investigations and Results BARIUM SWALLOW APPEARANCE IS CHARACTERISTIC Esophageal dilatation Spastic non-peristaltic contractions Retention of contrast above poorly relaxing LES at G-E junction ‘bird’s beak’ with obstruction UGI ENDOSCOPY IS NECESSARY TO RULE OUT CANCER (PSEUDOACHALASIA) AND PEPTIC STRICTURE Evidence of stasis Dilated esophagus with retained food, liquid, saliva Mucosal inflammation ‘retention esophagitis’ ESOPHAGEAL MANOMETRY IS NECESSARY TO CONFIRM THE DIAGNOSIS Incomplete or absent relaxation of LES Absence of normal peristalsis in body of esophagus

Diagnosis of Achalasia Suspect diagnosis: from symptoms Support diagnosis: from esophagogram see “Birds Beak” deformity Confirm diagnosis: from UGI Endoscopy and Manometry

Achalasia and Epiphrenic Diverticulum Always suspect underlying cause for epiphrenic diverticulum The cause must be treated as well

Complications of Achalasia ESOPHAGUS Malnutrition Progressive dilatation Retention esophagitis Epiphrenic diverticulum Esophageal cancer: squamous (due to retention esophagitis) adenocarcinoma ( due to post treatment reflux – Barrett’s epithelium) RESPIRATORY Aspiration pneumonia, empyema, lung abscess, fibrosis, bronchiectasis Dyspnea due to extrinsic tracheal compression PSYCHOSOCIAL Unable to eat in public withdrawn

What is the treatment for Achalasia? Chronic condition, no cure for it Aim of Treatment: relieve distal esophageal functional obstruction Choices of treatment: Pneumatic “Balloon” dilatation, initial success rate of 80% decreases to 50% at 10 years; esophageal perforation risk of 5% Intra-sphincteric injection of Botox, symptomatic relief of 60% decreases to 30% at 2.5 years Distal esophagomyotomy and partial fundoplication gives the best sustained result of 90%, postoperative reflux is about 15% over time

Distal Esophago-Myotomy and Partial Fundoplication

Distal Esophageal Spasm

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 Treatment 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

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 What condition is shown? How does it affect the patient? What serious problem can occur?

Complications of Hiatus Hernia 1. Incarceration  strangulation  ischemic perforation  death 2. Anemia – chronic blood loss due to mucosal congestion 3. Dyspnea – large hernia 4. Cardiac Arrhythmias – extrinsic pressure 5. Volvulus obstruction 6. Perforation 7. Massive Bleeding

Type I Type II Type III

Type IV hiatus hernia Intrathoracic stomach with risk of volvulus, associated herniation of transverse colon, small bowel

Management of Hiatus Hernia Classification Type I – most common Type II – very rare Type III – mixed Type I and II Type IV INCIDENCE 85% to 90% Pure is rare < 1% About 6% Least common SYMPTOMS May be asymptomatic or have GERD Asymptomatic 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 of Open Pneumothorax 1. If the chest wall defect is large  the effect is very serious  immediate respiratory distress  ACUTE VENTILATORY FAILURE  death occurs rapidly 2. If the chest wall defect is small  the effect is less serious and outcome will depend on vital capacity

Treatment of Open Pneumothorax How is open pneumothorax treated? Treatment in the ER should be immediate Cover the chest wall defect with sterile occlusive airtight dressing Insert intercostal chest tube as soon as feasible Alternate treatment is endotracheal intubation and assisted positive pressure ventilation

Patient involved in MVA is found to be markedly hypoxic in the ER Patient involved in MVA is found to be markedly hypoxic in the ER. CXR was performed. What is illustrated on CXR? Why is there a change in oxygen saturation? What is the reason for NGT insertion? 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 chest b. pulmonary hematoma c. subcutaneous emphysema d. pulmonary contusion e. 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 restriction b. intravenous albumin c. assisted ventilation with pressure support d. diuresis e. methylprednisone

discussion Fluid restriction is certainly indicated giving <1500mls/day Antibiotics only for sepsis complicating contusion Serum albumin to reduce alveolar edema The single most effective modality for treatment of pulmonary contusion is mechanical ventilation with addition of PEEP Improves FRC Improves oxygenation by keeping alveoli open Insert chest tube to prevent tension pneumothorax

Immediately life-threatening chest injury – Flail Chest WHAT IS FLAIL CHEST INJURY? Due to two separate fractures in three or more rib Anterior, Lateral, or Posterior location Indicative of severe blunt chest trauma

Immediately life-threatening chest injury – Flail Chest HOW IS IT DIAGNOSED? PARADOXICAL RESPIRATION Flail segment of chest wall sucks in with inspiration and pushes out with expiration opposite the rest of the chest wall Respiratory compromise is not due to paradoxical respiration TRAUMA VICTIM CHEST INJURY BRUISING ON CHEST WALL SURGICAL EMPHYSEMA ACUTE CHEST PAIN BREATHING DIFFICULTY

Flail Chest Injury  Hypoxia 1. Damaged painful unstable chest wall 2. Underlying lung contusion 3. Pleural space problems 4. Chest wall muscle damage and spasm Paradoxical respiration is not the cause of deranged physiology

What is the cause of respiratory compromise in Flail Chest Injury? 1.Damaged painful unstable chest wall Normal ventilatory force is lost  lung expansion decreases  FRC falls Cough is impaired  retention of secretions  retention atelectasis  V/Q mismatch  hypoxia 2. Underlying lung contusion Hemorrhagic, edematous, non-compliant lung  impaired diffusion  hypoxia 3. Pleural space problems Hemothorax and/or pneumothorax  compressive atelectasis  V/Q mismatch  hypoxia 4. Chest wall muscle damage and spasm, increased work of breathing and oxygen demand, hypoxia  muscle fatigue and oxygen debt

Flail Chest Injury Lung contusion is always present Multiple rib fractures

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-ray b. insertion of an endotracheal tube c. cricothyroidotomy d. stat arterial blood gas analysis e. Immediate needle decompression and chest tube insertion

Pathophysiology of Tension Pneumothorax Progressive accumulation of air in pleural space under pressure Tension Pneumothorax is life-threatening 2. Ipsilateral lung collapse V/Q mismatch  hypoxia 6. Rapid cardio-respiratory collapse 5. Impaired venous return ↓CO* 3. Contralateral mediastinal shift and lung compression V/Q mismatch  hypoxia 4. Severe impairment of ventilation*

This is a Clinical Diagnosis Tension Pneumothorax Death may occur relatively rapidly due to combination of HYPOXIA and HYPOTENSION HYPOXIA due to V/Q Mismatch Ipsilateral lung collapse Mediastinal shift contralateral lung collapse HYPOTENSION due to positive intra-thoracic pressure Impaired venous return Reduced stroke volume  reduced cardiac output  hypotension This is a Clinical Diagnosis

Problem 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. What are the clinical features of this condition? What is the reason for P140/min,R40/min, BP80/60, O2 sat 87%? Was CXR absolutely necessary for diagnosis? 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 Acidosis Pneumothorax 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 Hypoxia and Respiratory Acidosis

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 pneumothorax b. systemic air embolism c. cardiac tamponade d. tension pneumothorax e. 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 Impending airway obstruction 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 18%

Massive Hemoptysis and threat of Asphyxiation Gas exchange is impaired by 2 mechanisms Bronchial obstruction by blood clots: as little as 150 mls of blood clot can fill the anatomical dead space causing proximal airway obstruction  asphyxiation 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 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 Immediate clinical assessment – with patient upright Urgent resuscitation – administer supplemental oxygen, secure intravenous access, IV antibiotic 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 Obtain immediately: CBC, serum electrolytes, arterial blood gas analysis, PTT and INR, EKG, type and x-cross match blood, and consent for OR PRIORITY 1 in the OR Inform interventional radiology for urgent angiogram and possible embolization of bleeding vessel

Key to the management is Bronchoscopy Remove obstructing blood clots in the airways Restore oxygenation Temporarily arrest bleeding with endobronchial control measures: with cold saline (4°C) or dilute epinephrine solution irrigation (200mcg of 1:1000 epinephrine in 500 mls N/S) SEPARATE TWO LUNGS with double lumen tube to protect the good lung from aspiration of blood

Bronchoscopy should be done in the OR RIGID BRONCHOSCOPY FIRST Ventilate patient easily Suction effectively to remove obstructing blood clots and restore oxygenation Good optics to visualize and determine SIDE of bleeding Flexible bronchoscopy after rigid bronchoscopy to determine SITE of bleeding and possible cause Implement endobronchial control measures to protect good lung and to arrest bleeding: cold saline and dilute epinephrine solution irrigation Lung separation with double lumen tube to protect good lung and then come out of the OR Don’t leave the OR until patient is completely stable

General Principles of Treatment Early Bronchoscopy Clear the Airway Secure the Airway Separate the Two Lungs Handle the Cause

Endobronchial Control Measures Emergency Bronchoscopy Tray Rigid bronchoscope Flexible bronchoscope Cold N/S – 4 Celsius Bronchial Blocker and Double Lumen Tube Dilute epinephrine solution Oxygen saturation monitor

Rigid Bronchoscopy Optics - excellent for Visualization Channel - excellent for Suctioning ETT – excellent for Ventilation “ A situation where the margin between life and death is narrow, it will save the patient’s life”

Lung Separation Single Tube and Bronchial Blocker

Blocker in the Left Lung

Lung Separation Double Lumen Tube

Interventional Radiology for Angiogram and Embolization Safe after patient has been completely stabilized in OR Look for abnormal bronchial artery and non-bronchial collaterals Arrest bleeding - important component of medical treatment Thoracic aortogram (bronchial and intercostal arteries) and subclavian arteriogram (non-bronchial collateral arteries from intercostal, internal mammary, acromiothoracic and lateral thoracic arteries) Permits elective definitive operation under more safe conditions and with low mortality – resect diseased portion of lung in operable patients Complication of embolization: spinal cord ischemia

Bronchial artery angiogram and embolization Important component of medical treatment Safe after patient has been stabilized in OR and the healthy lung has been separated from bleeding lung Thoracic aortogram and subclavian arteriogram Need to look for abnormal bronchial (aorta) and 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 graft Pulmonary Fistula

Pneumothorax Because of the subatmospheric pressure in the pleural space, whenever the pleural membrane is breached so as to allow communication with the atmosphere, air will enter the space and a pneumothorax will result Classification according to the cause

Spontaneous Pneumothorax Due to spontaneous rupture of the visceral pleura either because of some local defect or because of underlying diffuse lung disease Local defect usually near the lung apices either a small bulla due to tractional emphysema associated with small scar or a bleb which is a localized collection of air within visceral pleura due to ruptured distended alveoli beneath the visceral pleura commonest cause in young Diffuse lung disease usually emphysema Older patient, chronic smoker

Simple Closed Secondary Spontaneous Pneumothorax Commonest cause is pulmonary emphysema Others are 1. asthma 2. interstitial lung disease 3. cystic fibrosis 4. active tuberculosis 5. histiocytosis X 6. pulmonary metastases from sarcoma 7. lymphangioleiomyomatosis (LAM) 8. Birt-Hogg-Dube syndrome 9. catamenial (related to menstruation)

Spontaneous Pneumothorax PRIMARY spontaneous pneumothorax Local defect usually near the lung apices small bulla >1cm (due to scar and tractional emphysema) bleb <1cm (a localized collection of air within the visceral pleura from ruptured distended alveolus) SECONDARY spontaneous pneumothorax Underlying lung disease is present Most common is emphysema

Spontaneous Pneumothorax – 3 types 1. Simple closed: primary and secondary 2. Tension or valvular in any closed pneumothorax 3. Complicated - associated with 1. infection – chronic, trapped lung, empyema 2. bleeding - hemothorax 3. open: broncho-pleural fistula between the bronchial tree and pleural cavity esophago-pleural fistula complicating post-emetic ruptured esophagus

Spontaneous Pneumothorax Simple pneumothorax tear in the pleural surface is small, resulting retraction of lung allows hole to close and prevent further egress of air while the intrapleural pressure is still below atmospheric Complicated pneumothorax Tear is larger and persists, mean intrapleural pressure becomes atmospheric, and risk of secondary infection, causing entrapment of lung and empyema; associated bleeding from the chest wall

Simple Closed Primary Spontaneous Pneumothorax CAUSE: an emphysematous bulla or a bleb ruptures and air leaks into the pleural cavity AGE incidence: young adults are especially liable CLINICAL POINTERS: 1. sudden onset 2. unilateral pleuritic chest pain; mild dyspnea 3. diminished breath sounds over the affected lung 4. dry cough is usually but not always present INVESTIGATIONS: Chest x-ray on inspiration and expiration confirms diagnosis; sometimes CT scan needed

Management of Simple Closed Spontaneous Pneumothorax Duration of pneumothorax depends on treatment: 1. Expectant observation - depends on the degree of lung collapse and assuming that the air leak has sealed immediately  the rate of re-expansion of the lung is 1.25% per day: 10% lung collapse will resolve in 8 days and 20% in 16 days 2. Intercostal chest tube drainage: about 72 hrs Complications: 1. small risk of becoming tension type 2. recurrence affecting the same lung is 20% to 30% after 1st episode; 50% after 2nd episode; 80% after 3rd episode 3. sepsis (empyema), trapped lung 4. associated hemothorax

Tension or Valvular Pneumothorax Cause 1. any simple closed pneumothorax has the potential to become tension under the right circumstances 2. communication between the lungs and the pleural cavity allows unidirectional passage of air and transmission of positive airway pressure into pleural cavity but not out of it  allows considerable tension to be built up inside the pleural cavity Precipitating factors 1. valve action at the site of air leak persists 2. severe coughing generates positive airway pressure 3. assisted ventilation with positive airway pressure

Tension or Valvular Pneumothorax Clinical pointers 1. sudden onset 2. severe unilateral chest pain worse on breathing 3. increasing respiratory distress, hypoxia and tachycardia are early signs 4. cyanosis (not always present), hypotension, distended neck veins, and tracheal deviation are late signs of a tension pneumothorax 5. increased resonance and absent or diminished breath sounds on affected side of chest (hyperinflated) 6. evidence of contralateral mediastinal shift

Life-threatening situations in Spontaneous Pneumothorax Tension Pneumothorax Clinical diagnosis Respiratory distress, tachycardia, cyanosis Hypotension and hypoxia Mediastinal displacement to opposite side Hyper-inflated chest and absent air entry Associated 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 Simple 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: Local spread (from infected lung) – pneumonia, lung abscess Implantation – at operation (pulmonary resection, esophagectomy, chest wall resection, mediastinal operation, hiatus hernia repair) Lymphatic trans-diaphragmatic spread (from subphrenic abscess) 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 Clinical Findings 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 30-09-2009 27-10-2009

Clinical Presentation Acute versus Chronic Phase Complications by extension, by secondary infection, by fibrosis Empyema necessitans Septic chondritis Osteomyelitis Broncho-pleural fistula Pericarditis Mediastinal abscess Septicemia fibrothorax

Diagnosis of Empyema Radiology CXR, U/S, CT scan Thoracentesis Cultures 50% positive pH<7 Glucose<2 WBC>15,000 Protein>2.5 Bronchoscopy Barium swallow/esophagoscopy

Treatment of Pleural Infection 1. Treat the Infection Antibacterial drugs Look for primary site of infection and treat 2. General Supportive Treatment Rest, treat toxemia, supplement oxygen, relieve pain 3. Remove the Pleural Effusion to allow Lung to expand completely to eliminate infection and restore lung function Insert intercostal (closed) catheter, intrapleural fibrinolytic agent –streptokinase, TPase Open drainage once pus is too thick, multiple loculations present, and lung is trapped – decortication, rib resection