CPB 101. Anterograde, Retrograde and Integrated Cerebral Perfusion

Anterograde, Retrograde and Integrated Cerebral Perfusion

Antegrade Cerebral Perfusion

Antegrade perfusion of the brain through cannulae inserted in the innominate (or more distally in the right common carotid artery) and left common carotid artery provides the most physiologic and efficient perfusion of the brain. Perfusate temperature is usually set at 18°C and flow is set between 10 and 20 mL/kg/min or adjusted to maintain a pressure between 40 and 50 mm Hg in the right radial artery. Clinical results, especially regarding swift recovery of cerebral function, have been outstanding with this method of perfusion. The necessity to cannulate relatively small and often diseased arch arteries and the presence of additional cannulae in the operating field constitute the main drawbacks of the technique. Cannulation of the common carotid arteries can result in dissection of the arterial wall and embolism of atheromatous plaque material or air. Furthermore, the flow in the artery is dependent on proper positioning of the tip of the cannula within the vessel. For these reasons, many surgeons rely on a unilateral perfusion of the brain, with the sole cannulation and perfusion of the right subclavian artery. The right vertebral and right common carotid artery territories are perfused in an antegrade fashion. The blood reaches the left cerebral hemisphere through the circle of Willis and, to a lesser extent, through cervicofacial connections. It is, therefore, important that the left common carotid and left subclavian arteries be occluded to avoid a steal of blood down these arteries. Occlusion (usually with an inflatable balloon) of the descending aorta is also a useful maneuver to improve overall body perfusion. Effective somatic perfusion (including the abdominal organs, spinal cord, and lower limb musculature) has been documented with this maneuver.

The presence of an aberrant right subclavian artery (also called arteria lusoria) is obviously a contraindication to the use of this perfusion method. The aberrant origin of the artery is usually readily identified by computed tomography or magnetic resonance. The burst of blood from the descending aorta during the opening of the aortic arch should alert the surgeon to this anatomic variation, and prompt a direct cannulation of the ostium of the right and left common carotid arteries.

Sequential perfusion of the cerebral arteries provides additional safety to unilateral cerebral perfusion, and avoids cannulation of small or diseased arch arteries. The right subclavian artery remains perfused during the whole procedure. A vascular graft is immediately sewn on a common patch of aortic wall including all the arch vessels, or the second branch of a multiple-arm prosthesis is anastomosed to the left common carotid artery. Perfusion is then instituted through this additional graft and enhances, after a short period of time, cerebral perfusion. 

 
Retrograde Cerebral Perfusion

The value of retrograde cerebral perfusion in protecting the human brain has still not been clearly elucidated. No animal model truly replicates the complex anatomy and physiology of the human brain, and none allows a fine neuropsychologic evaluation. Conflicting results and conclusions in clinical and experimental studies have, therefore, been reported. Accepted facts include a deep and homogenous cooling of the brain hemispheres (the cooling scalp effect) and the expulsion of solid particles or gaseous bubbles from the arch arteries. Controversies surround the possible nutritive value of retrograde perfusion. The nutritive value has been demonstrated in rabbits but not in dogs, pigs, or baboons. In humans, signs of cerebral perfusion and oxygen uptake have been documented, but the amount of perfusate providing cerebral nutrition is low, corresponding to about 5% of total retrograde flow. The blood delivered in the superior vena cava flows preferentially in the low-pressure inferior vena cava, via the azygos system, the perivertebral venous plexus, and the thoracic wall veins. Even within the brain, the distribution of retrograde flow is uneven, with a preferential distribution in the sagittal sinus and hemispheric veins. The large steal of blood to the inferior venous territory is corroborated by the clinical finding of an extremely small proportion of perfused blood flowing out of the arch arteries. Occlusion of the inferior vena cava to decrease the pressure gradient between the two venous territories effectively reduces the amount of stolen blood, but increases the sequestration of fluid in the interstitial tissue. Interstitial edema is another potential problem of retrograde perfusion, which can lead to cerebral edema and hypertension, particularly when the perfusion pressure exceeds 25 mm Hg. Finally, the finding that the human jugular system may contain competent valves casts definitive doubts regarding the reliability of retrograde cerebral perfusion.

Clinical series, however, have reported encouraging results. A reduction in both mortality and incidence of neurologic damage has been regularly documented with the adjunctive use of retrograde cerebral perfusion to classical hypothermia. Some studies confirmed the limited capacity of retrograde perfusion to sustain cerebral metabolism, and stressed the fact that the occurrence of neurologic damage was only delayed. Indeed, the risk rises sharply after 60 minutes of deep hypothermic circulatory arrest, perhaps at the extinction of intracellular energy substrates. If most surgeons acknowledge the capacity of retrograde cerebral perfusion to prolong the period of safe circulatory arrest, they consider the method a valuable but not an alternative adjunct to conventional methods when long periods of circulatory arrest are contemplated. 

Integrated Perfusion

Probably the safest approach to a patient requiring a long period of circulatory arrest resides in the integration of complementary methods of perfusion and monitoring. Retrograde perfusion of the aorta through the femoral artery should be avoided in the presence of a thoracic aortic aneurysm in order to reduce the risk of particulate dislodgment with embolization in the brain and myocardium. Antegrade perfusion of the aorta is performed with cannulation of the ascending aorta or right subclavian artery. The body is cooled to 18°C. Electroencephalogram and venous jugular saturation are monitored to ensure adequate reduction of cerebral metabolism. Circulatory arrest is established only after electrocerebral silence is obtained and jugular venous saturation is superior to 95%. During the 10 to 20 minutes preceding circulatory arrest, the temperature of the perfusate can be lowered to 13°C to further reduce brain temperature and metabolism. The arch arteries are connected to a graft (either with the use of a patch of aortic wall or separately), and antegrade perfusion of the brain is resumed before more extensive resection and repair of the aorta is performed. When the risk of particle embolization to the brain is substantial (old age, severe atherosclerosis of the aorta, arch aneurysm with thrombotic material), a short period of retrograde cerebral perfusion can be performed to wash out the arch arteries before antegrade perfusion is definitively reestablished.

Residency in Cardiothoracic and Vascular Surgery: My viewpoint

Obstacles Faced by the Resident 

I have recently completed my cardiothoracic and vascular surgery (CTVS) residency. It not only taught me the techniques and art of surgery but also enriched me spiritually. There are many things which I think can make our training programmes highly successful and beneficial. We as residents should learn to take maximum benefit from our residency, as this prepares the foundation on which our future will be built. The details of an ideal resident training programme will always be debated, and it’s not always possible to achieve the ideal. Residents will continue to expect many things from their course of instruction, and the demands of residency training will continue to create obstacles.

Various hurdles and obstacles may arise in our lives; these may hinder our path of training. Most of them are either in the form of health and family related issues or at times various aspects of the hard and rigorous training which test the resident’s psychological strength. From time to time residents may develop negative thoughts about the decision to become a Cardiothoracic Surgeon.

We should learn to minimize the loss and distraction that these situations inflict on our learning and career. There are many ways of doing so. Exercise is one of the best ways to shed one’s worries and increase physical and psychological strength.





The meals should be taken in a relaxed atmosphere whenever possible, not just to push in something for the sake of filling our stomach. If we can be careful about the protection of our patients’ myocardium, why cannot we practice protection of our own stomach and myocardium?

Nothing is more relaxing than a good sound sleep. Deprivation of sleep is a big enemy for all residents, but it is the call of the duty that keeps us awake for long hours. Resting areas in the hospital should be comfortable and peaceful, so that even a short nap is refreshing. Residents should try to have a good sound sleep the night before their call day.

Almost all of us have one or another hobby, but most of us are not able to pursue it. Some time should be set aside in our busy routine for hobbies. They have a very good relaxing and refreshing effect.

Another way of relieving stress is socializing together, going out for a dinner or picnic. Departments should have their own protocol for such get-togethers at least once a month. Apart from cementing the unity between team members, these occasions also let everyone know each other in a relaxed atmosphere. Such get-togethers don’t lead to loss of working hours; rather they increase the productivity of the team members.




Music at the working place has been proven to improve the atmosphere. Lots of musical compositions which suit such places are available and should be played.

Reading popular books or magazines on technology of today such ad ipad, windows, blackberry  and many others written on related issues especiali sport (martial art is my favorit)  have a very positive impact on our thinking and behavior.

Last but not least a supportive family is of great assistance in helping us to become a Cardiothoracic surgeon. Their contribution is no less than anyone else is because they sacrifice a lot to enable us to remain busy during our training and throughout our career.



During residency which is difficult, demanding and exhausting, when the hours are long and days unpredictable, many times a negative thought comes into our mind. One might question why I chose this endeavor. But then thinking about the challenges, excitement, and rewards that lie ahead will help remind you that the choice was correct.

Rewards are immeasurable after the hard work of residency. The future is full of opportunities in our specialty, we have to recognize and seize them. Many life saving opportunities that this profession provides are very gratifying.

Cardiothoracic surgeons are frequently given special respect. They are almost uniformly considered leaders among the surgical specialties. Heading a team of skilled healthcare providers of many types is satisfying and stimulating. We should be proud that we will be trusted and called upon to treat some of the sickest patients with the most complex problems in the hospital. We will be dealing with the most vibrant and dynamic organ, i.e., the heart. It will be our privilege to touch and mend the heart, to work inside its chambers and restore the health of a gravely ill patient. 
It is an honor which few people ever get to experience. 
The joys of being a Cardiothoracic and Vascular Surgeon will certainly greatly outweigh the frustrations and irritations that lie in the path of becoming one.

Ideas about an ideal CTVS residency programme will remain different and will continue to be debated at various levels. Nevertheless, training residents with the best and latest knowledge in an environment which is cordial, friendly, disciplined and honest, is essential. We as residents should try to make our learning as productive as possible. Frustrations should not be allowed to creep in. The whole idea of residency training should be not only to produce the best of surgeons but also the best of ‘humane’ surgeons. Let us all work together to accomplish this goal.

 

I will always be extremely grateful and thankfull to all my teachers who have always taught me the art and science of this specialty and encouraged me to realize my dreams. Many thanks to my great parents, sweet and caring wife and son, wonderful friends and colleagues, family members and all the staff of  the hospital who supported and loved me all throughout my CTVS residency.

Avoiding Pitfalls: “do not stumble over the same stone, learn from the experts"

European Cardiothoracic Residents' Meeting 2010

Avoiding Pitfalls: “do not stumble over the same stone, learn from the experts"

24th EACTS Annual Meeting
Palexpo Centre Geneva, Switzerland
Monday, 13 September 2010, 15:30-16:30
Residents’ Meeting Room E

Organisers	Surgical Training and Manpower Committee
Chairmen	Dr. Peyman Sardari Nia, Nieuwegein, Netherlands Dr. J Rafael Sádaba, Pamplona, Spain
Moderators	P. Sardari Nia, Antwerp; M. Siepe, Freiburg
Program 15:30 Adult cardiac surgery Complications: from present to prevent A. Brutel de la Riviere, Amsterdam 15:45 Thoracic surgery How not to do it: mistakes I have made and that you can avoid D. Wood, Seattle 16:00 Vascular surgery Pitfalls in thoracic and thoracoabdominal aortic aneurysm surgery M. Schepens, Brugge 16:15 Congenital cardiac surgery Pitfalls in operative techniques of congenital cardiac surgery V. Tsang, London Following the meeting residents are cordially invited to a dinner. The dinner is by invitation only, which will be allocated on a first-come, first-served basis.

Hemorrhage and Thrombosis

Hemorrhage and Thrombosis

COAGULATION BASICS

1. Overview

A. Primary hemostasis

1) Platelet (a) adhesion, (b) activation, (c) aggregation

B. Secondary hemostasis

1) Activation of plasma coagulation (form fibrin)

a) Extrinsic pathway (via tissue factor)

b) Intrinsic pathway (subendothelium or foreign contact)

c) Common pathway

2) Inhibition of systemic clotting

a) Natural anticoagulants (AT III, Protein C & S)

b) Fibrinolytic system, i.e. Plasmin (degrades fibrin(ogen))

C. Other reactions

1) Complement activation (increased permeability, cell lysis)

2) Kinin generation (vascular dilation, increased permeability)

2. Platelet Function

A. Contact

1) With subendothelium after endothelial injury

2) With proteins adsorbed onto synthetic surfaces

B. Adhesion

1) Via attachment mechanisms i.e. Glycoprotein Ib/IX

2) (GP Ib/IX) receptor

C. Activation

1) Begins as platelets spread with a conformational change

2) Release TxA2, ADP, serotonin, (PF4, BTG)

D. Aggregation

1) ADP induced change in GpIIb/IIIa receptor permits binding of adhesive proteins, like fibrinogen, between platelets

PHARMACOLOGY

3. Anticoagulants

A. Heparin

1) Glycosaminoglycan, MW 3K - 100K

2) Acts by binding enzyme AT III

a) (AT III inhib's IIa,Xa,IXa,XIa,XIIa)

3) Half life is 60-90 minutes

4) Monitored with aPTT or ACT

5) Complications: bleeding; HIT => thrombosis, "white clot"

6) (Ab versus Hep-PF4 complex); osteoporosis

4. Alternatives to heparin (future)

A. Hirudin (Hirulog, synthetic analog)

1) From leeches, direct inhibitor of thrombin

2) Does not require ATIII

3) Prolongs TT, aPTT, PT, and ACT

B. Ancrod

1) From venom of Malayan pit viper

C. Others

5. Warfarin

A. Acts as Vitamin K antagonist

1) (Vitamin K required for Fx II, VI, IX, X; Prot C,S)

B. Half-life is 36 to 42 hours

C. Monitored w/ INR = Pt. PT / Control PT

D. Reversed w/FFP (immediate); Vit K (8-24 hrs)

E. Complications

1) Bleeding, skin necrosis (Protein C & S deficiency), fetal abnormalities

6. Antiplatelet Agents

A. Aspirin

1) Inhibits cyclo oxygenase (rate-limiting enzyme for PG's)

a) Reduces TxA2 from platelets (causes aggregation)

b) (Low dose inhibits Plt cyclo oxygenase but not endothelium)

2) Irreversible inhibition for Plt lifetime (7-10 days)

B. Ticlopidine (ASA substitute)

1) Blocks fibrin-GpIIb/IIIa interaction

2) Onset slow, 2-3 days

C. Dipyridamole

1) Inhibits Plt adhesion

D. IV Dextran (40 - MW 40,000 daltons)

1) Decreases Plt-vascular endothelial interaction

2) Decreases von Willebrand factor

7. Hemostatic Agents

A. Protamine

1) Basic protein, binds heparin

2) 1 mg protamine = 100 U heparin

3) Adverse reactions

a) Transient systemic hypotension

(1) Related to infusion rate, total dose

b) Anaphylaxis - pulmonary hypertension, systemic hypotension, bradycardia

(1) (Risk factors - prior exposure, DM's/NPH)

8. Aprotinin

A. Mechanism: proteolytic enzyme inhibitor

1) Inhibits fibrinolysis, kinin activation, platelet activation

B. Benefits

1) Decreased blood loss, decreased systemic response to CPB

C. Risks

1) Prothrombotic effects, renal failure (?)

2) Anaphylaxis with re-exposure (cutaneous testing, predose)

D. Usage guidelines

1) Patient risk should influence use - high risk patients (reoperations, long procedures, coagulopathy, need to avoid transfusions)

2) ACT monitoring

E. Other agents

1) Amicar (Epsilon-amino caproic acid)

2) Desmopressin (DDAVP)

ANTICOAGULATION FOR CPB

9. Heparin

A. Standard initial dose = 300 U/kg

B. Maintain ACT > 300-350 (>300?)

C. Monitor with ACT

1) (or direct Heparin concentrations)

D. Redose to maintain therapeutic level

1) 100 U/kg every 60 - 90 minutes (approx.)

2) Use dose-response curve

E. Protamine for heparin reversal

1) Estimate heparin present (dose response curve)

2) Give 1.1 - 1.5 mg protamine : 100 U heparin

3) Confirm reversal to baseline

HEMOSTASIS WITH CPB

10. Basic Considerations with Cardiopulmonary Bypass (CPB)

A. Cardiopulmonary bypass leads to:

1) Activation of clotting cascades

2) Activation of fibrinolytic system

3) Platelet activation and removal

4) Kinin system activation

5) Complement activation

B. Results in hemostatic derangement

C. Results in systemic inflammatory responses

11. Blood Conservation Options

A. Cell saver recycling

B. Hemoconcentration of excess CPB blood

C. Reinfusion of shed blood from chest tubes

1) (Consider time, volume, infection hazard)

D. Prevention/reversal of bleeding diathesis

1) Optimization of heparin/protamine use

2) Autologous plasma, fresh whole blood

3) Aprotinin (Trasylol)

4) Epsilon-amino caproic acid (Amicar)

E. Heparinzed CPB circuits

1) More biocompatable, more thrombo resistant

D. Autologous blood donations (with erythropoietin)

HEMORRHAGE

12. Post-CPB

A. Consider

1) Surgical bleeding

2) Heparin excess

a) Incomplete neutralization; reinfusion of anticoagulated blood; heparin rebound

3) Clotting cascade procoagulant deficiency

5) Platelet dysfunction or thrombocytopenia

4) DIC, depleted fibrinogen (preop thrombolytics)

B. Exploration (< 3 - 5%)

1) >500/h x1 hr; >400/hr x 2 hrs; >300/hr x 3 hrs;

2) >1000 total in 4 hrs; >1200 total in 5 hrs

THROMBOSIS

13. CABG Graft Patency

A. Vein patency rate = 75-90% at 1 year

B. Technique is important

1) Avoid endothelial injury

C. Antiplatelet therapy

1) ASA, before or within POD 1 to > 1 year

2) Ticlopidine if allergic to ASA, or with coronary endarterectomy

3) Persantine, likely adds nothing

14. Prosthetic Valves

A. Mechanical valves

1) T-E rate = 2 - 4% per patient-year

2) Coumadin, INR=2.5-3.5, any position

a) (ACCP/NHLBI consensus opinion)

b) Bleeding complication rate = 2-3% per patient-year

3) Adding anti-platelet drug => decreased T-E, increased bleeding

a) Reserved for T-E despite therapeutic coumadin

3) Bioprosthetic valves

a) T-E: greatest 6-12 wks post-op then 2% per patient-year

b) Coumadin, INR=2-3 x 3 months (Opt for AVR)

c) With large, LA, LA clot, prior CVA - extend x 3-12 mos

4) Valve thrombosis

a) Thrombolytics emerging as front-line therapy

15. CAD

A. Acute MI

1) Heparin => decreased LV thrombus/embolism

a) Especially large (anterior) MI's, LV dysfunction

2) Coumadin - possibly beneficial

B. Unstable angina

1) Heparin + ASA

THROMBOSIS - DVT

16. General

A. Risk factors (Virchow's triad)

1) Stasis - immobility, surgery, CHF/atrial fibrillation, obesity

2) Hypercoagulable states, BCP's, malignancy

3) Vein injury

B. 48% incidence after CABG

C. Prophylaxis

1) Mechanical, SQ Heparin

2) (ASA, Persantine - ineffective)

17. Therapy

A. Distal DVT - low risk for pulmonary embolism

B. Proximal DVT - Anticoagulate

1) Heparin => Warfarin (INR 2-3) x 3-6 mos

2) IVC filter if anticoagulation contraindicated or ineffective

PULMONARY EMBOLISM

18. Incidence

A. 630,000/year with 200,000 deaths/year

B. Origin

1) DVT (above calf), tumor, foreign body

C. Pathophysiology

!) Combination of mechanical and reflex effects

2) Cardiodynamic effects, cyanosis, pulmonary vasoconstriction

D. Pathologic sequelae

1) Most resolve spontaneously

2) May lead to pulmonary infarction

19. Diagnosis of Pulmonary Embolism

A. Clinical

1) SOB, tachycardia, increased P2

2) Classic hemoptysis, pleural rub, S3/4, cyanosis - 1/4 of patients

3) Signs & symptoms of DVT - 1/3 of patients

B. Examinations

1) CxR: normal +/- decreased vascularity (Westermark's sign)

2) ECG: dysrhythmia, ST depression, T-inversion (III,AVF,V1,V4-5)

3) V:Q scanning

4) Pulmonary arteriography

20. Management

A. Anticoagulation

1) Heparin x 8-10 days (until DVT adherent)

2) Coumadin x 6 weeks-6 months

B. Thrombolytic therapy

C. Percutaneous extraction

D. Surgical management

1) IVC Interruption

a) Anticoag contraindicated, recurrent pulmonary emboli on anticoagulation, multiple small pulmonary emboli, pulmonary hypertension, after pulmonary embolectomy

E. Pulmonary embolectomy

1) Indications: persistent hypotension, hypoxia despite medical Rx

PULMONARY EMBOLECTOMY

21. Indication for operation

A. Hypotension, hypoxia, despite medical therapy (O2, anticoagulation, inotropes)

B. Operation

1) Median sternotomy, cardiopulmonary bypass, bicaval cannulation, pulmonary artery exploration, lung compression

C. Results

1) 25% mortality (major cause - cardiac complications)

EXTENDED OUTLINE

Hemorrhagic and Thrombotic Complications of Cardiac Surgery

1. History

A. 1953 - Gibbon - -first use of CPB for open heart surgery in a human - screen oxygenator

B. Early screen, bubble, and disc oxygenators were traumatic to blood à frequent bleeding diatheses

2. Pre-op hemotsatic disorders

A. Personal/family history and PE are most important tools for identifying a bleeding diathesis

B. Hereditary bleeding disorders

1) Hemophilia

a) X-linked recessive

b) A = Factor VIII deficiency - tx= factor VIII concentrates

c) B = Factor IX deficiency - tx=prothrombin complex or FIX

d) Factor XI - less common

e) aPTT prolonged, PT, platelet (plt) fxn, bleeding time (BT) are normal

2) von Willebrand’s Disease

a) Most common inherited bleeding disorder

b) von Willebrand’s factor stabilizes FVII essential for plt fxn

c) Mucocutaneous bleeding and bruising

d) Prolonged bleeding time, impaired plt aggregation to ristocetin

e) Frequently a prolonged aPTT

3) Treatment

a) A (FVIII deficiency )-FVIII concentrates

b) B (FIX deficiency) - prothrombin complex or FIX

c) Emergency - FFP or cryoprecipitate (for FVIII or vWf deficiency)

4) “Acquired hemophilia” - autoantibodies to FVIII

C. Acquired bleeding disorders

1) Plt dysfunction 2° to abnormal heart valves or assist devices

a) BT helpful

b) Plt transfusions will only be transiently helpful

c) Plt transfusion after discontinuation of CPB

2) Congenital cyanotic ht dz

a) Impaired plt aggregation in 14% in acyanotic CHD, 38% cyanotic

b) More profound with ­ hypoxemia and hemoconcentration

c) Hepatic synthesis of clotting factors may be impaired

d) Phlebotomy and hemodilution to Hct 50-60% improves plt number and fxn

3) Drugs

a) Most common cause of impaired hemostasis in cardiac surgery

b) Anticoagulants

(1) Coumadin - hold for 1-2d pre-op, give Vit K or FFP

(2) Heparin - response may vary after pre-op heparin

c) Drugs that affect plts

(1) ASA

(a) Increases post-op blood loss

(b) D/C 5-7days pre-op

(c) Prolonged BT - correct w/8-12U plts

d) Fibrinolytics

(1) tPA, urokinase, streptokinase

(2) Can reduce fibrinogen levels below safe (100mg/dl)

(3) FDP’s interfere w/plt fxn

(4) Heparin can compound the effect

4) Renal, hepatic failure and disseminated intravascular coagulopathy (DIC)

a) Uremia

(1) Defect in plt fxn due to plasma factors and anemia

(2) vWf-plt interacions impaired

(3) Plt transfusions ineffective due to uremic plasma

(4) Tx= correct anemia, dialysis, cryo (for vWf), DDAVP

b) Hepatic insufficiency

(1) Impaired synthesis of clotting factors (esp. vit K dependent - II,VII,IX,X)

(2) Tx= vit K if PT prolonged, plts if thrombocytopenic

3. Effects of cardiopulmonary bypass on hemostasis

A. Initial events of blood-surface interactions

1) Adsorption of fibrinogen and other plasma proteins to foreign surface is initial event

2) Contact activation of factor XII (intrinsic pathway)

3) Platelet adherence, release of cytoplasmic granules, thromboxane A-2

4) Contact activation initiates complement cascade and kallikrein/kinin system

5) Decreased velocity from hemodilution may ß damage to formed elements in blood, ß net blood loss, improve capillary perfusion

6) Frothing, high shear rates, and turbulence in pump damage formed elements àhemolysis, plt activation

7) Bubble oxygenator (blood-gas)contributes significantly to impaired hemostasis after 2-3 h. total bypass time

8) Intracardiac suction, “pump sucker”

B. Dynamics of plasma coagulation during CPB

1) Significant amounts of plasma proteins are not lost in extracorporeal circuit

2) Though diluted (£50%), clotting factor levels remain adequate

3) Prolonged clotting times post-op correlate poorly w/bleeding

4) Fibrinolysis

a) ??responsible for derangements of clotting tests early post-op

b) Activated plasmin degrades fibrin and fibrinigen

c) FDP’s act as anticoagulants

d) Aprotinin (see below)

C. Platelet dynamics during CPB

1) Number

a) ¯ to 40-50% baseline in 1st 10-15 min, then stabilizes

(1) “Passivation” of foreign surfaces after initial exposure

(2) Reduced plt adhesiveness

b) Rarely < 75,000/mL

c) Plt ct returns to normal 3-5d post-op (?sequestration in liver)

d) Microembolus formation contributes to platelet consumption

2) Function - substantially altered

a) Plasma levels of Tx A2, plt-specific proteins rise at onset of CPB

b) Plt stores of ADP & ATP depleted

c) Fxn returns to normal 3-5d post-op

d) Clot retraction impaired by heparin

(1) High concentrations of heparin impair vWf-platelet binding

(2) Reduction in clot retraction correlates w/post-op bleeding

e) Hypothermia, plasmin, other proteases

f) Neutrophil activation by surface glycoprotein (GMP-140 or P-selectin)

g) Attempts to inhibit plt activation during CPB (ASA, dextran) à excessive hemorrhage

4. Conduct of cardiopulmonary bypass

A. Heparin

1) Heterogenous family of glycosaminoglycans, not protein (6,000-20,000 dalton)

2) Accelerates by 2,500-fold the neutralization of thrombin by antithrombin III (ATIII)

3) Affects factors IX, X, XI, XII, activation of heparin Cofactor II, inhibition of smooth muscle proliferation, cytoprotective

4) Source of heparin (porcine gut mucosa or bovine lung) has little effect on anticoagulation, but long-term bovine lung heparin more frequently associated w/HIT

5) Platelet factor 4 is an anti-heparin compound

6) Monitoring

a) ACT or equivalent whole-blood clotting time at least q1h - maintain 300-350 sec

7) Heparin rebound - coagulopathy and increased clotting times

a) Pathogenesis not understood - ?protein-bound heparin unavailable to protamine

b) Tx=protamine

c) FFP will not reverse effects of residual heparin

B. Protamine- the sole effective heparin antidote

1) Small, highly positively charged protein, binds heparin

2) Derived from fish sperm

3) 1mg protamine /100U heparin (0.6-0.7 per Dr. Hurst)

4) Toxicity

a) Excess can have anticoagulant effect - overrated

b) Myocardial depression

c) Vasodilitation

5) Heparin-protamine complexes - mediators of inflammation and anaphylaxis - granulocytopenia, pulm sequestration of leukocytes, vasodilitation

6) Allergic reaction (rare) - pulm edema, hypoxia, hypotension more common in DM exposed to NPH

5. Perioperative adjuncts to hemostasis and blood conservation

A. Intra-op (topical agents)

1) Bovine thrombin - platelet activation and direct fibrinogen clotting-neutral pH

2) Oxidized cellulose(Surgicell) - contact activation of coagulation cascade - surface for fibrin polymerization

3) Microcrystalline bovine collagen (Avitene, Instat)-plt activation and adhesion

4) Hemostatic glues

a) Cyanoacrylate

b) Fibrin glue=cryo (for fibrinogen)+bovine thrombin

B. Autotransfusion

1) Pre-op phlebotomy and reinfusion post-bypass

2) Cellsaver - washes red cells (no plts or clotting factors)

3) Shed mediastinal blood - no study has shown reduction in use of banked, homologous blood

C. DDAVP

1) Vasopressin analog

2) Transiently increases vWf and FVIII

3) Probably only useful w/impaired vWf-dependent hemostasis (low vWf, drugs, plt receptor)

D. Aprotinin

1) Protease inhibitor from bovine lung

2) Inhibits kallikrein activity, and in turn, contact activation of coag cascade

3) Inhibits conversion of plasminogen to plasmin

4) ?secondary preservation of plt fxn

5) Most effective in preventing initial contact activation of blood and plts

6. Evaluation of post-op bleeding

A. <3% require early re-exploration

B. 1-3 u PRBC in uncomplicated cases

C. How much is acceptable? - author >100ml/hr for several hours; see chart from Kirklin

D. Transfusion: indications and risks

1) Hct 24%, Hb 8g/dl may be acceptable - individualize

2) Hepatitis in 7% (mostly hepatitis C)

3) HIV - 0.25% of donor pool is HTLV-III antibody +

E. Differential diagnosis of excessive bleeding

1) Plt ct, PT, PTT in all pts post-op

2) Heparin excess, integrity of coagulation cascade, plts

F. Excess anticoagulants

1) Heparin or FDP

2) Protamine trial - aPTT or ACT will normalize if heparin-related

3) Thrombin time +/- protamine - protamine will not correct FDP-related coagulopathy

G. Thrombocytopenia and plt dysfunction

1) Plt ct <75,000 + bleeding - tx w/8-12U plts

2) Normal plt count, normal coags + bleeding - DDAVP, plts

3) Bleeding time inaccurate post-op

H. Pathologic fibrinolysis

1) All clotting times abnormal, thrombocytopenia, hypofibrinogenemia - tx = transfusions + antifibrinolytics (amicar, aprotinin)

2) Cryoprecipitate (supra normal finbrinogen, vWf, FVIII concentrations) - for fibrinogen <100mg/dL

I. Massive transfusion

1) Plasma protein dilution (1-1.5 blood volume transfusion)

2) Thrombocytopenia most frequent derangement

7. Special hemostatic challenges

A. Jehovah’s Witnesses

1) Tx pre-op w/vitamins, iron, erythropoietin

2) 7% mortality

B. Heparin-induced thrombocytopenia (5% receiving continuous heparin)

1) Autoantibody to heparin-plt factor 4 complexes

2) Thrombocytopenia (<100,000) resolves within days of heparin withdrawl

3) Dx by plt aggregate testing

4) Strategy: elective - in vitro testing and postpone surgery - ab’s go away

5) Heparin-like substances, LMW heparin have high cross-reactivity

6) Org 10172 - rarely induces aggregation

7) Post-op - D/C all heparin

8. Future trends

A. Specific indications for DDAVP, aprotinin

B. Novel heparins - chemically modified

1) Hirudin - family of direct thrombin inhibitors

C. Anti-plt drugs

1) Ab’s to glycoprotein Iib/IIIa)

2) Synthetic peptides mimic fibrinogen

9. Thromboembolic complications of prosthetic valves

A. INR

1) DVT - 2.0-3.0

2) Prosthetic valves - 2.5-3.5

B. Mechanical valves

1) Thromboembolic rate

a) 0.5-3%/PT-yr - overall

b) MVR = 1-3

c) AVR = 0.5-2

2) Addition of an antiplatelet agent further reduces risk (ASA 160mgQD or dipyridamole 400mgQD)

3) Bleeding complications 0.7-6.3%/pt-yr

C. Bioprosthetic valves

1) Thromboembolism - 2%/pt-yr

2) More common in first 6-12 wks after operation

3) Recommendation - INR 2.0-3.0 for 3 months

4) ? Benefit from long-term ASA

D. Complicating

1) Child-bearing

a) Warfarin is teratogenic, crosses placenta - bad for fetus

b) Self-administration of SC heparin to PTT 1.5-2 x control

c) Antiplt tx alone?

2) Vascular and prosthetic grafts

a) SVG - 75-90% 1-yr patency

b) ASA + dipyridamole helps - ASA early post-op, dipyridamole pre-op

c) ASA alone may be effective

Assisted Circulation

Assisted Circulation

1. Advanced Mechanical Support

A. Indications

1) Post-cardiotomy cardiogenic shock

2) Post-MI cardiogenic shock

3) Post-transplant graft failure

4) High-risk PTCA support

5) Cardiopulmonary resuscitation (CPR)

6) Hypothermia rewarming

7) Alternative to transplantation(clinical trials)

2. Circulatory Support

A. Mechanical cardiac assist

1) Intra-aortic balloon pump (IABP)

2) Ventricular assist devices (VAD)

3) Cardiopulmonary support (CPS, ECMO)

B. Mechanical cardiac replacement

1) Total artificial hearts (TAH)

C. Others

1) Biologic cardiac assist- cardiomyoplasty

2) Ventricular remodeling

3) Pacing

3. Mechanical Circulatory Support- Characterization

A. Output hemodynamics

1) Pulsatile

2) Non-pulsatile

B. Drive mechanism

1) Pneumatic; electric (hydraulic, mechanical)

C. Configuration

1) TAH, BVAD, RVAD, LVAD

D. Status/availability

1) Approved for market, IDE trials, in development

4. Placement position

A. Orthotopic; heterotopic; extracorporeal

B. Paracorporal; transcutaneous

C. Implantability

1) Fully; partially; not at all

D. Application/ permanence

1) Temporary; bridge-to-transplant, cardiogenic shock; bridge-to-recovery

2) Permanent; alternative-to-transplantation

5. Device Selection for Bridge-to-Transplantation

Criteria	LVAD	RVAD	BVAD	TAH
LV failure	++	--	--	+
RV failure	--	++	--	+
LV & BV failure	--	--	+	+
Unresectable trombus	--	--	--	+
S/P mechanical valve	--	--	--	+
AI (or PI)	--	--	--	+
Irreparable intracardiac shunts	--	--	--	+
Uncorrectable arrhythmias	?	?	+	+
Refractory ischemia, angina	--	--	--	+
Transplant heart rejection	--	--	--	+
Acute MI at cannula site	?	?	?	+
Unresectable cardiac tumor	--	--	--	?

6. Bridge-to-Transplant

A. Problems

B. Cardiovascular

1) Failure on non-supported ventricle

2) Arrhythmias

3) Cyanosis/shunting with PFO

4) Ischemia/angina

C. Systemic

1) Hemorrhage

2) End-organ failure

3) Infection

4) Infection

5) Immune sensitization

6) Compromised quality of life

D. Device related

1) Thromboemboli

2) Obstruction/compression

3) Improper orientation

4) Device infection

5) Device failure

6) Hemorrhage

7) Air entrianment/embolus

8) Hemolysis

E. Results

1) 65-75% successfully bridged (90+% possible)

2) 90+% of those transplanted are discharged

7. Mechanical Circulatory Support– Issues for the future

A. Technological improvements

1) Size, biocompatibility, control, reliability, power and durability

B. Clinical effectiveness

1) Longevity, quality of life, complications, recovery, expertise

C. Cost-effectiveness

1) Of technology and implementation

D. Societal and ethical concerns

1) Allocation of resources; patient populations

E. Permanent Implantation– future NEED

1) By the year 2010

a) Number or patients: 35,000- 70,000 per year for long-term support

b) Devices:10,000-20,000 TAH and 25,000-60,000 VAD

8. Total Artificial Heart

A. Results– Bridge-to-transplant

	TAH	Control
	N	%	N	%
Pateints	27	--	18	--
Transplanted	25	93	8	44
Discharged home	28	89	7	39
Neurologic-embolic	9	33	--	--

B. Copeland et al

9. Summary

A. May be life saving in selected patients with end-stage heart disease

B. Need for this intervention is increasing with decreasing donor availability

C. May ultimately become an alternative to transplantation

ACABG.....Awake CABG

Awake coronary artery bypass grafting ? a simple and effective surgical procedure, that can be performed everywhere in the world !
Our institution, as a large academic center, has evaluated a variety of surgical techniques for minimally invasive CABG. Starting with MIDCAB operations via left-sided mini thoracotomy in 1996 moving to multiple vessel grafting on the arrested heart via mini thoracotomy using Port Access technology we changed our surgical approach to the more convenient partial lower sternotomy technique. This approach provides several advantages.
A paralell research effort was made evaluating the pros and cons of totally endoscopic robotically assisted technique. As an academic institution we analysed precisely the advantages and disadvantages of awake CABG surgery (ACAB). As a University Hospital performing more than 1800 cardiac procedures yearly, it was not our primary goal to pick up a new technique just for marketing purposes, but rather evaluate the most innovative techniques available in scientific manner.
Since March 2001 we performed ACAB in 68 patients. Besides of MIDCAB operations multiple vessel grafting procedures were performed in 12 patients via complete sternotomy in the awake setting.
With more than a 4 year experience in awake surgery it is my intention to communicate one important message not only to collegues, but also to all coronary patients who have to undergoe some type of revascularisation: ?The taboo of a heart operation as a risky and dangerous procedure has been broken.?���� There are severeal ways to achieve a good and long lasting revascularization of the heart. If we can offer the possibility of receiving a LIMA to LAD graft without standard anesthesia for cardiac surgery, we schould let the patient decide on the procedure! A stent with uncertain long term patency or a life time LIMA to LAD?
Let����s look at the critical issues:
Is there a true benefit of ACAB versus other surgical or interventional techniques?
Yes. For the first time in the history of cardiac surgery we have seen patients, who are able to eat a full lunch 2 hours postoperatively and walk over the ward the same afternoon, pain free,���� and able to go home on the first postop. day. Independent of the activity score that is used, such a fast track mobilization cannot be achieved by any other surgical techniques.
We perform fast track cardiac surgery routinely every day. As a surgeon who has a vast experience with both techniques I would like to state the following: the difference between awake surgery and fast track surgery is like the difference between day and night.
With the aging of the population, nowadays we have more and more elderly patients in their 80ies, who have considerable comorbidity����with impaired pulmonary function. Weaning such patients from the respirator is more and more difficult and dependent on the effects of drugs.
The same procedure performed under general anesthesia is also a good technique. But, the drawbacks are: hemodynamic compromise during induction of anesthesia, mechanical risk vocal chord injury, tracheal injury, malpositioning of the tube with ventilation of the stomach, etc.
Furthermore I have a question for the anesthesiologist: How long does it take to extubate a patient on the table while the next patient is waiting in line? What is the risk of transfer of fast track patients from the OR to the ICU? What about the reintubation rate? What about postoperative nausea and vomiting with the risk of aspiration?
The main aim of awake surgery is to increase the patient comfort during and after surgery. I believe, they have high comfort.
Isn����t it terrible to undergoe CABG and cardiac manuplation in fully awake condition?
Well, it really depends on which pair of eyeglasses you use when you look at this issue. And, dear collegues, it is time to visit your ophthalmologist and get a new pair of eyeglasses and look objectively at the trends, that are taking place in medicine:
What about a pecutaneous implantation of an AICD in a severely sick patients with low LVEF and an inclination for arrythmia. This procedure is nowadays performed in the cath lab even by the cardiologist, who has no surgical background or standby?
What about pace maker implantations in patients with symptomatic bradycardia and the endocardial manipulation during probe placement? Or explantation of pacer maker probe after several years? This procedure is done routinely, even though everybody knows, that in some cases we even observe ventricular perforation with all the consequences?
What about multiple stent implantation in one patient into the coronary vessels every day in many cath labs worldwide in the awake setting. It is done routinely enfacing the possible complications of such procedures in heavy calcified vessels. Sometimes more than 3, 4 even 5 hours procedure times?? What about left main stenting in the awake setting?
Why do interventionalists start to stent carotid arteries in awake patients enfacing a big neurologic risk. Are these guys crazy or are they practising latest state of the art medicine ?
Do not the ortopedic surgeons do arthroscopy and meniscus resection of 2 hours duration in spinal anesthesia? Many neurosurgical procedures are performed also in awake settings. In most of medical branches, the trend is towards patient comfort and ambulatory surgery.
I would like to hear from experienced OPCAB surgeon, if the LIMA-LAD in awake setting more dangerous than the above mentioned procedures?
What happens if the patient has episode of ventricular fibrilattion during the operation?
In such a scenario, with the surgeon and the anesthesiologist by the side, as well as the other members of the OR team, with the chest open, and the heart in your hands, one has the best and most optimal conditions to treat this complication. Internal massage can be started in 2 seconds, and internal defibrillation in 10-15 seconds.
What happens in the same patients undergoes Robotic revascularisation and sustains the same complication? How long before the thorax is open, hand massage and internal defibrillation are employed?
Or in the ICU? Or, even worse, on the normal patient ward? Or during PCI in cath lab in awake setting? It seams to me that cardiologists have more boldness than we, the surgeons.
Would I like to have an Awake CABG?
A classic question, and a classic response: yes. It is to me important the the anastomosis is well performed and the LIMA is nicely harvested. And one more contra-question: would you like to have your 80% stenotic left main stented in awake setting?���� Maybe you don����t like it, but it may well become a routine in a short time.
Some say that Awake CABG is not comfortable for the surgeon?
Many cardiac surgeons emphasize that suturing coronary anastomoses on the arrested heart and under general anesthesia is more comfortable than surgery on the beating heart. They say : ?Why schould I ride a Fiat Punto if I can afford a Mercedes??����
In my opinion surgical comfort is dependent on experience. The more cases one surgeon does in the same manner the safer it gets. I would like to ask one key question to all cardiac surgeons: The times are changing and I think it is time to make a decision what is more important: patient comfort or surgeons comfort.
Comfort is whatever keeps the surgeons adrenalin level in a normal range.
If one center follows the OPCAB philosophy all residents, OR nurses and anesthesiologists consider this bypass technique to be normal and standard.
Knowing that a certain procedure has potential benefit for the patient, we as a cardiac surgical community schould not be ignorant to refuse such innovation. At least we schould look into this new technique systematicly in multicenter trials before we ignore.
As an answer for the colleges: even if I have a Mercedes Maybach in my garage, for LIMA to LAD bypass I would prefer to ride my bicycle.
Come on guys, it just a matter of the perspective, that you take and how you want to look at a certain procedure !
Tayfun Aybek, MD
Cardiothoracic Surgeon
Thoracic and Cardiovascular Surgery
University of Frankfurt
Theodor Stern Kai 7
60590 Frankfurt/Main
GERMANY

What is Minimally Invasive Cardiac Surgery Anyway?

Minimally invasive clearly means many different things to different people. Some people are obsessed by small incisions, to achieve surgical success then they may need much longer bypas times. Others are obsessed by off-pump surgery, in return they may need much larger incisions to achieve adequate re-vascularisation. Do we really understand the trade-offs? Is an on-pump strategy with a very low blood product useage actually worse than an off-pump strategy in a unit that doesn't cell save and therefore has a higher transfusion rate. (yes it is true, you can be on-pump and still have a very low blood product useage. You do have to CARE about your transfusion levels though!) I have been struck looking at photographs of lower hemi-sternotomy that you can achieve, with care, a full sternotomy through the same skin incision. It is difficult but you can do it. Do we all wear headlights? I find it very difficult to use a small incision without a headlight, the corollary could be no head light therefore big incision, could it not?

We have to remember that we do live in a competitive world, cardiologists and patients are pushing us down routes that we consider might not be in the best interests of the patient. Outcome, survival and long term quality of life must be our drivers. Where we do things well we must market. If we truly believe in what we do then we must take up the challenges to demonstrate that what we do, be it, on or off pump, maximally or minimally invasive is of the highest currently attainable quality, but that we continue to strive to improve. If there are problems that we have not yet solved then we must solve them. At the end of the day we will have to transform our skills to meet the challenges as they arise, always realising that we must keep improving as cardiac suregry develops.

The Mediastinum

The Mediastinum

1. Anatomy
A. Compartments
1) Mediastinal borders: thoracic inlet (superior), diaphragm (inferior), sternum (anterior), spine (posterior), pleura (lateral)
2) Anterosuperior compartment is anterior to pericardium
3) Contents include thymus and great vessels
4) Middle, or visceral, compartment is between anterior and posterior pericardial reflections
5) Contents include heart, phrenic nerves, tracheal bifurcation, major bronchi, lymph nodes
6) Posterior, or paravertebral, compartment is posterior to posterior pericardial reflection
7) Contents include esophagus, vagus nerves, sympathetic chains, thoracic duct, descending aorta, and azygos/hemiazygos

2. Mediastinal Conditions
A. Mediastinal Emphysema
1) Introduction of air from esophagus, tracheobronchial tree, neck, or abdomen
2) Causes include penetrating or blunt trauma, or spontaneous mediastinal emphysema
3) Presents as substernal chest pain, crepitation, and pericardial crunching sound
4) May result in tamponade
5) Treat underlying cause; may require chest tube placement for pneumothorax
B. Mediastinitis
1) Occurs in about 1% of patients after median sternotomy
2) Risk factors include prolonged surgery or CPB, re-exploration, wound dehiscence, shock, and use of bilateral internal mammary artery grafts in patients who are older or have diabetes
3) Presents as fever, elevated WBC, and tachycardia
4) Best treatment results with wound debridement and tissue flaps
C. Mediastinal Hemorrhage
1) Caused by trauma, aortic dissection, aneurysm rupture, or surgical procedures
2) May result in mediastinal tamponade, which is more insidious than pericardial tamponade
3) Meticulous hemostasis and adequate chest tube drainage will prevent this syndrome
4) Spontaneous mediastinal hemorrhage can result from mediastinal masses, altered coagulation status, and severe hypertension
D. Superior Vena Cava Obstruction
1) Acute and chronic syndromes occur
2) See CTSN lecture on SVC Syndrome

MEDIASTINAL TUMORS

1. Location

1) Lesions are predictable to some degree predictable
2) Most common tumors are neurogenic (20%), thymomas (20%), primary cysts (20%), lymphomas (13%), and germ-cell tumors (10%)
3) Most are located in anterosuperior compartment (54%), followed by posterior (26%) and middle (20%) tumors

Tumors and Cysts by Location
Anterior Middle Posterior
Thymoma Enterogenous cyst Neurogenic origin
Germ cell tumor Mesothelial cyst Neurenteric cyst
Lymphoma Lymphoma Lymphoma
Hemangioma Thoracic duct cyst
Parathyroid adenoma Granuloma
Thymic cyst Hamartoma
Lipoma
Aberrant thyroid
Lymphangioma

4) A significant portion (25-40%) of mediastinal tumors are malignant
5) Anterosuperior tumors are more likely to be malignant, as are tumors of patients between the ages of 10 and 40
6) Neurogenic tumors and non-Hodgkin's lymphomas are the most common tumors in children

2. Clinical Presentation

1) About two-thirds of patients will have symptoms at the time of diagnosis
2) The absence of symptoms is a reasonably good indicator that a diagnosed tumor is benign
3) Most common symptoms include chest pain, cough, and fever
4) Signs of mechanical compression or invasion of mediastinal structures are more common with malignant tumors
5) Paraneoplastic syndromes are not uncommon and include Cushing's syndrome, thyrotoxicosis, hypertension, hypercalcemia, hypoglycemia, diarrhea, and gynecomastia

3. Diagnosis
A. CXR will localize the tumor and give information on calcification and relative density of the tumor
B. CT scanning identifies chest wall invasion, multiple masses, and extension into spinal column
C. MRI is more accurate for vascular involvement and intracardiac pathology
D. Echocardiography is useful for patients with middle compartment tumors to localize between intracardiac and pericardial tumors
E. Guided needle biopsy can make a diagnosis of malignancy in 80-90% of patients
F. Mediastinoscopy/mediastinotomy may be necessary to make a diagnosis and establish resectability

4. Thymoma
A. Features
1) Represents 20% of all mediastinal masses in adults
2) Peak incidence is in 3rd to 5th decades of life; rare in children
3) About half are of mixed cell type, followed by epithelial (28%) and lymphocytic (20%) types
4) Between 15 and 65% of thymomas are benign
5) Frequently associated with paraneoplastic syndrome, most commonly myasthenia gravis
6) Myasthenia gravis is diagnosed in 30-50% of patients with a thymoma, and 15% of myasthenia patients will have a thymoma
7) Autoimmune reaction directed against the postsynaptic nicotinic receptors results in skeletal muscle fatigability and weakness, especially in axial muscles
B. Operative Technique
1) Remove all anterior mediastinal tissue and any invasive disease, including involved lung, pleura, pericardium, and SVC/innominate vein
2) Thymic blood supply arises from the internal mammary arteries
3) Patients with stage IIa or higher disease should receive postoperative radiation
4) Chemotherapy is indicated for stage III or IV disease
5) Debulking may be appropriate for stage IV disease, although there is no evidence for increased survival · At 5 years after resection, 25-30% of patients will have complete resolution of myasthenia symptoms and 30-50% will be improved
6) Prognosis is dependent on stage of tumor, not on presence of myasthenia gravis

5. Thymic Carcinoid
A. Most occur in males and about two-thirds are symptomatic
B. Originate from Kulchitsky cells in the thymus, but are not associated with myasthenia gravis or the carcinoid syndrome
C. May cause other paraneoplastic syndromes, however, most commonly Cushing's syndrome (33%)
D. Presence of such syndromes is a very poor prognostic factor
E. Up to 75% will develop local recurrence or metastases
F. Low overall cure rate and mean survival is 3 years

6. Lymphoma
A. Between 40 and 70% of lymphoma patients will have mediastinal involvement during their disease course
B. Only 5-10% of lymphoma patients will have isolated mediastinal disease, and are usually symptomatic
C. Characteristic Hodgkin's lymphoma symptoms are chest pain after alcohol consumption and cyclic Pel-Ebstein fevers
D. Nodular sclerosing and lymphocyte predominance forms of Hodgkin's lymphoma are the most common to cause mediastinal involvement
E. Up to 40% of patients with lymphoblastic non-Hodgkin's lymphoma will have mediastinal disease
F. Surgery is indicated if fine-needle aspiration is inconclusive or to evaluate residual mass after chemotherapy
G. Surgical options include cervical mediastinoscopy, parasternal mediastinotomy, and thoracoscopy

7. Germ Cell Tumors
A. Comprise 15-25% of anterior mediastinal masses
B. Most common in children and young adults
C. Includes teratomas, teratocarcinomas, seminomas, embryonal cell carcinomas, choriocarcinomas, and endodermal cell or yolk-sac tumors
D. Identical to germ cell tumors originating in the gonads, but are not metastatic lesions from primary gonadal tumors
E. About 60% are benign and 40% are malignant
F. Predominantly Benign Tumors
1) Teratomas are complex, multiple tissue element tumors
2) Symptoms are related to mechanical effects
3) Simplest form is the dermoid cyst, which consists of mostly dermal and epidermal tissue
4) More complex teratomas may have well-differentiated bone, cartilage, nerve, or glandular tissue
5) Malignant tumors are differentiated upon histologic identification of embryonic tissue
G. Malignant Tumors
1) Male predominance and most patients are symptomatic
2) 40% are seminomas and 60% are nonseminomas (embryonal cell, choriocarcinoma, yolk-sac, and teratocarcinoma)
Seminomas Non-seminomas
AFP/B-HCG rare 90%
Associated syndromes none Klinefelter's, trisomy 8, 5q deletion
Radiosensitivity High Insensitive
Metastatic behavior Remain intrathoracic Frequently disseminated
Treatment Radiation Cis-platinum chemotherapy
Remission Over 80% CR in 55-60%, PR in 30-35%
5-year survival 50-80% 50-60%
Remission CR=complete PR=partial

3) Initial surgical intervention typically only for diagnosis due to high radiosensitivity of seminomas and frequent metastatic disease in non-seminomas
4) Surgical resection after induction of chemotherapy may have a role in non-seminomatous tumors

8. Endocrine Tumors
A. Intrathoracic Thryoid
1) 80% are substernal extensions of a cervical goiter
2) True intrathoracic thyroid (derives blood supply from thoracic vessels) comprises only 1% of all mediastinal tumors
3) More common in women and in the 6th to 7th decades, most are adenomas
4) Usually presents with tracheal or esophageal compression; thyrotoxicosis is uncommon
5) I-131 scanning should be done to identify presence of functioning cervical thyroid tissue before resecting these tumors
6) Resect substernal extensions through a cervical incision and true intrathoracic lesions through the chest
B. Parathyroid
1) Most are adenomas and are found by the superior pole of the thymus due to common embryogenesis from the third branchial cleft
2) Symptoms are usually due to hyperparathyroid syndrome
3) Parathyroid cysts are not usually hormonally active

9. Primary Cysts
A. Bronchogenic Cysts
1) Most common primary cysts in the mediastinum (5%)
2) Arise from ventral foregut and are usually located in the subcarinal or right paratracheal region/a>
3) Two-thirds are asymptomatic; symptoms include tracheobronchial or esophageal compression and infection from tracheobronchial communication
4) Complete excision is recommended, even if asymptomatic, to prevent late complications
B. Esophageal/Enteric Cysts
1) Comprise 3-5% of mediastinal tumors
2) More common in children and tend to occur in the lower third of the esophagus
3) Dysphagia is the most common symptom
4) CT scanning is essential in patients with vertebral anomalies to evaluate for possible spinal cord involvement (neuroenteric cyst)
5) Avoid endoscopic biopsy, as this may cause cyst perforation and infection
6) Complete excision is indicated; a thoracoscopic approach can be used for uninfected cysts
C. Pleuropericardial Cysts
1) Uncommon, classically occur at the pericardiophrenic angles, 70-80% on the right side
2) Usually asymptomatic and may communicate with the pericardium
3) Guided needle aspiration is the initial therapy of choice
4) Surgical excision is indicated if the cyst recurs or if the diagnosis is in doubt

10. Neurogenic Tumors
A. Etiology and Diagnosis · Most posterior mediastinal masses are of neurogenic origin
1) 95% of these tumors in adults are benign and are usually asymptomatic
2) In children, most neurogenic tumors are malignant
3) Classified according to cell origin; most arise from intercostal nerve or sympathetic chain
Intercostal nerve Sympathetic ganglia Paraganglia cells
Neurofibroma Ganglioma Paraganglioma
Neurilemoma Ganglioneuroblastoma (pheochromocytoma)
Neurofibrosarcoma Neuroblastoma

4) Neurilemomas are the most common and originate from Schwann's cells
5) These are encapsulated tumors which stain with S-100 protein immunostain
6) Two primary types: Antoni A (organized pallisading pattern) and Antoni B (loose reticular pattern)
7) Neurofibromas originate from peripheral nerve
8) Form a pseudocapsule and have more variability with the S-100 stain
9) Both types of tumors are associated with von Recklinghausen's disease, although more commonly neurofibromas
10) Chest CT is sufficient for diagnosis of most of these tumors, and MRI should be used when an intraspinal component is present

B. Operative Indications
1) Benign tumors (neurofibroma, neurilemoma, ganglioneuroma) can be effectively treated with local excision
2) Combined thoracic and neurosurgical approach is indicated for tumors with intraspinal extension
3) Recurrence is rare for benign tumors
4) Local recurrence is common for malignant tumors and overall prognosis is poor

Esophageal Diagnostic Procedures

Esophageal Diagnostic Procedures

1. Definition
A. There are several procedures utlitized for the diagnosis of esophageal disease, and the approach must be tailored to the specific disease entity. Contrast swallow and esophagoscopy are commonly used for most patients with esophageal disorders, with CT scanning, endoscopic ultrasound, and reflux testing reserved for more specific indications. MRI and nuclear medicine scans may have additional limited roles.

2. Esophagoscopy
A. Indications
1) Dysphagia, odynophagia, regurgitation, hematemesis, chest pain, foreign body ingestion, or history of traumatic esophageal tear
2) Should usually be preceded by contrast swallow/cineesophagogram to help localize the site of disease
3) Contraindications include aortic aneurysm (can rupture), recurrent nerve paralysis, esophageal diverticulum (can perforate blindly), corrosive strictures (can perforate - stop when you see the stricture), and kyphoscoliosis (may be impossible)
4) Use rigid technique when Zenker's diverticulum or disease of the upper third is suspected, as flexible esophagoscopy is done blindly and can perforate in these areas
B. Technique - Rigid Esophagoscopy
1) Topical or general anesthesia may be used; general anesthesia generally provides better relaxation, lowering the risk of perforation
2) The 9mm scope is adequate for most adult patients
3) The patient is positioned supine with head and shoulders over the end of the table
4) Introduce the esophagoscope into the right side of the mouth and rest the shaft on your left thumb
5) The scope is advanced behind the right arytenoid cartilage into the right pyriform fossa
6) Lower the patient's head as the scope is advanced past the cricopharyngeus
7) Lower the head further and move to the right to pass through the gastroesophageal junction
8) Full examination is done on withdrawal, as folds of mucosa may hide pathology during advancement of the scope
C. Technique - Flexible Esophagoscopy
1) Topical anesthesia with sediation is usually adequate
2) The patient is placed in the left lateral position
3) The esophagoscope is introduced blindly with gentle pressure as the patient swallows
4) Insufflation of air distends the esophagus for complete visualization
5) Advance scope into upper stomach and perform thorough examination upon withdrawal
D. Complications
1) Perforation occurs in 0.1-0.25% of patients
2) Most commonly occurs posteriorly at the upper opening of the esophagus when forceful pressure is applied against the cricopharyngeus
3) Other sites include the diaphragmatic hiatus and diverticuli
4) Perforation can also occur after deep biopsy, forceful dilation of strictures, or during removal of foreign bodies
5) Chest pain after esophagoscopy is an indication of perforation and should be promptly evaluated
E. Findings in Disease
Reflux Esophagitis
Stage I localized spots of erythema, some with exudate
Stage II confluent areas of erythema
Stage III circumferential areas of erythema, friable, bleeds readily when touched
Stage IV deep ulcers, stenoses and columnar metaplasia

1) Barrett's esophagus: stratified squamous epithelium replaced by columnar epithelium and may become discrete ulcer; biopsy should be performed to look for malignancy
2) Stenosis: congenital stenoses usually have normal mucosa; acquired stenoses are usually associated with esophagitis or ulcers
3) Corrosive esophagitis: acute inspection shows edematous, friable walls which are easily perforated; stop at first area of injury
4) Diverticulum: exclude ulcers and neoplasms at the site of the diverticulum
5) Varices: range from small bluish elevations to large dilated veins at the lower end of the esophagus--commonly found in cirrhotics
6) Hiatal hernia: redundant folds in the lower esophagus and lack of diaphragmatic support are characteristic only in true hiatal hernia
7) Achalasia: markedly dilated, inflamed esophagus with thickened walls; GE junction has normal tone but may be hard to negotiate
8) Carcinoma: typically large fungating mass that bleeds easily, less commonly a smooth stenosis with edematous mucosa. Microinvasive carcinoma presents as slight discolorations of the mucosa, known as leukoplakia or erythroplakia.
9) Benign neoplasms: leiomyomas, fibromas, and lipomas are all covered with normal mucosa

3. Endoscopic Ultrasound
A. Particularly applicable in defining tumors and varices
B. May become useful in staging of esophageal cancer
C. 5 layers are identified: mucosa, deep mucosa, submucosa, muscularis, and adventitia
D. Extension of tumors into periesophageal structures and lymph nodes can be evaluated
E. Carcinomas appear as indistinct, echo-poor lesions; varices appear as round, echo-poor lesions

4. Gastroesophageal Reflux Evaluation
Note: Radiographic tests for GE reflux are not highly reliable for pathologic reflux, as up to 25% of patients will have reflux without associated pathology. Such tests can rule out patients with no reflux, however.
A. Manometry
1) Intraluminal pressures are measured using a continuous infusion catheter system while the patient is lying supine
2) This catheter is withdrawn at 1-cm intervals to obtain resting pressures
3) The catheter is reinserted, and pressures measured after swallowing at 1-cm intervals
4) This test is essential in delineating the various esophageal motility disorders
B. pH Reflux Test
1) A pH probe is placed 5 cm above the GE junction
2) 200 to 300 ml of 0.1N HCl is instilled in the stomach
3) A fall in pH below 4.0 during various maneuvers indicates GE reflux
C. Acid Perfusion Test
1) The distal esophagus is perfused in an alternating fashion with 0.1N HCl and saline
2) The test is positive if atypical chest pain occurs during acid perfusion and resolves during saline perfusion
3) High rates of false positivity and false negativity make the test somewhat unreliable
D. 24-hour pH Monitoring
1) a pH probe is placed 5cm above the GE junction
2) The patient records any symptoms and pH changes are monitored constantly over 24 hours
3) Analysis includes percentage of time pH was less than 4.0, and percentage of time patient was upright and supine
4) The number of reflux episodes, the duration of the episodes, and the longest episode of reflux are also evaluated
5) This test gives the most objective evidence of reflux

5. Therapeutic Esophagoscopy
A. Removal of Foreign Bodies
1) Rigid esophagoscope is best
2) Most common sites are just below the cricopharyngeus and at the diaphragm
3) Sharp objects carry the highest risk of perforation
B. Dilation of Strictures
1) Savary-Gilliard dilators are the safest
2) A metal guidewire is passed through the stricture using the esophagoscope
3) The stricture is then dilated using progressively larger dilators passed over the guidewire
4) Retrograde dilation may also be done using Tucker dilators over a string passed through a gastrostomy and out the mouth
C. Corrosive Esophagitis
1) Esophagoscopy should be performed to confirm the burn, but do not pass the injured area
2) Dilation can be performed after burn have healed (usually 3-4 weeks) if strictures have formed
D. Carcinoma
1) Palliative dilation usually is only temporary, and should be followed with either laser resection or stenting
2) The Nd:YAG laser can be used from above or below to core a passage through tumor and permit swallowing
3) Brachytherapy can be applied after endoscopic dilation for inoperable carcinoma
E. Achalasia
1) Dilation can be performed of the GE junction if surgical myotomy is contraindicated
2) Perforation, however, is a definite risk and can present as either chest or abdominal pain
F. Variceal bleeding
1) Electrocautery and laser therapy of bleeding varices do not prevent rebleeding
2) Sclerotherapy is probably best and obliterates current varices; however, rebleeding occurs in 40% of patients

6. Radiographic Examples
A. Schatzki's ring
B. Achalasia
C. Diffuse Esophageal Spasm
D. Leiomyoma
E. Carcinoma