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