Management of thoracic duct injury following radical neck dissection.

PAPER IV JUNE 2008
Q. Management of thoracic duct injury following radical neck dissection.

Chyle Leak
Chyle leaks have been reported to occur following neck dissections in 1–2.5% of cases, with 25% occurring on the right. Chyle is a mixture of lymph from interstitial fluid and emulsified fat from interstitial lacteals. It is mildly alkaline and on standing forms three layers, a cream top layer, milky middle layer, and a lower layer of cellular sediment. The fat content is 1–3%, largely triglycerides, which are responsible for the milky appearance and greasy feel. The daily drainage may reach two to four litres.
Anatomy
The thoracic duct begins at the cisterna chyli and continues upwards into the thorax posterior to the aorta through the aortic hiatus of the diaphram. It runs in the posterior mediastinum along the right anterior aspect of the vertebral bodies between the aorta and the azygous vein. The thoracic duct crosses the midline at the fifth or sixth thoracic vertebra and continues to extend superiorly along the left posterior border of the oesophagus. It exits the thorax posterior to the left common carotid artery between this vessel and the left subclavian artery. As it enters the neck, it arches superior, anterior and lateral to form a loop that terminates into the venous system. This loop is anterior to the vertebral artery and the thyrocervical trunk. It courses between the internal jugular vein and the anterior scalene muscle superficial to the deep cervical fascia overlying the phrenic nerve. The loop is always found within 2 cm of the internal jugular-subclavian vein junction, and its maximal height is usually 3–5 cm above the clavicle. The right jugular, subclavian, and the tracheobronchial trunks form the right lymphatic ducts. These usually terminate separately in the region of the right internal jugular — subclavian vein junction. A single duct on the right is thought to be rare.
Presentation
A chyle leak may present in the neck, chest or abdomen. If left untreated, it may result in a metabolic, nutritional and immunologic complication. Patients will eventually become weak, dehydrated, oedematous, and emaciated. Chylothorax can result from injury in the chest or neck. It may progress from the neck by tracking along fascial planes to the mediastinum, where it causes tissue maceration and inflammation, resulting in rupture of the pleura. The dangers of a chylothorax include cardiopulmonary compromise because of compression of the lungs, leading to a mediastinal shift with distortion of the great vessels. The diagnosis of a chyle leak can be intra or postoperative. During dissection of the lower left portion of the neck, chyle may macroscopically be recognised as a milky substance, or the thoracic duct itself may be seen with a tear in it. If a leak is suspected it can be confirmed by asking the anaesthetist to apply a continuous positive airway pressure and place the patient in the Trendelenburg position. Postoperatively, chyle may present in the drainage bottle, but if it is a low volume leak, it can be missed initially because it is mixed with blood. Even chemical analysis of the fluid may not be conclusive. However, >100 ng/dL triglycerides or >4% chylomicrons indicate possible chylous leakage.
Management
It is universally accepted that the optimum management of a chylous fistula is by prevention. If the leak is identified during surgery, every effort should be made to arrest it immediately. Ligation with 3-0 or 4-0 non-absorbable suture without going through the duct wall should be performed. It has been suggested that inclusion of the medial edge of the anterior scalene muscle will help prevent duct laceration during ligation. Leakage may continue to occur postoperatively, even when the procedure is apparently successful because of unidentified injuries to the duct or additional terminations. Medical management involves an elemental diet supplemented with medium chain triglycerides (MCT). These are absorbed directly into the portal circulation, bypassing the lymphatic system.Total parentral nutrition (TPN) is an alternative, but is not recommended by all. In theory, interruption of entral alimentation should reduce intestinal peristalsis and lymph flow.However, the disadvantages are the need for central venous access, associated morbidity, and cost. The application of pressure dressings to encourage closure and the formation of chyle collection are usually futile, as the anatomy is not contoured for such an efficient dressing to be applied continuously. Instead, the use of continuous suction drainage is recommended to prevent chyloma formation and avoid the associated intense inflammatory reaction. The indications and timing for surgical intervention, when a chyle leak is diagnosed in the postoperative phase, remain controversial. Surgery is appropriate if the leak is in excess of 500 ml per day for four or more consecutive days, or if a chyloma formation could not be controlled with pressure dressings or serial aspirations. Surgery is also recommended when chyle drainage is in excess of 500 ml per day after one week of medical management, in case of persistent low-output drainage for a prolonged period, or if complications develop. In these situations, a thorascopic approach to the thoracic duct, on the right side of the chest is considered the definitive management option, with minimal morbidity.

Ref: surgical complications 2007

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What are pressure sores? What are the common sites and how would you prevent development of these sores?

PAPER I DEC 2010
Q. What are pressure sores? What are the common sites and how would you prevent development of these sores?

Pressure Ulcers
Pressure sores, decubitus ulcers and bed sores are some of the different terms referring to the consequences of unrelenting pressure on vulnerable skin points. The commonest areas where they occur are the sacrum, heels and ischial tuberosities, and the greater trochanteric areas. The normal capillary pressure which has to be overcome to result in tissue ischaemia is 32 mmHg.12 This capillary pressure is easy to overcome over boney prominences. If one recalls the vascularity of the skin and subcutaneous fat...


























Fig:The basic mechanism for the development of a pressure ulcer.
...it can be seen that an extensive plexus exists within the subcutaneous fat and the dermis. Thus although this pressure is overcome in everyday life, due to a good layer of subcutaneous fat and intact interconnections between the blood capillaries, true ischaemia of the tissue does not occur. In the conscious patient with normal sensibility and mobility, however, there will also be conscious and subconscious efforts at relieving the pressure from the vulnerable points. In contra-distinction, when there is poor nutrition, when the patient is unconscious, and when there is poor sensibility/mobility, tissue necrosis followed by local sepsis will results.Ultimately there will be loss of integument as well as loss of any underlying muscle with possible exposure of underlying bone/joints. A grading system exists to help in management plans for patients suffering from pressure ulcers. It is graded 1–4 as follows13:
(1) Non-blanchable erythema of the intact skin. This is a red or violaceous
area that does not blanch upon pressure with the finger, indicating blood
has escaped form the capillaries into the interstitial tissue.
(2) Partial-thickness skin loss.
(3) Full-thickness skin loss and extension into the subcutaneous fat.
(4) Extension into the muscle and bone. Prevention is far better than any attempts to cure these ulcers. It is incumbent on the attending surgeon to ensure appropriate nursing care such that pressure is relieved from the commonest points and the patient is turned regularly. The patient must be placed on an appropriate pressure relieving mattress. Malnourishment needs to be alleviated. If there is loss of continence of bowel or bladder then the effluent needs to be controlled either by diversion into reservoir bags (stoma, urinary catheterisation) or by regular cleaning. The development of pressure ulcers in otherwise normal surgical patients has been used by some as an indicator of the quality of medical care delivery.There has been a schema developed to assess the risk of pressure sore development in patients with the intention that resource allocation be rationally made to those most at risk. Independent risk factors are: general physical health, mental state, activity, mobility, incontinence and nutritional status. A common problem with the management of pressure ulcers is the lack of recognition of the problem when the ulcers develop. Typically a grade 4 ulcer carries significant morbidity. Lack of recognising the fact that the wound surface will have many deep fissures/sinuses means that they are inadequately treated and therefore recur rapidly. The apparent wound surface will only be a small portion of the true wound surface. This is explained by the fact that during their natural history, the skin and subcutaneous fat are destroyed, but the fat is destroyed to a greater extent than the skin and thus there will be some amount of undermining. Colonised or frankly infected ulcers will lead to further fat necrosis to differing depths surrounding the ulcer. Surgical management of pressure ulcers must be undertaken if the patient is acutely septic from an infected pressure ulcer and/or when the patient has been optimised for surgery. Again the principle of “tumour” excision of the wound has to be applied. Various aids have been developed to ensure complete wound excision. In essence all the aids to a comprehensive excision relate
to revealing the true extent of the wound surface. The so-called bursa of the wound needs to be excised. Thus sewing a gauze swab soaked in either betadine or hydrogen peroxide and India ink will delineate the bursa.Tumour excision can then be effectively undertaken by excising around this construct and ensuring that no pigmented tissue is seen. After a comprehensive excision one must remember that primary and reactionary haemorrhage is common and these must be anticipated during and after the surgery. In paraplegic patients, there is profound hypotension during anaesthesia and thus during wound excision cut blood vessels may be concealed and a reactionary bleed will occur post-op. When considering the reconstruction of pressure ulcers one must apply the KISS principle. A defensive approach will ensure that should the ulcer recur, options have not been exhausted. The usual reconstructive ladder/elevator/ toolbox can be applied in these cases. An algorithm is shown and the important aspect is to diagnose the condition accurately.

ref: surgical complications 2007

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Classify skin flaps

PAPER III DEC 2009
Q. Classify skin flaps.
The Reconstructive Ladder
Traditionally reconstructive plastic surgeons approach tissue reconstruction by paying due attention to the reconstructive ladder. This was viewed as a ladder with each successive rung representing an increasingly complex mode of treatment. This concept was principally introduced as an aid to obtaining wound closure. Thus the simplest method represented on the ladder is by primary closure and the most sophisticated is by way of free tissue transfer. It was envisaged that one “climbed” this “ladder” when attempting to close wounds. Thus only after the simplest technique has failed should one try the next level of complexity. Free tissue transfer is in essence an autotransplantation of blocks of tissue. An increased level of anatomical knowledge and surgical skill are required when undertaking free tissue transfer. Whilst undoubtedly the reconstructive ladder principle was of help, modern reconstructive plastic surgeons suggest that one gets to the most appropriate rung of the ladder at the beginning. This represents a shift in the attitudes in modern reconstructive plastic surgery and some have re-named the ladder as a “toolbox” or “elevator”. We should do the right operation for the patient at the outset rather than the simplest. Clearly these may be inclusive.
ref: Surgical Complications 2007



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What is familial adenomatous polyposis? How will you manage such a patient?

PAPER II DEC 2010
Q. What is familial adenomatous polyposis? How will you manage such a patient? 






Management of 30 years old man with hematuria following blunt trauma to flanks

PAPER III JUNE 2010
Q.    Management of 30 years old man with hematuria following blunt trauma to flanks.

Management of 40yrs old lady with arterial insufficiency in right hand

PAPER I JUNE 2010
Q. Management of 40yrs old lady with arterial insufficiency in right hand.

Patho-physiology of "Septicemic Shock"

Various parameters to assess the nutritional status of a surgical patient

1.PAPER I JUNE 2008

Q. Various parameters to assess the nutritional status of a surgical patient.



Describe the classifications of lymphomas

PAPER I JUN 2007
Q.           Describe the classifications of lymphomas.   
 2008 WHO classification.
 Mature B-cell neoplasms
·         Chronic lymphocytic leukemia/small lymphocytic lymphoma
·         B-cell prolymphocytic leukemia
·         Splenic marginal zone lymphoma
o   Hairy cell leukemia
o   Splenic lymphoma/leukemia, unclassifiable    
o   Splenic diffuse red pulp small B-cell lymphoma*  
·         Hairy cell leukemia-variant*
·         Lymphoplasmacytic lymphoma    
o   Waldenström macroglobulinemia
·         Heavy chain diseases    
o   Alpha heavy chain disease    
o   Gamma heavy chain disease    
o   Mu heavy chain disease Plasma cell myeloma
·         Solitary plasmacytoma of bone
·         Extraosseous plasmacytoma
·         Extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma)
·         Nodal marginal zone B-cell lymphoma (MZL)    
o   Pediatric type nodal MZL
·         Follicular lymphoma    
o   Pediatric type follicular lymphoma
·         Primary cutaneous follicle center lymphoma
·         Mantle cell lymphoma
·         Diffuse large B-cell lymphoma (DLBCL), not otherwise specified    
o   T cell/histiocyte rich large B-cell lymphoma    
o   DLBCL associated with chronic inflammation    
o   Epstein-Barr virus (EBV)+ DLBCL of the elderly
·         Lymphomatoid granulomatosis
·         Primary mediastinal (thymic) large B-cell lymphoma
·         Intravascular large B-cell lymphoma
·         Primary cutaneous DLBCL, leg type
·         ALK+ large B-cell lymphoma
·         Plasmablastic lymphoma
·         Primary effusion lymphoma
·         Large B-cell lymphoma arising in HHV8-associated multicentric Castleman disease
·         Burkitt lymphoma
·         B-cell lymphoma, unclassifiable, with features intermediate between diffuse large B-cell lymphoma and Burkitt lymphoma
·         B-cell lymphoma, unclassifiable, with features intermediate between diffuse large B-cell lymphoma and classical Hodgkin lymphoma
·         Hodgkin Lymphoma
·         Nodular lymphocyte-predominant Hodgkin lymphoma
·         Classical Hodgkin lymphoma    
o   Nodular sclerosis classical Hodgkin lymphoma
o   Lymphocyte-rich classical Hodgkin lymphoma
o   Mixed cellularity classical Hodgkin lymphoma
o   Lymphocyte-depleted classical Hodgkin lymphoma
Mature T-cell neoplasms
·         T-cell prolymphocytic leukemia
·         T-cell large granular lymphocytic leukemia
·         Chronic lymphoproliferative disorder of NK-cells*
·         Aggressive NK cell leukemia Systemic EBV+ T-cell lymphoproliferative disease of childhood (associated with chronic active EBV infection)
·         Hydroa vacciniforme-like lymphoma
·         Adult T-cell leukemia/lymphoma
·         Extranodal NK/T cell lymphoma, nasal type
·         Enteropathy-associated T-cell lymphoma
·         Hepatosplenic T-cell lymphoma
·         Subcutaneous panniculitis-like T-cell lymphoma
·         Mycosis fungoides Sézary syndrome
·         Primary cutaneous CD30+ T-cell lymphoproliferative disorder
o   Lymphomatoid papulosis    
o   Primary cutaneous anaplastic large-cell lymphoma
·         Primary cutaneous aggressive epidermotropic CD8+ cytotoxic T-cell lymphoma*
·         Primary cutaneous gamma-delta T-cell lymphoma
·         Primary cutaneous small/medium CD4+ T-cell lymphoma*
·         Peripheral T-cell lymphoma, not otherwise specified
·         Angioimmunoblastic T-cell lymphoma
·         Anaplastic large cell lymphoma (ALCL),
·         ALK+ Anaplastic large cell lymphoma (ALCL), ALK–*

Post-operative pain analgesia ladder.

PAPER IV JUNE 2009
Q. Post-operative pain analgesia ladder.
Managing patients in the postoperative period is often challenging. The spectrum of challenges depends on:
1. Patient factors: age, comorbid conditions etc
2. Surgical factors: site and nature of surgery, fluid and blood loss, nil by mouth
status etc
3. Local factors: availability of resources, man power, drugs, equipments etc.

There is an endless list of problems that can be encountered in the postoperative period. This section will focus on some commonly occurring ones in the postoperative ward.

Management of postoperative pain:
The effective relief of pain is of paramount importance to anyone treating patients undergoing surgery. This should be achieved for humanitarian reasons, but there is evidence that pain relief has significant physiological benefit.

Clinical factors
The site of the surgery has a profound effect upon the degree of postoperative pain a patient may suffer. Operations on the thorax and upper abdomen are more painful than operations on the lower abdomen which, in turn, are more painful than peripheral operations on the limbs. However, any operation involving a body cavity, large joint surfaces or deep tissues should be regarded as painful. In particular, operations on the thorax or upper abdomen may produce widespread changes in pulmonary function. The result will be an inability to cough and clear secretions which may lead to lung atelectasis and pneumonia. Matters are made worse by postoperative bowel distension or tight dressings.

Effects of pain
Pain causes an increase in the sympathetic response of the body with subsequent rises in heart rate, cardiac work and oxygen consumption. Prolonged pain can reduce physical activity and lead to venous stasis and an increased risk of deep vein thrombosis and consequent pulmonary embolism. In addition, there can be widespread effects on gut and urinary tract motility which may lead, in turn, to postoperative ileus, nausea, vomiting and urinary retention. These problems are unpleasant for the patient and may prolong
hospital stay.