Thoracic Surgery Flashcards

1
Q

Massive hemoptysis definition

A

expectoration of large amount of blood and / or rapid rate of bleeding (>500cc over 24 hours or >100cc / hour)

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2
Q

How to rule out GI source of upper bleed (presenting with hemoptysis)

A

blood with alkaline pH, foaminess, pus makes GI source unlikely

endoscopy rules out GI source bleeding

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3
Q

How to rule out upper airway bleeding presenting with hemoptysis

A

no source of bleeding on examination of nose & mouth and laryngoscopy rules out upper airway bleeding

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4
Q

Source of massive hemoptysis

A

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

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5
Q

What is the most common cause of hemoptysis

A

Pulmonary (bronchiectasis)

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6
Q

Bronchiectasis causing hemoptysis pathophysiology

A

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

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7
Q

Causes that can lead to bronchiectasis

A

cystic fibrosis

prior bacterial or viral infection

TB

impairment of mucociliary clearance

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8
Q

Tuberculosis causing hemoptysis pathophysiology

A

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

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9
Q

Bronchogenic carcinoma causing hemoptysis pathophysiology

A

typically large centrally located tumour that invades bronchial artery

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10
Q

Aspergilloma causing hemoptysis pathophysiology

A

invasion and destruction of parenchymal and vascular structure within the lung

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11
Q

Complicated pneumonia (nec pneumonia, lung abscess) causing hemoptysis pathophysiology

A

cavitation from necrotizing pneumonia or abscess from lung abscess can cause ulceration and necrosis of adjacent bronchial vessels

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12
Q

Differential diagnosis of hemoptysis (pulmonary causes)

A
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
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13
Q

Hemoptysis mechanism of death

A

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

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14
Q

Risk factors for mortality due to hemoptysis

A

underlying cause for hemoptysis

low cardiopulmonary reserve: underlying cardiac or pulmonary disease

area of chest alveolar hemorrhagic infiltrate

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15
Q

Hemoptysis diagnosis

A

bronchoscopy = diagnostic procedure of choice to visualize and localize bleeding site

high resolution CT and arteriography if negative bronchoscopy

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16
Q

Hemoptysis management

A

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

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17
Q

Differential diagnosis for oral dysphagia

A

neurologic: dementia

inflammation / infection: tonsillitis, xerostomia

neoplasm: squamous cell carcinoma
other: poor dentition

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18
Q

Differential diagnosis for pharyngeal dysphagia

A

neurologic: dementia, stroke, multiple sclerosis

infection / inflammation

neoplasm: squamous cell carcinoma
structural: Zenker’s diverticulum

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19
Q

Differential diagnosis for esophageal dysphagia

A
  1. 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
  2. Motility (Neuromuscular) disorder
    a) primary motility disorder
    achalasia
    diffuse esophageal spasm
    nutcracker esophagus (hypertensive peristalsis)
    hypertensive lower esophageal sphincter
    b) secondary motility disorder
    scleroderma
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20
Q

What is succussion splash

A

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

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21
Q

What does succussion splash indicate

A

Achalasia

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22
Q

What is CREST syndrome

A
Calcinosis
Raynaud’s phenomenon
Esophagitis
Sclerodactyly
Telangiectasia
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23
Q

Dysphagia investigations

A

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

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24
Q

Oral dysphagia presentation

A

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

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25
Q

Pharyngeal dysphagia presentation

A

difficulty initiating swallow, coughing, choking, repeated attempts at swallowing, wet & gurgling voice, wet breath sounds

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26
Q

Esophageal dysphagia presentation

A

food stopping or sticking retrosternally after swallowing

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27
Q

dysphagia with solids alone suggests…

A

mechanical obstruction

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28
Q

dysphagia with solids and liquids suggests…

A

motility (neuromuscular) disorder

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29
Q

for mechanical obstruction, intermittent dysphagia suggests…

A

lower esophageal ring

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30
Q

for mechanical obstruction, progressive dysphagia suggests…

A

peptic stricture or carcinoma (especially if old age >50 years and weight loss)

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31
Q

for motility (neuromuscular) disorder, intermittent dysphagia suggests…

A

diffuse esophageal spasm, especially if associated with chest pain

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32
Q

for motility (neuromuscular) disorder, progressive dysphagia suggests…

A

scleroderma (associated with chronic heart burn) or achalasia (associated with bland regurgitation and weight loss)

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33
Q

Zenker’s diverticulum epidemiology

A

common in elderly male typically age >75 years

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34
Q

Zenker’s diverticulum pathophysiology

A

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

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35
Q

Zenker’s diverticulum clinical presentation

A

symptoms: oropharyngeal dysphagia, halitosis, gurgling in throat, food regurgitation into mouth
signs: mass in neck

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36
Q

Zenker’s diverticulum complications

A

pulmonary aspiration

aspiration pneumonia

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37
Q

Zenker’s diverticulum investigations

A

barium swallow: visualization of diverticula

neck ultrasound: visualization of outpouching

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38
Q

Zenker’s diverticulum diagnosis

A

patient diagnosed based on Zenker’s diverticulum visualized on barium swallow

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39
Q

Zenker’s diverticulum management

A

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

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40
Q

Peptic stricture etiology

A

peptic stricture is a complication of GERD (in 10-20% of untreated GERD)

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41
Q

Peptic stricture pathophysiology

A

GERD cause esophagitis followed by sub-mucosal collagen deposition and fibrosis

the scarring cause smooth, circumferential tapered luminal narrowing usually at lower esophagus

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42
Q

Peptic stricture clinical presentation

A

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)

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43
Q

Peptic stricture diagnosis

A

diagnosis based on visualization of stricture on EGD

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44
Q

Peptic stricture treatment

A

EGD dilation (to diameter >15mm) by balloon dilators, Maloney or Savary method

PPI to treat GERD

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45
Q

What is achalasia

A

disorder of motility with some mechanical obstruction

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46
Q

achalasia epidemiology

A

common in adults age 30-50

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47
Q

achalasia pathophysiology

A

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

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48
Q

achalasia clinical presentation

A

symptoms: progressive dysphagia for solids and liquids, weight loss, bland regurgitation, chest pain / heart burn

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49
Q

achalasia complications

A

pulmonary aspiration

aspiration pneumonia

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50
Q

achalasia investigations

A

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

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51
Q

achalasia treatment

A

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)

  1. 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
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52
Q

Esophageal cancer epidemiology

A

affect elderly age >50

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53
Q

Esophageal cancer risk factors

A

squamous cell carcinoma: smoking, alcohol, diet

adenocarcinoma: gastroesophageal reflux disease (GERD), obesity, smoking, diet

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54
Q

Esophageal cancer pathophysiology

A

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

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55
Q

Esophageal cancer clinical presentation

A

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

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56
Q

Esophageal cancer complications

A

aspiration pneumonia

upper GI bleed from esophagus

trachea-esophageal fistula

broncho-esophageal fistula

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57
Q

Esophageal cancer common metastasis locations

A

trachea, liver, lung, bone, celiac & mediastinal lymph nodes

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58
Q

Esophageal cancer investigations

A

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

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59
Q

Esophageal cancer treatment

A

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

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60
Q

Esophageal Leiomyoma epidemiology

A

<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

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61
Q

Esophageal Leiomyoma pathophysiology

A

leiomyomas = neoplasm arising from smooth muscle cells (intra-mural growth), usually along distal 2/3 of esophagus

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62
Q

Esophageal Leiomyoma clinical presentation

A

esophageal leiomyoma need to be large >5cm to cause symptoms

symptoms: dysphagia, regurgitation, vague retrosternal discomfort, chest pain

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63
Q

Esophageal Leiomyoma complications

A

rare risk of upper GI bleed due to erosion through mucosa

64
Q

Esophageal Leiomyoma investigation

A

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

65
Q

Esophageal Leiomyoma treatment

A

if symptomatic or size >5cm, then surgical resection of tumor via thoracotomy

66
Q

Hiatus hernia risk factors

A

older age

increased intra-abdominal pressure: obesity, pregnancy, coughing, heavy lifting

smoking

67
Q

Hiatus hernia pathophysiology

A

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

68
Q

Hiatus hernia clinical presentation and complications

A

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

69
Q

Hiatus hernia investigation

A

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

70
Q

Hiatus hernia treatment

A

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

71
Q

Hiatus hernia incarceration and strangulation definitions, presentation, investigation, treatment

A

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

72
Q

Spontaneous pneumothorax epidemiology

A

primary spontaneous pneumothorax usually in young adults 20-40

73
Q

Spontaneous pneumothorax risk factors

A

primary spontaneous pneumothorax: smoking, family history of spontaneous pneumothorax, tall height, Marfan syndrome, homocystinuria, thoracic endometriosis

74
Q

Spontaneous pneumothorax etiology

A

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

75
Q

Spontaneous pneumothorax clinical presentation

A

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

76
Q

Spontaneous pneumothorax complications

A

Tension pneumothorax (1-2% cases)

Hemopneumothorax (1% risk)

77
Q

Spontaneous pneumothorax investigations

A

chest X-ray: collapsed lung with visible white visceral pleural line, which is usually sufficient for diagnosis

78
Q

Management of primary spontaneous pneumothorax

A

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

79
Q

if recurrent pneumothorax or first pneumothorax requiring tube thoracotomy or VATS, then patient should have prevention for future pneumothorax by any of the following:

A

VATS pleurodesis

chemical pleurodesis via tube thoracotomy or pigtail catheter with Tetracycline or Talc

open thoracotomy pleurodesis

80
Q

Management of secondary spontaneous pneumothorax

A

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

81
Q

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:

A

VATS mechanical pleurodesis

chemical pleurodesis via tube thoracotomy or pigtail catheter

open thoracotomy mechanical pleurodesis

82
Q

Spontaneous hemopneumothorax pathophysiology

A

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

83
Q

Spontaneous hemopneumothorax clinical presentation

A

symptoms and signs of pneumothorax

may have signs of volume depletion and hypotensive shock from bleeding

84
Q

Spontaneous hemopneumothorax investigations

A

chest X-ray: pneumothorax + hemothorax (pleural effusion), which is sufficient for diagnosis

85
Q

Spontaneous hemopneumothorax management

A

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)

86
Q

Esophageal perforation etiology

A

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

87
Q

Esophageal perforation pathophysiology

A

perforation / tear of esophagus resulting in leakage of esophageal contents and air into thoracic cavity

88
Q

Esophageal perforation clinical presentation

A

symptoms: hematemesis, neck pain, dyspnea, odynophagea, respiratory distress, chest pain
vitals: fever, tachycardia, hypotension, tachypnea, hypoxemia
signs: subcutaneous emphysema

89
Q

Esophageal perforation complications

A

sepsis

abscess

empyema

fistula

mediastinitis

death (10-50% mortality risk)

90
Q

Esophageal perforation investigation

A

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

91
Q

Esophageal perforation diagnosis

A

diagnosis based on chest CT or esophagram

92
Q

Esophageal perforation management

A

NPO, NG suction, fluid resuscitation, IV broad spectrum antibiotics (e.g. Ceftriaxone & Flagyl)

indication for surgery:

  1. thoracic esophagus perforation
  2. 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)

93
Q

Esophageal perforation post- surgical complication

A

esophageal leak

94
Q

Descending Necrotizing Mediastinitis pathophysiology

A

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

95
Q

Descending Necrotizing Mediastinitis clinical presentation

A

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

96
Q

Descending Necrotizing Mediastinitis investigations

A

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

97
Q

Descending Necrotizing Mediastinitis management

A

ABC: intubation & mechanical ventilation, fluid resuscitation

IV antibiotic therapy

source control: drainage of abscess, surgical closure of any perforation, debridement of necrotic tissue

98
Q

What is Hamman sign

A

auscultatory crunch during cardiac systole

99
Q

Pleurisy etiology

A

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

100
Q

Pleurisy pathophysiology

A

inflammation of the pleura

101
Q

Pleurisy clinical presentation

A

symptoms: pleuritic chest pain that may radiate to shoulder or back, dyspnea, cough

102
Q

Pleurisy complications

A

atelectasis

pleural effusion

103
Q

Pleurisy investigation

A

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

104
Q

Pleurisy management

A

analgesia for pain, pulmonary rehabilitation to prevent atelectasis

if pleural effusion, chest tube drainage

address underlying cause

105
Q

Pericarditis/pericardial effusion typical history

A

pericarditis risk factors include recent upper respiratory tract infection

pericardial effusion / cardiac tamponade risk factors include trauma, cardiac procedure, malignancy, uraemia, pericarditis

106
Q

Pericarditis and cardiac tamponade presentations

A

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

107
Q

Pericarditis/pericardial effusion physical exam

A
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

108
Q

Pericarditis/pericardial effusion/cardiac tamponade investigations

A

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

109
Q

Pericarditis/cardiac tamponade diagnosis

A

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

110
Q

Pericarditis/pericardial/cardiac tamponade effusion treatment

A

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

111
Q

Pericarditis definition and etiology

A

inflammation of pericardium

most commonly idiopathic or viral

112
Q

Pericardial effusion definition and etiology

A

increased pericardial fluid

can be caused by pericarditis, congestive heart failure, cirrhosis, renal failure, tumor

113
Q

Cardiac tamponade definition

A

pericardial effusion constricting heart, impeding diastole and systole causing cardiogenic shock

114
Q

Tietze’s syndrome pathophysiology, clinical presentation, treatment

A

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

115
Q

Lung atelectasis etiology

A

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

116
Q

Lung atelectasis pathophysiology

A

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

117
Q

Lung atelectasis clinical presentation

A

symptoms: dyspnea
vitals: low fever, tachycardia, tachypnea, hypoxemia
signs: respiratory distress, dullness on percussion, decreased air entry

118
Q

Lung atelectasis investigations

A

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

119
Q

Lung atelectasis prevention

A

smoking cessation

deep breathing and coughing

change in position, ambulation

incentive deep breathing, breathing exercise

120
Q

Lung atelectasis treatment

A

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

121
Q

Pleural effusion clinical presentation

A

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

122
Q

Pleural effusion diagnosis

A

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

123
Q

Thoracocentesis routine evaluation

A

routine evaluation of pleural fluid from thoracocentesis include

  1. appearance of pleural fluid
  2. cell count and differential
  3. biochemistry: LDH, protein, albumin, glucose, pH
  4. gram stain, acid fast stain, culture
  5. cytology
124
Q

Transudative vs exudative

A

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

125
Q

Transudative pleural effusion differential diagnosis

A

CHF

nephrotic syndrome

hypo albumin states including liver failure

hepatic hydrothorax

peritoneal dialysis

126
Q

Exudative pleural effusion differential diagnosis

A

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

127
Q

Treatment of pleural effusion

A

if fluid >1cm thickness on lateral decubitus chest X-ray, then chest tube drainage

address underlying cause

128
Q

What is a para-pneumonic effusion

A

any pleural effusion related to bacterial pneumonia, lung abscess or bronchiectasis

129
Q

Progression of para-pneumonic effusion

A

simple para-pneumonic effusion (exudative) -> complex para-pneumonic effusion (fibropurulent) -> empyema (organized)

130
Q

Simple para pneumonic effusion (exudative) pleural fluid qualities

pH

Glucose

LDH

Gram stain and culture

Pus

A

pH 7.2+

Glucose 3.33 mmol/L+

LDH <1000IU/L

Gram stain and culture Negative

Pus - no frank pus

131
Q

Complex para pneumonic effusion (exudative) pleural fluid qualities

pH

Glucose

LDH

Gram stain and culture

Pus

A

pH <7.2

Glucose <3.33 mmol/L

LDH >1000 IU/L

Gram stain and culture Positive

Pus No frank pus

132
Q

Empyema para pneumonic effusion (exudative) pleural fluid qualities

pH

Glucose

LDH

Gram stain and culture

Pus

A

pH <7.2

Glucose <3.33 mmol/L

LDH >1000 IU/L

Gram stain and culture Positive

Pus frank pus

133
Q

Complicated para-pneumonic effusion and empyema complications

A

high complication rate of causing scarring resulting in an inelastic pleural peel encasing the lung

134
Q

Complicated para-pneumonic effusion and empyema management

A

requires chest tube drainage and long term antibiotic therapy

135
Q

Empyema definition

A

pus in pleural space or effusion with bacterial organism on staining or culture

136
Q

Empyema pathophysiology

A

usually lung infection or chest wall infection that extends contiguously into pleural space

137
Q

Empyema management

A

antibiotic for at least 4-6 weeks

complete pleural drainage with chest tube, consider video-assisted thorascopic surgery (VATS) to drain loculated empyema

138
Q

Stridor definition

A

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

139
Q

Clinical presentation of upper airway obstruction

A

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

140
Q

Stridor investigations

A

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)

141
Q

Differential diagnosis of stridor adults

A

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)

142
Q

Stridor management

A

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

143
Q

Pediatric differential diagnosis and approach to stridor

A

Tony’s pg 63

144
Q

Solitary lun g nodule differential diagnosis

A

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 
  1. Pulmonary carcinoid
145
Q

Lung nodule definition

A

<3 cm

146
Q

Lung mass definition

A

> 3 cm

147
Q

Characteristics of benign lung lesions on CXR

Size
Margins
Features
Doubling time

A

<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

148
Q

Characteristics of malignant lung lesions on CXR

Size
Margins
Features
Doubling time

A

> 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

149
Q

Lung nodule/mass low risk definition and work-up

A

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

150
Q

Lung nodule/mass high risk definition and work-up

A

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)

151
Q

Lung cancer epidemiology

A

1 cause of cancer related death

152
Q

Lung cancer risk factors

A

85% of all lung cancer cases are attributable to smoking

chemical exposure: asbestos, arsenic, chromium, nickle

radiation

lung scarring: granulomatous disease, pulmonary fibrosis, scleroderma

153
Q

Lung cancer pathology

A

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

154
Q

Lung cancer clinical presentation

A

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

155
Q

Lung cancer management

A

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