Thoracic Surgery Flashcards
Massive hemoptysis definition
expectoration of large amount of blood and / or rapid rate of bleeding (>500cc over 24 hours or >100cc / hour)
How to rule out GI source of upper bleed (presenting with hemoptysis)
blood with alkaline pH, foaminess, pus makes GI source unlikely
endoscopy rules out GI source bleeding
How to rule out upper airway bleeding presenting with hemoptysis
no source of bleeding on examination of nose & mouth and laryngoscopy rules out upper airway bleeding
Source of massive hemoptysis
all cases of massive hemoptysis are from bronchial artery, because bronchial artery is systemic circulation and have high pressure that would cause more bleeding
than pulmonary vasculature with lower pressure
What is the most common cause of hemoptysis
Pulmonary (bronchiectasis)
Bronchiectasis causing hemoptysis pathophysiology
bronchiectasis with chronic airway inflammation cause hypertrophy and tortuosity of bronchial arteries as well as submucosal / peri-bronchial plexus of blood
vessels, which may rupture causing bleeding into bronchus
Causes that can lead to bronchiectasis
cystic fibrosis
prior bacterial or viral infection
TB
impairment of mucociliary clearance
Tuberculosis causing hemoptysis pathophysiology
pathophysiology:
active TB have cavitary with bronchiolar ulceration and necrosis of adjacent bronchial vessels
inactive TB have bronchiectasis or erosion of healed calcified lymph node into bronchial artery
Bronchogenic carcinoma causing hemoptysis pathophysiology
typically large centrally located tumour that invades bronchial artery
Aspergilloma causing hemoptysis pathophysiology
invasion and destruction of parenchymal and vascular structure within the lung
Complicated pneumonia (nec pneumonia, lung abscess) causing hemoptysis pathophysiology
cavitation from necrotizing pneumonia or abscess from lung abscess can cause ulceration and necrosis of adjacent bronchial vessels
Differential diagnosis of hemoptysis (pulmonary causes)
B = bronchitis, bronchiectasis A = aspergilloma T = tumor T = TB L = lung abscess E = embolism, pulmonary C = coagulopathy A = autoimmune vasculitis (Behcet’s, Lupus, Good pasture’s), arterio-venous malformation, alveolar hemorrhage M = mitral stenosis, congenital heart disease from pulmonary hypertension P = pneumonia
Hemoptysis mechanism of death
massive hemoptysis is life threatening due to asphyxiation, not exsanguination
asphyxiation due to blood in alveoli impairing gas exchange across alveolar membrane, resulting in hypoxemia
Risk factors for mortality due to hemoptysis
underlying cause for hemoptysis
low cardiopulmonary reserve: underlying cardiac or pulmonary disease
area of chest alveolar hemorrhagic infiltrate
Hemoptysis diagnosis
bronchoscopy = diagnostic procedure of choice to visualize and localize bleeding site
high resolution CT and arteriography if negative bronchoscopy
Hemoptysis management
1) Stabilize
identify side that is bleeding and position patient with bleeding lung in dependent position (i.e. right lung bleeding = right side down decubitus position)
bleeding side can be based on history of lung disease, gurgling sound on auscultation or imaging
establish patent airway by endotracheal intubation with large bore (size >8) tube
protect non-bleeding lung from spillage by unilateral lung ventilation or double lumen endotracheal tubes
unilateral lung ventilation = single lumen endotracheal tube into mainstream bronchus of non-bleeding lung
double lumen endotracheal tube = 2 lumens (longer lumen into and inflated at left bronchus to ventilate left lung; shorter lumen into and inflated at trachea to ventilate right lung), which can ventilate both lungs while preventing aspiration of blood from one lung to another
2) Control Source of Bleeding
1st line = bronchoscopy techniques (in OR as priority 1)
balloon tamponade: balloon catheter into segmental or sub-segmental bronchus of bleeding site to limit bleeding to the segment
ice saline lavage: lavage of bleeding source using 50mL aliquots of cold saline causing local vasoconstriction, reducing blood flow and promoting hemostasis
topical medication: infusion of topical vasoconstrictive agent (Epinephrine or Vasopressin) or topical coagulant (Thrombin or Fibrinogen Thrombin) onto bleeding site
laser therapy, electrocautery, argon plasma coagulation or cryotherapy to stop bleeding form mucosal lesion
2nd line = interventional radiology techniques
focal injection of IV contrast to define intended arterial circulation bleeding, then insert occlusive material to embolize bleeding vessel or proximal vessel that supply bleeding vessel
3) Definitive Treatment
definitive therapy = surgery and addressing underlying cause
a) thoracic surgery
patient should have early evaluation by thoracic surgeon and expedited for surgical intervention (first priority)
surgery = pulmonary resection of bleeding segment or cavernostomy & packing of bleeding cavity
b) addressing underlying cause
TB / Aspergilloma / complicated pneumonia: antimicrobial treatment
bronchiectasis and bronchogenic carcinoma usually have no short term definitive treatment
Differential diagnosis for oral dysphagia
neurologic: dementia
inflammation / infection: tonsillitis, xerostomia
neoplasm: squamous cell carcinoma
other: poor dentition
Differential diagnosis for pharyngeal dysphagia
neurologic: dementia, stroke, multiple sclerosis
infection / inflammation
neoplasm: squamous cell carcinoma
structural: Zenker’s diverticulum
Differential diagnosis for esophageal dysphagia
- Mechanical obstruction
a) intrinsic mechanical obstruction
peptic stricture
esophageal webs
lower esophageal ring (A or B (Schatzki’s ring))
eosinophilic esophagitis
esophageal carcinoma
foreign body
b) extrinsic obstruction
vascular compression
mediastinal abnormalities
cervical osteoarthritis
hiatus hernia - Motility (Neuromuscular) disorder
a) primary motility disorder
achalasia
diffuse esophageal spasm
nutcracker esophagus (hypertensive peristalsis)
hypertensive lower esophageal sphincter
b) secondary motility disorder
scleroderma
What is succussion splash
Succussion splash also known as a gastric splash, is a sloshing sound heard through the stethoscope during sudden movement of the patient on abdominal auscultation. It reflects the presence of gas and fluid in an obstructed organ, as in gastric outlet obstruction
What does succussion splash indicate
Achalasia
What is CREST syndrome
Calcinosis Raynaud’s phenomenon Esophagitis Sclerodactyly Telangiectasia
Dysphagia investigations
EGD is investigation of choice for esophageal dysphagia for mechanical obstruction, which can be therapeutic by interventions (dilation, stenting, thermal ablation)
barium swallow looks for mechanical obstruction, but less sensitive and specific than EGD
esophageal manometry is gold standard for evaluating esophageal motility (neuromuscular disorder), usually as follow up to negative EGD after ruling out mechanical obstruction
Oral dysphagia presentation
difficulty manipulating bolus in mouth, difficulty containing bolus in mouth (spillage), lengthy chewing time, pocketing of food in oral cavity, oral
residue in mouth, drooling
Pharyngeal dysphagia presentation
difficulty initiating swallow, coughing, choking, repeated attempts at swallowing, wet & gurgling voice, wet breath sounds
Esophageal dysphagia presentation
food stopping or sticking retrosternally after swallowing
dysphagia with solids alone suggests…
mechanical obstruction
dysphagia with solids and liquids suggests…
motility (neuromuscular) disorder
for mechanical obstruction, intermittent dysphagia suggests…
lower esophageal ring
for mechanical obstruction, progressive dysphagia suggests…
peptic stricture or carcinoma (especially if old age >50 years and weight loss)
for motility (neuromuscular) disorder, intermittent dysphagia suggests…
diffuse esophageal spasm, especially if associated with chest pain
for motility (neuromuscular) disorder, progressive dysphagia suggests…
scleroderma (associated with chronic heart burn) or achalasia (associated with bland regurgitation and weight loss)
Zenker’s diverticulum epidemiology
common in elderly male typically age >75 years
Zenker’s diverticulum pathophysiology
1) uncoordinated swallowing, impaired relaxation / spasm of cricopharyngeus muscle increase pressure within pharynx
2) increased pressure cause pharyngeal mucosa to pouch at the weakest point (Killian triangle) above the cricopharyngeus muscle forming a diverticulum
Zener’s diverticulum = out pouch of the pharyngeal mucosa just above the cricopharyngeal muscle
Zenker’s diverticulum clinical presentation
symptoms: oropharyngeal dysphagia, halitosis, gurgling in throat, food regurgitation into mouth
signs: mass in neck
Zenker’s diverticulum complications
pulmonary aspiration
aspiration pneumonia
Zenker’s diverticulum investigations
barium swallow: visualization of diverticula
neck ultrasound: visualization of outpouching
Zenker’s diverticulum diagnosis
patient diagnosed based on Zenker’s diverticulum visualized on barium swallow
Zenker’s diverticulum management
definitive treatment = surgery or endoscopic intervention
surgical options include:
mobilization of Zenker’s diverticulum and excision at later stage when granulation has formed around the diverticulum
excision of Zenker’s diverticulum in 1 step
cricopharyngeal myotomy leaving Zenker’s diverticulum undisturbed
cricopharyngeal myotomy with diverticulectomy or diverticulopexy
Peptic stricture etiology
peptic stricture is a complication of GERD (in 10-20% of untreated GERD)
Peptic stricture pathophysiology
GERD cause esophagitis followed by sub-mucosal collagen deposition and fibrosis
the scarring cause smooth, circumferential tapered luminal narrowing usually at lower esophagus
Peptic stricture clinical presentation
symptoms:
progressive solid food dysphagia with heartburn but without weight loss
food bolus impaction (food getting stuck where any food, liquid or saliva cannot go through)
Peptic stricture diagnosis
diagnosis based on visualization of stricture on EGD
Peptic stricture treatment
EGD dilation (to diameter >15mm) by balloon dilators, Maloney or Savary method
PPI to treat GERD
What is achalasia
disorder of motility with some mechanical obstruction
achalasia epidemiology
common in adults age 30-50
achalasia pathophysiology
decreased activity of inhibitory ganglion of myenteric plexus innervating the esophagus, resulting in lack of peristalsis in esophagus and failure to relax the lower esophageal sphincter
achalasia clinical presentation
symptoms: progressive dysphagia for solids and liquids, weight loss, bland regurgitation, chest pain / heart burn
achalasia complications
pulmonary aspiration
aspiration pneumonia
achalasia investigations
barium swallow: Bird’s beak (dilated esophagus with narrow lower esophageal sphincter) due to failure in relaxation of lower esophageal sphincter, which is specific for achalasia
esophageal manometry: gold standard for diagnosis of achalasia
achalasia treatment
1st line = laparoscopic or open surgery Heller myotomy (incision to cut lower esophageal sphincter) with fundoplication (gastric fundus wrapped around esophagus to decrease reflux after loss of lower esophageal sphincter)
- alternative treatments = medication, EGD interventions
a) medication to relax lower esophageal sphincter: calcium channel blocker Nifedipine, Nitrate, PDE inhibitor Sildenafil
b) EGD intervention: botox injection into lower esophageal sphincter, pneumatic dilation of lower esophageal sphincter with balloon
Esophageal cancer epidemiology
affect elderly age >50
Esophageal cancer risk factors
squamous cell carcinoma: smoking, alcohol, diet
adenocarcinoma: gastroesophageal reflux disease (GERD), obesity, smoking, diet
Esophageal cancer pathophysiology
squamous cell carcinoma (~60% esophageal cancer) is more common than adenocarcinoma (~40% of esophageal cancer), but squamous cell carcinoma incidence is decreasing and adenocarcinoma incidence is increasing
Barrett’s esophagus -> adenocarcinoma arise from mucosal glandular cells at gastroesophgeal junction (5 year survival ~20%)
squamous cell carcinoma arise from mucosal squamous cell at mid to lower esophagus
Esophageal cancer clinical presentation
elderly age >50 with progressive solid food dysphagia and unintentional weight loss is esophageal cancer until proven otherwise
esophageal cancer usually is asymptomatic for a long period, therefore present at advanced stages
symptoms: GERD, progressive solid food dysphagia, odynophagia, regurgitation, unintentional weight loss, anorexia, retrosternal discomfort, iron deficiency anemia from bleeding, hoarseness, sialorrhia
Esophageal cancer complications
aspiration pneumonia
upper GI bleed from esophagus
trachea-esophageal fistula
broncho-esophageal fistula
Esophageal cancer common metastasis locations
trachea, liver, lung, bone, celiac & mediastinal lymph nodes
Esophageal cancer investigations
EGD: biopsy for tissue diagnosis, can determine extent and resectability of tumour
CT chest & abdomen +/- PET: metastasis staging
endoscopic ultrasound: regional staging (visualize local disease, regional nodal involvement)
bronchoscopy and thoracoscopy: rule out airway invasion
Esophageal cancer treatment
treatment depend on stage, age, comorbidities, patient preference, local expertise
treatment options include
esophagectomy and lymphadenectomy = surgical removal of esophagus with anastomosis in neck or chest and reconstruction with stomach or colon via transthoracic or transhiatal approach; ~5-8% operative mortality rate; post-surgical risk of dysphagia, cough, reflux
endoscopic mucosal resection = resection via EGD usually in poor surgical candidates
chemotherapy = Cisplatin and 5-FU
radiotherapy = external beam radiotherapy
treatment is curative for stage 1-3
stage 1 or 2: (surgical esophagectomy or endoscopic mucosal resection) with post-operative chemotherapy or radiotherapy
stage 2 or 3: (surgery or palliation) with chemotherapy and / or radiotherapy
stage 4: palliation with chemotherapy and / or radiotherapy; EGD esophageal dilation / stenting to allow food passage and tumor ablation to relieve symptoms
Esophageal Leiomyoma epidemiology
<1% of esophageal cancer are benign neoplasms; esophageal leiomyoma is most common benign neoplasm of esophagus
typically occur in patients age 20-50 years of age
Esophageal Leiomyoma pathophysiology
leiomyomas = neoplasm arising from smooth muscle cells (intra-mural growth), usually along distal 2/3 of esophagus
Esophageal Leiomyoma clinical presentation
esophageal leiomyoma need to be large >5cm to cause symptoms
symptoms: dysphagia, regurgitation, vague retrosternal discomfort, chest pain
Esophageal Leiomyoma complications
rare risk of upper GI bleed due to erosion through mucosa
Esophageal Leiomyoma investigation
barium swallow: smooth concave mass underlying intact mucosa
EGD: non-specific tumor in wall of esophagus without mucosal involvement
esophageal ultrasound: smooth round mass in muscularis without spread to adjacent tissue
Esophageal Leiomyoma treatment
if symptomatic or size >5cm, then surgical resection of tumor via thoracotomy
Hiatus hernia risk factors
older age
increased intra-abdominal pressure: obesity, pregnancy, coughing, heavy lifting
smoking
Hiatus hernia pathophysiology
90% hiatus hernia = type 1 sliding herniation (herniation of stomach and gastroesophageal junction into thorax)
<10% hiatus hernia = type 2 para-esophageal hernia (herniation of all or part of stomach through esophageal hiatus into thorax with an undisplaced gastroesophageal junction
mixed hernia = combination of type 1 and 2 hiatus hernia (GE junction in thorax with herniation of additional loop of stomach)
type 4 hernia = herniation of other abdominal organs (colon, spleen, small bowel) into thorax
Hiatus hernia clinical presentation and complications
type 1 symptoms: GERD
type 1 complications: esophagitis (dysphagia, heartburn) -> peptic stricture, Barett’s esophagus, esophageal cancer
type 2 symptoms: dysphagia, pressure sensation in lower chest, may have nausea / burping / post-prandial fullness
type 2 complications: upper GI bleed, incarceration, strangulation, volvulus, obstruction, gastric stasis ulcer
Hiatus hernia investigation
barium swallow: visualization of herniation
EGD: visualization of hernia; biopsy to document type of herniation, extent of tissue damage, rule out esophagitis / Barrett’s esophagus / esophageal cancer
Hiatus hernia treatment
Type 1:
lifestyle modification = address risk factors (smoking cessation, weight loss), minimize reflux (elevate head of bed, no eating within 3 hours prior to sleeping, smaller & frequent meals, avoidance of alcohol / coffee / mint / fat)
medication = GERD medication including antacid, anti-histamine, proton pump inhibitor, profinetic agent
surgical option = anti-reflux laparoscopic Nissen fundoplication (fundus of stomach wrapped around lower esophagus and sutured in place) to stop reflux with 90% success rate
indication for surgery: reflux failing medical therapy, peptic stricture, severe nocturnal aspiration, Barrett’s esophagus
Type 2:
usually for all type 2 hernia, surgery = reduction of hernia and excision of hernia sac, repair defect at hiatus and anti-reflux procedure (Nissen fundoplication), may suture stomach to anterior abdominal wall (gastropexy)
if patient is not a good surgical candidate, then feeding by percutaneous endoscopic gastrostomy (PEG) tube
Hiatus hernia incarceration and strangulation definitions, presentation, investigation, treatment
only type 2 para-esophageal hernia can have complication of incarceration and strangulation, which can lead to gastric perforation
incarceration = irreducible hernia
strangulation = lack of blood supply from incarceration leading to obstruction and ischemia
clinical presentation: epigastric or chest pain radiating to back, dysphagia
investigation: chest & abdominal CT with IV contrast: hiatus hernia with narrow neck and signs of ischemia and possible perforation, which is essential for diagnosis
treatment: emergency laparotomy with reduction of hernia and resection of necrotic esophagus or stomach followed by anastamosis of esophagus with stomach and repair of defect
Spontaneous pneumothorax epidemiology
primary spontaneous pneumothorax usually in young adults 20-40
Spontaneous pneumothorax risk factors
primary spontaneous pneumothorax: smoking, family history of spontaneous pneumothorax, tall height, Marfan syndrome, homocystinuria, thoracic endometriosis
Spontaneous pneumothorax etiology
1) Primary spontaneous pneumothorax
primary spontaneous pneumothorax = pneumothorax without known lung disease
2) Secondary spontaneous pneumothorax
secondary spontaneous pneumothorax = pneumothorax in context of underlying disease
almost any lung disease can be complicated with pneumothorax, but the following ones are the most common
infection: necrotizing pneumonia (bacterial, fungal, PCP, TB)
neoplastic: lung cancer, lung metastasis
congenital / genetic: cystic fibrosis
structural: COPD
Spontaneous pneumothorax clinical presentation
symptoms: sudden onset dyspnea and pleuritic chest pain
vitals: tachypnea, hypoxemia
signs: may have respiratory distress, ipsilateral decreased chest expansion, hyper-resonance on percussion, decreased air entry
risk of recurrence of primary spontaneous pneumothorax: 25-50% recurrence over 1-5 years follow up period with highest risk in the first 30 days
risk of recurrence of secondary spontaneous pneumothorax: 50% recurrence in 3 years in COPD
Spontaneous pneumothorax complications
Tension pneumothorax (1-2% cases)
Hemopneumothorax (1% risk)
Spontaneous pneumothorax investigations
chest X-ray: collapsed lung with visible white visceral pleural line, which is usually sufficient for diagnosis
Management of primary spontaneous pneumothorax
1) Initial Management
supplemental oxygen to maintain oxygen saturation and facilitate absorption of air from pleural space
if clinically stable and small asymptomatic pneumothorax <3cm rim of air on chest X-ray, then observation for up to 6 hours and discharge home if repeat chest X-ray show no progression of pneumothorax
if large or symptomatic pneumothorax (>3cm rim of air on chest X-ray or symptomatic with chest pain or dyspnea), needle aspiration of intra-pleural air
needle aspiration = 14 gauge needle at 2nd or 3rd intercostal space at mid-clavicular line
if needle aspiration fails, chest tube insertion (tube thoracotomy)
if recurrent spontaneous pneumothorax or hemopneumothorax, then chest tube insertion followed by video-assisted thoracoscopy (VAT)
via video-assisted thoracoscopy (VAT), one can perform pleurodesis (adhesion of visceral and parietal pleura) by pleural abrasion or partial parietal pleurectomy, resection of bullae
if patient clinically unstable, then chest tube insertion
2) Long-Term Management
if persistent air leak >3 days and lung >90% expanded, then patient can have any of the below
uni-directional flutter valve (Heimlich valve) attached to chest tube
autologous blood patch infusion into pleural space
VAT to oversew area of leak and mechanical pleurodesis
if recurrent pneumothorax or first pneumothorax requiring tube thoracotomy or VATS, then patient should have prevention for future pneumothorax by any of the following:
VATS pleurodesis
chemical pleurodesis via tube thoracotomy or pigtail catheter with Tetracycline or Talc
open thoracotomy pleurodesis
Management of secondary spontaneous pneumothorax
1) Initial Management
almost all patients with secondary spontaneous pneumothorax should be hospitalized due to higher risk of adverse outcome from underlying lung disease
supplemental oxygen to maintain oxygen saturation and facilitate absorption of air from pleural space
if very small pneumothorax (pleural line <1cm from chest wall), observation with repeat chest X-ray in 12-24 hours
if large pneumothorax (pleural line >1cm from chest wall) or symptomatic (dyspnea), then chest tube placement
chest tube preferred over needle aspiration due to higher success rate
2) Long-Term Management
if persistent air leak >3 days, then patient can have any of the below
VAT to oversew area of leak and mechanical pleurodesis
autologous blood patch infusion into pleural space if patient is not a surgical candidate
chemical pleurodesis via chest tube with Tetracycline or Talc
Secondary spontaneous pneumothorax: for all patients, intervention to prevent future pneumothorax in same hospital stay, due to high risk of recurrence from underlying lung condition by any of the following:
VATS mechanical pleurodesis
chemical pleurodesis via tube thoracotomy or pigtail catheter
open thoracotomy mechanical pleurodesis
Spontaneous hemopneumothorax pathophysiology
complication of spontaneous pneumothorax
small blood vessel in adhesion band between visceral and parietal pleura, which is torn during collapse of lung in pneumothorax -> bleeding into pleural space
Spontaneous hemopneumothorax clinical presentation
symptoms and signs of pneumothorax
may have signs of volume depletion and hypotensive shock from bleeding
Spontaneous hemopneumothorax investigations
chest X-ray: pneumothorax + hemothorax (pleural effusion), which is sufficient for diagnosis
Spontaneous hemopneumothorax management
1) Stabilize and chest tube
2) Surgery
VATS or open thoracotomy: hemostasis, oversewing of bleeding vessel, irrigation of pleural cavity, resection of bullae or pneumorrhaphy (suture of lung)
Esophageal perforation etiology
iatrogenic: endoscopy, endoscopic procedure (dilation, biopsy), intubation, surgery, NG tube placement
barogenic: trauma, repeated & forceful vomiting (Boerhaave’s syndrome), convulsion, defecation, labour
ingestion injury: foreign body, caustic agent ingestion
esophageal cancer
Esophageal perforation pathophysiology
perforation / tear of esophagus resulting in leakage of esophageal contents and air into thoracic cavity
Esophageal perforation clinical presentation
symptoms: hematemesis, neck pain, dyspnea, odynophagea, respiratory distress, chest pain
vitals: fever, tachycardia, hypotension, tachypnea, hypoxemia
signs: subcutaneous emphysema
Esophageal perforation complications
sepsis
abscess
empyema
fistula
mediastinitis
death (10-50% mortality risk)
Esophageal perforation investigation
Chest X-ray: pneumothorax or pneumo-mediastinum or free peritoneal air, pleural effusion, widened mediastinum
chest CT: visualization of esophageal perforation, pneumomediastinum
contrast swallow (water soluble then thin barium): contrast escaping from esophagus into thoracic cavity
Esophageal perforation diagnosis
diagnosis based on chest CT or esophagram
Esophageal perforation management
NPO, NG suction, fluid resuscitation, IV broad spectrum antibiotics (e.g. Ceftriaxone & Flagyl)
indication for surgery:
- thoracic esophagus perforation
- free (i.e. not contained) perforation (with free air)
if perforation within 24 hours, then primary closure of esophagus or resection of diseased esophagus with anastomosis
if perforation >24 hours or non-viable wound edges, diversion and exclusion followed by delayed reconstruction (i.e. esophagostomy proximally, close esophagus distally, gastrostomy / jejunostomy for decompression / feeding)
Esophageal perforation post- surgical complication
esophageal leak
Descending Necrotizing Mediastinitis pathophysiology
pathogen usually polymicrobial
1) infection source from oropharynx
odontogenic is most common infection source
other sources: pharyngeal abscess, sinusitis, tumour necrosis, esophageal perforation
iatrogenic: thoracic surgery / instrumentation
2) infection from oropharynx that extends inferiorly into mediastinum
Descending Necrotizing Mediastinitis clinical presentation
history of infection source: dental infection, thoracic surgery / instrumentation, sinusitis
symptoms: neck pain / swelling, odynophagia, trismus, dyspnea, cough, pleuritic retrosternal chest pain radiating to neck and interscapular region
systemic symptoms: fever, chills, confusion
vitals: fever, tachycardia, hypotensive shock, tachypnea, hypoxemia
signs: face / neck swelling, stridor, crepitus of neck or chest, Hamman sign
Descending Necrotizing Mediastinitis investigations
labs: CBC, electrolytes, BUN, creatinine, ESR, CRP
blood culture
imaging: chest X-ray, head & neck & chest CT
chest X-ray mainly rule out other causes, but may show widening or haziness of mediastinum or pneumomediastinum
chest CT is gold standard for diagnosis of mediastinitis
Descending Necrotizing Mediastinitis management
ABC: intubation & mechanical ventilation, fluid resuscitation
IV antibiotic therapy
source control: drainage of abscess, surgical closure of any perforation, debridement of necrotic tissue
What is Hamman sign
auscultatory crunch during cardiac systole
Pleurisy etiology
infection: viral infection (influenza, Epstein-Barr virus, cytomegalovirus, para-influenza), bacterial pneumonia, fungal infection, TB
autoimmune: rheumatoid arthritis, systemic lupus erythematosus
trauma: chest wounds, rib fracture
vascular: pulmonary embolism, sickle cell crisis
iatrogenic: post thoracic / cardiac surgery, medication, radiotherapy
neoplasm: lung cancer, mesothelioma, lymphoma
Pleurisy pathophysiology
inflammation of the pleura
Pleurisy clinical presentation
symptoms: pleuritic chest pain that may radiate to shoulder or back, dyspnea, cough
Pleurisy complications
atelectasis
pleural effusion
Pleurisy investigation
chest X-ray: pleural effusion
chest CT: to look for lung / pleura pathology as potential causes of pleuritis
if pleural effusion, thoracentesis for diagnosis and theurapeutic purposes
Pleurisy management
analgesia for pain, pulmonary rehabilitation to prevent atelectasis
if pleural effusion, chest tube drainage
address underlying cause
Pericarditis/pericardial effusion typical history
pericarditis risk factors include recent upper respiratory tract infection
pericardial effusion / cardiac tamponade risk factors include trauma, cardiac procedure, malignancy, uraemia, pericarditis
Pericarditis and cardiac tamponade presentations
pericarditis: sharp pleuritic pain located at central or left chest, which is typically positional (worse with lying down), may have dyspnea
cardiac tamponade: chest fullness, dyspnea, fatigue, peripheral edema, syncope
Pericarditis/pericardial effusion physical exam
vital signs: tachycardia, tachypnea and hypotension in cardiac tamponade pulsus paradoxus (decrease in blood pressure >10mmHg with inspiration) in cardiac tamponade
general appearance: acute distress and shock in cardiac tamponade including cyanosis, cool extremities, decreased urine output
cardiovascular exam:
decreased heart sounds & pericardial rub in pericarditis
increased JVP, peripheral edema and quiet heart sounds in pericardial effusion / cardiac tamponade
Pericarditis/pericardial effusion/cardiac tamponade investigations
ECG: diffuse ST elevations (concave, not tombstone) and PR depressions for pericarditis; low voltage and QRS alterans in pericardial effusion / cardiac tamponade
chest X-ray: enlarged cardiac silhouette in pericardial effusion / cardiac tamponade
bed side echocardiogram: pericardial effusion visualized in pericardial effusion / cardiac tamponade; heart chamber collapse in cardiac tamponade
Pericarditis/cardiac tamponade diagnosis
pericarditis diagnosed on ECG with diffuse ST elevations (concave, not tombstone) and PR depressions
pericardial effusion and cardiac tamponade diagnosed based on clinical presentation, physical findings and echocardiogram findings
Pericarditis/pericardial/cardiac tamponade effusion treatment
pericarditis: aspirin, NSAID, systemic steroids if refractory, Colchicine for recurrent pericarditis
pericardial effusion / cardiac tamponade: drainage of pericardial fluid by pericardiocentesis (catheter with echocardiogram guidance) or surgical drainage
Pericarditis definition and etiology
inflammation of pericardium
most commonly idiopathic or viral
Pericardial effusion definition and etiology
increased pericardial fluid
can be caused by pericarditis, congestive heart failure, cirrhosis, renal failure, tumor
Cardiac tamponade definition
pericardial effusion constricting heart, impeding diastole and systole causing cardiogenic shock
Tietze’s syndrome pathophysiology, clinical presentation, treatment
Pathophysiology: inflammation of costal cartilage (costochondritis), commonly caused by injury or physical strain
clinical presentation: sharp chest pain, tenderness on palpation of chest wall, signs of chest wall inflammation (swelling, erythema, warmth)
treatment: analgesia (Tylenol, NSAID), rest and stretching exercise
Lung atelectasis etiology
atelectasis caused by blockage of a branch of bronchial tree
intra-luminal blockage: foreign body, mucus plug, tumor
extra-luminal blockage: lymphadenopathy, tumor, pleural effusion, pneumothorax
shallow breathing and suppression of cough -> mucus plugging & closure of alveoli -> atelectasis
Lung atelectasis pathophysiology
blockage of branch of bronchial tree prevent ventilation of alveoli downstream from the bronchial branch
air in alveoli beyond alveoli is abosrbed by blood, resulting in shrinkage and collapse of alveoli
collapsed alveoli cannot participate in gas exchange, decreasing oxygen and increasing carbon dioxide in blood
collapsed alveoli increases risk of bacterial infection, resulting in pneumonia
Lung atelectasis clinical presentation
symptoms: dyspnea
vitals: low fever, tachycardia, tachypnea, hypoxemia
signs: respiratory distress, dullness on percussion, decreased air entry
Lung atelectasis investigations
chest X-ray: opacity with volume loss (classically linear border triangular shaped), which is sufficient for diagnosis of atelectasis
chest CT and bronchoscopy may be done to find cause for atelectasis
chest CT for extra-luminal causes
bronchoscopy for intra-luminal causes
Lung atelectasis prevention
smoking cessation
deep breathing and coughing
change in position, ambulation
incentive deep breathing, breathing exercise
Lung atelectasis treatment
1) stabilize ABC if necessary
2) Addressing underlyng cause
a) shallow breathing / suppression of cough
deep breathing, chest physiotherapy, mechanical insufflation - exsufflation, intrapulmonary percussive ventilation, intermittent positive pressure breathing
b) intraluminal causes
bronchoscopy interventions for intra-luminal causes
suctioning of mucus plugging or secretions
retrieval of foreign body
for mucus plugging, consider DNase and N acetylcysterine as mucolytic therapy
c) extraluminal causes
surgery, chemotherapy or radiotherapy for tumor
chest tube for pleural effusion or pneumothorax
3) Treat existing infection
if fever, leukocytosis or other signs of infection, then antibiotic therapy for pneumonia
4) Prevent recurrent atelectasis
if recurrent or chronic infection due to atelectasis or bleeding, then surgical lobectomy
Pleural effusion clinical presentation
may be asymptomatic
symptoms: dyspnea, pleuritic chest pain
systemic symptoms: fever, chills, weight loss, malaise, anorexia
vitals: tachypnea, hypoxemia
signs: contralateral tracheal deviation, asymmetric chest expansion, dullness on percussion, decreased tactile fremitus, decreased air entry, pleural rub on auscultation
Pleural effusion diagnosis
diagnosis based on blunting of costal phrenic angle, opacity with meniscus, and / or contralateral mediastinal shift on chest X-ray PA and lateral
thoracocentesis possible if fluid >1cm thickness on lateral decubitus chest X-ray
Thoracocentesis routine evaluation
routine evaluation of pleural fluid from thoracocentesis include
- appearance of pleural fluid
- cell count and differential
- biochemistry: LDH, protein, albumin, glucose, pH
- gram stain, acid fast stain, culture
- cytology
Transudative vs exudative
exudative pleural fluid usually have pleural fluid protein >30g/L
transudative vs. exudative diagnosed based on thoracocentesis pleural fluid according to Light’s Criteria
exudative diagnosed based on any of the following
pleural fluid protein / serum protein >0.5
pleural fluid LDH / serum LDH >0.6
pleural fluid LDH > 2/3 upper normal limit of serum LDH
Transudative pleural effusion differential diagnosis
CHF
nephrotic syndrome
hypo albumin states including liver failure
hepatic hydrothorax
peritoneal dialysis
Exudative pleural effusion differential diagnosis
infectious including bacterial, TB, fungal, parasitic, viral
maligancy including metastatic pleural disease, mesothelioma, body cavity lymphoma
pulmonary embolism
connective tissue disease
lymphatic (chylothorax)
blood (hemothorax)
GI source
endocrine
inflammatory
Treatment of pleural effusion
if fluid >1cm thickness on lateral decubitus chest X-ray, then chest tube drainage
address underlying cause
What is a para-pneumonic effusion
any pleural effusion related to bacterial pneumonia, lung abscess or bronchiectasis
Progression of para-pneumonic effusion
simple para-pneumonic effusion (exudative) -> complex para-pneumonic effusion (fibropurulent) -> empyema (organized)
Simple para pneumonic effusion (exudative) pleural fluid qualities
pH
Glucose
LDH
Gram stain and culture
Pus
pH 7.2+
Glucose 3.33 mmol/L+
LDH <1000IU/L
Gram stain and culture Negative
Pus - no frank pus
Complex para pneumonic effusion (exudative) pleural fluid qualities
pH
Glucose
LDH
Gram stain and culture
Pus
pH <7.2
Glucose <3.33 mmol/L
LDH >1000 IU/L
Gram stain and culture Positive
Pus No frank pus
Empyema para pneumonic effusion (exudative) pleural fluid qualities
pH
Glucose
LDH
Gram stain and culture
Pus
pH <7.2
Glucose <3.33 mmol/L
LDH >1000 IU/L
Gram stain and culture Positive
Pus frank pus
Complicated para-pneumonic effusion and empyema complications
high complication rate of causing scarring resulting in an inelastic pleural peel encasing the lung
Complicated para-pneumonic effusion and empyema management
requires chest tube drainage and long term antibiotic therapy
Empyema definition
pus in pleural space or effusion with bacterial organism on staining or culture
Empyema pathophysiology
usually lung infection or chest wall infection that extends contiguously into pleural space
Empyema management
antibiotic for at least 4-6 weeks
complete pleural drainage with chest tube, consider video-assisted thorascopic surgery (VATS) to drain loculated empyema
Stridor definition
stridor is harsh high pitched wheezing or vibrating sound best heard above neck, typically occurs with inspiration, which is specific for severe upper airway obstruction
inspiratory stridor is a medical emergency
Clinical presentation of upper airway obstruction
symptoms: altered voice, dysphagia, odynophagia
vitals: tachycardia, tachypnea, hypoxemia
physical exam: altered mental status, respiratory distress, stridor, decreased air entry bilaterally on auscultation
complete airway obstruction -> asphyxiation -> cyanosis, bradycardia, hypotension -> cardiovascular collapse
Stridor investigations
pulmonary function test, which can confirm presence of upper airway obstruction
imaging: neck X-ray, CT of neck, chest X-ray, chest CT
neck X-ray (AP and lateral) as 1st screening imaging to rule in foreign body, croup, epiglottis, retropharyngeal abscess
chest X-ray to identify tracheal deviation, extrinsic compression, foreign body
CT of neck and chest for suspected structural abnormality such as upper airway tumor or tracheomalacia or vascular structure to foreign body
direct laryngoscope for vocal cord abnormalities, structural abnormalities and tumors
direct laryngoscope under general anesthesia usually necessary as definitive diagnosis of upper airway obstruction
rigid or flexible bronchoscopy can have direct visualization of airway below larynx for definitive diagnosis
flexible bronchoscopy can be therapeutic (laser therapy, photo resection, electrocautery electrosurgery, balloon bronchoplasty, tracheal stunting)
Differential diagnosis of stridor adults
trauma: facial trauma, oropharyngeal laceration, laryngeal or tracheal fracture, edema of upper airway, subglottic stenosis, foreign body, inhalation injury
vascular: bleeding into upper airway
malignancy: laryngeal tumor, head and neck tumor, laryngeal papillomatosis, any tumor compressing on upper airway or trachea
infection: suppurative parotitis, Ludwig angina, tonsillar hypertrophy, peri-tonsillar abscess, epiglottitis, laryngitis, deep neck space abscess (para-pharyngeal, retro-pharyngeal, prevertebral)
inflammatory: anaphylaxis, laryngitis, GERD causing laryngospasm, angioedema (ACE inhibitor)
iatrogenic: post-extubation complications (laryngeal edema, laryngospasm, arythenoid dislocation), tracheal stenosis (post tracheostomy or post intubation), medication causing
laryngospasm, mucous ball from transtracheal catheter
neuromuscular: bilateral vocal cord paralysis / dysfunction (post-surgical)
Stridor management
1) Stabilize ABCs
A: secure airway
medication include nebulized racemic epinephrine and IV corticosteroids to decrease airway mucosal edema
1st line = endotracheal intubation (nasal or oral), which can be aided by fiberoptic bronchoscopy
2nd line = cricothyroidotomy (converted to formal tracheotomy if >72 hours of use)
B: helium and O2 (Heliox) to improve airflow and reduce work of breathing
2) Surgical Intervention
after stabilization with secure airway, surgical intervention to treat obstruction
interventions via bronchoscopy
laser therapy for intra-luminal tracheobronchial lesions
tracheal stent for tracheal obstruction due to benign or malignant causes
dilatation with or without laser resection of benign disease
core out of tumor followed by laser, photodynamic therapy, brachytherapy, cryotherapy or electrocautery for malignant lesion
3) Address Underlying Cause
Pediatric differential diagnosis and approach to stridor
Tony’s pg 63
Solitary lun g nodule differential diagnosis
Benign - 70%
Infectious granuloma - histoplasmosis, coccidiomycosis, TB, atypical mycobacteria
Other infections - bacterial abscess, PCP, aspergilloma
Benign neoplasms - hamartoma, lipoma, fibroma
Vascular - AV malformation, pulmonary varix
Developmental - bronchogenic cyst
Inflammatory - Wegener’s granulomatosis, rheumoatoid nodule, sarcoidosis
Other - hematoma, infarct, pseudotumour, rounded atelectasis lymph nodes, amyloidoma
Malignant - 30% 1. Bronchogenic carcinoma Adenocarcinoma Squamous cell carcinoma Large cell carcinoma Small cell carcinoma
2. Metastatic lesions Breast Head and neck Melanoma Colon Kidney Sarcoma Germ cell tumours
- Pulmonary carcinoid
Lung nodule definition
<3 cm
Lung mass definition
> 3 cm
Characteristics of benign lung lesions on CXR
Size
Margins
Features
Doubling time
<3cm, round, regular
Smooth margin
Features
Calcified pattern: central, popcorn pattern if hamartoma, usually no cavitation
If cavitated, wall is smootha nd thin
No other lung pathology
Doubling Time
Doubles in <1 month or >2 years
Characteristics of malignant lung lesions on CXR
Size
Margins
Features
Doubling time
> 3 cm, irregular, spiculated
Ill-defined or notched margin
Usually not calcified
If calcified, pattern is eccentric, no satellite lesions, cavitation with thick wall, may have pleural effusions, lymphadenopathy
Doubles in >1 months or <2 years
Lung nodule/mass low risk definition and work-up
low risk = benign features on chest X-ray or unchanged from previous chest X-ray
low risk work-up = repeat chest X-ray in 3-6 months then yearly and observe, where any change on chest X-ray would require chest CT
Lung nodule/mass high risk definition and work-up
high risk = change from previous chest X-ray, malignancy features on chest X-ray, or significant risk factors (i.e. smoking) on history
high risk work up = chest CT
if clinical evaluation and chest CT cannot differentiate between begin and malignant lesion, then biopsy (bronchoscopic biopsy, percutaneous biopsy, thoracoscopy excision or thoracotomy excision)
Lung cancer epidemiology
1 cause of cancer related death
Lung cancer risk factors
85% of all lung cancer cases are attributable to smoking
chemical exposure: asbestos, arsenic, chromium, nickle
radiation
lung scarring: granulomatous disease, pulmonary fibrosis, scleroderma
Lung cancer pathology
90% primary lung cancer are bronchogenic cancer, which include
small cell lung cancer (SCLC)
non-small cell lung cancer (NSCLC): adenocarcinoma (which include bronchioalveolar cancer), squamous carcinoma, large cell carcinoma
10% primary lung cancer include lymphoma, sarcoma, carcinoid and other malignancies
Lung cancer clinical presentation
1) General symptoms
respiratory: cough (75% cases), dyspnea (60% cases), hemoptysis (35% cases)
chest: chest pain (45% cases)
other: clubbing (20% cases), other pain (25% cases)
constitutional symptoms: anorexia, weight loss, fever, anemia
2) Local extension symptoms
lung, hilum, mediastinum: ateletasis, wheezing
lung apex (Pancoast tumor): Horner’s syndrome (miosis, anhydrosis, ptosis), brachial plexus palsy usually involving C8 and T1
pleura: pleural effusion
pericardium: pericarditis, pericardial effusion, pericardial tamponade
esophagus: dysphagia
phrenic nerve: paralysis of diaphragm
recurrent laryngeal nerve: hoarseness
superior vena cava: facial & neck swelling, dyspnea, cough, dilated neck vein, increased collateral vein on anterior chest, cyanosis, face / neck / chest / arm edema, Pemberton’s
sign (facial flushing, cyanosis and neck vein distention upon raising both arms above head)
rib and vertebrae: bony pain and pathologic fracture if erosion
3) Metastasis
commonly metastasis to brain, bone, liver and adrenals
4) Paraneoplastic Syndromes
para-neoplastic syndrome = disorders associated with malignancy that are not related to physical effect of tumor itself
small cell lung cancer most commonly associated with para-neoplastic syndrome due to origin from neuro-endocrine cells
Lung cancer management
Surgery
indication: curative intent for stage 1 and 2 NSCLC
contraindication: spread to mediastinal lymph node or contralateral lymph node
procedure = resection of tumor, which can be a segmentectomy, lobectomy or pneumonectomy
peri-operative mortality of 1% for segmentectomy; 3% for lobectomy; 6% for pneumonectomy
Chemotherapy
chemotherapy can be curative or adjuvant or palliative
indication for curative chemotherapy: limited stage SCLC (with radiotherapy)
indication for adjuvant chemotherapy: NSCLC post curative surgical resection depending on pathology report and margin
indication for neo-adjuvant chemotherapy: stage 3 NSCLC as potential surgical candidate post chemotherapy
indication for palliative chemotherapy: high stage SCLC or NSCLC where cure is not possible
chemotherapy = Cisplatin & Etoposide; Paclitaxel; Vinorelbine; Gemcitabine; biologics for EGFR muutation (Geftinib)
acute complication: tumor lysis syndrome, infection, bleeding, immune suppression, hemorrhagic cystitis (Cyclophosphamide), cardiotoxicity (Doxorubicin), renal toxicity (Cisplatin), peripheral neuropathy (Vincristine)
chronic complication: neurologic damage, leukaemia, additional primary neoplasms
Radiotherapy
radiotherapy can be curative or adjuvant or palliative
indication for curative radiotherapy: stage 1 and 2 NSCLC in poor surgical candidates, limited stage SCLC
indication for adjuvant radiotherapy: prophylactic cranial irradiation if good response to chemotherapy + radiotherapy for limited stage SCLC
radiotherapy = external beam radiation, stereotactic radiation
