SURGICAL AUDIT

surgical audit is a process used by clinicians who seek to improve patient care.

The process involves comparing aspects of care(structure, process and outcome) against explicit criteria. keeping track of personal outcome data and contributing to a clinical database ensures that a surgeon's own performance is monitored continuously and can be compared with a national data set to ensure compliance with agreed standards

  If the care falls short of the criteria choosen, some change in the way that care is organised should be proposed . This change may be required at one of many levels. it might be an individual who needs training or an instrument that needs replacing. at times, the change may need to take place at the team levels.

  

         Sometimes, the only appropriate action is change at an institutional level(eg-a new antibiotic policy), regional level (provision of a tertiary referral centre) or indeed, national level (screening programmes and health education campaigns).

     

     Essentially two types of audits may be encountered: national audits( eg- in the UK, the national institute for health and clinical excellence-NICE) and local/hospital audits.

   Both are designed to improve the quality of care.

In an ideal world, national audits should be driven by needs identified in local and hospital based audits that are closest to the patient. For example, hospital topics are often identified at the departmental morbidity and mortality meetings, where issues related to patient care are discussed .

   The reporting process might identify a possible national issue, and a national audit could be designed to be completed by the local audit department and surgical teams.

Audits are formal processes that require a structure . the following steps are essential to establish an audit cycle:-

1.                   Define the audit question in a multidisciplinary teams.

2.                  Identify the body of evidence and current standards.

3.                  Design the audit to measure performance against agreed standard based on strong evidence. Seek appropriate advice(local audit department in UK)

4.                  Measure over an agreed interval.

5.                  Analyse results and compare performance against agreed standards.

6.                  Undertake gap analysis- a) if all standards are reached, reaudit after an agreed interval. b) if there is a need for improvement, identify possible interventions and agree with the involved parties.

Reaudit.

Hand Spaces and Infection

The arrangement of fascia and the fascial septa in the hand is such that many spaces are formed. These spaces are of surgical importance because they may become infected and distended with pus.

The important spaces are named below:

(A) PALMAR SPACES

1.The pulp space of the fingers
2.The digital synovial sheaths
3.The ulnar bursa
4.The radial bursa
5.The midpalmar space
6.The thenar space

(B) DORSAL SPACES

1.Dorsal subcutaneous space
2.Dorsal subaponeurotic space

(C) THE FOREARM SPACE OF PARONA

1.The pulp space of the fingers:-The tips of the fingers and thumb contain subcutaneous fat arranged in tight compartments formed by fibrous septa which pass from the skin to the periosteum of the terminal phalanx. Infection of this space is known as WHITLOW. The rising tension in the space gives rise to severe throbbing pain. Infection s in the pulp space(Whitlow) can be drained by a lateral incision which opens all compartments and avoids damage to the tactile tissue in front of the finger.

If neglected, a Whitlow may lead to necrosis of the distal 4/5 of the terminal phalanx due to occlusion of the vessels by the tension. The proximal 1/5 (epiphysis) escapes because its artery does not traverse the fibrous septa.

Cell cycle

Cell-Cycle Dysregulation in Cancer

The proliferative advantage of tumor cells is a result of their ability to bypass quiescence. Cancer cells often show alterations in signal transduction pathways that lead to proliferation in response to external signals. Mutations or alterations in the expression of cell-cycle proteins, growth factors, growth factor receptors, intracellular signal transduction proteins, and nuclear transcription factors all can lead to disturbance of the basic regulatory mechanisms that control the cell cycle, allowing unregulated cell growth and proliferation.

The cell cycle is divided into four phases.

During the synthetic or S phase, the cell generates a single copy of its genetic material, whereas in the mitotic or M phase, the cellular components are partitioned between two daughter cells.

The G₁ and G₂ phases represent gap phases during which the cells prepare themselves for completion of the S and M phases, respectively.

When cells cease proliferation, they exit the cell cycle and enter the quiescent state referred to as G₀.

In human tumor cell-cycle regulators like INK4A, INK4B, and KIP1 are frequently mutated or altered in expression. These alterations underscore the importance of cell-cycle regulation in the prevention of human cancers.

Describe the scientific basis to "Hormone therapy in cancers". Describe the limitations of hormone therapy and its side effects.

• Endocrine therapy with its minimal toxicity is considered a primary option over cytotoxic chemotherapy in patients with hormone receptor-positive disease.
• It has the advantages of good efficiency, low toxicity, and low impact on quality of life.
• Their efficacy depends on the expression of both steroid hormone receptors (ER and PR positive: remission rate (RR) 50–75%; only ER or PR positive: RR 20–50%; ER and PR negative: RR < 10%). Treatment should be continued until disease progression or occurrence of relevant side effects.
• On average, first-line treatment is associated with 8 to 12 months of tumor control, and second-line treatment with 4 to 6 months. Individual patients may experience substantially longer time to progression. Sequential single-agent second- and third-line endocrine treatments are often effective, although typically for shorter durations than initial therapy..

• Endocrine therapy can cause even regression of soft tissue and bone and visceral metastases.
• Eventually many patients with hormone-receptor positive metastatic breast cancer will progress despite first-line endocrine therapy.

Induction Chemotherapy is to be considered in patients presenting with extensive visceral metastases or profound symptoms from breast cancer (visceral crisis) which should then be followed with endocrine therapy.

ENDOCRINE THERAPIES AVAILABLE FOR METASTATIC BREAST CANCER

Commonly Used Endocrine Regimens in the Metastatic Setting

                        Ovarian suppression/ablation (premenopausal women)

                        Selective estrogen receptor modulators - tamoxifen, toremifene

                        Aromatase inhibitors (postmenopausal women)

                        Non-Steroidal- anastrozole, letrozole,

                        steroidal - exemestane

                        Antiestrogens - fulvestrant; postmenopausal women

                        Progestins - megestrol and medroxyprogesterone

                        Other steroid hormones (high-dose estrogens, androgens; only of historical interest)

INITIAL ENDOCRINE THERAPY OPTIONS: (for breast ca)

No prior endocrine therapy or over one year since endocrine therapy

Premenopausal ➙ Antiestrogen or Ovarian Function Suppression (OFS) with endocrine therapy like postmenopausal women

Postmenopausal ➙ Aromatase inhibitor or antiestrogen

Prior endocrine therapy

Second-line endocrine therapy (see below

SUBSEQUENT ENDOCRINE THERAPY OPTIONS

Premenopausal patients

Add OFS and treat like postmenopausal women

Postmenopausal patients

Nonsteroidal (anastrozole, letrozole) or steroidal (exemestane)

aromatase inhibitor ,fulvestrant, tamoxifen,megasterol, fluoxymesterone,ethinyl estradiol.

*Consider chemotherapy if no clinical benefit (response or stable disease) after three endocrine regimens or symptomatic visceral disease

Selective Estrogen-Receptor Modulators

Tamoxifen is the historic standard as treatment for ER-positive metastatic breast cancer, associated with a 50% response rate and median duration of response of 12 to 18 months among treatment-naive patients .Tamoxifen, 20 mg daily is the most

commonly used SERM in many countries. Toremifene has also been approved but has a similar profile and is cross-resistant with tamoxifen.

Aromatase Inhibitors:

In postmenopausal women with no or distant previous exposure to antiestrogen agents, the aromatase inhibitors show similar or modestly superior efficacy compared with tamoxifen. These drugs are ineffective in premenopausal women and should be avoided as single agents in this setting. Aromatase inhibitors are more active and less toxic than megestrol acetate as second-line therapy; they also are more active and less toxic than the first-generation drug aminoglutethimide.

Letrozole is a more potent suppressor of total-body aromatization and plasma estrogen levels than anastrozole in patients with breast cancer12. However in metastatic breast cancer there is no convincing clinical advantage of one aromatase inhibitor over another.

Exemestane is a steroidal compound with the activity of aromatase inhibition.

Antiestrogens:

The nonsteroidal pure antiestrogen fulvestrant downregulates ER without the agonistic activity of tamoxifen. It appears to have inhibitory effects in breast and uterus with neutral effect in bones and lipids, and clinical effects appear similar to aromatase inhibitors.15 It is currently only approved in postmenopausal women as a monthly, deep IM injection

In premenopausal women with metastatic breast cancer, combined endocrine therapy with ovarian suppression and tamoxifen can improve survival compared to treatment with either tamoxifen or ovarian suppression alone. Premenopausal women with metastatic tumor despite tamoxifen use are candidates for ovarian suppression/ablation and aromatase inhibitor therapy.

In Postmenopausal women either tamoxifen, aromatase inhibitors, fulvestrant or progestational agents are used as palliation for metastatic breast cancer. Aromatase inhibitors are preferred as initial agents for women who received prior tamoxifen treatment in the adjuvant setting. 

Health to Happiness

Ca Rectum

Q. Describe the surgical anatomy of mesorectum and its importance in management of Carcinoma rectum.

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

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

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

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"

2.PAPER I JUNE 2008
Q. Patho-physiology of "Septicemic Shock". 








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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–*