CARDIOTHORACIC SURGERY

Student Handbook
For Medical Year 6
2018/ 2019

8th Edition

Division of Cardiothoracic Surgery

Department of Surgery
Prince of Wales Hospital
The Chinese University of Hong Kong

23 May 2018

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 CARDIOTHORACIC SURGERY: STUDENT HANDBOOK

Contents:

Introduction

Schedule

Selected Topics:
1. Cardiac Surgery
2. Lung Cancer
3. Video Assisted Thoracic Surgery
4. Blunt Thoracic Trauma
5. Pneumothorax
6. Chest Drainage
7. Pleurodesis
8. Pleural Space Infections

Further Reading
Other thoracic topics to consider:
Anterior Mediastinal Mass, Posterior Mediastinal Mass, Chest Wall Deformity

This handbook is NOT a textbook nor a syllabus for Cardiothoracic Surgery

- the aim of this handbook is to give you some background reading so that you can make the
most of your attachment with us and to guide your own reading around the subject
- much of the information is far more detailed than you need for your exams
- there may be topics not covered in this handbook that may turn up in your exams
- your examiners may or may not agree with some of the information in this handbook

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INTRODUCTION

Welcome to Cardiothoracic Surgery!

Cardiothoracic Surgery is a highly specialized and often very technical surgical specialty. Many students
may find our specialty ‘too advanced’ and are intimidated. However, when you consider the sheer number
of patients with Cardiothoracic problems (more people die of lung cancer and ischaemic heart disease
than any other diseases) and the many different specialties in various hospitals that are interdependent
with our team (e.g. cardiologists, respiratory physicians, ICU intensivists, interventional radiologists,
oncologists and many more) you can see that Cardiothoracic Surgery may encompass many subjects you
already know quite well. There is no need to feel intimidated. Rather, you should take a fresh look at how
many common chest conditions can be managed surgically. Hopefully, you may then realize that this very
dynamic field may be relevant to you and helpful in your clinical practice long after you have passed your
exams !

What you should learn:

It is not realistic to expect that you will learn all there is to know about Cardiothoracic Surgery during your
brief attachment with us. Therefore, you should aim to learn selectively. For example:
- learn what Cardiothoracic Surgery can offer to patients from all specialties
(i.e. when other specialties should make referrals to us)
- practice your chest and cardiovascular examination technique on our patients, and familiarize
yourself with the presentations and signs of common chest diseases
(our patients on the wards may be your short & long cases in the exams !)
- learn to identify and react to common Cardiothoracic emergencies

What you should do to learn:

Don’t try to memorize lists of facts and figures or details of operative techniques at this stage: these come
later in your career (if you want to be a Cardiothoracic Surgeon)! Try instead to:
- clerk and present as many patients as you can: pre-op patients will show you common
symptoms & signs of chest disease; post-op patients will show you how such conditions
are managed (e.g. chest drain management)
- look at all CXR’s, CT’s, angiograms: get some idea what looks normal and abnormal
- ask if there is anything you don’t know or are curious about

Remember: Cardiothoracic Surgery is a small, busy team but we are all very happy to teach
- if you have any questions at any time about anything, please ask !

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Must do:

1. Thoracic Surgery teaching will be through e-learning videos and “flip-classroom” case discussion
tutorials (frequency and schedule as yet to be decided upon revision of this handbook). Everyone
must attend and groups may be expected to clerk some thoracic cases (common conditions) on Ward
7C before the sessions and present the cases on powerpoint for discussion (topics to be included: 1)
lung mass/ CA, 2) anterior mediastinal mass, 3) chest drain/ box management and airleak with video,
4) pneumothorax, 5) trauma, 6) hemoptysis, 7) Empyema, others)

2. Thursday OPD
- best chance to see new patients with presenting symptoms and signs
- clinics are quite busy and we may not be able to stop and discuss every single patient, but
please ask at any time if you have any questions

3. Friday Cardiac Surgery tutorials twice per module (i.e., for two different four sub-groups of students),
at the Arthur Li Surgical Library from 17:30:
Everyone must attend and those who are rotating with the CTS team over that particular week of the
tutorial will be expected to clerk some cardiac cases on Ward 7C and present them at the tutorial for
further discussion. The clinical cases should include ischemic heart disease and valvular disease,
unless otherwise instructed by the tutor.

performance at the tutorials is an essential part of your assessment for this module !
Make sure you are prepared to present the cases at each tutorial.

Try to do:

1. Bronchoscopy sessions (Thursday start around 2:30 or 3 p.m. – dependent on when OPD ends)
- try to come at least once
- best way to see bronchial anatomy and uses/limitations of bronchoscopy
- if lucky you will see Endobronchial Ultrasound (EBUS) biopsy

2. OT sessions:
- if you are keen to come to OT: you are most welcome but please ask one of us first

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CHAPTER 3: ADULT CARDIAC SURGERY

In PWH, we perform mainly adult cardiac surgery:

 80% Coronary artery surgery & Heart valve surgery
 20% Others: Aortic surgery, Cardiac Tumor, ECMO support, adult congenital cardiac conditions and
cardiovascular trauma etc.

CARDIOPULMONARY BYPASS (CPB)

 CPB is required for almost all cardiac surgery
 Purpose
1. Bypass of blood flow ⇒ BLOODLESS operative field
2. Cardioplegia ⇒ STILL operating field
3. Provide cerebral and visceral organs support during cardiac / aortic surgery
 Performed by specially trained Perfusionists

 Essential Components of CPB

 Standard circuit:
1. Systemic venous blood siphoned from IVC/SVC or RA into venous reservoir by gravity
2. Oxygenator: oxygenation of blood
3. Heat exchanger: temperature regulator
4. Blood pumped back into aorta via aortic / arterial cannula (Centrifugal / Roller)
 Important technical aspects
 Aorta is cross-clamped proximal to the site of aortic cannula
 Systemic heparinization is mandatory to keep Activated Clotting Time (ACT) > 400 sec

Myocardial protection
1. CARDIOPLEGIA
2. COOLING
3. LV VENTING (⇒ reduce wall distension)
4. Drugs: e.g. Adenosine

 Cardioplegia:
 Purpose:
1. Still operative field
2. Reduce and replenish metabolic demand of heart during OT
 Category
a. By temperature
1. ‘cold’ cardioplegia: electrolyte solution with high K+ content at 4 oC
2. ‘warm’ cardioplegia
b. By content
1. Crystalloid
2. Blood

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 Harmful Physiological Disturbances
1. Triggering of systemic inflammatory response
2. Trauma to blood components
3. Consumption coagulopathy
4. Organ damage: e.g. stroke, renal failure
 Microemboli
 Regional hypoperfusion
 Inflammatory response
 ↑ Interstitial oedema

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CORONARY ARTERY BYPASS GRAFTING (CABG)

Ischaemic Heart Disease

 Coronary artery stenosis
 50% loss of arterial diameter in two perpendicular planes in angiogram⇒ ~75% stenosis (Cross-sectional
area reduction)⇒ symptoms of angina with activity
 75-80% loss of diameter ⇒ 90% stenosis ⇒ reduced blood flow at rest

 Manifestation of ischaemic heart disease

A. Acute myocardial ischaemia
 Acute coronary thrombosis due to plaque rupture
 Presentation:
1. New-onset or increasing angina to at least CCS Class III Canadian Cardiology Society (CCS)
2. Ventricular arrhythmia classification of severity of angina
3. Heart block Class I: symptom on heavy exertion only
4. Mechanical complications: Class II: symptom on moderate exertion
- Acute ischaemic mitral regurgitation Class III: symptom on mild exertion
- Ventricular septal rupture Class IV: symptom at rest
- Ventricular free wall rupture
- Ventricular/septal aneurysm
B. Chronic myocardial ischaemia
 Static imbalance of myocardial blood supply and demand
 Presentation:
1. Heart failure: Ischaemic cardiomyopathy
2. Ischaemic mitral regurgitation
C. Episodic myocardial ischaemia
 Dynamic imbalance of myocardial blood supply and demand
 Presentation: Angina
- Brought on by exertion / emotional stresses
- May RADIATE to arm or shoulder
- RELIEVED with rest or sublingual nitrate within 5 minutes.

 Treatment of Ischaemic heart disease: General pointers

 Medical therapy and risk factor control are the mainstays of treatment
 Coronary Angiogram is essential to anatomically characterize the extent of coronary disease (preferably
with cardiac catheterization)
 Revascularization in stable angina or silent ischaemia
1. Left main stem disease >50%
2. Proximal LAD >70 stenosis or >50% stenosis with demonstrable ischaemia
3. Angina with any coronary stenosis >50%
4. Large area (>10%) LV territory ischaemia
 Revascularization in acute STEMI /NSTEMI is in general by Cardiologists:
1. Thrombolysis
2. Percutaneous coronary intervention
Surgical revascularization is indicated only in certain clinical conditions
1. Cardiogenic Shock
2. Post MI angina
3. Ischaemic Malignant Ventricular Arrhythmia
4. Mechanical complications of MI

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Indications for CABG over PCI

A. ANATOMICAL Consideration
1. PROXIMAL LAD disease (≥70% stenosis)
2. TRIPLE-VESSEL disease (≥70% stenosis), especially in patients with:
- Impaired LV function
- Diabetes mellitus
- Chronic kidney disease
3. LEFT MAIN disease (≥50% stenosis)
- LEFT MAIN-equivalent disease: Proximal LAD + Proximal LCx disease
B. Post-MI MECHANICAL COMPLICATIONS
1. Ventricular septal rupture (VSR)
2. LV free wall rupture / LV aneurysm
3. Acute severe ischaemic mitral regurgitation (IMR)
C. Symptomatic patients not suitable for PCI with revascularizable targets

Procedure of CABG

1). Incision: Median sternotomy

- Alternatives: Mid-CAB, Minimally-invasive, Robotic
2). Conduits harvested and used for bypass grafting
- Approach: Open or Endoscopic
3). Systemic heparinization
- Reversed with protamine at end of CPB
4). CPB with warm blood cardioplegia
- Alternatives: On-pump beating-heart CAB; Off-pump CAB
5). Grafting: usually distal anastomosis to the coronary artery first, then proximal anastomosis to the ascending
aorta
6). Procedure can be combined with other procedures
- e.g. LV aneurysm excision, valve repair/replacement etc.
7). Sternum closed with stainless steel wires

 Typical post-operative course:

1. 4-24 hours stay on ICU (usually extubated same day)
2. 5- 7 days in-hospital stay
3. Can resume activities of daily living upon discharge and resume non-manual work 4-6 weeks and manual
work at 3 months
4. Take-home medication on discharge:
 Antiplatelets: Aspirin ± Clopidogrel/Ticagrelor
 Statins
 Anti-ischaemic: Beta blockers
 Anti-heart failure: ACEi/ARB

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Conduits
A. Great Saphenous Vein
- used in 80% of all grafts
- advantages: long length available for many grafts; easy to harvest & use
- disadvantages: 70-85% early patency; 50%-70% late (10 years) patency (Studies showed statin improves
long term vein graft patency)
B. Internal Mammary Artery
ENDOSCOPIC VEIN HARVEST
- usually left IMA
1. Less wound complications especially
- sometimes right IMA is also harvested (i.e. bilateral IMA harvest) in high risk patients such diabetics,
- almost always used for grafting to LAD neuropathy and peripheral vascular
- advantages: Excellent early and late patency (95% at 10 year) disease
2. Less painful, Better wound cosmesis,
C. Other Arterial Conduits
Shorter hospital stay
- e.g. radial artery, gastroepiploic artery, inferior epigastric artery 3. Vein quality & patency rate non-
inferior to traditional open technique
Results of CABG
Outcome of CABG tends to be very good: > 90% relieved of angina without need for medication
In patients with LM or TVD and impaired LVEF <50%, CABG achieved 10% better survival benefit than PCI with
less need of re-intervention

 Risk
 Mortality 1-2%
 Perioperative stroke 1-2.5%
 Common complications:
1. Atrial fibrillation (up to ⅓ patients)
2. Post-op bleeding 1-2%
- may require re-exploration if severe bleeding
3. Wound infection
- Leg wound infection 5-8% ( higher in DM patients )
- Deep sternal wound infection < 1%
- if mediastinitis develops, it is potentially life-threatening
4. Post-op Low Cardiac Output Syndrome (LCOS)
- may require circulatory support with inotropes, IABP or even ECMO
 High risk factors include: poor LV function, DM, emergency operation, other medical comorbidities

Important preparations before referral for CABG

A. History
1. Severity of symptoms
2. Comorbidities
B. Physical Examination
1. Varicose veins
2. Carotid bruit
3. Peripheral pulses
4. Ulnar collaterals (Allen’s test)
C. Investigations
1. CXR ± CT Thorax (plain) for aortic calcifications
2. Lung Function Test, Renal Function Test
3. Coronary Angiogram (preferably by cardiac catheterization)
4. Echocardiogram: for LV function and concomitant valvular diseases
5. Carotid Duplex: if history of TIA/stroke or positive carotid bruit

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VALVULAR HEART SURGERY

In Hong Kong, valve diseases are COMMON

- 50% caused by rheumatic heart disease
- 50% other causes: e.g. degenerative or infective endocarditis

Pathophysiology of Valvular Heart Disease

A. Valvular Stenosis:
1. Hypertrophy of the proximal chamber [PRESSURE OVERLOAD]
2. Dilatation occurs later as the chamber fails
B. Valvular Regurgitation: Dilatation of the chambers on BOTH side of the valve [VOLUME OVERLOAD]

 Symptoms New York Heart Association (NYHA)

1. Progressive exertional dysponea: Left heart failure classification of heart failure symptoms
2. Ankle oedema / RUQ discomfort: Right heart failure Class I: symptom on heavy exertion only
3. Palpitations: Commonly atrial fibrillation Class II: symptom on moderate exertion
4. Easy fatigability: Low cardiac output Class III: symptom on mild exertion
5. Chest pain: Myocardial ischaemia (esp. in aortic stenosis) Class IV: symptom at rest

 Symptomatology of diseased valves

 Stenosis
− Impairment to outflow ⇒ ↑ intraventricular pressure ⇒ ↑ cardiac workload
− Imbalance between supply and demand
 Regurgitation:
− Ventricle accommodates the increased volume load
− Often already severe and irreversible myocardial damage upon onset of symptoms
 Principle of surgery: To correct the defect before irreversible damage to myocardium occurs

 CRITERIA for surgery (as isolated procedure):

Severe Aortic Stenosis Symptomatic: Angina, Syncope, Dyspnoea
Impaired LVEF
Low Flow Low Gradient AS
Severe Aortic Regurgitation Symptomatic
Impaired LVEF
LV dilatation
Aortic root disease with dilated ascending aorta
Severe Mitral Stenosis Symptomatic
Percutaneous mitral commissurotomy contraindicated
Severe Mitral Regurgitation Symptomatic
Impaired LVEF (≤ 60% but >30%)
LV dilatation
New-onset atrial fibrillation or pulmonary hypertension
Tricuspid Regurgitation Severe TR
Absence of RV dysfunction

 Two types of surgery can be done:

A. Repair (mainly mitral or tricuspid valves)
B. Replacement

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 Valve Repair
 In general, repair is performed whenever possible to avoid complications of prosthetic valve
 Advantages: no long-term anticoagulation, better haemodynamics, autologous tissue preserved
 Disadvantages: technically not always possible, risk of recurrence in the long-run

 Valve Replacement
 Two types of valve prostheses:
1. Mechanical (carbon/graphite) (not metal)
2. Biological (usually porcine aortic or bovine pericardium)
 Complications of prosthetic valves:
1. Thrombosis (‘jam valve’)
2. Thromboembolism
3. Degeneration: >50%/15 years for biological valve
4. Infection
- Prosthetic valve infection is very serious: 20% mortality; usually requires re-replacement

 Comparison of Mechanical & Tissue Valve

Mechanical Biological
Life long Durability >50% failure at 15 yrs
Excellent Haemodynamic Theoretically better (∵ unobstructed laminar flow)
3 months post-op (∵ re-endothelialization)
Essential & Life long Anticoagulation
Unless large atrial thrombus & chronic AF
ELDERLY > 66 year of age
YOUNG who can take warfarin Choice
Warfarin Contraindicated (e.g. pregnancy)

 Post-op care of prosthetic valves:

 Antibiotic cover when having invasive procedures (e.g. dental procedures)
 Anticoagulation (esp. mechanical valve):
- Usually with Warfarin (NOACs are NOT proven to be safe and effective alternatives!)
- Replace Warfarin with IV Heparin as bridging anticoagulation for invasive procedures
- Keep INR 2-2.5 for most mechanical valves (aim higher for mechanical mitral valve)
- Female of child-bearing age should be advised on the issues of teratogenic effect of warfarin and the
risk of valve thrombosis during pregnancy and chance of massive peri-partum bleeding

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Important preparations before referral for valvular surgery

A. History
1. Severity of heart failure symptoms
2. Comorbidities
B. Investigations
1. Echocardiogram: Etiology, severity of valve disease, ventricular functions, chamber size, intracardiac
thrombus
2. Lung Function Test, Renal Function Test
3. Coronary Angiogram: Concomitant ischaemic heart disease
4. Dental examination

Appendix: Remember to revise and practice your physical examination skills!

Pathology Typical Physical Signs

Left ventricular failure
Right ventricular failure
Atrial fibrillation
Mitral Stenosis
Mitral Regurgitation
Aortic Stenosis
Aortic Regurgitation
Tricuspid Regurgitation
S3, S4
Bilateral pulmonary basal fine crepitation
JVP: Prominent ‘a’ wave and ‘v’ wave
Dependent oedema
Pulsatile liver
Ascites
Parasternal heave
Pulse: irregular in rate and volume
JVP: loss of ‘a’ wave
Apex: Tapping, Diastolic thrill
Loud S1, Opening snap (Absent in AF patients)
Mid-diastolic rumbling murmur
Beware of Austin-Flint Murmur
Apex: Displaced hyperkinetic (‘thrusting’), Systolic thrill
Soft S1, S2 obscured by murmur
Pansystolic murmur best heard at apex radiating to axilla
Slow-rising pulse
Sustained (‘heaving’) apex
Systolic thrill at aortic area
Weak A2
Ejection systolic murmur best heard at aortic area and apex with radiation to
bilateral carotid area
Collapsing pulse
Displaced hyperkinetic apex
Diastolic thrill at left lower sternal border
Ejection systolic flow murmur at aortic area
High-pitch blowing early diastolic murmur loudest at left lower sternal
border in full expiration & leaning forward
JVP: Giant ‘v’ wave
Pansystolic murmur over lower sternal border, louder with inspiration

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AORTIC SURGERY

 Acute Aortic Syndrome

1. Classical Aortic Dissection
2. Intramural Haematoma (IMH)
3. Discrete dissection
4. Plaque rupture / Penetrating atherosclerotic ulcer (PAU)
5. Iatrogenic/ traumatic

Aortic Dissection
 Pathophysiology
 Sequence of events
1). Intimal tear
2). Separation of the layers of media layer (NOT intima!)
3). Formation of flap separating the true lumen and false lumen
4). Propagation of dissection in antegrade and/or retrograde direction
 Development of complications
1. Compression of aortic side-branches ⇒ Acute myocardial infarction, Organ malperfusion
2. Rupture of intrapericardial part of aorta ⇒ Haemopericardium with acute pericardial tamponade
3. Involvement of aortic annulus ⇒ Acute aortic regurgitation
4. Weakness of aortic wall against blood pressure ⇒ Free rupture

 Classification
Stanford DeBakey
Type A: Dissections involving Type I: Originate at ascending aorta, propagates to at least the aortic arch
the ascending aorta Type II: Originates in and confined to ascending aorta
Type B: Dissections not Type III: Originates in the descending aorta and extends distally
involving the ascending aorta
** By definition, for an aortic dissection originating at the descending aorta and spanning from the ascending aorta down to
the abdominal aorta, it is called a Stanford Type A dissection, or a DeBakey Type III dissection with retrograde involvement of
the ascending aorta

 Aetiology
A. Chronic uncontrolled hypertension
B. Connective tissue disorder
- e.g. Marfan syndrome, Ehlers-Danlos syndrome, Bicuspid aortic valve
C. Vascular inflammation
- e.g. Giant cell arteritis, Takayasu arteritis, Behcet’s disease, Syphilis
D. Deceleration trauma
E. Iatrogenic
- e.g. catheter/instrument intervention, open heart surgery

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 Investigations
 Physical Examination
- Radial-radial or radial-femoral delay
- Absent of radial or femoral pulse
- Muffled heart sound (Signifying pericardial effusion)
 ECG
- LVH: chronic poorly-controlled hypertension
- ST segment abnormalities: may represent acute coronary syndrome
- Remember: Inferior lead ST elevation may reflect type A aortic dissection with involvement of the
right coronary ostium
 CXR
- Widened mediastinum is neither sensitive or specific for aortic dissection!
- Look for other causes of acute chest/abdominal pain: e.g. pneumothorax, pneumoperitoneum
 Transthoracic Echo / V-scan
- Present of AR
- Pericardial effusion
- Dissection flap
- Any RWMA suggesting coronary involvement
 CT Aortogram (with contrast)
- Diagnosis of aortic dissection, classify the extent of involvement
- Look for organ malperfusion
- Planning for sites of cannulation
 Other adjuncts: Trans-Oesophageal Echocardiogram, MRI Aortogram etc.

Treatment of Aortic Dissection

Traditionally:
 Type A: Surgical management to prevent life-threatening complications
 Type B: Medical treatment with blood pressure control to prevent progression

 Treatment for Type A Aortic Dissection

 Aim
- Resection of primary tear
- Restore blood flow within the true lumen
 Extent of surgical repair depends on the extent of disease involvement
 Ascending aorta replacement
 Aortic root + ascending aorta replacement
 Ascending aorta + Hemiarch replacement
 Total arch replacement ± Elephant trunk

 Treatment for Type B Aortic Dissection

 Uncomplicated Type B
 Definition: No distal malperfusion syndrome, no rapid disease progression
 Treatment: Medical (effective, with 80% 5 year survival)
 Complicated Type B
 Definition: Presence of distal malperfusion syndrome or rapid disease progression
 Indications for emergency intervention:
1. organ or limb ischemia
2. aneurysm expansion and risk of rupture
3. periaortic blood collection
4. intractable pain

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 5. uncontrolled hypertension
 Treatment: Medical + Surgical
 Thoracic Endovascular Aortic Repair (TEVAR)
 Open descending aorta replacement

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Management of Type A Aortic Dissection
 Natural History of Type A Aortic Dissection
 High mortality
 Mortality ↑ 1-2% per hour during first 24-48 hours
 Mortality without surgical treatment: 20% by 24 hours, 30% by 48 hours, 40% at 1 week, 50% at 1
month
 Surgical mortality: 10-35% ( 20-25% from IRAD, 17-20% GERRADA, 5-10% PWH )
 Complications
a. Immediately life-threatening
1. Acute pericardial tamponade
2. Acute severe aortic regurgitation
3. Acute myocardial infarction
4. Aortic rupture
b. Organ malperfusion
1. Stroke
2. Renal, liver and mesenteric malperfusion
3. Paraplegia
4. Acute limb ischaemia

 Immediate Management
1. ECG: evidence of ACS
2. Pain control (e.g. IV Morphine)
3. Invasive arterial blood pressure monitoring
4. IV Antihypertensives to control systolic BP
- IV Beta-blocker (e.g. Labetalol) is mandatory (to reduce the ΔP/Δt)
- Do NOT give pure vasodilator without adequate beta blockade
5. Urgent CT Aortogram: to establish diagnosis and assess the extent of aortic dissection
6. Urgent transthoracic echocardiogram: look for pericardial effusion, aortic regurgitation, RWMA
7. Urgent Cardiothoracic Surgery consultation

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Thoracic Aortic Aneurysm
 Definitions
 Definition of aneurysm: PERMANENT LOCALIZED DILATATION of an ARTERY with >50% increase in
diameter compared to its adjacent normal segment
 Types of aneurysm
a. By location
- ascending aorta (45%)
- arch of aorta (10%)
- descending aorta (55%)
- thoracoabdominal (10%)
b. By histology
 True aneurysm: aneurysm wall still contains all histological layers of normal aortic wall
 False aneurysm: walls do not contain all histological layers
- usually results from chronic aortic dissection or trauma

 Aetiology
A. Degenerative
B. Chronic dissection
C. Trauma
D. Aortitis
E. Infective

 Investigations
 CT scan and MRI
 Echocardiogram: evaluation of valvular functions and ventricular function

 Indications for operation:

1. Size: diameter >5.5 cm (ascending aorta) / 6 cm (arch) / 6.5 cm (descending aorta)
2. Progressively increase in size (more than 5mm in 6 months)
3. Symptomatic
4. Evidence of rupture or leak

 Operations: Approach depends on the extent of aneurysm involvement

a. Open surgery
 Ascending: Graft replacement ± Aortic root replacement
 Arch: Total arch replacement ± Elephant trunk
- under circulatory arrest and cerebral protection
 Descending/thoracoabdominal: Graft replacement
- with left heart bypass & spinal cord protection
b. Endovascular surgery (TEVAR)
- Zone of landing of stent graft: Zone 0/I/II/III/IV
- Head and neck vascular bypass if origin of the BCT/LCCA/LSCA covered by the stent graft

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CHAPTER 4: CONGENITAL HEART SURGERY

Atrial Septal Defect

 Embryology
 Failure of septal growth or excessive reabsorption of tissue leads to ASDs
 Classifications
1. Secundum ASD (70%): defect in the middle of the septum; best outcomes post-op
2. Primum ASD (20%): defect in inferior atrial septum; abnormal endocardial cushions
3. Sinus venosus defect (10%): defect in upper atrial septum, above fossa ovalis

 Pathophysiology
 Shunting from LA to RA  ↑ flow through Tricuspid Valve during diastole  RV Volume overload
 The amount of shunting depends on the size of defect and the relative compliance of RV & LV.
 Usually remains asymptomatic till fourth decade
– except ostium primum defect: usually causes symptoms in childhood

 Physical signs
1. Parasternal heave (RV volume overload)
2. Wide FIXED splitting of S2
3. Soft (grade I or II) Ejection Systolic Murmur in RVOT
4. Mid-diastolic murmur LLSB: larger shunt  increased volume passing across tricuspid valve.

 Investigations
 ECG: Incomplete RBBB, RA enlargement, RAD, RVH
 CXR: RA & RV enlargement, Increased pulmonary vascularity
 Cardiac catheterization: degree of shunting (Qp:Qs), pulmonary vascular pressure

 Management
 Treatment consideration
− Small ASD: 80% spontaneous closure in first few years
− Complications of large ASD
1. Arrhythmia
2. Eisenmenger syndrome
 Modalities
 Catheter occlusion device
 Surgical closure
 Indication for closure of ASD: Symptomatic ASD with left to right shunt (Qp:Qs) >1.5

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Ventricular Septal Defect

 Pathophysiology
 Most common congenital cardiac defect (~2/1000 live births)
 Isolated VSD accounts for 20 - 25% of all congenital heart disease
 ↑ pulmonary blood flow  ↑ pulmonary venous return  LA & LV Volume overload

 Presentation
 Presenting symptoms
 Shortly after birth: MURMUR
 6-8 weeks later: HEART FAILURE symptoms
 Chronic VSD: Eisenmenger syndrome
 Physical signs
1. Apical impulse
2. Parasternal heave
3. PANSYSTOLIC murmur heard best at LLSB
4. Splitting of S2 and ↑ intensity of P2

 Investigations
 CXR: Cardiomegaly, Increased pulmonary vascularity
 ECG: RVH, LA enlargement, LVH
 Echocardiogram: location, type and size of VSD; pressure gradient across VSD
 Catheterization: Qp:Qs, pulmonary pressure

 Management issue
 50-70% VSD can shrink or heal at age of 6-12 months
 Less than 10% large VSD can close spontaneously
 Surgical closure indicated if
 Intractable symptoms with Qp:Qs > 1.5 and pulmonary resistance <4 Wu
 Asymptomatic child without signs of closure by 2 years’ old
 Operative mortality rate: < 3%

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Patent Ductus Arteriosus

 Pathophysiology
 Closure of ductus arteriosus: usually within the first few days of life
1. Increase in blood oxygen content
2. Withdrawal from maternal prostaglandin
3. Release of bradykinin from lung
 More common in premature infants: usually presents as heart failure in the premature neonate/infant
 Small PDAs are asymptomatic. Moderate to larger shunts produce the symptoms of CHF as the pulmonary
vascular resistance decreases over the first 6 to 8 weeks of life.
 PDA may also be seen in combination with other defects: e.g. VSD / AR /aortic coarctation etc.
 May be complicated by Eisenmenger’s syndrome

 Physical signs
1. Widened pulse pressure
2. Hyperdynamic precordium
3. Continuous machine-like murmur heard at left infraclavicular area & left back

 Management issues
 Small and moderate PDA: spontaneous closure
 Treatment modalities
 Indomethacin
 Catheter occlusion
 Surgical ligation
 Indications for surgical ligation:
1. Premature infants with severe pulmonary dysfunction
2. Heart failure within first year of life
3. Asymptomatic child with patent ductus >2 year old

20
2. LUNG CANCER
Epidemiology

In HK, malignant neoplasms of all types remain the leading cause of death.
Of all malignant neoplasms: lung cancer is still the commonest cancer in men.
- accounted for 3867 deaths in Hong Kong in 2013 (28.5% all cancer deaths)
- incidence exceeds all other cancers (including liver ca and colorectal ca combined)
- In 2012, there were 4610 new cases of lung cancer in HK.

Lung cancer is still more common in men than in women. However, incidence of lung cancer
(adenocarcinoma) in young female non-smokers is rising quickly.
- Male: Female 1.8: 1 in 2012 Hong Kong

Note: surgery for lung cancer accounts for >90% of all lung resection operations in the Western world

Etiology

Tobacco smoke: undoubtedly the single most important risk factor

- >90% lung cancers are aetiologically related to smoking
- passive smoking is now a recognized carcinogen
- lung cancer can hence be regarded as a ‘preventable’ disease
- however, it takes 10 years for risk to start reducing after stopping smoking
and the risk never fully returns to that of a lifelong non-smoker

Other risk factors: - asbestos exposure - atmospheric pollution

- radiation exposure - metals (esp nickel & silver)
- certain chemicals (e.g. chloromethyl ethers)

There may be an element of genetic predisposition to lung cancer

- e.g. higher incidence of adenocarcinoma in non-smoking females in China/Japan
- research still being conducted in this respect especially EGFR mutation

WHO classification of malignant lung neoplasms (modified)

a) Small cell carcinoma

- ~10-20% all lung cancers
- metastasize early, hence inoperable; overall 5 year survival ~10%
b) Squamous cell carcinoma
- strongest association with smoking
- typically metastasize later than other lung cancers
- variant: spindle cell carcinoma
c) Adenocarcinoma
- most frequent histological type in Hong Kong/Asia ?
- variant: bronchoalveolar carcinoma (old term – but still used in textbooks )- replaced by
nomenclatures such as MIA (minimally invasive adenocarcinoma)
d) Large cell carcinoma
- aggressive, but relatively less common (<5%)
- variants: giant cell ca, clear cell ca
e) Others
- carcinomas: adenosquamous ca, carcinoid tumour, adenoid cystic ca, mucoepidermoid ca etc
- also (rarely): sarcomas and lymphomas

Important: because of strong tendency for small cell ca to metastasize early ...
“Surgery is for NON-small cell lung cancers only”

is the general statement in many textbooks and management protocols, but new evidence
suggest that surgery for small cell ca has a role in the earliest forms of the ca (Stage 1a)

21
 The rest of this chapter will deal only with non-small cell lung cancers

Presentation

Typical patient: male, smoker in 6th - 7th decade of life

Many patients are asymptomatic at presentation: mass discovered ‘incidentally’ on chest x-ray
- more typically: patient symptomatic for 3 to 6 months at time of first presentation

a) Bronchopulmonary Symptoms
- caused by irritation, ulceration or obstruction of a bronchus
- e.g. cough, hemoptysis, dyspnoea, chest pain, chest infection, wheeze/stridor
b) Extrapulmonary Intrathoracic Symptoms
- result from growth/invasion of the tumour beyond the confines of the lung
- e.g. hoarseness (laryngeal nerve), Horner’s syndrome (sympathetic chain),
chest pains (direct chest wall invasion), raised hemidiaphragm (phrenic nerve),
malignant pleural effusion, SVC obstruction etc
c) Extrathoracic Metastatic Symptoms
- e.g. neurological (brain mets), bony pains (bone mets), jaundice/ascites (abdo mets) etc
d) Extrathoracic Nonmetastatic Symptoms
- e.g. clubbing, scleroderma, hypertrophic osteoarthropathy, SIADH etc
e) Nonspecific symptoms
- weight loss, weakness, anorexia, malaise etc

Diagnosis

1) Chest X-ray
- every chronic smoker with recent onset of pulmonary symptoms should be offered a CXR
- if CXR shows a lesion, try to exclude a benign lesion
(e.g. long-standing shadow without any change in size compared to old films)
- if any suspicion of malignancy exists: proceed to establish histological diagnosis
2) Sputum cytology
- also routinely send sputum for culture and TB to exclude infection as cause of lung shadow
- if negative: proceed for bronchoscopy +/- biopsy , or image guided FNA
3) Bronchoscopy
- tissue diagnosis by washings, brushings, biopsy
- some centres perform transbronchial biopsy
- useful for centrally-located lesions
4) Fine Needle Aspiration
- performed with imaging (CT, ultrasound, fluoroscopic) guidance
- safer and more useful for more peripheral lesions
- chance of causing pneumothorax
5) Electromagnetic Navigational Bronchoscopy (ENB) – allow navigation of small biopsy catheter to the
more peripheral aspects of the lung for tissue acquisition.
6) Operative biopsy
- when all else fails, biopsy can be done operatively (esp. Video-Assisted Thoracic Surgery (VATS))
- can be done as a ‘frozen section’ of a Trucut biopsy or lung wedge excision
(allowing proceeding to curative surgery, for example lobectomy, if lung cancer confirmed)

When diagnosis of non-small cell lung cancer (NSCLC) confirmed, surgery is the treatment of choice
- surgery is the only chance of ‘cure’ with best survival data (chemo- and RT essentially “palliative”)
However, operability depends on:
i) disease staging (see below)
ii) patient factors (see below)
iii) technical considerations: e.g. surgeon’s expertise, intraoperative staging & complications etc

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Staging
Divided into Clinical staging (use of CT imaging/ PET, mediastinal biopsy before surgery) &
Pathological staging (after resection of the tumour, and all the surrounding lymph nodes). The latter
is the more accurate.

“Staging at operation is the most accurate predictor of long-term survival”

From al-Kattan et al (1996) Thorax 51:1266-1269

TNM Staging 7th edition [students need not memorise this !]

Tis Carcinoma in-situ

T1 <3cm
T2 >3cm or distal atelectasis caused by tumour, or invades visceral pleura, or involves the main bronchus ≥ 2
cm distal to the carina
T2a >3cm but ≤ 5cm
T2b >5cm but ≤ 7cm
T3 > 7cm, or parietal pericardial/parietal pleural/chest wall involvement (include superior sulcus tumours) or
tumour within 2cm of carina
T4 mediastinal organs involved (heart/ great vessel, trachea, recurrent nerve) or separate satellite nodule in
different ipsilateral lobe

N1 ipsilateral bronchopulmonary or hilar nodes

N2 ipsilateral mediastinal or subcarinal nodes
N3 contralateral mediastinal or supraclavicular nodes

M1 distal metastasis (including pulmonary mets to contralateral lung, pleural nodules/ malig effusion,
pericardial mets/ effusion)

Stage TNM 5 year Survival with surgery & adjunct

therapies
Ia T1 68.5%
Ib T2a N0
IIa T1N1, T2aN1, T2bN0 46.9%
IIb T2bN1, T3N0
IIIa T3N1, T(1-3)N2, T4N0, 26.1%
T4N1
IIIb T4N2, any N3 9.0%
IV any M1 (negligible)

a) Operable: stages Ia to IIb

- only ~30-40% patients are in this group at presentation
- survival with surgery significantly improved compared to survival without surgery

b) Inoperable: stages IIIb and IV

- over 55% patients in this group at presentation
- surgery offers no survival benefit at all, hence not for surgical resection
- for palliative radio/chemotherapy (including targeted/ immunotherapy) or supportive care only

c) Controversial: stage IIIa

- if stage IIIa is due to chest wall invasion by tumour (T3), some surgeons perform lung resection
en bloc with chest wall resection
- if stage IIIa due to N2 spread, combination chemo/radiotherapy may be given (many unknowns!)

23
 (a proportion of selected patients may subsequently benefit from lung resection following neo-
adjuvant treatment, if good response and tumour significantly “down-staged”)

Pre-operative Staging Evaluation is hence essential to establish operability:

1) Blood tests (CBP, RLFT etc)

- in particular, raised ALP may be suggestive of bone mets
(if ALP raised, check ALP isonenzymes)
- CEA
2) Fibre-optic Bronchoscopy
- to assess endobronchial involvement (e.g. airway occlusion, proximity to carina)
3) CT thorax with contrast enhancement
- a recent set of CT scans is essential for all cases of NSCLC for which surgery is planned
- contrast helps reveal any mediastinal lymph node enlargement
- CT must include cuts through liver and adrenals (common sites of mets)

4) Abdominal USG
- Not done routinely: indicated if CT or blood tests suggest suspicion of abdo mets
- ultrasound may be more specific than CT in differentiating between liver mets and cysts

5) Bone scan
- not done routinely: indicated if patient has recent bone pains or raised ALP bone isoenzymes
6) CT brain
- not done routinely: indicated if patient has recent onset of neurologic symptoms
7) Mediastinoscopy
- indicated if CT suggests mediastinal lymph node enlargement / PET +ve mediastinal Ln
- surgery performed under GA
8) PET scan
- measures glucose metabolism of tissues with Standard Uptake Value (SUV) measured (i.e. a
functional scan, as opposed to a CT which gives a structural/ anatomical picture only)
- International Guidelines suggest should be done for all lung cancer patients.
- use in lung cancer staging still and detection of distal metastasis is useful
- advantages: can determine metabolic activity of suspicious lesions seen on CT and
hence suggest whether or not they may be benign / malignant /metastases
- disadvantages: not always highly specific (e.g. inflamed tissues also shown as hotspots), and
not sensitive for smaller lesions. False positive for TB and infection, false negative for small lesion
(esp. < 1cm) and low grade (low metabolism) malignancy e.g. MIA /Lepidic types Ca.
9) Endobronchial Ultrasound (EBUS)
- Proven to be useful for USG image guided biopsy of mediastinal LNs for pre-op staging. A
negative EBUS does NOT rule out mediastinal LN metastasis and mediastinoscopy is still the gold
standard. EBUS can be combined with EUS for complete mediastinal staging.

In addition, occasionally intrathoracic/pleural mets may not be found until surgery

- routine VATS exploration performed as intraoperative staging procedure (before opening more
ports or opening a thoracotomy) to exclude pleural mets

Preoperative patient evaluation

1) Arterial blood gases
- many patients are smokers who may have concomitant COAD or other lung disease
- ABG’s essential to exclude significant respiratory failure in these patients
- in particular, high pCO2 indicates high surgical risk
2) Pulmonary function test
- typically, lung function required depend on extent of surgery (wedge , segmentectomy, lobectomy,
pneumonectomy): FEV1 value is the most predictive of post-op complications/ morbidity:
For example: FEV1 55-60% predicted, needed for lobectomy

- poor figures may be due to poor technique: also must consider patient’s exercise tolerance
- DLCO should also be evaluated in the current guidelines
3) Exercise tolerance & mobility

24
 - important because patient must be able to undergo post-op physiotherapy & pulmonary rehab
4) Other medical comorbidities
- as patients are often old and chronic smoker, other medical conditions may co-exist
(e.g. ischaemic heart disease, vascular disease, hypertension, DM etc)
- all medical comorbidities must be investigated and be under satisfactory control prior to surgery

Patients with borderline or poor lung function should receive pre-op optimization
- pre-op chest physiotherapy may be beneficial
- use of regular nebulized bronchodilators in the perioperative period (for COAD patients)

Those patients who have suboptimal FEV1 & DLCO for lobectomy may undergo other types of
pulmonary function assessment to further establish their operability. (for example, shuttle walk test, 6-
min walk, cardiopulmonary exercise test (CPET) etc.)

Surgery for Lung Cancer

Surgery is only offered for operable non-small cell lung cancer in patients with sufficient physiological
reserve to withstand the resection [see above]

Surgery represents only potential chance of cure for early stage NSCLC
- chemo/radiotherapy can only offer very modest survival benefit

1) Anaesthesia: GA with double lumen endotracheal intubation

- allows one lung ventilation (affected side deflated during surgery)
2) Position: full lateral (affected side up) with table ‘broken’/ in “jack-knife” position to open up rib spaces
3) Incision:
-80-90% of lobectomies in PWH are by minimally invasive video-assisted thoracic surgery (VATS)
requiring small incisions.
- for open surgery, the standard incision is posterolateral thoracotomy (usually 4/5th intercostal space)
- may or may not require rib cutting and/or resection to improve access
- this is a traumatic incision and one of the most painful surgical wounds
4) Procedure: aim to achieve complete removal of tumour with clear margins
- depending on size, location (peripheral vs central), invasiveness of the tumour and
on fitness of patient to undergo major resection, the options include:
a) Lobectomy [mortality ~1%]
(variations include bilobectomy, lobectomy with sleeve resection)
b) Pneumonectomy [5-10% mortality (R>L)]
c) Wedge Resection / Segmentectomy
(role is controversial: for very small GGOs / sometimes used for elderly with poor lung function)

- we routinely explore with VAT to exclude pleural mets before embarking on resection
- systematic mediastinal lymph node sampling is an essential part of the procedure for Pathological
Staging. Pathology from the dissected LN needed to guide the need for post-op adjuvant chemo-
and/or radio-therapy

5) Chest drains: always placed after resection via stab wounds made just below main wound/ through
VATS ports
a) after lobectomy: a drain is usually placed and connected to low suction
- in some more complex operations, 2 drains may be placed: anterior apical drain to drain air,
‘back’ basal drain for blood/fluid
- drains removed when remaining lung re-expanded with no air leak and minimal drainage
b) after pneumonectomy: single drain connected to no suction (applying suction may kill the patient!)
- mainly used to monitor for reactive post-op bleeding and removed the day after surgery
- pleural space allowed to fill up with fluid which eventually fibroses

6) Post-operative care:
- close monitoring is essential initially, but usually does not require ICU/HDU stay
- patients can resume full diet once effects of GA wears off (usually next morning)
- we strongly encourage mobilization and aggressive chest physio as soon as possible
(patients are at risk of sputum retention/atelectasis if they stay immobile in bed)

25
 - aids to breathing/expectoration can be given to reduce risk of atelectasis
(e.g. incentive spirometer, nebulized bronchodilators, mucolytics, steam inhalation, etc)
- ensure adequate analgesia: if not, patient mobility reduced and risk of complications increased
- patients discharged as soon as all drains off and fully mobile (often 3-5 days post-op)

Potential post-operative complications

1) Sputum retention: common; may initially present with desaturation/dyspnoea

- leads in turn to atelectasis, then pneumonia, then even ARDS and death
- can be prevented with aggressive chest physio and early mobilization
- may require urgent bronchoscopic toileting if acute
2) Cardiac complications: not very common but leads to significant morbidity. Higher risk after
pneumonectomy.
- including dysrhythmias (esp. AF), MI. Less common: heart failure, pulmonary oedema, PE.
3) Air leak: may be either from bronchial stump (bronchopleural (BP) fistula) or from lung parenchyma
- parenchymal leaks tend to stop spontaneously (esp. as residual lung fills haemohorax)
- severe air leaks from BP fistula may require re-operation
- BP fistula after a pneumonectomy is very serious and can be a life-threatening emergency
(lie patient with affected side down to prevent pleural fluid flooding into unaffected lung)
4) Bleeding / Haemothorax: re-explore if very severe
5) Pleural space infection: requires aggressive management
- may develop into life-threatening empyema
- [see below section on ‘Pleural Space Infection’]

In addition, there are two important and inevitable sequelae:

6) Pain: standard thoracotomies are very painful

- usually requires epidural/paravertebral infusion and/or PCA for first few days post-op
- poor pain control can give rise to other complications (e.g. sputum retention, shoulder stiffness)
- a minority of patients suffer persistent chronic pains after surgery which is very difficult to
treat (known as ‘Post-thoracotomy syndrome’)
7) Reduced lung function: simply as a result of removing lung tissue, pain, incision

Video Assisted Thoracic Surgery (VATS) for Lung Cancer

For many years, VATS has been used in lung cancer patients for:
- diagnosis: e.g. operative staging, lung / mediastinal biopsy
- palliation: e.g. pleurodesis, pericardial window (for malignant pleural/pericardial effusions)

Since 1993 in PWH: VATS has been used for therapeutic lobectomies and even pneumonectomies
- for selected patients: smaller tumours (<5cm), non-centrally located tumours
- Different variations of the technique include the:
- Conventional 3 port technique: 2 small camera/instrument ports + 1 ‘utility thoracotomy’ (3-5cm
long, needed for specimen retrieval)
- 2-port technique (the posterior port of the 3-port technique is eliminated)
- single port (uniportal) technique (only one small 3 to 5 cm incision is used
- lobectomy and LN surgery is done virtually same way as open technique except for smaller
wounds
- advantage of VATS: smaller incisions, and avoids rib-spreading thoracotomy and hence pain
significantly reduced (in turn giving less blood loss, shorter hospital stay and earlier return to full
ADL / work)

In PWH: ongoing studies being conducted to compare survival, post-op quality of life, and pain in
patients having single port VATS with those having traditional 3-port VATS.

Some difficulties/dilemmas/ controversies have been found regarding use of VATS in lung cancer:
- some surgeons still doubt adequacy of mediastinal LN sampling/clearance by VATS

26
 - incomplete fissures contraindicate VATS resection: conversion to open procedure required
- port site recurrence has been reported: wound protection needed when delivering specimen out
- surgeons need specific training (overseas surgeons now coming to PWH for VATS training)

In fact, over the past 2 decades, VATS resection for lung cancer has proven to be superior to open
surgery, and is now the RECOMMENDED SURGICAL APPROACH in US and UK guidelines.

27
3. VIDEO ASSISTED THORACIC SURGERY (VATS)
VATS is defined as the performing of ‘traditional’ thoracic surgery with the aid of video camera and
endoscopic instruments, avoiding the use of large painful thoracotomy and rib-spreading
- VATS is to thoracotomy what laparoscopy is to laparotomy

VATS is minimal access surgery: i.e. same basic operation, but using smaller, less traumatic wounds
(minimally invasive is another commonly used term, but is more ambiguous and tends to imply wrongly
that the basic operation is different or smaller in scale – it is usually not)

VATS is still ‘major’ surgery: performed under GA with same principles as ‘traditional’ surgery
- one lung ventilation with double lumen ET tube (allows deflation of affected lung during surgery)
- lateral decubitus position with affected side up
- operating table flexed 30 degrees to spread ribs on affected side
- typical ‘three port’ technique: 1 camera + 2 instrument ports (others include 2-port, single port)
- usually no CO2 insufflation necessary (in contrast to laparoscopy)
- bupivicaine LA applied to wounds on closing

All patient preparations, theatre set-up, instruments readied same as for open thoracotomy
- if difficulties arise, procedure can be converted to ‘open’ quickly

Advantages
- main advantage: no rib-spreading = less pain, smaller wound
- HD cameras with magnification provide excellent visualization (often even better views than
thoracotomy)
- less blood loss / less transfusion
- shorter in-hospital stay / earlier return to work
- better cosmetic result
- reduced postoperative inflammatory response (CRP, interleukin, immunochemokine etc)
- some evidence suggest better survival (in VATS resection for lung CA compared with open
procedure)

Indications
This list is not exhaustive, and shows only the more common VATS indications

Diagnostic
- biopsy or wedge resections of suspicious lung or mediastinal lesions
- investigation +/- biopsy for pleural conditions (e.g. effusions of unknown origin)
- operative staging of ca lung (e.g. pleural mets, mediastinal LN’s)

Therapeutic / palliative
- mechanical pleurodesis and bleb excision for pneumothorax
- bullectomy and Lung Volume Reduction Surgery for emphysematous/bullous disease
- drainage and decortication of empyema and loculated effusion
- drainage and clot evacuation for haemothorax
- sympathectomy for peripheral vascular disease or palmar hyperhidrosis
- excision of virtually any intrathoracic mass/ pathology:
e.g. thymectomy for MG, paraspinal neurofibroma
- pericardial window surgery
- major lung resection for CA lung [see ‘Lung Cancer’ section above]
- assistance in other thoracic surgeries (e.g. oesophagectomy, thoracic spinal surgery)
- Trauma (assessment & therapeutic – hemostasis of injured intercostal / IMA artery or suturing of
lung)

28
Relative contraindications
- excessive pleural symphyses/adhesions (e.g. from previous lung surgery)
- inability to tolerate one lung ventilation
- poor interlobar fissures in lobectomies
- surgeon’s inexperience with VATS techniques
- unstable massive trauma

29
4. BLUNT THORACIC TRAUMA
Epidemiology
20-25% of deaths due to trauma are attributed to thoracic injury
Immediate deaths: usually due to major disruption of heart or great vessels
Early deaths (within 30 minutes to 3 hours after the injury – the ‘Golden’ period)
- mainly from cardiac tamponade, airway obstruction and aspiration etc.
- two thirds of these patients reach the hospital alive and potentially can be saved
10-15% blunt chest trauma require thoracic surgery (~15-30% for penetrating injuries)
- the rest can be managed by non-surgical lifesaving management

Pathophysiology
Blunt forces applied to the chest wall cause injury by three mechanisms:
i) Rapid deceleration
- e.g. high speed motor vehicle accidents and falls from a height
ii) Direct impact
- localised fractures of the ribs, sternum or scapula
- lung injury & contusion, cardiac contusion, even valvular injury pneumothorax.
iii) Compression
- increase in venous BP in upper thorax, may give traumatic asphyxia
- may cause multiple bony fractures

These cause death and pathology in the acute phase by:

a) Respiratory insufficiency:
- pneumothorax (simple, tension, open)
- pulmonary contusion
- flail chest (note: often damage due to underlying lung contusion contribute more than paradoxical
movement)
- aspiration
b) Haemorrhage:
- haemothorax / haemomediastinum / haemopericardium
- hameorrhagic shock

Subsequently, further sequelae may develop (e.g. atelectasis/chest infections, ARDS, MODS, DIC etc)

(a) Life-threatening injuries requiring immediate treatment

“Always give priority to Airway, Breathing, Circulation !!!”

Open Pneumothorax
- if defect is large, air enters wound (since lower resistance) rather than normal airways
- patient cannot ventilate that lung hence VQ mismatch +++
- if spontaneously breathing: apply occlusive dressing then insert chest drain at different site
- if unstable: intubate and positive pressure ventilation (often surgical repair then required)

Tension Pneumothorax
- air enters the pleural space and creates increasing intrathoracic pressure
- impaired central venous return: haemodynamic instability
- mediastinum shifts to opposite side, compressing contralateral lung
=> immediately decompress (e.g. wide-bore Angiocath), then insert chest drain
- this is an emergency: do NOT wait for CXR !!

30
Massive Haemothorax
- causes shock, compromised central venous return (increased intrathoracic pressure),
lung compression (massive blood accumulation)
- diagnosis made from clinical picture and CXR
- requires placement of a large (32-36 French) chest tube for monitoring:
a. moderate haemothorax (500-1500 ml) that stops bleeding after
chest drainage may be treated by drainage alone (depending on mechanism of injury)
b. > 1500 to 2000 ml or with continued bleeding > 200 ml per hour:
emergency thoracotomy or thoracoscopy is indicated

Cardiac Tamponade
- Beck’s Triad: auscultation: muffled heart tones
hypotension (systolic-diastolic gradient <30 mmHg)
elevated central venous pressure (e.g. distended neck veins)
- CXR and echocardiography (FAST scan) helpful, pericardiocentesis diagnositic
- requires prompt Tx: resuscitate, ?pericardiocentesis, ?emergency thoracotomy

(b) Common injuries from blunt thoracic trauma

Chest Wall Injuries

Rib fractures: usually occur at the point of impact, often laterally
- also: look for possible associated sternal & costovertebral fractures
- pointed fragment may be pushed inward, tearing pleura and lung
- diagnosis: abnormal movement of ribs/fragments, ecchymosis, crepitus, hypoventilation
- CXR: identify the number and the extent of rib fractures
look for associated pneumothorax, haemothorax, pleural effusion
- conservative Mx: fairly stable in 10-15 days; callus formation after about six weeks
- but pain associated with the fracture can prevent proper ventilation and coughing,
which can lead to atelectasis and pneumonia (esp. elderly, smokers)
- intractable pain from multiple rib fractures can be treated by intercostal or
paravertebral block (call anaesthetic Pain team)
Flail Chest:
- diagnosis by physical examination & CXR (multiple #s- usually require 2 ribs and 2-point fractures in
the ribs)
-respiratory compromise by underlying lung contusion may be more significant than the compromise
from paradoxical movement
- if respiratory decompensation: intubation and ventilation
- otherwise, conservative Mx with analgesia, chest physio, early mobilisation
- rarely: stabilisation of the chest wall by external surgical fixation (titanium plates and screws)

Pneumothorax
[see below section on ‘Pneumothorax’]

Pulmonary Contusion
- potentially life-threatening: onset of symptoms is insidious
(e.g. dyspneoa, hypoxaemia, cyanosis, tachycardia, decreased or absent
breath sounds and rib fractures)
- CXR: patchy, undefined densities or homogenous consolidation
- if respiratory compromise results: needs intubation, ventilation, and antibiotic therapy

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(c) Other significant injuries

Injury to major intra-thoracic vessels (esp. aorta)

- if not diagnosed and treated (urgent surgery) many will die in a few hours
- shock and/or respiratory distress (due to large haemothorax +/- tamponade)
- CXR: haemo/pneumothorax, widened mediastinum
- CT with contrast or transoesophageal echo if haemodynamically stable
(although the traditional “gold standard” is aortic angiography, this is rarely done, because high
resolution multi-phase contract CT can provide needed information)
- if chest drain blood loss >1 litre and bleeding continues, consider urgent thoracotomy

Myocardial contusion
- associated with fractures of overlying sternum or ribs
- high index of suspicion in young, fit patient with fractured sternum
(since force to fracture sternum is great)
- Ix: ECG changes and elevation of serial cardiac enzymes, check Tnt (can mimic MI)
- may need echocardiography to confirm
- needs close observation with cardiac monitoring

Rupture of Trachea or Major Bronchi

- estimated mortality ~30%
- most occur near carina
- presents as: large pneumothorax, haemoptysis, dyspnoea, surgical emphysema
- after insertion of chest drain: continuous air leak, and suction fails to reexpand lung
- bronchoscopy should be carried out promptly when rupture is suspected
- if tear is large, respiration compromised, or persistent air leak: surgical repair via thoracotomy

Trauma to Oesophagus
- excruciating neck/chest/epigastric pain, dyspnoea, cyanosis and shock
- CXR: surgical emphysema and (hydro)pneumothorax /pneumomediastinum
- OGD visualisation is diagnostic
- early surgical closure and drainage of mediastinum is preferable

Diaphragmatic Injuries
- herniated abdominal viscera into thorax: dyspnea, chest/shoulder pain, cyanosis
- diagnosis suspected on CXR
- barium meal, ultrasound, CT or laparoscopy will confirm the diagnosis
- treatment: surgery by an abdominal approach (urgently if in distress or shock)

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5. PNEUMOTHORAX
Presence of gas within pleural space
- by losing the surface tension between pleurae, and in the confines of the thoracic cavity (ribcage),
the air thus causes lung to collapse

Classification
a) Spontaneous
i) Primary
- usually in young (teens to twenties), M> F
- thought to result from rupture of lung blebs/bullae (usually apical and congenital)
- chance of recurrence after 1st episode ~30-50% but increases after
each subsequent episode
- presents as acute dyspnoea and/or acute chest pain
(symptoms may sometimes be very minimal and diagnosis missed)
- may occur after heavy coughing or exertion, or very commonly at rest
ii) Secondary
- typically older age group
- with pre-existing lung disease e.g. COAD, malignancy, infection
(lung bullae from emphysema can be very large mimicking pneumothorax on CXR ! )
- also associated with connective tissue disease e.g. Marfan’s syndrome
b) Traumatic
- sharp penetrating injuries
- blunt injuries: rib fracture spicules can lacerate lung
c) Iatrogenic
- e.g. FNA biopsies in the chest, central line insertions

Management

Management should be considered in two steps:

1) Acute treatment
i) Small pneumothorax (<15%)
- can be managed conservatively (air may be absorbed)
- there is increasing role for percutaneous needle aspiration of air within many A&E /
respiratory guidelines, which may shorten hospital stay / observation period
- if patient is symptomatic with SOB : have low threshold for chest drain insertion
ii) Tension pneumothroax
- this is an emergency: do not wait for CXR if clinical signs suggest tension !!!
- remember: diagnosis is clinical, not radiological
- pleural defect acts as flap valve allowing air to escape into pleural space but not out
=> rapid accumulation of air in pleural space
- cardiorespiratory compromise caused by inability to ventilate compressed lung
and mediastinal shift (may distort major vessels)
- insert a large bore needle (at least 19G) into the side of pneumothroax
(typically 2nd intercostal space midclavicular line)
- then insert chest drain as soon as possible after patient more stable
iii) Chest Drainage [see below section on ‘Chest drainage’]
- indications for chest drainage in pneumothorax:
.significant lung compromise / collapse (e.g. >15%)
.symptomatic , ie SOB (irrespective of pneumo size)
.pneumothorax increasing in size
.tension pneumothorax
.primary spontaneous hemopneumothorax

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2) Definitive management [see below section on ‘Pleurodesis’]
- i.e. pleurodesis as prophylaxis against recurrence
- indications for pleurodesis in pneumothorax:
.recurrent episodes of pneumothorax
(risk of recurrence after 1st episode 30-50%, but >60% for subsequent episodes)
.tension pneumothorax or complete lung collapse on first presentation
.bilateral pneumothorax (synchronous or within 1 year of each other)
.failure of lung to reexpand after chest drainage
.persistent air leak after chest drain insertion (typically >3 days)
.special considerations (e.g. patient is airline crew)
.haemothorax associated with the spontaneous pneumothorax

Pleurodesis can be mechanical or chemical

Mechanical (i.e. VATS) preferred for young, fit patients
- surgery should be done at specialist Cardiothoracic Surgery centres only
- if VATS pleurodesis not done properly first time, and Pneumothorax recurs : redo VATS operations
for recurrent pneumothorax technically difficult, less effective and more hazardous
- hence we strongly advise that candidates for VATS be referred directly to Cardiothoracic
Surgeons at tertiary centres (and not to inexperienced surgeons)
- Postop analgesic after VATS pleruodesis surgery : NSAID should be avoided (reduces inflammation
and pleurodesis effect, may increase pneumo recurrence)

If patient not fit for GA: can consider chemical pleurodesis

- but beware: chemical pleurodesis is itself associated with a very small risk of mortality
from CP arrest, especially in elderly patients with poor GC

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6. CHEST DRAINAGE
Chest drainage is a type of surgical drain
- closed drainage system with underwater seal

Can be used with or without suction

- fluids can often be drained by gravity without suction
- pneumothorax may require suction to overcome pressure gradient to drain air
(remember: pleural pressures negative with respect to atmosphere)

Indications
Like with any other drain, a chest drain can be used to drain something from the chest, monitor
something or allow us to put something into the chest.
- drainage of air from pleural cavity (pneumothorax)
- drainage of fluid from pleural cavity (e.g. haemothorax, empyema, malignant effusion)
- after surgery to promote/maintain lung expansion (e.g. thoracic surgery)
- after multiple trauma where chest or lung injury is suspected
(e.g. if pneumothorax is a probability once patient is intubated & ventilated)
- to monitor blood loss from chest from haemothorax (from trauma or any other cause), and post-op
- chemical pleurodesis (esp talc)

Chest drain tubes

- types: with or without trocar; straight or curved (general consensus that trocar drains should be
avoided except when used by experts)
- typical sizes 16F to 36F depending on what you are draining
(e.g. 24F for pneumothorax, 32F for thick empyemas)
- last hole is on the radioopaque white line printed on drain
- numbers on drain indicate distance to last drainage hole in cm

Insertion (for housemen)

- give prophylactic analgesia: e.g. IM Pethidine 50mg prior to procedure
- typically 4th / 5th intercostal space, between anterior or mid axillary line - the ‘safety triangle’
(apical pneumothorax may require 2nd ICS, mid clavicular line)
- lie patient in lateral position on flat bed with affected side up and hand placed on top of head
(this helps spread rib spaces facilitating insertion)
- prepare aseptic field
- generous local anaesthesia to skin, rib periosteum, pleura
- always perform needle aspiration to confirm air/fluid present before proceeding to insert drain
(if in any doubt: it is safer to abandon procedure and seek help than to continue)
- 2cm incision made above and parallel to upper border of rib: cut down carefully until
subcutaneous fat seen then stop (further sharp dissection is very bloody)
- blunt dissection through muscles and pleura with artery forceps: stay near upper border of rib
- it is easy to ‘lose your tract’: can avoid this by using a pair of forceps in each hand and using
one pair to hold open the tract at any one time whilst dissecting down with other pair
(it also helps to dissect vertically down rather than going for a very oblique tract)
- once pleural space entered insert one finger to palpate & free for adhesions digitally
- insert chest drain: aim apical for air / basal for fluid (insert using trocar is now strongly discouraged)
- immediately connect to underwater seal with bottle below patient level
(lifting too high can cause fluid from water seal to rise up the tubing and even into chest)
- check for swing ( can ask pt to cough)
- anchor drain to chest wall with suture
- check all connections and dressings are correctly applied yourself before leaving
- always confirm drain position with CXR

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Warning: chest drain insertion is an invasive procedure and potentially dangerous
- always obtain informed consent
- housemen should never attempt insertion unless supervised by an experienced senior
- if any difficulty or doubt arises: stop immediately and seek help (no heroics please !)

Management

Drain Suction Systems

‘2 bottle system’ = reservoir + underwater seal
‘3 bottle system’ = reservoir + underwater seal + suction control
- all 3 ‘bottles’ actually in one box (disposable unit)

‘Leak’
- bubbling seen at the underwater seal indicates air leaking upstream from the seal
- always check drain tubing to exclude leak from loose connections, drain that has “shifted out”, or
leak at skin wound
- if these are excluded, leak must be from inside chest (e.g. lung surface, bronchopleural fistula)

‘Swing’
- water level at underwater seal should rise & fall with deep breathing and coughing
- if it fails to ‘swing’: need to exclude blocked drain, kinked drain, drain slipped out etc
- if blockage excluded: failure to ‘swing’ may be due to fully re-expanded lung,
drain inside a loculated pocket etc
- exaggerated swinging is often seen when there is still a large pneumothorax in situ

Pain
- drains in situ can be painful: ensure patient has adequate regular and/or prn analgesia
- often pain is from movement of drain at the wound: this can be reduced by ensuring a wide,
well-positioned ‘mesentery’ tape is applied

Monitoring
- after a chest drain is inserted: sudden re-expansion of lung can result in pulmonary oedema
(actually quite rare, and even rarer to be clinically significant)
.monitor SaO2 until stable
.if large effusion: do not release excessive volume too quickly
(e.g. clamp drain after ~1 litre drained then release clamps after delay e.g. 500mls q6h)
- output should be charted regularly (e.g. Q4H; more frequently after trauma/surgery)
- in-charge doctor must review drain (swinging, leaking, output etc) and CXR on daily ward round

Infection
- pleural space infection is very dangerous and difficult to treat
- always use sterile technique when manipulating drain
(e.g. when inserting/removing drain, shifting drain, infusing fluids via drain)
- drain wound should be checked regularly for infection
- if drain in situ for long time: change drain bottle at least once weekly
- if drain wound infection occurs: may need drain removal and reinsertion at different site
- chest drains should be removed as soon as their purpose has been completed

Other general considerations

- unless large air leak, we encourage mobilization with drain in situ: NO need for bed rest
(suction can be disconnected temporarily while patient walking around)
- chest physiotherapy and use of incentive spirometer (‘Triflow’) can help re-expand lung
- when patient transported: do not raise underwater seal above patient level, DO NOT clamp drain,
and DO NOT turn off the tap on the suction tube extension of the CD box)

To clamp or not to clamp – that is the question !

- old teaching: clamp drains and repeat CXR to check for air leak before removing chest drain
(if there was still a leak, CXR would show recurrent pneumothorax after clamping)
- new teaching: never clamp drain as this is potentially dangerous

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 (if there is an air leak, severe tension pneumothorax can develop while waiting for CXR)

Removal (for housemen)

- ask for assistance (e.g. from a nurse)
- prepare aseptic field
- switch off suction (never shift or remove a drain with suction on)
- place purse-string or closing stitch around wound if not already present
- release anchoring stitch
- ask patient to inhale as deeply as possible, then hold his breath, then exhale through his mouth
(why? think of the physiology !)
- at start of exhalation*, pull out drain as quickly as possible to avoid air entry through wound
(this step is the most critical: if necessary, ask an assistant to help)
- compress edges of wound firmly to allow tissue re-expansion to close the ‘hole’
- tie the wound-closing/purse-string stitch to close wound firmly
- confirm with CXR that no pneumothorax has accumulated

* (there are still controversies regarding at which point of respiratory cycle to pull out drain
- this is just one way to do it: other doctors may have other techniques)

Conditions for chest drain removal:

- when original purpose completed (e.g. effusion fully drained, pneumothorax fully resolved):
may need CXR to confirm this before removal
- no air leak for >24 hours
- fluid output <100ml/day (this is an arbitrary but widely accepted rate – controversy exists) (for post-
op patients <200ml/day is ok for removal if fluid is not too heavily blood stained)

Many (if not most) ‘recurrent’ pneumothoraces are really due to poor chest drain removal technique
- e.g. air entry while drain pulled out, poor wound closure etc
- such ‘recurrences’ may need drain re-insertion and is distressing to the patient
- housemen should treat each drain removal seriously and perform removal carefully

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7. PLEURODESIS
Aim: induce inflammation of parietal pleura, ‘gluing’ lung visceral pleura to chest wall parietal pleura
- pleural space obliterated, hence no potential space for air/fluid to collect
- the ‘scarred’ pleura is also less likely to leak or produce effusion
Remember: pleurodesis does not treat the underlying condition leading to the air/fluid collection
(e.g. the emphysema causing pneumothorax, or malignancy causing effusion)

Indications
Pneumothorax
[see above section on ‘Pneumothorax’]
Pleural Effusions
- recurrent symptomatic malignant pleural effusions
- chylothorax not resolving on conservative management
Post-operative
- after pericardial window surgery for malignant pericardial/pleural effusions (if persistent
high output)
- prophylactically on discovery of pleural metastases during thoracic surgery
- in persistent air leaks post-op

Parapneumonic effusions and pleural empyemas are a contra-indication to pleurodesis

- these require prompt drainage +/- surgical decortication [see ‘Pleural Space Infection’ section]
- any attempt to give pleurodesis may make drainage/decortication difficult or impossible
(causes multiple loculations of exudative, infected fluid), and worsen the infection
- hence should exclude pleural infection (e.g. by pleural fluid Gram stain/ CST) before giving
pleurodesis
Adhesions from pleurodesis can be dense & extensive: subsequent chest surgery would be very difficult
- carefully consider if pleurodesis is truly necessary in any patients who may need subsequent
chest surgery before proceeding

Types
a) Chemical Pleurodesis
- preferred for malignant effusions and patients unfit for surgery (e.g. severe COAD, elderly)
- sometimes used to stop air leaks in post-op patients
- chest drainage, then apply sclerosing agent via drain when lung re-expanded
- many types of sclerosing agent are used : e.g. talc powder; tetracycline; bleomycin
- there may be risk of provoking CP arrest in elderly or very ill patients with poor GC, therefore a
safer agent such as autologous blood should be considered.

b) Mechanical Pleurodesis
- now preferred for all pneumothorax patients who can undergo surgery
- much lower recurrence rates than chemical pleurodesis but more major procedure
(recurrence rates for pneumothorax after VATS pleurodesis typically <5%)
- virtually all done by VATS nowadays (traditionally by open thoracotomy):
. lung bleb(s) identified, stapled, resected
. mechanical abrasion to parietal pleura to induce pleurodesis
- some center’s perform pleurectomy (peeling away of parietal pleura) instead of abrasion

Regardless of which type of pleurodesis used: lung must be kept fully expanded following the procedure
for the fibrinous exudate and blood on the pleura to achieve the pleurodesis effect.
- chest drain inserted/kept in situ & keep suction on drain and encourage deep breathing by patient

Drain can be removed usually when lung has been fully re-expanded for 48 hours, and
with no air leak, drain output not excessive (<200ml/day) via the chest drain in last 24 hours

Note: induced inflammation is often painful

- chemical pleurodesis usually given in mixture with a local anaesthetic
- adequate analgesia should always be ensured afterwards

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8. PLEURAL SPACE INFECTIONS

Common causes:
i) underlying chest infection (most common)*
ii) following thoracic surgery or invasive thoracic procedure (e.g. pleural tap, FNA)
- less common causes include prolonged chest drainage (ascending drain infection), trauma,
mediastinal or subdiaphragmatic infection (e.g. subdiaphragmatic abscess) etc

Typical natural history starts with initial pleural space infection by one of the above causes
- exudative pleural effusion is produced by the inflamed lung
- initially this is clear and sterile and known as a ‘Parapneumonic (Pleural) Effusion’
- if the fluid becomes infected, it may become purulent: ‘Empyema thoracis’
- fibrous septae form giving rise to ‘loculation’ of the effusion/empyema
- as inflammation progresses, a layer of fibrous pleural ‘peel’ is deposited on the lung
- after 3-4 weeks: the peel becomes firm ‘entrapping’ the lung and preventing re-expansion

If left undrained, a parapneumonic effusion or empyema can lead to consequences, most notably:
i) chronicity and even further progression of the sepsis
ii) entrapped lung with resulting decreased lung function
iii) persisting pleural air/fluid space which may later become (re)infected
iv) peel itself may be a ‘reservoir’ of micro-organisms that can give recurrent infections (e.g. TB)

Management

Pneumonia related pleural space infections are usually first managed by chest physicians
- CT Surgeons can collaborate in management of parapneumonic effusions and/or empyema

We strongly advocate that should a parapneumonic effusion/empyema develop, the patient should be
referred to a CT Surgeon early for consideration of surgery
- any delay in surgery (e.g. 2 weeks or more after effusion first seen) may result in very dense
peel and adhesions in the pleural space, making surgery technically much more difficult and
hazardous, with reduced chance of complete evacuation of infected material

Treatment algorithms vary & controversies still exist (e.g. persist with (repeated) drainage or go for early
surgery ?)
- hence, the below simply lists some of the options available to clinicians:

1) Aggressive medical management of underlying infection

- using combination of antibiotics (according to sensitivities if available), chest physiotherapy etc
- aim to prevent progression of pleural disease and treat underlying cause

2) Thoracocentesis (pleural tapping)

- useful for differentiating between different types of effusion
(e.g. transudate vs exudate, infective vs malignant, chylothorax etc)
- in loculated effusions: may require guidance by imaging (e.g. ultrasound)

3) Chest drainage (options include pigtail, Seldinger drains, formal Chest drains)
- using large-bore drains, usually with relatively high suction achieve best results
- effective if effusion is free, and source of infection (e.g. pneumonia) controlled
- if effusion fails to completely drain away, suspect loculation
=> will need ultrasound or CT to define loculations
- imaging-guided drain insertion may be possible/necessary for loculated effusions
- in some cases where dense peel formation has set in, fibrinolytic agents (e.g. Streptokinase)
can be infused via chest drain to breakdown the peel/septae
- in the past, when condition stabilized, can convert to open drainage via empyema tube or
percutaneous window for longer-term management of chronic empyemas (e.g. TB) but
this is nowadays seldom required, especially with more aggressive surgical therapy

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4) Surgical drainage and/or decortication
- aim: evacuate infected material and allow re-expansion of entrapped lung
- can be done via thoracotomy or VATS (we now regularly perform the latter)
- all septae are broken down and all loculations drained
- decortication: fibrous peel is removed off the entire lung surface, ‘releasing’ it from entrapment
and allowing full lung re-expansion under direct vision. At the same time some of the thicken cortex
on parietal pleura is also removed.

5) Thoracoplasty and airspace filling procedures

- despite all above measures, sometimes a large residual pleural airspace persists
- if problematic (e.g. recurrent pleural space infections or impaired breathing mechanics)
the space should be surgically reduced
- thoracoplasty: resection of several ribs to collapse chest wall, reducing dead space size
- airspace can also be ‘filled’ with a surgical flap (e.g. latissimus dorsi muscle flap)

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FURTHER READING
This student handbook is not a textbook of everything you need to know, nor do you have to know
everything in this handbook! You should add your own notes to it to make it more useful to you in your
own revision.

Cardiothoracic Surgery is a large, complex specialty, so it is not realistic to read exhaustively on the subject
in the little time you have. For your exams, you will need a solid understanding of the basic principles
behind the investigations, monitoring and indications for surgical management for chest diseases: this
should guide what and how much you read. Do not try to learn excessive details.

Recommended for medical students:

1. ‘Minimal Access Cardiothoracic Surgery’ by Yim et al
- focuses on minimal access surgery, but comprehensively covers all the basics of
CT Surgery with an easy-to-read, attractively illustrated style
- one of the best and most up-to-date reference books available: highlighting modern
controversies and different approaches to surgery in this field
2. ‘Essential Surgery’ by Burkitt, Quick & Gatt (2nd Edition):
- the chapter on Cardiothoracic Surgery is simple to understand and well illustrated
- about the right depth of knowledge needed for medical students: highly recommended
3. ‘Bailey & Love’
- the chapters on Thoracic & Cardiac surgery are detailed and a good foundation
4. ‘Essential Surgical Practice’ by A.Cuschieri
- very detailed and well presented chapters (but probably more than you need to know)

For reference only: ‘Thoracic Surgery’ by Pearson

‘Cardiac Surgery’ by Kirklin
- definitely excessive detail for students, but these are the ‘bibles’ of CT Surgery if you want to
read up more about any specific points

Review articles in Journals (we recommend Annals of Thoracic Surgery, Journal of Thoracic and
Cardiovascular Surgery, Chest, European Journal of Cardiothoracic Surgery)
- for the most up-to-date news & views
- but of course too excessive for your exams

Students are strongly advised to make full use of the Dept of Surgery Intranet
 all CT Surgery Grand Round slides and many useful Teaching Notes will be uploaded there

Remember: Cardiothoracic Surgery is better learnt from the ward and from teaching by seniors - spend
more time on the ward instead of just ploughing through textbooks!

Above all, enjoy your attachment with Cardiothoracic Surgery!

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