The robotic system used now is DaVinci system.
Parts
y Master surgeon console: On which the surgeon sits, uses his hands to manoeuvre instruments via master controllers and sees 3 -dimensions vision through the stereoviewer y Patient cart: Patient lies on this cart and the instruments are docked (fixed) into the
ports on the robot wheel cart over this table. There are 4 arms for instruments with one of them being camera port. Ports are placed as in laparoscopy and then the instruments inserted in ports through robot arms to connect them to the master console control y Vision cart: Has a binocular vision through 3-D endoscope connected to camera.
Advantages
y Stereoscopic depth perception (3-D vision)
y More range of motion due to wrist like motion present in robotic instruments which give some degrees of freedom in movement
y Improved hand eye co-ordination as the robotic camera is controlled by the surgeon and is held in steady position by robotic cart so no fatigue or tremors
y Less surgeon fatigue due to excellent ergonomics (sitting surgery) y Comparably less prolonged learning curves than with laparoscopy.
Limitations y Cost
y Learning curve
y Duration of surgery is prolonged compared to open surgery Commonly performed robotic procedures
y Gastrointestinal—cholecystectomy, pancreatic resections, bariatric surgery, colectomy, mesorectal excision, fundoplication, gastrectomy
y Urology—radical cystectomy, prostatectomy, pyeloplasty, nephrectomy y Thoracoscopic—esophageal surgery and thymectomy
y Head and neck—transoral robotic surgery (TORS) for nasopharyngeal cancer, robotic thyroidectomy
y Gynecology—hysterectomy
Malignancy y Lymphoma y Leukemia
Autoimmune disorders y SLE
y Rheumatoid arthritis y Sarcoidoses y Amyloidoses
Other y Metastasis from various malignancies.
Tubercular cervical lymphadenopathy
y It is a very common cause of cervical lymphadenopathy and should be ruled out in all cases of it
y Caused by M. tuberculosis
y Children are more commonly involved but, it can affect individuals from any age group.
Clinical features
y Fever with evening rise, anorexia, weight loss, chronic cough with sputum production might precede the appearance of cervical lymph nodes
y Initially, the nodes are enlarged and discrete. This is due to lymphadenitis without periadenitis
y Then, lymph nodes become matted due to periadenitis and adhesions y There is no sign of inflammation and the nodes are nontender
y Upper jugular cervical nodes are most commonly involved. Other groups and lymph nodes in other areas can also be involved.
Natural history
y If the disease progresses unhindered, then after matting of lymph nodes, caseous necrosis leads to abscess formation which is known as cold abscess.
y Further progression lead to tracking of this pus along the fascial layers of neck. Because of the plane of lymph nodes deep to deep cervical fascia, the pus also travels down deep to this fascial layer
y Further increase in pus leads to increased tension and rupture of deep cervical fascia with tracking of pus in superficial fascia. This is known as collar- stud abscess. It shows cross- fluctuation due to presence of two abscess cavities on either side of the deep fascial rupture y Finally, the pus ruptures through the superficial fascia and skin and presents as
tubercular sinus or ulcer.
Investigations
y Evaluation for tuberculosis—chest X-ray, sputum for AFB and culture, mantoux test, ESR, total leukocyte count with differential count, hemoglobin level.
y FNAC of the lymph node and if it is inconclusive, excision or incision biopsy can be done y CECT neck and chest will show the entire extent in cases with cold abscess.
Treatment
y Antitubercular medications as described in the question on ATT
y Local management of abscess is done by antigravity aspiration that is aspiration from higher level than the most dependent part if it is large or if it does not resolve on anti- tubercular treatment.
Contd...
y Excision is done for enlarged lymphnodes if they do not resolve with antitubercular treatment.
Q41. Discuss the medical management of a patient of TB.
Define the various types of drug resistant TB categories and discuss their management.
Ans.
y DOTS categories
Category 1 New case pulmonary or
extrapulmonary 2HRZE+ 4HR
Category 2 Relapse, failure, default 2HRZES + 1 HRZE + 5HRE
Category 3 MDR TB 6 drug IP for 6–9 months
4 drug CP for 18 months H – isoniazid, R – rifampicin, Z – pyrazinamide, E – ethambutol, S – streptomycin
y MDR-TB suspect
– Any patient who fails category 1 treatment
– Category 2 patients who remain sputum positive at 4 months of treatment or later – Close contacts of MDR TB patients with smear positive pulmonary TB
y MDR TB suspect patient—start appropriate ATT first according to class of the patient
MDR TB case: MDR TB suspect with sputum culture positive with resistance to atleast H and R. All patients with MDR TB and all patients with rifampicin resistance are treated with category 3.
Management of MDR TB
y Follow-up smear and culture of specimens collected at the end of 3, 4, 5, 6, 7 months, then at 9th month end, 12th,15th,18th, 21th, 24th month end.
y 2 consecutive smear and culture negative samples obtained then patient is called smear/
culture converted.
Regimen (category 3)
Intensive phase Kanamycin
Ofloxacin/levofloxacin Ethionamide
Ethambutol Pyrazinamide Cycloserine
6–9 months
Continuation phase Ofloxacin/levofloxacin Ethionamide
Ethambutol Cycloserine
18 months
PAS can be substituted if any of the above drug is not tolerated.
Groups of anti-TB drugs
1 Oral 1st line HRZE
2 Injectable aminoglycoside Streptomycin, kanamycin, capreomycin, amikacin, viomycin 3 Fluroquinolones Ciplox, oflox, levoflox, moxiflox, gatiflox
4 Oral 2nd line PAS, ethionamide, cycloserine 5 Other drugs with unclear
efficacy Linezolid, amoxicillin, thiacetazone
XDR TB
y Extensive drug resistant TB
y H, R resistance + any fluroquinolone resistance + at least one of three injectable anti-TB resistance
y Treat with category 3 treatment as per sensitivity
Totally drug-resistant TB (XXDR- TB/ virtually untreatable TB/ extremely drug-resistant TB)
y All first line oral + second line oral + all injectable
y These are also treated like XDR TB with maximum possible culture sensitive drugs for
> 2 years.
Q42. Write a note on Ludwig’s angina.
Ans.
Definition
Rapidly spreading cellulitis of floor of mouth and submandibular space (submaxillary or submental and sublingual divided by mylohyoid) secondary to:
y Soft tissue infection y Tonsil infection
y Lower premolar or molar infection (80%) y Submandibular sialadenitis
y Injuries to the oral mucosa
Symptoms
y Trismus, odynophagia y Excessive salivation
y Tongue is pushed upwards and backwards due to edema of the floor of the mouth.
Extent
y Can go to parapharyngeal and retropharyngeal spaces y Laryngeal edema
y Aspiration pneumonia y Septicemia
On examination
y Tongue is pushed backwards
y Woody hard feel of submandicular and submental spaces Organisms
y Mixed infection of aerobes and anaerobes y Dental origin—streptococcus viridians and E. Coli Treatment
y Systemic antibiotics
y Tracheostomy if airway is endangered
y Incision and drainage should be delayed as long as possible, as pus is seldom found y Submaxillary space (superficial to mylohyoid)—transcutaneous drainage through
submandibular skin fold
y Sublingual space (deep to mylohyoid)—drained through floor of mouth Q43. Write a note on tetanus.
What is tetanus neonatorum? Discuss its preventive measures.
Write the measures to be taken for prophylaxis of tetanus after an injury.
Ans.
y Tetanus is caused by clostridium tetani—a gram positive, anaerobic, terminal spore bearing organism
y It produces exotoxin called tetanospasmin which on reaching the neural tissue acts on spinal cord, brain, sympathetic system and motor end plate of muscles to block the normal inhibitory pathways of these nerves and lead to the characteristic muscular rigidity and spams
y The spores reside in soil and dust and enters body through contaminated wound and injuries or chronic ulcers or dental extraction sites or in injection drug abusers through injection sites from where they germinate, produce exotoxin and bind their neuroreceptors tocause the disease. This entire life cycle takes around 5 to 10 days in the body
y Some specific modes of transfer give the tetanus its name.
– Tetanus neonatorum—infection through infected cut surface of umbilical cord
– Puerperal or postabortal tetanus—infection through unsterile uterine instrumentation.
– Otogenic tetanus—infected material to clean ear can introduce infection y Clinical features
– Most early symptom—trismus (Lock jaw)
– Anxious expression of face (Risus sardonicus or sardonic grin) – Opisthotonus
– Constitutional symptoms such as elevated temperature, tachycardia, tachypnea, cyanosis
– Rigidity of muscles of lower limb and abdomen. Gradually all the muscles develop rigidity and death is due to respiratory arrest, due to laryngeal spasm and spasm of respiratory muscles.
– Other causes of death include aspiration pneumonia, lung infections or hyperpyrexia.
Management of established case
y Patient should be admitted to a quiet, dark and well ventilated room y Care of airway, breathing
y Sedation with diazepam/barbiturate is frequently used to avoid provocation of spasms y Foley catheter, feeding tube, muscle relaxation and tracheostomy, IV fluids and antibiotics
as per requirement. These are needed in severe cases. Mild cases can be managed with conservative measures and supportive care alone
y General nursing care of the patient till he stabilizes and is out of the ventilator.
Specific treatment
y Passive immunisation with human anti-tetanus globulin, 4000 units or equine anti- tetanus serum, 1 lac units half IV and half IM should be administered with tetanus toxoid (active immunisation).
y Crystalline penicillin 20 lac unit 6 hourly or 10 lac unit 4 hourly should be given y Wound debridement.
Prophylaxis
Means: Immunization, antibiotic and wound cleansing and debridement (most important).
Active immunization Passive immunization
y Aluminium phosphate adsorbed tetanus toxoid 0.5 mL in left deltoid is the best agent for active immunization y 3 doses at 4 weeks interval and then
booster after 1 year completes the routine mandatory immunization requirement.
Booster is given at every 4–5 years to maintain immunity. Immunization schedule is 6,10,14 weeks age, 18 months age, 5 year age and 10 year age
y Equine anti-tetanus serum 1500 units SC/
IM after negative sensitivity testing
y Human anti-tetanus globulin 250–500 units IM is a homologous antitoxin and does not require sensitivity testing. It is many times more protective than equine serum and is therefore preferred
Plan of immunization after injury
y A patient who has been completely immunized as above within past 5 years needs no tetanus immunization prophylaxis. It should be managed only with wound debridement
y A patient who has been completely immunized in past with a clean non-penetrating wound < 6 hours duration needs only a single tetanus toxoid injection and wound debridement
y A patient who has been completely immunized in 5–10 years range with a dirty, penetrating or old wound needs only a single tetanus toxoid injection and wound debridement but, if it is > 10 years then he needs single shot tetanus toxoid with anti-tetanus globulin.
y A patient whose immunization history is not known needs complete tetanus immunization course if he has a clean nonpenetrating wound < 6 hours duration and complete tetanus immunization course with anti-tetanus globulin for old, penetrating or dirty wounds.
y Tetanus neonatorum can be prevented by using aseptic techniques and surroundings during delivery and aseptic means to cut the cord. Also 2 maternal immunizations at 16 and 20 weeks serve to prevent both maternal and neonatal tetanus in nonimmunized mothers and a single booster dose in immunized mothers. The immunization can be given any time the mother is seen but atleast three weeks before delivery. If the mother is seen directly during delivery, then the infant can be given 750 units Equine ATS or 250 units human serum within 6 hours of birth to prevent tetanus neonatorum.
Q44. Write a note on gas gangrene.
What is gas gangrene? Discuss its management.
Ans. Gas gangrene is caused by clostridium perfringens/clostridium welchii and other clostridia species such as C. septicum, C. histolyticum, etc., anaerobic organisms also called “flesh eating bacteria”.
Pathogenesis
y These organisms enter the body through wounds which are grossly contaminated with soil/foreign bodies which provide the low tissue resistance, low pH, anaerobic environment and high calcium due to cell lysis in the wound necessary for clostridial growth
y The organisms are also present in stools and female genital organs and therefore wounds that come in contact with these areas and body fluids are more predisposed
y The organism then produce exotoxins which cause the characteristic gas gangrene.
These include lecithinase (Alpha toxin), hyaluronidase, collagenase, other hemolytic and leukocidal toxins
y Occlusion of end arteries supplying the wound, accumulation of wound exudates and inadequate wound debridement are all factors that increase the risk of occurrence of gas gangrene
y Diabetes and chronic arterial occlusive diseases also predispose.
Stages of disease progression
1. Stage of contamination—no symptoms and signs.
2. Stage of anaerobic clostridial cellulitis—no systemic symptoms.
3. Spreading cellulitis and fascitis with systemic symptoms and signs.
4. Clostridial myonecrosis.
5. Bacteremia and septicemia.
Clinical features
y It presents as rapidly spreading infective gangrene with accumulation of gas in muscles and subcutaneous tissue and is called clostridial myonecrosis
y Initially it can be present as clostridial cellulitis with edema of subcutaneous tissue and spreads rapidly to involve the muscles and subcutaneous tissue rapidly
y Can affect the liver (Foaming liver)
y Constitutional symptoms such as pyrexia, anxiety, tachycardia, vomiting and hypothermia are initial symptoms
y Pain out of proportion to the appearance of wound, swelling and edema of the affected part, profuse, foul smelling, brown or grey color discharge called “dishwater pus” are also the characteristic features. Finally, the wound becomes black in color marking the phase of gas gangrene
y On examination, crepitus is almost always present and is pathognomonic.
Investigations
y Gram stain of wound exudates reveal the organisms y Anaerobic cultures are positive
y Nagler’s reaction is used to detect C. welchi.
Management
Treatment of a diagnosed case
y Wound drainage and debridement can extend from extensive debridement to even guillotine type amputation as a life saving measure in cases of severe myonecrosis y Crystalline penicillin 10 lac unit 4 hourly or 20 lac unit 6 hourly
y Anti-gas gangrene serum 22,500 IU (contains 9000 units C. welchii, 4500 units C. septicum and 9000 units Cl. oedematiens) stat and repeated at 6-hour interval for 3 consecutive doses y Hyperbaric oxygen therapy is also used once the wound is non-infective and healthy
to aid healing.
Prophylaxis
y Wound drainage and debridement to remove all devitalized tissues and foreign bodies y Crystalline penicillin 10 lac unit 4hrly or 20 lac unit 6hourly
y Anti gas gangrene serum 22,500 IU (contains 9000 units C. Welchii, 4500 units C. septicum and 9000 units Cl. oedematiens) stat single dose is suggested but not of proven role in prophylaxis.
Q45. What is carbuncle? Discuss its management.
Ans. Carbuncle is caused by staphylococcal infection (S. aurues)—aerobic, gram positive cocci in clusters and is an infection of subcutaneous tissue.
Pathogenesis
y The organism penetrates deep into subcutaneous tissue and produces multiple interlinked abscesses that open separately on surface to produce a sieve like appearance y They coalesce in center and produce the wound
y This can extend peripherally and assume large sizes
Clinical features
y Patients are commonly diabetic males
y Common sites are nape of neck, back, dorsum of hand, shoulder, chest and abdomen y Constitutional symptoms mark the onset
y Begins as a painful, edematous subcutaneous swelling and progresses to a sieve like appearance which is characteristic of carbuncle
y The openings can finally enlarge, coalesce and form an ulcer.
Investigations
y Wound smears and culture sensitivity y Blood culture
y Diabetic work up Treatment
y Control of diabetes
y Wound debridement and dressing—cruciate incision and deroofing y Culture specific antibiotic therapy
Q46. Write a note on madura foot.
Ans.
y Madura foot is an infectious condition affecting foot y It is also known as mycetoma.
Causes are as follows:
Eumycetoma Actinomycetoma
y Organism—Madurella mycetomeii.
y Disease is slowly progressive type y Treatment is antifungal therapy for
prolonged periods
y Organism—Actinomyces, Nocardia y Disease is rapidly spreading and extensive.
y Treatment is amikacin + co-trimoxazole (first line) or rifampicin or amoxyclav (second line)
Entry and route of spread y Inoculation from trauma site
y From here the disease localizes in the site and further spread is via lymphatics as well as along the fascial planes
Clinical features
y Triad of noncontagious multiple sinuses, multiple painless subcutaneous masses and seropurulent discharge
y Site: Foot is the disease site in most cases. Other sites are perineum, arm, leg, head, neck, thigh and hand
y Tendons and nerves are spared till very late in the disease y Secondary bacterial infection can complicate the local disease
y The disease spreads along the fascial planes so what is a small lesion superficially might be extending for large areas deeply.
Diagnoses
y X-ray—areas of calcification can be seen. Also, areas of punched out lesions in bone can be seen.
y Ultrasound
y MRI—shows “dot in circle” sign.
y Biopsy:
– Type 1 mycetoma: Multiple neutrophils surrounded by lymphocytes and mononuclear cells surrounded by fibroses.
– Type 2 mycetoma: There are no neutrophils in the lesion. It only contains macrophages.
– Type 3 mycetoma: It contains epitheliod granulomas with giant cells.
y FNAC can also be done but biopsy is more reliable.
y Culture-sensitivity is done to help in selection of culture specific antibiotics.
Treatment
y Antibiotics or antifungals as written above
y Surgical debridement under general or spinal regional anesthesia. Use of local anesthesia is contraindicated.
Q47. Write a note on anatomy of palmar spaces.
Ans.
y Arrangement of the fascia and fascial septa in the hand is such that it forms many spaces y Spaces are of surgical importance because they may become infected and distended
with pus
y The three palmar septa divide the palmar space into thenar and midpalmar spaces.
Midpalmar and thenar spaces
y These are triangular spaces of which base lies distally and the apex is directed proximally y The thenar space lies between the lateral and intermediate palmar septa
y The midpalmar space lies between the intermediate and medial palmar septa.
Boundaries of thenar space
y Medially: Intermediate palmar septum y Laterally: Lateral palmar septum
y Anteriorly: Lateral part of palmar aponeurosis, and flexor tendons to index finger y Posteriorly: Adductor pollicis, transverse head.
Boundaries of midpalmar space y Medially: Medial palmar septum y Laterally: Intermediate palmar septum
y Anteriorly: Medial part of palmar aponeurosis and flexor tendons to medial three fingers y Posteriorly: Fascia covering the medial three metacarpal bones and intervening
interosseous muscles.
Fig. 1: Anatomy of palmar spaces
Extent of spaces
y Proximally, the midpalmar and thenar spaces extend up to the distal margin of the flexor retinaculum
y Distally, the thenar space extends up to the proximal transverse crease of the palm and the midpalmar space extends up to the distal transverse crease
y Incisions are made through these creases to drain the spaces.
Communications of spaces
y The spaces are normally closed at the proximal end
y However, occasionally the midpalmar space may communicate with the forearm space through the carpal tunnel
y The two spaces of the palm quite frequently communicate with each other, and infection can pass from one to the other.
Contents of the thenar and midpalmar spaces
y Normally filled mainly with loose connective tissue. When infected they can be distended with pus
y They are closely related to the lumbrical muscles. The thenar space contains the first lumbrical muscle, while the midpalmar space contains the second, third and fourth lumbrical muscles, the tendon of each lumbrical muscle is surrounded by a lumbrical canal.
Clinical Correlations
y Infection of the midpalmar space may result from tenosynovitis of the middle and ring fingers or from a web infection which has spread proximally through the lumbrical canals y When this happens the normal concavity of the palm is obliterated and the swelling
extends to the dorsum of the hand
y The space can be drained by an incision in either the 3rd or 4th web depending on where the pus points.
Q48. What is the difference between acute paronychia and felon? Discuss its features.
Write a note on acute paronychia.
Ans. Definition
y Acute paronychium is the infection of the nail fold whereas felon or whitlow is terminal pulp space infection
y Acute paronychium is the most common hand infection whereas felon is the second most common infection.
Etiology
y Small pricks and abrasions and cuts in hand especially in people involved with household work, manual laborers, gardeners is the commonest etiological factor
y Unsterile manicure instruments can also result in paronychium y S. aureus is the most common organism.
Clinical features Paronychia
y Painful swollen nail folds is the most common presentation
y Examination reveals tenderness, redness and swelling of the nail fold which increases on pressing the nail
y Suppuration can extend deep to nail and reach upto base of nail.
Felon
y The pulp of finger is painful and swollen
y Examination reveals tenderness, redness and swelling of pulp which increases on pressing.
Complications Acute paronychium y Chronic paronychium
y Paronychium can extend into pulp space and result in felon.
Felon
y Suppurative flexor tenosynovitis
y Septic arthritis of distal interphalangeal joint y Osteomyelitis of terminal phalanx.
Treatment Acute paronychium
y Conservative management with antibiotics and analgesics in mild cases y Elevation of nail fold and release of pus
y Bilateral cuticular incision and pus drainage y Nail excision and pus drainage