7fa437dbb6a5404d9bf72521f65c6631

Section : E: Surgical Specialty Topics
Acknowledgement for this section
1. Dr. Prasanth Bylapudi, NRI institute of medical sciences, Visakapatinam, Andhrapradesh
2. Dr. Mohammed Shiyas
RRM’S SURGERY SIXER APP BASED WORK BOOK 1

Chapter 1: Urology
Part : 1: Kidney, Ureter, Bladder and Urethra
BRODELS LINE-Avascular line on the greater curvature of the kidney
Narrow points in the ureter:
• Length of ureter - 20cm
KIDNEY INVESTIGATION
CYST IN KIDNEY

● IOC- CECT ABDOMEN
BOSNIAK CLASSIFICATION
Category I- Simple Cyst Clear cyst

No septum
Category II- Benign Cyst Hair Line Septations+
No soft tissue component or calcification
Category IIF- Complex Cyst Hair line septations++
No soft Tissue component
Septations have no enhancement
<5% risk of malignancy
Category III- Indeterminate Cyst Cyst wall thick enhancement+
Septations enhancements*
50% risk of malignancy
Category IV- Malignant Cystic mass Soft Tissue components are seen
100% risk of malignancy
• Category I, II - no risk of malignancy
• Category IIF- <5% risk of malignancy
• Category III- biopsy is done

• Category IV- Resection
SPECIAL SCANS IN KIDNEY
● DMSA(Dimercapto succinic Acid)- IOC- for accessing the Morphology of kidney

● DTPA (Diethylene Triamine Penta Acetate)-For accessing the Perfusion: Physiological study of
kidney. PUJ obstruction can be detected.
● MAG-3 (Mercapto Acetyl Triglycine Scan)- IOC FOR PUJ OBSTRUCTION**
RENAL STONES
CLINICAL FEATURES
● Mostly asymptomatic
● Based on the location of the stone the symptoms are :
■ Renal-back pain
■ PUJ- pain radiating from loin to testicles ( Genital branch of
Genitofemoral nerve)
■ Mid ureter-mimics pain like appendicitis
■ VUJ- pain radiating from loin to groin or mid thigh ( ilioinguinal
nerve>iliohypogastric )**
■ Intramural ureteric stone- strangury
Figure: Symptoms related to Location of Stone
DIETEL'S CRISIS- After an attack of acute renal pain following an alcoholic binge, a swelling in loin is
found, some hours later following the passage of stone large amount of urine is passed , pain is
relieved and swelling disappears.

Clinical features-
● Hematuria
● Increase frequency
● Strangury
● Pain
**Worst pain experienced by a male in his life time- Ureteric Stone pain- DOC for him is Injection
Diclofenac**
Types of stones
Calcium Oxalate (Calcium oxalate Monohydrate and Dihydrate)

• Also known as Mulberry stone
• M/c type of stone overall
• M/c stone to cause haematuria
Triple Phosphate ( Calcium , magnesium ,NH4,PO4 / Struvite )
Cystine
● Hard stone
● Cystinuria
● SH=SH (disulphur bond makes it radiopaque); without calcium they are still radio opaque due
to the Bond**
Uric acid
● Only radiolucent stone
● Yellow colour
● Associated with hyperuricemia in Gout, cancer
Rare stones
● Indinavir (HIV patients)- Radiolucent
● Xanthine ( In Xantine Oxidase deficient patients)- Radiolucent

Urinary crystals
Image Description
Calcium oxalate monohydrate:

• Dumbbell shaped or Hour glass
shaped crystals

Cystine crystals:
• Hexagonal
• Benzene ring like
Struvite:
• Coffin lid shape
Brushite:
• Needle shaped
By ESWL- Hardest stone to break- MBC ( Calcium oxalate Monohydrate> Brushite> Cystine)

Drug causing renal stone ( mnemonic- TIMES- CALL)
• T-Triamterine
• I-indinavir
• M-Mg trisilicate ( Antacids)**
• E-ephedrine
• S- Septran
• C-ciprofloxacin
• A- Acetazolamide
• L-loop diuretic
• L- laxatives containing Mg**
MANAGEMENT OF STONE
● < 5mm - No treatment needed

● Fluid intake :>2.5 l/urine
● Restrict : Protein, salt , oxalate diet
● Increase consumption - Calcium supplements**
● Juice - Cranberry juice** is used in management of renal stones**
BLADDER STONE
Primary Bladder stone Secondary Bladder stone

• • Secondary to some pathologies like
BOO, BPH and Stenosis
• Formed in Bladder itself**
• • This is the most common Bladder
stone**
• Ammonium Urate is the MC secondary
bladder stone.
• The calcium Apoplexy ( Coating of
Calcium over the ammonium urate
stone) results in radio opaque

MANAGEMENT
● ESWL-EXTRACORPOREAL SHOCK WAVE LITHOTRIPSY
● PCNL- PERCUTANEOUS NEPHROLITHOTOMY
● RIRS- RETROGRADE INTRA RENAL SURGERY ( Via Ureter the Stone removed from kidney)
● Open Nephrolithotomy- Opening the kidney along the Brodel’s line and remove the Stone
● Open Pyelolithotomy- Opening the renal pelvis and removing the stone.
ESWL
• Passing Piezo electric waves and breaking the stones.
Indication
● <1.5cm size
● Mainly done for stone in kidney, pelvis, upper ureter ( Cannot use it for lower ureteric stone
(d/t pelvic brim bone hindrance))
Contraindications
● Absolute- pregnancy, bleeding diathesis
● Relative:
○ Obstruction / distally
○ Infection
○ Hematuria
○ Renal dysfunction
Complications
● Hematuria
● Incomplete clearance
● If stone >1.5 cm a rare complication known as stein strasse ( Stone Street)** happens. To
prevent this problem happening we must keep a 20 cm Double J stent before ESWL.
PCNL
Indication
● Stone >2cm
● Infected
● Obstructed

● Cysteine
● Failed ESWL
● Anatomical abnormality- Calyceal Diverticulum containing Stones**
Procedure:
• Trans costal approac
• Subcostal Approach
• We insert a guidewire under
fluoroscopic Guidance- we dilate the
tract and insert the Nephroscope via
the tract and remove the stone.
Complications
● Bleeding
● Sepsis
● Perforation of bowel
● Trans costal approach- Pleural injury and Hydrothorax can happen
● Subcostal Approach- Duodenal injury, Colon injury and Liver and spleen injury
● Injury to renal artery /vein/IVC**
Staghorn Stone:
• Sandwich technique- ESWL followed by PCNL
• If this technique is not mentioned – go with PCNL**
RIRS
● For renal pelvis stone
● For mobile stone
● By retrograde method we use ureteroscopy to remove intra renal stones.
Management of Ureteric stones:
● <5mm - it will pass
● >5mm/impacted somewhere- Removed by Dormia basket technique

Figure: Dormia Basket removal
• For upper ureteric stone- PUSH BANG technique** we push the upper ureteric stone back
into the renal pelvis by Ureteroscope and break the stone by ESWL**
Bladder stone
● Old technique- Open Cysto lithotomy
● Latest- Transurethral Cysto lithotripsy
● Lasers used now- HO:YAG(best) Nd:YAG
Image Based question:
• The image shown below is asked in AIIMS- please note the Doube J stent in right Ureter**
• The left kidney is having a Percutaneous DJ stent- for percutaneous nephrostomy**

Image : Right Ureteric Stent and left Percutaneous stent**
RENAL CELL CARCINOMA @ Grawitz Tumor @ Hypernephroma

● a/k/a Clear cell adenocarcinoma
● M/c site- Upper pole
● Origin- Proximal convoluted tubule
● MC in 50-60yrs
● MC in men 2:1 ratio
● M/c malignant neoplasm
● MC arises from Proximal Convoluted tubule**
● M/c presentation – RCC Triad
o Hematuria (MC symptom)

o Pain
o Loin mass

Pathology
Clear cell type Papillary type Chromophobe type Medullary type
o Most common o Trisomy of o Best prognosis

type 7,16,17
o M/c type o Chromosome 7
o Von Hippel mutation
Lindau Gene o M/c in PCKD
mutation patients ON
o 3p mutation** DIALYSIS
Clinical Features-
● Earliest and m/c feature – HAEMATURIA**
● Mass can grow inside renal vein- it can grow up to Right atrium- it is still operable.
● Young male patient can present with left side varicocele which is irreducible on lying down**
● Hematogenous metastasis- Pulsatile Skull secondaries and Cannon Ball Secondaries can
develop
Paraneoplastic syndrome in
• Increased ESR (M/C)**
● Hypertension (2nd m/c)
● Anemia (3rd m/c)
● Hypercalcemia (5%)
● Polycythemia (3%)
● Stauffer's syndrome- non metastatic liver enzyme elevation**
● Other features- Neuropathy, Amyloidosis, PUO and weight loss
GRADING and SCORING SYSTEMS from Bailey and Love:

• FUHRMANS - Nuclear grading system
• LEIBOVICH SCORE -Histological scoring
STAGING
● Stage I- mass <7 cm within the kidney
● Stage II- mass >7 cm within the kidney

● Stage III- Involving Renal Vein,,IVC or even upto Right atrium /nodes/ adrenal gland**.
Tumor not spread out of Gerota’s Fascia**
● Stage IV- Out of Gerotas fascia
Radical nephrectomy Partial nephrectomy (nephron sparing

procedure)
● Structures removed: ● Indication

○ Kidney ○ T1 - <7cm (even with normal
○ Adrenal gland opposite kidney)
○ Perinephric pad of fat ○ Single functioning kidney
○ Regional nodes ○ VHL mutation- B/L RCC** cases
○ Ureter ○ Renal failure (DM,HTN)
○ Gerota’s fascia
Renal cell cancer Wilm’s Tumor

Chromosome 3p mutation 8/11th Chromosome Mutation
Age: 50-60 years Age: 1- 5 years
MC tumors in Adults MC primary tumor in Children
C/F: C/F
Hematuria ( MC presentation) Hematuria
Mass Mass ( MC presentation)
Pain Pyrexia
Associated with
• Beckweith Wiedman syndrome-
Macroglossia+ Visceromegaly+
Hyperinsulinemia
• WAGR syndrome- Wilms, Aniridia, GU
anomalies and Renal anomalies
MC distant mets- Lung MC distant Mets- Lungs
No need of preop Biopsy Preop Biopsy is must
Surgery is TOC Surgery is TOC
Chemo and Radioresistant Chemo sensitive and Radio sensitive
Sunitinib** - ( monoclonal antibody) used for Chemo- Vicristine, Actinomycin
metastatic RCC
Bad prognosis Good Prognosis

2 protocols in Wilm’s Tumor management:
NWTSG- National Wilm’s tumor study group
• Advise surgery first followed by Chemotherapy
• Pre chemotherapy based staging**
SIOP- ( International Society of Paediatric Oncology)-
• Chemotherapy followed by surgery
• Post Chemotherapy Based staging system**
Overall survival is same for both.
Surgery- Radical nephroureterectomy

• For Bilateral Wilms - chemo is done first, then following the shrinkage of the tumor- nephron
sparing surgery is done
ANGIOMYOLIPOMA
● Hamartoma
● 50% of Tuberous sclerosis ( EPILOA- Epilepsy+ Low Intelligence+ Adenoma Sebaceum)
● This contains- Blood vessels+ Muscles+ Fat content inside**
● IOC- CT SCAN (Fat inside lesion)
● Tumor marker: HMB 45 +ve
● Clinical features:
○ Hematuria
○ Hypertension
○ Mass
○ Pain
○ Anemia
○ Wunderlich syndrome-spontaneous Retro peritoneal hemorrhage- self limiting
Treatment
● <4 cm- no treatment

● >4 cm- partial nephrectomy
● Selective embolization

BLADDER CANCER
● M/c type: Transitional cell cancer(90%)
● 2nd m/c- SCC
● 3rd m/c – Adenocarcinoma ( Arises from Urachal remnants)
Risk factors:
TCC Squamous cell cancer

● M/C risk factor- smoking • Stones
● Schistosomiasis • Schistosomiasis
● Occupational • Special diseases- Diverticula diseases,
○ Beta naphthylamine (coal) Long term catheters
○ Diaminobiphenyl (Aniline)
○ Aminobiphenyl
○ Nitrophenyl
• M/c presentation- painless terminal haematuria
• M/c site - Dome and Lateral wall of bladder**
• Cancer from anterior wall producing spread to posterior wall is known as KISSING cancer**
Investigation
● Urine examination: Screening test for

○ NMP-2 Protein
○ MCM Protein
● IOC FOR STAGING- CECT ABDOMEN / PELVIS
● IOC FOR DIAGNOSIS-CYSTOSCOPIC BIOPSY
STAGING
● Ta- Non invasive papillary cancer
● Tis- Cancer in situ

● T1- Subepithelial connective tissue
● T2- Muscularis propria
● T3- Peri vesical tissue
● T4- adjacent organs - prostate, seminal vesicles, vagina , abdominal wall

Intravesical therapy agents:
● Mitomycin -C
● Doxorubicin
● Thiotepa
● BCG (BEST)
RADICAL CYSTECTOMY : STRUCTURES REMOVED
● Bladder+ fat
● Prostate + seminal vesicles
● Uterus+ cervix+ fallopian tube +anterior vaginal wall
● +/- Urethrectomy
● Pelvic lymphadenectomy

Ileal conduit Colon Conduit
○ M/c type ○ Drained into Sigmoid Colon
○ M/c complication- ureteroilial ○ M/c complication-infection
stricture ○ Risk of malignancy++
• Important pre-requisite for this

procedure- Patient must be able to hold
200 ml saline in Rectum with continence
• Neobladder can also can be created if urethra is not involved using ileum.
● Continent Urinary diversion procedure – Kock’s Ileostomy ( Ileum made like a valve)
● Mitranoff procedure- appendix can be used as a drainage of urine procedure from Bladder.
Figure: Mitranoff procedure
Conduit associated metabolic problems:
● Ileal - metabolic acidosis+ hyperchloremia
● Jejunum- metabolic acidosis+ hypochloremia**
● Colon- metabolic acidosis+ hyperchloremia
● Stomach- Metabolic alkalosis** + hyperchloremia- Stomach conduit is used in Renal failure
patients**

Management of the above problems:
• IV SALINE + NaHCo3
• Oral { potassium citrate+ NaHCo3} – Three times daily
Chemotherapy
• Indicated in ≥T3a, LN positive, Margin +ve
• GC regimen- Gemcitabine+ Cisplatin
• MVAC regimen (Old)- Methotrexate+ Vinblastin + Actinomycin+ Cisplatin
• Post op RT is not useful
URINARY TRACT INFECTION

● M/c organism- E.coli
● Kass criteria
○ Men: >105 Colony forming units/ ml (mid steam urine)

○ Female: >103 CFU/ml (catheterised urine)
● MC cause of prostatitis- E.Coli
RENAL TB
● M/C - KIDNEY; other sites- URETER and BLADDER
● Route of entry- Hematogenous route
● Earliest and m/c features of renal TB - Increased frequency** ( DD for increased frequency-
DM, UTI, TB)
● O/E of urine in Renal TB- Sterile pyuria** (Bacteria is absent but WBC count is increased)
● **Early morning urine specimen for 3 days – Acid Fast Bacilli to diagnose TB
IOC to diagnose early TB:
• Earliest feature in TB kidney- Blunting of Calyx**
● OLD modality- IVP
● NEW modality- CT PYELOGRAM**
Complications of chronic TB:
• Cement or putty kidney
• Golf hole ureter
• Thimble small bladder

Figure: Golf hole ureter and Blunting of calyx
Treatment of chronic TB – Resection and reconstruction(optimum after 6-12 weeks after ATT
started)
Trauma to urinary system

Renal trauma
● M/C mechanism - BLUNT INJURY
● Haematuria (omnious sign)
● IOC- CECT ABDOMEN
Grades of Renal Trauma:
• Grade 1- Subcapsular; Non Expanding Perirenal hematoma

• Grade 2- Laceration <1cm, Non Expanding Perirenal hematoma confined to retroperitoneum
and Gerota fascia

• Grade 3- Laceration > 1cm, No urine extravasation
• Grade 4- Laceration with Urine Extravasation**, Injury to Main renal artery and Vein**
• Grade 5:
• Shattered kidney.
• Avulsion of renal hilum: Devascularisation of a kidney due to hilar injury.
• Uretero pelvic avulsions**
• Complete laceration or thrombus of the main renal artery or vein.

● IOC- CECT abdomen (stable pt)
● Laparotomy (unstable) , nephrectomy done if needed
● 90% conservatively treated
● 10% need surgery
● In a stable patient one Clinical Scenario:
o In CT abdomen ,if there is injury of kidney IVP is a must, if it is normal patient can
be discharged
o In IVP- If a kidney is not visualized suspect renal artery compression by a perirenal
hematoma, immediately explore the hilum and repair the renal artery on the table
and repeat the IVP on the table and confirm normal flow into that kidney( AIIMS PG
question)
Ureteric injury
● Usually during surgery

● Ureter can be identified by looking for the – Peristalsis**
● On table ureteric injury- Repair it end to end by using 3'0 vicryl**
Repaired by
o keeping a stent in ureter
o Boari’s flap using the urinary bladder as shown below
o Auto transplant of kidney or ureter- 1st done by Hardy**
Figure: Boari Flap operation (Image question)

Bladder injuries
Intraperitoneal rupture of bladder Extraperitoneal rupture of bladder

● ●
● Cause uremic peritonitis ● Superficial extravasation of urine with
● Immediate surgery needed urine extravasated from nipple level to
Holden’s line level.
● Catheter inserted immediately.
● Wait and watch- gradually the injury
heals
IOC for Bladder injury -Retro Grade Cystography**
Urethral injury:
4 parts of urethra:
• Most dilatable part- prostatic urethra
• Least dilatable part- Membranous urethra
• Anterior urethra- Penile and Bulbar
• Most narrowest part of urethra- External urethral meatus
Clinical feature of Urethral injuries:
• Blood at urethral meatus
• Retention of Bladder

Membranous Urethral injury Bulbar Urethral injury
• Mainly due to fracture pelvis ● Mainly due to straddle injury
• Per rectal examination: ● Typical presentation of urethral injury
Prostate: high lying and Floating seen.
(Vermooten sign)**
• The above examination is not advised
in latest guidelines of ATLS
• Deep extravasation +++ of Blood seen
• Bladder shape - Inverted tear drop
Figure: Straddle injury causing Bulbar urethral injury
Steps to be done in Urethral injury:

• Never put Foley’s catheter as it will cause more damage of the urethra
• Put Suprapubic catheter ( SPC)
• Via SPC we can do Descending cystourethrogram / Micturating Cysto urethrogram
• Other Investigation-Retrograde urethrogram ( Via Foley’s inserted only upto penile urethra
and push contrast)
NEET PG 2020 Image based Question:
For understanding purpose in X ray- to say the In MCU we have;

image is RGU we will have: • Bladder will be full; and will be
• Cannulated penis appearing like below: with Bladder being
• Incomplete bladder filling filled with Contrast by Supra pubic
catheter.
Management:
o Wait for 6-8 weeks after SPC insertion

o Gradually the urethral injury goes for stricture
o If stricture is short and single- we can use Dilators
o If stricture is multiple and long- we plan Stricturoplasty using Buccal mucosa**
Figure: RGU shows Urethral stricture

Congenital anomalies of Urinary System
Disease Sex
Polycystic kidney Disease No sex predilection
Ectopic Ureter Females
Congenital PUJ obstruction Males
Ureterocele Females
Horse Shoe kidney Males
Congenital VUR Males (Acquired VUR in Females)
Ectopia Vesica Males
ECTOPIC URETER
● M/C anomaly of Urinary system-Duplication of renal pelvis and ureters**
● Unilateral > bilateral
● Ectopic ureter arises from upper pole, it runs lateral, outwards and joins distal to normal ureter**
● Scenarios in Ectopic Ureter are:
WEIGERT - MAYER RULE: 2nd type: 3rd Type

- Upper pole ectopic it's orifice
inserts infero medially to - Upper ectopic ureter - YoY o Reflex
normal ureter . gets obstructed. Urine - Ureter draining
gets collected inside into the ureter
Ectopic ureter opens into: resulting in itself.
- Boys- Prostatic urethra Ureterocele**
- Girls- Distal to External - Lower ureter which is
urethral sphincter. normal results in VUR
in normal ureter
Hence girls will have Paradoxical
urinary incontinence and continuous
dribbling of urine seen

• IVP- diagnostic of ectopic ureter
• Drooping Lilly appearance ( Ectopic ureter with ureterocoele)
POLYCYSTIC KIDNEY DISEASE
INFANTILE PKD
● <1yr
● Autosomal recessive
● Child won't survive more than 1 year
AUTOSOMAL DOMINANT Polycystic Kidney Disease Adult type ( ADPKD):
Criteria to diagnose ADPKD is based on usg
● On USG one kidney: 3 cysts
● B/L kidney : 2 in each

Clinical features
● PKD - Bilateral (95%)
● Incidence 1 in 400 to 1 in 1000
● Before 40 years - Presentation- hypertension (from 20yr onwards),
● kidney failure from 40year onwards
● The renal tissue is progressively replaced by Cysts and results in renal failure.
● Rare- Haematuria , kidney stone (20%)- MC type of Renal stone is URIC ACID STONE**
● End stage renal failure - M/c in male than female
IVP shows- Spider leg appearance**
Associated anomalies
Cysts seen in Berry aneurysm Mitral valve Colonic Liver fibrosis

● Liver - Sudden prolapse diverticulitis
● Spleen headache - Sudden
● Pancreas cardiac
● Ovary failure
● Not seen
in lungs
Treatment-
● Rovsing’s operation (olden days,not used now)
● Tolvapton ( NEET PG 2020)
○ Vasopressin receptor antagonist
○ 1st approved drug

○ Increased urine excretion
○ Increase sodium content in the body
● Treatment of choice- Renal Transplant

● Until transplant they survive by Dialysis
CONGENITAL PUJ OBSTRUCTION
● M/c cause of congenital hydronephrosis** is PUJ obstruction
● Cause unknown
● Aberrant renal vessels may be seen- but they are not the cause of obstruction**
● M/c in boys
● Unilateral mostly
● Bilateral in 40% cases
● Whitaker test - pressure measurement of renal pelvis and bladder. High pressure in Pelvis
and low in bladder
● MAG-3 (Mercapto Acetyl Triglycine Scan)- IOC FOR PUJ OBSTRUCTION**
● Treatment : Anderson Hynes Pyeloplasty operation**
VESICOURETERIC REFLUX
● Congenital - m/c in boys
● Acquired- m/c in girls
● Main problem is the longitudinal bladder muscle deficiency**
● The urine from the bladder refluxes into the ureter on micturition.
International classification of VUR
● I and II - Non dilated ureter
● III, IV and V – Dilated ureter seen

IOC – Micturating Cysto urethrogram**
Management:
● I and II - No surgery needed, Only medical treatment
● For UTI - antibiotics (*if not responding to antibiotics surgery recommended)

● III (Bilateral),IV (Bilateral) ,V (Unilateral) - Surgery is recommended
● Surgical Treatment- Reimplantation of ureter
HORSESHOE KIDNEY
● 1 in 1000
● M/c in men
● Lower pole fusion at L4
● Most of them are Asymptomatic
● The isthmus is cut only in one Surgery- Abdominal Aortic Aneurysm Surgery
● Blood Supply is from Major arteries nearby.

● Pregnancy is not a Contraindication- but Urinary infection is common for them**
● IVP- FLOWER VASE or HAND SHAKE APPEARANCE**
Figure: Flower vase appearance in Horse Shoe Kidney
ECTOPIA VESICA ( EXSTROPHY of BLADDER)
• Embryology- the basic defect in Exstrophy bladder is abnormal over development of the
cloacal membrane and its rupture.
• Associated anomalies
Males Females
○ Umbilical hernia ○ Umbilical hernia
○ Inguinal hernia ○ Epispadias
○ Epispadias ○ Split Clitoris
○ Undescended testis ○ Wide open pelvis (duck like waddling gait)
○ Wide labia
○ Urinary incontinence
○ Increased risk of bladder cancer

• C/F- total urinary incontinency with dribbling and risk of bladder cancer
• Treatment- Plastic surgery Reconstruction
Figure: Ectopia Vesica reconstructed
URETEROCELE
● M/C in females
● 10% bilateral
● M/c : Urinary tract infection due to stagnation of urine in Dilated part of ureter
● IVP- cobra head appearance
● Treatment- Ureteric Reimplant
Figure: Cobra Head deformity on IVP

Part 2: Prostate and Seminal Vesicles
Basic anatomy: Mc Neal’s 3 Surgical zones
● Transition zone
● Central zone
● Peripheral zone
In BPH - Transition zone is more involved*

In Cancer- Peripheral zone is more involved**
5 lobes in prostate:
• 2 lateral lobe
• 1 median lobe
• 1 posterior lobe
• 1 anterior Lobe
BPH arises from Median Lobes
Cancer arises from Posterior Lobe
(Remember : Cancer- P -P : Peripheral zone, Posterior lobe)
Prostatitis:
• MC organism causing – E.Coli
• C/F- Low grade fever+ perineal pain
• PR- Soft Boggy swelling of prostate due to conversion to abscess
• Treatment: Antibiotics for 4 weeks

Most common type of stones:
• MC stone in Prostate :
• MC stone in Kidney-
• MC stone in Bladder-
• MC stone in Salivary gland-
• MC stone in Gall bladder-
Benign Prostatic Hyperplasia:
● Mc in Old age
● Symptoms of BPH is given by bladder outlet obstruction
● Symptoms associated with bladder outlet obstruction
Irritative symptoms Obstructive

o Increased frequency ( MC symptom) • Dribbling
o Nocturia • Thin stream urine
o Urgency • Retention
o Hesitancy
o Haematuria
• IOC to detect bladder outlet obstruction- uroflometry**
• USG abdomen :
o Prostate enlargement
o Post void residual urine
o B/l hydroureteronephrosis

Medical treatment
Alpha 1 a Blockers: 5 Alpha reductase inhibitors

• Tamsulosin • Finasteride 5 mg
• Decreases smooth muscle tone • Slow action – needs 6 months
• Quick action • Decreases the volume (upto 40%)
Other drugs like Prazosin and terazosin will Remember Finasteride is used in 1 mg dosage.
cause postural hypotension
Indication of Surgery
● Retention
○ Acute
○ Chronic ( PVR >200 ml)
● Complications
○ Diverticula
○ B/L HUN
○ Bladder stone
○ Haematuria
○ UTI
● Uroflometry value
○ <10ml/s
○ >80 cm H20
SURGERY
TURP( gold standard ( 1)
Open
○ Retropubic – MILIN’s operation (2)
○ Trans vesical- Freyers operation (3)
○ Perineal - Young operation (4)

TURP
● Distal limit of TURP -Verumontanum**
● IUS is under involuntary control
● EUS is under voluntary control

● In TURP – using energy device we remove the prostatic tissue via cystoscopy.
Modalities used for TURP:

● Diathermy
● HO: Laser (Best )
● ND: Yag
During dissection:
• If you go beyond Verumontanum we can injure the EUS- Results in Incontinency**

• If you injure the IUS ( most common Complication)**- Retrograde ejaculation happens in
>50% cases
• If you injure the bladder neck- Bladder neck stenosis happens and symptoms will be same like
BOO**
During surgery
● Fluid of choice for monopolar diathermy-……………………………………..
● If not available distilled water
● Normal saline shouldn't be used as the current may get dissipated and wont cut and
coagulate properly if I use Monopolar diathermy (As NS is a good conductor of electricity)
● Bipolar diathermy or with LASERs- we can use normal saline

• HO laser - HOLEP -Holmium laser enucleation of prostate
• TULIP-. Transurethral USG laser induced prostatectomy
• Post op of fluid of choice for washing bladder and irrigation with Three lumen Foley’s
catheter 18 G catheter: Normal saline. We will get clear Pink urine during the irrigation.
Figure: 3 lumen Foley’s catheter for post op irrigation
Immediate post op complications-
● Hemorrhage- Usually arises from FLOCH arteries arising from Inferior Vesical arteries**
● TUR syndrome- patient confused, irrelevant words, if we use distilled water there is high
chance of dilutional hyponatremia and water intoxication
Delayed complication:
● Bladder neck stenosis
● Retrograde ejaculation (m/c complication overall) due to IUS injury
● Incontinence due to EUS injury
CANCER PROSTATE
● Clinical Presentation- bladder outlet obstruction + back pain
● Screening protocol : Digital rectal examination+ PSA
Prostate Specific Antigen
● Normal value: <4 ng/l
● Men 50-69 year :>4ng/l - Indication for biopsy

● >10ng/l : Localised Cancer+
● >35ng/l : metastatic Cancer prostate+

Other Values:
• PSA velocity
• PSA density
• Old – Acid phosphatase
Biopsy methods:
● TRUS guided biopsy ● Transperitoneal template biopsy(TPTBP)
○ Traditional
○ Increased risk of infection,
septicemia, Bleeding etc
○ Prophylactic antibiotics required
○ Less areas of biopsy possible
• IOC to stage prostatic cancer- CECT ABDOMEN/ PELVIS
• 1st node involved in Cancer prostate: Obturator Nodes*
T-STAGING

● T1:
○ T1a - <5% of TURP specimen
shows cancer
○ T1b ->5 % of TURP specimen
shows cancer
○ T1c- PSA increase
● T2-
○ T2a- involved one lobe
○ T2b - involved both love
● T3- seminal vesicle; involved beyond the
capsule
● T4- spread to rectum, bladder, Pelvic
bone
• T1 and T2: Early disease
• T3 and T4: Locally advanced
Management:
● T1,T2- Radical prostatectomy
○ <70yr
○ Fit for surgery
● >70 years , unfit- T1/T2 Prostatic cancer- wait and watch
● T3,T4,M1- Androgen ablation (1st step)
Androgen Ablation methods:

• Gold std method for androgen ablation: Subscapular orchidectomy or Conventional
orchidectomy+ testicular prosthesis kept
• If not willing for orchidectomy: Medical Castration methods : LHRH Agonist like
Flutamide; Leuprolide, Goserelin
GLEASON SCORE
● Grade 1 - Small uniform glands
● Grade 2- More space between glands and increase in stroma
● Grade 3- Distinct infiltration of cell margin
● Grade 4- Irregular masses of neoplastic cells
● Grade 5 - Lack of glandular pattern
● Old score- grade 1(well differentiated)-grade 5(poorly differentiated)

● New Gleason score: Extends from grade 1 to grade 10
• MC site of mets- Lumbar vertebra; More of Osteoblastic secondaries**
MALE INFERTILITY
Figure: Travel of Sperm: Testis- Vas- Seminal vesicles gives fructose- Ejaculatory duct- Prostatic
urethra- Penis- Ejaculated
Semen analysis findings
Decreased Volume of Semen (Sperms+) Azoospermia ( No sperm)

o Retrograde ejaculation o Ejaculatory duct obstruction
o Obstruction of vas deferns or o Testicular failure
Ejaculatory duct, Seminal vesicle o Vas obstruction bilateral
(unilateral)
Scenario: Patient with sperm count normal, decreased fructose level** - suggestive of seminal vesicle
obstruction
● M/ c cause of obstruction- TB
● IOC of ED obstruction- TRUS > Vasography ( Invasive). TRUS is non invasive and superior
● Final test - Testicular biopsy

URETHRA AND PENIS
Hypospadias
● m/c congenital anomaly ( lower urinary)

● I in 250
● Features:
○ Dorsal hood
○ Ventral opening of urethra

○ Ventral chordae
● Associated Cryptorchidism
● Associated Indirect inguinal hernia
Types
● Glandular (m/c type)- No treatment needed
● Coronal
● Penile
● Perineal
● Age group for surgery- 6 months - 1 year
● Circumcision is contraindicated
● Old method of Surgery- Dennis brown 2 stage
● New and used procedure- MAGPI (MEATAL ADVANCEMENT GLANULOPLASTY
INCORPORATION)
● Order of reconstruction of MAGPI
○ Orthoplasty ( Penile straightening)
○ Urethroplasty

○ Glanuloplasty
○ Meatoplasty
○ Scrotoplasty
○ Skin reconstruction and Circumcision is done as last step**
Epispadias
● Dorsal opening of urethra
● Rare
● M/c associated with ectopia vesica
Phimosis
● Unable to retract the prepuce backwards
● Smegma produced underneath from Tyson's gland gets collected inside. Smegma is
carcinogenic. Hence phimosis is premalignant**

● Congenital phimosis
○ Physiological adhesions up to 6 years
○ No need to operate before 6 years
○ Wait up to 5-6 years
● Acquired phimosis
○ Inflammation
○ Diabetes
○ BXO
○ Cancer
○ Trauma
○ Surgery is done for all acquired cases
● Less than 1 year child with severe Ballooning of prepuce will need surgery as this is causing
severe obstruction.
● Less than 1 year children can be operated by a HOLLISTER/ PLASTIBEL device- Sutureless
method.

Figure: Plastibel device
Conventional operations
● Dorsal slit method- safer method
● Guillotine method- Religious circumcision by Muslims use this method.
Types of circumcision
● Neonatal- at birth practiced by Jews, 100% protective of cancer penis
● Infantile- <1yearr practiced by Muslims ,decreases incidence of cancer of penis
● Adults: no relation with cancer
Paraphimosis
● Perpucial skin get retracted back and does not goes to the original position
● Treatment
○ Keep ice packs
○ Multiple punctures
○ Try to bring back manually
○ Circumcision - Dorsal slit method

Peyronie’s Disease
● Associated with Dupyutrens , Retroperitoneal fibrosis, Riedels
● C/F- Painful, persistent erection with deformity in a middle aged man.
● Penis gets curved (dorsal curvature usually**)
● Xray - Calcified penis
● NESBITT Procedure is done electively to straighten the penis**
Priapism
● Painful erected penis following sexual activity
High Flow Priapism Low Flow Priapism

• Increased Arterial Flow • Venous return Blockage
• Spinal Cord injury • Sickle cell anemia
• RP injuries • Leukemia and Lymphomas
• Papaverine injections
High Oxygen content on Penile Blood gas Low O2 Content on Penile Blood
analysis It’s like Strangulation ( Venous gangrene)
Less dangerous Urgent Treatment Needed
Treatment:
Immediate treatment
● Inj phenyl ephrine/ adrenaline ( **should be injected within 36 hours)
● >36 hours-Shunt operations are done

o Winter- Distal corpora spongiosum Shunt
o Sacher-proximal corpora spongiosum shunt
o Gray hack- corpora cavernosa with saphenous vein
Figure: Winter Shunt operation for Priapism
Congenital puv
● Cause of urinary outflow obstruction
● M/c boys
● Cystoscopy- normal
● IOC - MCU
Cancer penis
● MC in 4th decade of men.

● M/c type: SCC
● Rare types:
○ BCC
○ Adenocarcinoma ( Arises from Tyson glands)
○ Melanoma
○ Kaposi
● Common sites
○ Glans penis(50%)
○ Preputial skin (20%)

○ Other places- Shaft, Corona glandis etc
● Predisposing condition
○ M/c – Smegma**
○ Other risk factors:
■ Leukoplakia
■ BXO
■ Buschke Lowenstein tumor ( caused by Human Papilloma virus)
● Cancer in situ of Glans- Erythroplasia of Queyrat**
● Cancer in situ of Shaft of Penis- Bowen’s Disease
● Verrucous cancer:
o a variety of SCC
o Low malignant
o Aggressive growth on RT
Figure: Verrucous cancer penis
Clinical features
● Fungating growth
● Foul smelling odour (d/t secondary infection)
● Sentinel node of cancer penis- CABANA node** ( Superficial inguinal node)
Clinical staging (Jackson's staging)
● I-Glans and perpuce involvement
● II- shaft involved
● III- Node +
● IV - Mets +

TNM Staging
● T1- <2cm growth
● T2- 2-5cm
● T3- >5 cm can invade corpus spongiosum, cavernosum, urethra ( Usually urethra not
involved due to transitional epithelium inside)
● T4- adjacent structure
● N1 : Single LN +
● N2 : Multiple LN (unilateral/ bilateral)
● N3 :Deep inguinal / iliac node
One of the most common cause of death – Erosion of femoral artery by the nodes**
Management of primary:
Non surgical Surgical treatment is best

○ Radiotherapy ● 2cm margin is given and after resection
○ Interstitial brachytherapy atleast 2cm of stump must be available
○ 5FU Cream for Sexual activity and passing urine in
○ Moh's micrographic standing position.
○ Laser excision. ● Usually partial amputation of penis is
done for glans and distal growth
● Indication of total amputation:
○ <2cm shaft.
○ Urethral involvement++
● Young operation- partial penectomy+ Bilateral ilioinguinal dissection
● Piersey Gold operation-Total amputation + scrotum+ Testis ( EMASCULATION)- Not done **

Secondary nodal management:
● Node positive cases : lazy "S" incision done and Ilioinguinal block dissection done
● Node negative cases:
○ Sentinel node biopsy of Cabana done in olden days**
○ Superficial inguinal dissection of DASSLER- all superficial nodes removed and sent for
Frozen section: If positive ilioinguinal block is done
● Latest protocol for node negative cases
○ Modified ilioinguinal dissection of Catalona ( superficial + deep nodes removal in a
rectangular area) Send for Frozen section -if nodes are positive ilioinguinal block is
done.
Testicular pathologies
Testicular cancer
Pathological types:
Germ cell tumors Sex cord Tumors

Seminomas Leydig cell tumors
Non seminomas: Sertoli cell tumors
o Choriocarcinoma
o Yolk sac
o Teratoma
o Embryonal cell
Seminomas Non-Seminomas
o 4th decade
o Highly radiosensitive
o LN mets > hematogenous mets
o LDH increased
o Good prognosis
Clinical features
● 3rd decade- non seminomatous
● 4th decade-Seminomatous
● >5th decade - Lymphoma testis.

● Predisposing factors
○ Undescended testis(seminoma)- Please remember even by doing orchidopexy the risk
is not reduced; but helps in early diagnosis**
○ Klinefelter’s
○ Testicular feminisation syndrome
○ Maternal DES
○ Siblings history - h/o testicular cancer
● Painless lump+
● Testicular sensation lost ( Syphilis and Tumors have this clinical feature)
● Abdominal lump
○ Sentinel node on Right side- inter aortocaval node
○ Sentinel node on Left side- Preaortic node
● Hurricane tumour- aggressive choriocarcinoma**
● Sertoli cell tumors-Feminisation and Gynaecomastia

● Leydig cell tumors- Precocious puberty
Investigations for testicular tumors:
● IOC
○ To diagnose- Biopsy** ( Inguinal method- Chevasu manuever)
○ To stage- MRI**
○ Tumor markers-HCG, AFP, LDH
● For Biopsy testing-CHEVASU MANUEVER BIOPSY

○ Don’t do Trans scrotal biopsy (Violation of Tumor Principle will happen and you may
disseminate the tumor via Superficial inguinal nodes which is not it’s regular course)
○ Put an Inguinal incision, Pull the testis and examine the tumor and take biopsy from
tumor.
○ Do frozen section
○ If positive- High inguinal orchidectomy
○ If negative- keep testis back in scrotum
STAGING
● T1-Tumour confined to testis, no lympho vascular invasion
● T2-Tumour confined to testis with lympho vascular invasion(+) and Tunica albuginea(+)
● T3-Tumour goes to spermatic cord
● T4-Tumour goes to scrotal wall

● N1 - <2 cm nodal mass
● N2- 2-5 cm nodal mass
● N3 - >5cm nodal mass
● M 1 - Mets
Treatment
● After High Inguinal orchidectomy: Nodal secondaries must be managed.
● Seminoma is Radiosensitive and hence RT given to nodes
● Non-Seminoma is not Radiosensitive and hence we do Retro peritoneal Lymphnode dissection
(RPLND)
● N1,N2 cases:
○ Seminomatous- Radiotherapy to Lymph nodes
○ Non seminomatous-RPLND+ CHEMO
● N3 cases and M1
○ Seminoma-chemotherapy
○ Non seminoma- chemotherapy
● Radiotherapy in Seminomatous tumors:
○ Inverted "Y" field RT
● Chemotherapy
○ B-bleomycin
○ E-Etoposide
○ P - Cisplatin
VARICOCELE TESTIS
● MC in young tall thin males
● C/F - Bag of worms on palpation
● Cough impulse (+)
● Disappears on lying down
● M/c in left side**

Why varicocele is mc on Left side?
❑ Left testicular vein drains at right angle
❑ Left testicular vein is long
❑ Left adrenal vein is near left testicular vein and hence can cause increased spasm
❑ Sigmoid colon compresses Left testicular vein
❑ RCC can invade left renal vein and causes obstruction of left testicular vein
• The left varicocele not disappears on lying down- LEFT SIDE RCC**
● M/c cause of infertility in men**
● Paloma operation -Retroperitoneal ligation of Testicular veins
● Inguinal approach- Invanissevich procedure
● Transcortical approach
● After ligating vessels testis will drain through cremasteric vessel
Painful testis Causes: Torsion Vs Orchitis:
● 2 causes
○ Torsion- Emergency**
○ Orchitis
● Orchitis
○ Chlamydia (mc organism)
○ Follow urinary tract infection
● Torsion
○ Bell clapper deformity (m/c deformity associated with torsion)- Bilateral pathology
○ Other causes

- UDT
- Testicular inversion
○ Prehn’s sign-
▪ To differentiate between torsion and orchitis
▪ On lifting the testis
● If pain increases- suggestive of torsion
● If pain decrease - orchitis
○ Angel sign - Normal testis lying horizontally**
○ Deming sign- Affected testis lying higher up**
Management of torsion testis:
○ 1st hour- manual detorsion

○ <4 hours- save testis ( 4 hours is Golden period)
○ >4 hours- testis would be Gangrenous
● IOC - Colour Doppler scan**
● Bilateral exposure is done for Torsion testis always:
○ Affected testis removed
○ Unaffected testis may have pathologies like Bell clapper deformity and hence do
orchidopexy

Figure: Bilateral exposure for torsion testis
HYDROCELE
● Collection of fluid between tunica vaginalis
● Amber colour fluid
Clinical features:
● Transilluminant +
● Get above swelling +
● Fluctuation +
Types of Vaginal Hydrocele:

● Primary hydrocele - testis not palpable
● Secondary hydrocele- Testis palpable separately
○ Primary - cause unknown
○ Secondary:
■ Infection- Filariasis, Syphilis etc
■ Inflammation
■ Tumours
■ Trauma
Types of hydrocele based on closure of Tunica Vaginalis:
● Vaginal
○ Confined only to scrotum
○ Get above the swelling+
● Infantile hydrocele

○ Fluid collection seen up to superficial ring.
○ Get above swelling not possible
● Congenital hydrocele
○ Communicating with the peritoneum
○ Reduced on lying down overnight
○ INVERTED INK BOTTLE EFFECT is seen**
● Encysted hydrocele cord.
○ Decreased movement on traction
Figure: Vaginal- Infantile- Congenital- Encysted hydrocele types in order
Epididymal Cyst Spermatocele

❑ Congenital and derived from embryonic ❑ Acquired condition
remnant around the epididymis ❑ Due to retention of portion of sperm
❑ MC in Middle age conducting duct of epididymis
❑ Clear fluid ❑ Filled with fluid of barley water colour**
❑ Multilocular and contains spermatozoa
❑ Bilateral rarely ❑ Any age, Unilateral
❑ Cyst located behind testis ❑ Occasionally the swelling may enlarge
❑ Chinese Lantern Transillumination** and appear as three testicles**
❑ Transillumination may be negative or
positive.
Management Of Hydrocele
● Jaboulay’s Eversion of sac- bigger hydrocele
● Lords plication of sac - small hydrocele with thin sac
● Excision of thick sac

Complications of Hydrocele:
● Pyocele
● Hematocoele
● Rupture is not seen
UNDESCENDED TESTIS.
Testis is an organ of lumbar region
Course
● 2nd month - lumbar region

● 3rd month- iliac fossa
● 7th month- Deep ring.
● 7-8 month -travels in the canal
● 8th month - superficial ring

● 9th month - scrotum
Gubernaculum has 5 tails
● Public tail
● Perineal tail
● Femoral tail
● Inguinal tail- if inguinal tail- is taking the dominance it will reach superficial inguinal pouch (
most common site of ectopic testis)

● Gubernaculum tail - normal one reaching scrotum

Undescended testis Ectopic testis
● Arrest in normal path ● Deviation from normal path
● Underdeveloped ● Normal development
● Can cause ● Can cause trauma as only complication.
○ T- torsion ● Scrotum normal
○ E-Epididymo orchitis
○ S-sterility
○ T- trauma
○ I- indirect inguinal hernia
○ S-seminoma
● Scrotum not developed**
Retractile testis
● Cremasteric muscle overaction
● Testis will be retracted and lying in Superficial ring and we can manually pull it back to
scrotum which is impossible in ectopic testis.
● Scrotum normal
Clinical features:
● M/c location - inguinal canal
● 70% of it resolve by 2 months
● M/c preterm babies
● Right side
● Leydig cell normal, Sertoli cell affected- so secondary sexual characters normal**
Investigation
● Gold std - diagnostic laparoscopy
● Inguinal UDT- USG is enough ( Indirect inguinal hernia is also noted)
● On Diagnostic Laparoscopy: ( NEET PG 2020)
- Blind Ending testicular vessels means the testis has gone for atrophy and no
use of further exploration.
- If vessels are seen entering deep ring- we will explore the inguinal canal**
Management:
● BILATERAL UDT- Measure Beta HCG Level ( May be hypertrophied clitoris looking like penis
and the patient may be a female )

● Testosterone value
● Testis should be brought to scrotum back : Uses
○ To prevent trauma
○ To detect malignancy.
○ Normal spermatogenesis returns if done early.
● Orchidopexy + fixation
○ Sub dartus pouch (m/c)
○ Ombredanne procedure (kept in opposite side with normal tail)
○ Ladd and gross technique- 2 sutures applied ( Testis and Thigh)
○ Keetley torek- temporarily keep it in thigh- after 3 months bring it back
● Testis unable to bring it to scrotum

○ Silbar – Disconnect the testicular artery keep it in scrotum and do microvascular
anastomosis
○ Fowler Stephen – 2 stage procedure

Chapter 2: Vascular Surgery
Topic: 2a- Arterial System
Aneurysm:
• Def: blood vessel dilatation >50% is Aneurysm.
• Important DD is ECTASIA (def: blood vessel dilatation <50%).
One liners:
• m/c cause of aneurysm : Atherosclerosis
• m/c site of aneurysm : Circle of Willis
• m/c extra cranial site of aneurysm : Abdominal Aorta (Infra Renal AA is MC site)
• m/c peripheral artery aneurysm : Popliteal Artery
• m/c site of visceral artery aneurysm : Splenic Artery
• m/c site of Mycotic aneurysm : Femoral Artery
(Mycotic aneurysm is a misnomer it is caused by Bacteria)
Classification of aneurysm:
• True aneurysm: contains all the layers of blood vessel
• False aneurysm: lacks 1 or 2 layers of the blood vessel
• Fusiform aneurysm (Symmetric dilatation of Blood vessel)
• Saccular aneurysm (Asymmetric dilatation of Blood vessel; only one part of Blood vessel is
dilated; high chances of Rupture**)
• Dissecting aneurysm (Dissection happens in between the layers of B.V)
Abdominal Aortic aneurysm:

• m/c location : Infra renal A.A
• m/c presentation: Back pain
• Major issue with this aneurysm: it ruptures
• Anterior rupture (20%) Die on spot due to haemorrhage into abdominal cavity
• Postero-lateral (80%) presentation Back pain and Shock; high mortality
IOC for AAA: CT Angiography**

For follow up: USG
Indication of treatment:
• Symptomatic patient
• Asymptomatic patient: AP diameter >55mm (until 5.5cm if patient is asymptomatic follow
up)

Conventional Treatment:
• Resect the aneurysm out
• Replace it with DACRON PANT Type GRAFT
Figure: DACRON GRAFT
Complications:
• m/c cause of death : MI
• Renal failure
• Leak from graft
• Colonic ischemia (inferior mesenteric artery if not re implanted properly)
• Injury of artery of Adamkieklicz
- It arises from Posterior intercostal Artery
- Supplies : anterior part of spinal cord
- Injury leads to: Anterior Spinal Artery Syndrome (Paraplegia)
• Mortality
- Elective:2%
- Emergency: 50%
Endo Vascular Aneurysm Repair (EVAR)- Latest treatment

• A Stent is placed inside the blood vessel at the site of aneurysm.
• Blood flows through the stent and the aneurysm collapses.

Figure: EVAR
HUNTERIAN LIGATURE OPERATION:

• Leaving the blood vessel above and below, the aneurysm is ligated.
• The aneurysm collapses after ligation
• Not done in recent day because of various ischemias developing.
Material used in aneurysm repair: DACRON and Polytetrafluoroethylene

Suture material: 3’0 or 4’0 Prolene
AORTIC DISSECTING ANEURYSM:

• Aortic dissection is caused by a circumferential or less frequently, transverse tear of the
intima
• Most common site: Right lateral wall of the ascending aorta**
• Another common site: Descending thoracic aorta (just below the ligamentum arteriosum)
• Peak incidence: 6th and 7th decades**
• Men are more commonly affected**
• m/c Risk factor: HTN**
• other risk factors:
o Marfan’s syndrome
o EDS
o Takayasu arteritis
o Coarctation of Aorta
• Presentation: Severe pain; Hypotension; M.I ( if coronary ostium is involved in dissection)
• X-ray chest: Widened mediastinum

• Investigation of Choice
o Stable patients: CECT thorax

o Unstable patient: TEE (Trans Esophageal Echo)
De Bakey Classification STANFORD Classification

• Type I: • STANFORD A: De Bakey I &II (A –
Ascending aorta)
• Type II: • STANFORD B: De Bakey III
• Type III:
Classification of Dissection Aneurysm
Clinical Features
• Pain
• Shock
• BP: disproportionate BP between Upper limbs or disproportionate BP between UL & LL
Treatment: Emergency DACRON GRAFT repair**
CRAWFORD CLASSIFICATION OF THORACO-ABDOMINAL AORTIC ANEURYSM

• Type I: from Lt subclavian artery up to
renal artery.
• Type II: from Lt subclavian artery up
to bifurcation of aorta (largest**)
• Type III: from middle of descending
aorta up to bifurcation of aorta.
• Type IV: it involves supra renal aorta
+/- renal artery. ( Not present inside
Thorax)

Popliteal artery aneurysm:
• It is the m/c peripheral artery aneurysm
• 2/3rd of times bilateral
• Can wait up to 25mm (>25mm surgery)
• Distal occlusion ( Due to thrombus or embolus formation)
Mycotic aneurysm:
• Caused by Staphylococcus
• Site : Femoral Artery
• False aneurysm
Acute Limb Ischemia:

• M/C cause: embolus that comes from Lt atrial thrombus
• Clinical features: 6P
• Pain
• Paresthesia
• Pulselessness
• Poikilothermia
• Paralysis of limb
• Pallor
• It is an emergency: do embolectomy in 4-6hrs
Seldinger technique:
• Cannulate the artery in retrograde way using seldinger needle
• Pass the guide wire distal to the block
• Through guide wire a balloon (Fogarty balloon catheter) is passed distal to block, balloon is
inflated & withdrawn
• Through a small incision the embolus is removed

CHRONIC LIMB ISCHEMIA:
Peripheral Vascular Disease- Atherosclerosis of LL TAO
Causes: •
• DM
• HTN
• Hyper cholesterolemia
• Obesity....
Thrombus formed in vessel occludes the vessel
Involves :
Major vessels
• Aorta
• Common iliac artery
• External iliac artery
• Femoral artery
It is U/L or B/L
Common in Old age
Males > Females
UL not affected
Adjacent Veins & Nerves not affected
C/F: Intermittent claudication C/F:
• Pain not present at rest • Young male with bilateral leg claudication
• Pain stops on walking pain.
• Pain not present on standing • On CT angiography: symmetric lesion is
• Pain decreases on rest seen
(Neurogenic claudication pain increases on
standing)

• m/c site of claudication pain : Calf**
• m/c site of occlusion:
Superficial femoral artery
Q. Claudication pain in Buttock, both thigh, both calf. Site of occlusion? (NEET 2020 pattern)
• Ans. Aortoiliac occlusion.
Q. Claudication pain in Buttock(rare), one thigh & one calf. Site of occlusion?
• Ans. Unilateral Common Iliac artery occlusion.
Q. Claudication pain in thigh & calf. Site of occlusion?
• Ans. Externa Iliac Artry occlusion.
Q. Claudication pain in calf. Site of occlusion?
• Ans. Superficial femoral artery/ popliteal artery occlusion.
LERICH SYNDROME:
• Saddle shaped thrombus at bifurcation of aorta.
• Clinical Features:
- Buttock claudication
- Impotence
BOYDS CLINICAL CLASSIFICATION OF CLAUDICATION PAIN:

• Grade I: Pain relieved on continued walking
• Grade II: Walks in pain with limp
• Grade III: Pain compels to sit
• Grade IV: Rest pain
Other classification systems

• Fontaine
• RUTHERFORD
Ankle Brachial Pressure Index:

• ABPI= AP/BP = 0.9-1.1 (Normal)
• If Ankle pressure less than Brachial pressure: there is stenosis of vessel seen:
o <0.9 : Claudication
o <0.5 : Rest pain
o <0.3: Imminent necrosis
• False high AP/BP >1.3 seen in calcified arteries in DM & CKD
Investigations of vascular disease:

• 1st done: Colour Doppler (Duplex scan)

o Non invasive
o Repetitive
o Gold standard: CT Angiography (Road map)
TREATMENT:
Olden days:
• BYPASS OPERATION is done using
• DACRON (for Aortic bypass & Aortic- femoral bypass. Suture material 3’0 or 4’0
Prolene)
• PTFE (for Ileo femoral artery bypass. Suture material 5’0 Prolene)
• SAPHENOUS VEIN (for infra femoral bypass)
▪ INSITU do valvotome of the LSV valves. (Or)
▪ REVERSE LSV**
Figure: Bypass operations
ANGIOPLASTY: Gold standard treatment now

• Seldinger needle is passed beyond the block and an Intra-arterial stent is placed
Thromboangitis Obliteras ( TAO)- Buerger’s disease

Shionaya Criteria:
• History of smoking
• Onset should be before 50yrs

• Infra popliteal occlusion only
• UL involvement present
• Superficial phlebitis present
• No other risk factors Except Smoking
Pathophysiology:
• Occlusion is due to sympathetic over activity leads to vaso-spasm in infra popliteal arteries, it
is bilateral
Angiography demonstrates various collaterals
• Cork screw collaterals
• Tree root collaterals
• Spider leg collaterals
Figure: Angiography shows TAO
• TAO Patient: Young male with bilateral leg claudication pain.

• On CT angiography: symmetric lesion is seen
Treatment :
• Stop smoking
• Buerger’s exercises: collaterals in lower limbs increases
• Lifestyle modifications
Surgery: Lumbar sympathectomy

• On one side L1, L2&L3 are cut on the other side L2&L3 are cut.
• L1 on one side is preserved to prevent retrograde ejaculations
Indications of lumbar sympathectomy**

• Rest pain
• Ulcer
• Gangrene
Contraindications for lumbar sympathectomy
• Intermittent claudication
• ABPI > 0.3
• Diabetic patients
A-V FISTULA
• Abnormal communication between artery and vein is A-V fistula
• M/C cause: Iatrogenic
• CIMINO FISTULA: Surgically created fistula between Cephalic vein and Radial artery for
Dialysis purposes
• M/C acquired cause: penetrating trauma
• Genetic syndromes
o Sturge weber
o Beckwith weidmann
o Klippel trenanauy
Patho physiology:
o Arterialisation of vein
o Limb lengthening
o Temperature high on that limb
o Pulse rate high on that limb
o O/E: Machinery murmur (continuous thrill)
Figure: AV Fistula
NICOLDANI / BRANHAM’S SIGN: on compressing proximal to fistula
o Murmur disappears
o Swelling decreases
o Thrill absent
o Pulse rate decrease
RAYNAUD DISEASE
• Due to unknown cause
• If it happen due to Scleroderma, SLE it is called Raynaud’s phenomenon

• Vasospasm is due to
• Cold exposure
• Continuous Vibrations
Phenomenon seen:
W-B-C : initially limb colour is White later
Blue and then Crimson red
• White: due to spasm of both arteries
and veins
• Blue (cyanotic phase) : here arteries are
still in spasm and veins & capillaries
opens
• Crimson red: Arteries opens in an
extensive way, veins already in opened
state
Treatment:
• Calcium Channel Blockers
• Avoid cold
• Cervico dorsal sympathectomy (benefit is doubt full)

Image Based Questions:
Image 1: Seldinger Needle for Retrograde cannulation of vessels
Image 2: Miller cuff: interposition of vein between graft and Artery during anastomosis
Image: 3: Fogarty Balloon Catheter for Embolectomy

Topic: 2b – VENOUS SYSTEM
Anatomy of Venous system:

• Deep venous system: femoral vein (FV) that continuous as popliteal vein (PV) and that divides
into anterior tibial vein (AT) and posterior tibial vein (PT)
• Superficial venous system: medial side great saphenous vein (GSV) that enters deep system at
sapheno-femoral junction (SFJ). At lateral side short saphenous vein (SSV) drains into deep
system at popliteal vein
• Perforators: vessels that connect superficial and deep venous system
Perforators on medial side:

• Adductor canal
perforator or
Hunterian perforator :
At mid thigh: Connects
GSV to FV
• DODD: Above knee

perforator: Connects
GSV to FV
• BOYD: Below knee

GSV to PT
• COCKETT: Lower leg

Posterior arch vein(a
branch of GSV) to
Posterior Tibial vein
• MAY/KUSTER: Ankle
small perforator
Varicose veins:
Causes:
• DVT
• SFJ incompetence
• Perforator incompetence

C/F:
• Dilated tortuous veins of > 3mm
• Skin stretched
• Eczema, pigmentation
• Ulceration
• Loss of hair in LL
• Brittle nails
• Lipo Dermato Sclerosis: is skin pigmentation due to rupture of RBC releasing Hemosiderin
Types of Dilated veins:

• Telangiectasia: Vein size < 1 mm diameter
• Reticular veins: Vein size 1 – 3 mm diameter
• Varicose veins: vein dilatation > 3 mm diameter
TESTS
SF incompetence: Perforator Incompetence DVT:
• Trendelenburg I • Perthes test

• Morrissey’s cough • Modified Perthes test
impulse test • Homan’s test
• Moses test
• Pratt’s sign
Trendelenburg I test:
• The patient is made to lie down flat and superficial veins are emptied. With the thumb
compress SFJ (SFJ present 4 cm below & lateral to pubic tubercle) and make the patient
stand on taking the thumb out we can see the veins filling from above to below. It is due to
SFJ incompetence**
Trendelenburg II test:
• The patient is made to lie down flat and superficial veins are emptied. With the thumb
compress SFJ and make the patient stand and without removing the thumb we can see veins
filling from below to above it is due to perforator incompetence** ( THUMB Not taken out)
Multiple tourniquet test:

• The patient is made to lie down flat and superficial veins are empties. Multiple tourniquets
are tied 1st is below SFJ, tourniquets are tied in such a way that a tourniquet is present
above and below each perforator. Vein dilatation between two tourniquets indicates that
particular perforator incompetence

Perthes test: For DVT:
• Compress the superficial veins with tight elastic crape and ask the patient to walk. If he
complains pain it indicates DVT. It is a subjective test
Modified Perthes test:

• A tourniquet is tied below SFJ and patient is asked to walk if the veins become more dilated
and patient complains of pain it indicates DVT.
• Prerequisite to do this test: perforator incompetence should not be present**
PRATT’S TEST:
• Patient is made to lie down flat, superficial veins are drained and a tight elastic crape is
rolled from below upwards, another elastic crape is rolled from above downwards
simultaneously first band is removed loop by loop.
• Quick filling of veins between the bandages and a blowout is seen indicate that particular
perforator is incompetent. On removing the crape and on palpation of the blow out the deep
fascia will have a pit this is FEGAN’S TEST
SCHWARTZ TEST:
• Valve incompetency can be detected.
• Tap at lower end of the varicose vein and you can feel the impulse at the upper level
MORRISEY’s COUGH IMPULSE TEST:

• Patient is made to lie down flat and the superficial veins are drained and on coughing an
expansile impulse is felt at SFJ.
• Saphena varix: bulge in the SFJ before coughing
Homan’s sign: forceful dorsiflexion of the ankle (C/I due to chances of PE)
Moses sign: forceful compression at mid calf level (C/I due to chances of PE)
Pratt’s sign: lateral compression of calf
CEAP classification of varicose veins

Clinical classification:
• C1: Telangiectasia / reticular veins
• C2: Varicose veins
• C3: Edema in legs
• C4a:
• C4b:
• C5:

• C6:
Etiological classification:
• Ep: primary
• Ec: congenital
• Es: Secondary
Anatomical classification:
• As: superficial veins
• Ap: Perforators
• Ad: Deep veins
Pathological classification:
• Pr: Reflux
• Po: Obstructive
• Pro: Reflux + obstruction
Risk factors
• Family H/O
• Long standing job
• DVT
• Defective valves
• Mass in abdomen
• Pregnancy
• Congenital syndrome: KLIPPEL TRENANAY SYNDROME
o Port wine stain
o Lateral varicose veins
o Limb lengthening
Figures: Showing Klippel Trenanay Syndrome
Complications:

Skin complications:
• Eczema
• Pigmentation
• LDS
• Atrophic blanche
• Inverted champagne bottle appearance**
• Skin ulcer
• Bleeding from Varicose veins
Figure: LDS with inverted Champagne Bottle appearance
Skin ulcer: on medial malleolus the venous pressure is high that lead to venous ulcer
• Gaiter area
• Sloping edge
• Floor covered by granulation tissue
• Base formed by tibia

Figure: venous ulcer and Marjolin’s
Complications of Venous ulcer:

• Ulcer can bleed
• Ulcer can cause periostitis tibia
• Equinus deformity
• On long standing can go for Marjolins ulcer- Squamous cell cancer
Management: Bisgaard method of management of Venous ulcers.
Investigations:
• Hand Held Doppler:
o Obstruction: sound+
o Woosh sound on compression & Release
• IOC: color Doppler (Duplex scan)
o Normal flow Blue color
o Reflex Red color: incompetence
o MICKEY MOUSE SIGN: Face FEMORAL VEIN, Lateral ear: FEMORAL ARTERY,
Medial ear: GSA
o Duplex scan is done to
R/O DVT & To mark the perforators

Figure: Mickey mouse sign
Management:
Compression stockings
BRITISH CLASSIFICATIONOF STOCKINGS
o Class 1: give pressure of 14 -17 mm Hg (used prophylactically)
o Class2: gives pressure of 17 – 24mm Hg
o Class 3: gives pressure of 25 – 35 mm Hg (used for venous ulcer & varicose veins)
VENOUS ULCER:
BISGAARD METHOD:
• Leg lifting is advised
• Clean the ulcer with water / NS
• Pus C/S – Antibiotics
• Bleeding: lift the leg
• 4 layer bandage should be applied to seal the venous ulcer** ( NEET SS)
1. Cotton wool
2. Cotton Elastocrepe bandage
3. Elastic bandage
4. Cohesive bandage
• If ABPI is normal i.e 0.9 – 1.1 apply pressure of 35 – 40 mm Hg

• If ABPI is less: 0.5 - 0.8 apply pressure of 30mm Hg
• If ABPI is < 0.5: no compression, 1st revascularize the artery
• Clean the ulcer and put a split skin graft.

SURGICAL MANAGEMENT OF VARICOSE VEINS
Conventional treatment : TRENDLENBERG OPERATION:
• Identify the sapheno-femoral junction, flush ligation of the GSV close to SFJ & ligate all the
superficial veins at SFJ to prevent recurrence
• Insert a stripper (OESCH PIN STRIPPER) from midcalf level and tie the vein at SFJ and
withdraw the stripper the entire vein will come out
Figure: Stripped Veins
Note:
• If inserted below the mid calf level, Saphenous nerve will be injured medially and sural nerve
will be injured laterally
• Ensure there is no DVT before performing this surgery
• Surgery is contraindicated if DVT is present in the same limb
Perforator incompetence:
• Supra facial ligation of LINTON (in Lipodermatosclerosis Linton operation is not possible)
• Sub facial ligation of COCKETT & DOD (can be done in LDS)
• Sub Facial Endoscopic Perforator Surgery (SEPS):
- Perforators are clipped below the fascia on visualizing through a endoscope
• TRIVEX SYSTEM:
- Subcutaneous illuminator is used
- Veins are visualized
- By a minimally invasive method visible veins are Hooked and ligated
FOAM SCLEROTERAPY
• By using USG dilated veins are sclerosed by TESSARI METHOD
Foam Sclerosants used are:
• Sodium Tetra Decyl sulphate (M/C used)
• Sodium morrhuate
• Polidocanol
• Ethanolamine oleate

Figure: Tessari method of FOAM sclerotherapy
Recent Advances:
Endovenous laser ablation (EVLA) Radio Frequency Ablation
• A laser catheter is introduced into the A coil is inserted into the dilated vein,
dilated vein, 1470nm is applied veins Electromagnetic current is used to produce
are totally destroyed thermal energy and burn out all the vessels
Preset cycle of current application
Advantages
• Any size vein can be ablated Advantages:
• Can be used for Perforator** • Set standard protocol is available
incompetence • Easy for the beginners
• Cheaper than Radio Frequency Ablation • Less procedure time
• Less painful
• Laser protocol is not needed
Disadvantages:
• RFA fiber is costly
• RFA is not possible for tortuous veins
• RFA is not possible for perforators
DEEP VEIN THROMBOSIS

Clinical features:
• M/C pain and swelling in calf (Usually Unilateral)
• Low grade fever
• M/C site of DVT: calf veins
• M/C site of DVT causing PE is: Femoropopliteal veins
Signs of DVT
• Pratt’s sign can be done

• Perthes test
• Modified Perthes test
IOC: Duplex scan (Color Doppler)
Causes of DVT:
Patient factors Diseases:
• Old age • Trauma surgery
• Obesity • Surgery to orthopaedic fractures
• Immobilization • Malignancy
• Pregnancy / Puerperium / High dose of • Heart failure / MI
estrogen therapy • IBD
• Previous H/O of DVT • Nephrotic Syndrome / MI
• Thrombophilia • CVA
• PNH, Homocystinemia
Virchow’s triad: result in DVT

• Stasis
• Hypercoagulable stage
• Endothelial damage
Thrombophilia: group of diseases
Congenital Acquired
Anti Thrombin III deficiency Anti phospholipid antibody
Protein c / s deficiency Lupus anticoagulant present
Factor V leiden deficiency
Lupus anticoagulant present
Dysfibrinogenemia
Risk of DVT:
High risk Surgeries for DVT:
• Urology surgeries 40>Yrs
• Abdomen surgeries
• Pelvic surgery
• Orthopedic surgery
Moderate risk surgeries
• General surgery > 40Yrs
• Patients on OCP undergoing surgeries
• Surgery lasting for > 1 hour
Low risk
• Uncomplicated surgery < 40yrs
• Surgery duration < 30 min

Modified Well’s criteria to predict DVT (NEET DVT going to Pulmonary embolism can be
2020 TOPIC) predicted by another Modified Well’s criteria
• -2 to 0: low probability • >4: suggestive of PE
• 1 to 2: Moderate probability • <4: less chances of PE
• >2: High probability of developing DVT
Factors:
Factors 3 points :
• Lower limb injury / surgery / • C/E: signs & symptoms of DVT: 3
immobilization: 1 • Alternative diagnosis less likely then
• Bed ridden > 3days / any surgery <4 DVT: 3
weeks: 1 1.5 points each:
• Clinical examination • HR > 100/min: 1.5
o Tenderness:1 • Hemoptysis: 1.5
o Swollen limb: 1 • H/O DVT / PE: 1.5 points
o Calf diameter> 3cm: 1
o Pitting edema: 1 1 point each:
o Dilated superficial vein: 1 • H/O immobilization >3days / surgery in
• History points: < 4 weeks- 1 point
o H/O:DVT: 1 • H/O Malignancy ( Treated or palliation
o H/o Malignancy: 1 in 6 months)- 1 point
o H/o Drug abuse: 3
• Alternate diagnosis more likely: -2
Prevention of DVT:
Mechanical methods
• Early mobilization of patient
• Pneumatic compression devise
Pharmacological method (Best to prevent DVT)
• Inj Heparin (aPTT monitoring)
• Low molecular weight heparin(prophylaxis) (Warfarin not used in prophylaxis)
Treatment of DVT:
• First 5 days: Heparin + warfarin
• After 5 days: only Warfarin (monitor PT/INR)
• 1st episode: 3 months
• Recurrent: life long
• Thrombolytics are used for iliac vein involvement
International Normalised Ratio : INR

• INR = PT of patient / PT of controller usually 1 to 1.1

• Surgery is done only if INR < 1.4
• INR > 1.4: No surgery advise, give FFP before surgery
• DVT : on warfarin target INR: 2 – 3
• Mechanical heart valves on Warfarin target INR: 2.5 – 3.5
Surgical Treatment:
• Thrombectomy and place a IVC filter (Greenfield filter)
• Bypass operation: Palma operation
• Green field filter indication
o Anticoagulants contra indicated: Cerebral hemorrhage
o DVT + anticoagulants developing recurring PE
Palma Operation:
• In cases of DVT of the external iliac
vein on one side the contralateral
saphenous vein is anastomosed to
the femoral vein on the affected
site below the level of occlusion or
stenosis.
SYNDROMES RELATED TO DVT

May Thurner and cockett syndrome:
• Right common iliac artery is

running on Lt common iliac
vein and compressing it:
resulting in clinical feature
like DVT

Phlegmasia Alba Dolens (White leg/ Milk
Leg)
• Seen in pregnancy &
underlying malignancy
• Deep veins are thrombosed
• Superficial veins are patent
• Not much dangerous as the
blood is flowing
Phlegmasia cerulean Dolens (Blue leg)

• M/C seen in Malignancy
patients
• Deep veins thrombosed
• Superficial veins thrombosed
• Leg is in a gangrenous stage:
Venous gangrenous stage
• Immediate surgery is needed
TOPIC 2C: LYMPHATIC SYSTEM

LYMPHEDEMA:
• M/C cause worldwide: FILARIASIS
• M/C cause of upper limb Lymphedema: Post mastectomy
Classification:
Primary Lymphedema Secondary Lymphedema
Cause: Congenital • Filariasis(M/C)
• Fungal
• RT
• Malignancy
• Surgery (MRM)
• Trauma
• Superficial thrombophlebitis
• DVT
• Silica Exposure

PRIMARY LYMPHEDEMA:
Congenital Lymphedema praecox Lymphedema tarda
• Onset < 1 year • Onset > 35 years

• M/c Bilateral
• Involve whole leg
• Milroy’s disease.
Figure: Milroy’s disease
Malignancies associated with Lymphedema:

• Lymphangiosarcoma (Stewart Treves Syndrome)
• Kaposi sarcoma (HIV)
• SCC
• Liposarcoma
• Malignant Melanoma
• Malignant fibrous histiocytoma
• BCC
• Lymphoma
Clinical features of LYMPHEDEMA

• More confined to foot, toes and ankle
• Dorsum of foot looks like buffalo hump, toes look like square foot
• Skin is not pinchable: STEMMER’s SIGN
• Eczema
• Fungal infection: of skin: Dermatophytosis
• Fungal infection of nail: Onychomycosis
• Fissures, verrucae, wart

• Ulceration is unusual if present rule out venous insufficiency
• May get a problem: LYMPHANGIOMA
LYMPHANGIOMA
• Dilated Dermal Lymphatics- Forming Blisters
• Clear fluid present( Rarely Blood stained)
• Long term- Lymphangiomas- Thrombose and form nodules.
o < 5cm = Lymphangioma Circumscriptum
o More widespread- Lymphangioma Diffusum
o Forming Reticulate pattern of Ridges- Lymphedema ab igne.
• Weeping Lymphangioma- Lymphorrhea/ Chylorrohoea
• Protein-losing diarrhoea, chylous ascites, chylothorax, chyluria and discharge from
lymphangiomas suggest lymphangectasia (megalymphatics) and chylous reflux
Figure: Lymphangioma Circumscriptum
Figure: Lymphangioma Ab Igne
BRUNNER’s CLINICAL GRADING OF LYMPHEDEMA:

o Grade I: pitting edema, edema decreases on lying over nigh
o Grade II: STEMMER’s SIGN +ve: non pitting edema, not subsided on lying over night
o Grade III: Irreversible skin changes: Fibrosis & papillae
Management:
Lymphedema usually treated conservatively:
CONSERVATIVE management
o Pain management

o Infection (Lymphangitis in Lymphedema is due to Streptococcal) treated with antibiotics
o Skin management: Moisturisers, antifungal ointment
o Multilayer compression stockings are used > 35 mm Hg:
- at the level of ankle 100% pressure,
- at knee 70% pressure,
- at mid thigh 50% pressure and
- at groin 40% pressure is applied
Exercises:
o Vigorous exercise contraindicated
o Mild exercise is prescribed like swimming
o Rhythmic exercise is advised
DRUGS: not much available
Tab DEC is given in acute cases and acute exacerbation
Surgical option in Lymphedema:

Bypass procedures: not much successful
o Omental pedicle
o Skin bridge (GILLIES procedure)
o Ileal mucosa (KINMONTH surgery)
o Lymphatico venular anastomosis
o Lymph node to saphenal anastomosis (KINMONTH)
Limb reduction procedure: successful & M/C used

o Charles
o Sistrunk
o Thompson
o Homans
Charles procedure:
o Remove entire skin and subcutaneous tissue up to the muscles or fascia, place a split skin
graft. Continuous lymph ooze is present

Figure: Charles procedure
SISTRUNK operation:
o Wedge excision of skin and subcutaneous tissue + Reapproximation. No lymph ooze
ThomPson:
o Buried dermal flap operation, Pilonidal sinus is a complication
HOMAN’s Operation:
o Most satisfactory surgery, skin flap is raised all the subcutaneous tissues is removed and the
skin flap is closed. Skin flap necrosis is a complication
CHYLURIA:
• Filariasis is the MC cause of Chyluria.
• 1-2% cases of filariasis will get this complication after 20 years.
• Painless passage of milky White Urine, after a fatty meal
• Chyle may Clot leading to Renal Colicky and Hypoproteinemia may result.
• Chyluria may be caused by Ascariasis, Malaria, TB and Tumour also.
• IV urography or Lymphagiography may show the fistula ( Lympho Urinary)
• Low fat, High Protein diet, Plenty of liquids to avoid clots of chyle are advised.
• Laparotomy and ligation of Dilated lymphatics are advised.
• Sclerotherapy of lymphatics are attempted.

Chapter 3 – Plastic surgery and Skin lesions
Part 1: Skin lesions, Ulcers, Swellings etc
Topic 3a: Pressure sores / Bed sores

• Pathophysiology: as patient stays in one position capillary pressure becomes >30mm Hg that
results in ischemia. Ischemia leads to loss of skin subcutaneous tissue
Classification:
• Stage I: Erythema
• Stage II: Partial thickness (Epidermis & Part of dermis lost)
• Stage III: Full thickness (Epidermis & Dermis lost; raw area extends up to subcutaneous tissue
• Stage IV: involves Fascia, Muscles & Tendon
M/C sites of bed sore in sequence:

• Indra - m/c : ischium
• Gandhi- Greater trochanter
• Statue- Sacrum
• Has - Heel
• More- Malleoli(lateral> medial)
• Ornaments- Occiput
Figure: bed sore- MC site- Ischium
Prevention:
• Bed ridden patient :Change the position - 2 hrs once
• Wheel chair patient : lift him up for every 10 minutes once for 10 second
• BED- Aqua bed for quadriplegic patient

Management:
• Grade I & II: Moist dressings
• Grade III & IV: Debridement and use VAC devices at -120mm Hg negative suction.
• TOC : Vacuum Assisted Closure Device
Topic 3b: NECROTISING FASCITIS

• Definition: It is a rapidly progressing bacterial infection causing necrosis of skin, subcutaneous
tissue, fascia and underlying muscles.
• M/C organism: Group A Beta Hemolytic Streptococci**
• It is usually polymicrobial infection
• Seen in immune compromised patients like
o DM
o Cancer patients
o Patients on chemo-therapy
• Necrotising fasciitis involving scrotum : Fournier’s Gangrene** . Remove necrotic tissue on
debridement results in Shameful exposure of testis
• Necrotising fasciitis involving Abdominal wall: MELENEY’S Gangrene**
• Necrotising fasciitis involving Lower limb: M/C site of Necrotising Fascitis**
• Rarely involves head & neck
Figure: Fournier’s Gangrene

Treatment:
• Hyperbaric Oxygen therapy
• Immediate Debridement
• Higher antibiotics
Topic 3c: CELLUTLITIS VS ERYSIPELAS

CELLULITIS ERYSIPELAS
Caused by : Streptococcal pyogenes Caused by : Streptococcal pyogenes
Subcutaneous tissue (mainly) + Deeper tissues Skin + subcutaneous tissue involved
Poor demarcation between involved tissue and Well demarcation
normal tissue

Bacteremia Due to loss of skin multiple organisms attack &
Tenderness the patient will be in severe TOXAEMIA
Subcutaneous tissue absent in ear:
Hence Ear not affected Ear is affected(MILIANS EAR SIGN)**
Butterfly shaped lesion seen in face
Figure: Cellulitis and Erysipelas
Topic 3d: ABSCESS

PYOGENIC ABSCESS COLD ABSCESS
Caused by Bacterial infection
Staph aureus
Signs of inflammation present No signs of inflammation

Treatment
• Abscess drained by putting a CRUCIATE Cold abscess drained by non-dependent method
incision to prevent sinus formation
• If abscess present in parotid region, neck
& axilla or any place where neuro
vascular structure is present use
HILTONS METHOD to drain the abscess
(no cruciate incision use LISTER’S SINUS
FORCEPS)

Topic 3e: HIADRENITIS SUPPURATIVA
• It is apocrine sweat gland infection
• Caused by Staphylococcus aureus
• M/C site : Axilla > Pubis
• M/C in DM patients
• To prevent spread of infection advice not to shave axilla just cut the hair
• Extensive conditions may need split skin grafting
Figure: Hiadrenitis Suppurativa
CARBUNCLE
• Rapidly spreading cellulitis in diabetics
• Caused by S.aureus
• M/C site nape of neck
POTT’S PUFFY TUMOR:

• It is frontal bone osteomyelitis
• infection spreads from frontal sinusitis
• it can extend deeper and can cause subdural empyema
• I&D
Topic 3f: ULCER

Parts of ulcer:
• Margin
• Edge
• Floor : is seen on inspection (Slough or granulation tissue is seen)
• Base : is felt on palpating the ulcer

TYPES OF ULCER:
• Sloping edge: seen healing ulcer or venous ulcer
• Punched out edge: seen in Syphilis, trophic ulcer & arterial ulcer
• Undermined edge: seen in TB
• Rolled out edge: seen in BCC(rodent ulcer)
• Everted edge: seen in SCC
Venous ulcer:
• Seen in varicose veins
• Seen on medial malleolus
• A long standing venous ulcer converted into malignancy MARJOLINS ULCER(SCC)
MARJOLINS ULCER
• Arise from Burns scar, venous ulcer & keloid.
• Usually no LN mets
• If it crosses normal skin LN mets are seen
• Radiotherapy is contraindicated. Only Surgery Advised

Figure: Marjolin’s Ulcer
Topic 3g: SWELLINGS

LIPOMA SEBACEOUS CYST DERMOID CYST
• Also known as universal • Also known as Sequestration Dermoid:
tumor epidermoid cyst • Due to epithelium entering at
• M/C skin swelling • Formed due to the line of fusion
• DERCUM’S Disease: obstruction of
multiple painful lipomas sebaceous duct .It is a Seen in
retention cyst • Scalp (M/C)
Emergency presentation: • 70% punctum present • External angular dermoid
• GIT(Intussusception) • Content : bad smelling • Post auricular dermoid
• Respiratory pultaceous material
Tract(Obstruction) • M/C site : Head &
Neck**
Malignant conversion • It is absent in palms &
(Liposarcoma) soles
• Thigh
• Retroperitonium FORDYCE DISEASE:
• Presence of ectopic
sebaceous tissue in lips
Clinical Examination: Clinical Examination: Clinical Examination:
• Slip sign + • Skin is not pinchable** • Indentation + of Bone may be
• Pseudo fluctuation + • Putty consistency present
• Trans illumination+/-
Treatment: Treatment: Treatment:
• Enucleation • Elliptical incision made Excision
• Excision along with punctum
sebaceous cyst excised

• Infected sebaceous cyst: • Always take a CT scan before
cruciate I&D surgery to rule out intra
cranial extension
Complications of sebaceous cyst: Rare types of dermoid:
• Cock’s peculiar tumor- • Implantation dermoid m/c in
ulcerated sebaceous finger tips
cyst in scalp looks like • Tubulo dermoid: present at
a tumor midlines Eg: Thyroglossal
• Sebaceous horn- dried cyst, post anal dermoid
up sebum • Teratomatous dermoid:
• M/C complication: contains all 3 layers usually
Infection seen in ovaries(contains skin,
hair, teeth& muscle)
SYNDROMES ASSOCIATED
• FAP + sebaceous cyst =
GARDNER’S
• HNPCC+ sebaceous cyst
= MUIR TORRE
One liners
• DERCUM DISEASE -
• COCK’S PECULIAR tumor-
• WEN:
• DIMODEX FOLLICULARUM: Worm inside sebaceous cyst
• SEBACEOUS HORN: Widow Dimanche is the Bailey and Love Model**
Figure: Cock’s Peculiar Tumors

Figure: Sebaceous Horns
Topic 3h: SCARS

HYPERTROPHIC SCAR KELOIDS
Is due to proliferation of
• mature fibroblasts
• mature blood vessels
Limited only to previous scar It may happen from previous scar or anywhere
without scar
It extends to normal skin
More seen in flexor surfaces More seen in extensor surfaces
Eg: sternum, face
C/F : Itching+++++
No family Genetic: Negroes & young females
No genetic
Treatment: Treatment:
• Excision • No excision
• Intra lesional steroid (Triamcinolone
acetate) for preventing the growth of
keloid & to decrease itching.
Long standing keloid leads to Marjolin’s ulcer

Topic 3i: HEMANGIOMA OF SKIN
Classification of Hemangioma based on Involution
NICH RICH
• Non involuting congenital hemangioma • Rapidly involuting congenital
• Happens at 4-6 months hemangioma
• Doesn’t disappear • Happens at 4-6 months
• Disappears in 5-7 yrs
Classification based on depth of invasion

CAPILLARY HEMANGIOMA CAVERNOUS HEMANGIOMA
Superficial hemangioma of skin Deeper or in bigger blood vessel
Capillary hemangiomas:
SALMON PATCH STRAWBERRY (RICH) PORT WINE STAIN (NICH)
Appears: at Birth Appear:at Birth
Disappears: by 1 yr And never disappears
• M/C site : NECK in
New Bailey ( Errata )
Treatment not necessary Treatment needed: pulsed
wave laser therapy

Part 2: Plastic Surgery _ Reconstructive surgery
SKIN GRAFT FLAPS

Graft is a piece of tissue without its own blood Flap is a tissue carrying its own blood vessel
supply • Pedicle flap:
• Free flap: micro vascular anastomosis
needed
Partial thickness graft Full thickness graft Axial pattern flap Random pattern flap
• Involves • Involves • Contains • Leash of
epidermis + epidermis+ full named blood unnamed
part of dermis dermis vessel blood vessel
supply
Skin graft: survival

• First 48hrs: Plasma Imbibition
• 48hrs – 5 days: Inosculation (alignment of Blood vessels)
• >5 days : Revascularisation
Absolute contra indication for skin grafting- Beta haemolytic streptococci present on wound.
Partial thickness graft Full thickness graft

Also called as: Thiersch graft Also known as Wolf graft
Donor site: •
• Thigh
• Back

Advantage: •
• No need to cover donor area
• Wider areas can be taken
• Repeated grafting is possible from same
site
Disadvantage: •
• Cosmetically ugly
• Contractures present
Procedure: •
• Using Humby knife or Electrotome
At donor site:
• Punctuate spots & absence of fat
indicates a proper partial thickness
graft is taken
Figure: Humby Knife for SSG
Partial thickness graft

Thiersch graft: 0.006 – 0.012 inches ( Thin Partial Thickness graft)
• Most commonly used
• Thin graft
• High take up
• Low primary contraction
• Increased secondary contraction
Blair Brown graft: Intermediate 0.012- 0.018 inches
Padgett graft: 0.018 – 0.024 inches ( Thick Partial Thickness graft)
• Thick graft
• Poor uptake
• High primary contracture

• Low secondary contracture
Meshing: Split skin graft

• Size of the graft can be increased
• It helps to drain any fluid
Figure: Partial Thickness Split Skin Graft
Indications of Flap:
Flap is used instead of graft in the following condition
• Exposed Bone (graft can be placed on periostium but not on exposed bone)
• Exposed tendon (graft can be placed on tendon sheath but not on exposed tendon)
• Exposed joint
• Exposed prosthesis or metal plates
• Complex defects
• Radiation necrosis
Axial pattern flap (Based on a named Blood vessel)

• PMMC flap based on Thoraco acromian artery
• DP (Delto pectoral) flap based on Internal Mammary artery
• TRAM flap based on Superior Epigastric Artery or Inferior Epigastric Artery
• DIEP flap (Deep inferior epigastric artery free flap) based on Inferior Epigastric Artery
• PMMC & DP flap used in Oral cavity reconstruction
• TRAM & DIEP flap is used in Breast reconstruction

Figure: DIEP flap ( Free Flap)
Random pattern flap
• It is based on dermal & subdermal plexus
• Accepted length: Width ratio = 3:1
Types
Types of Random pattern Flaps Figures corresponding
Transposition flap:
• Flap rotated about a pivot point
into adjacent defect
Z plasty:
• A type of transposition flap, 1.7
times elongation of wound
happens in 60 degree angulation.
Used mainly for burns
contracture.
Rhomboidal flap (Limberg flap):

• a type of transposition flap, it can
be used in any place. Very
commonly used in pilonidal sinus
surgery.

Rotational flap: similar to transposition
flap but differ in that they are semi
circular
Advancement flap:
• Burrow’s triangle is made and the
flap slides forward or backward.
• Common variants include
Rectangular advancement flap, V-
Y advancement flap & Abbes flap
( to reconstruct lip cancer after
resection)
Interpolation flap:
• Like rotation flap they rotate
about a pivot point but they insert
into defects nearby area but not
into adjacent donor site (Eg:
thenar flap for finger tip)

Classification based on tissue included
• Cutaneous flap
• Fascio cutaneous flap
• Myocutaneous flap
• Osteo cutaneous flap
• Muscle flap + skin graft
• Fascia- fat flap
Types of MUSCULAR FLAPS

Mathes- Nahai classification ( NEET SS)**
• I - 1 vascular pedicle (Eg: Gastrocnemius)
• II - 1 dominant + minor pedicles (Eg: Gracilis muscle )
• III - 2 dominant pedicles (Eg: Rectus abdominus (TRAM flap))
• IV- Segmental pedicle (Eg: Sartorius muscle)
• V- Dominant pedicle + Segmental pedicles (Eg: Pectoralis muscle(PMMC flap))
Part 2: Plastic Surgery - Cosmetic surgery

Reduction mammoplasty: Principles
• Volume of breast reduced
• Ptosis is decreased
• Anatomical location corrected
• Reposition on nipple/ areola is done maintain blood & nerve supply
• Minimal scar
M/C technique used: inferior pedicle based technique
Other techniques:
• Superior pedicle
• Lateral pedicle
• Central mound
• Superomedial pedicle

Figure: Reduction mammoplasty- Inferior Pedicle Technique
ISSUES in reduction mammography:
• Can be done at any age (breast tissue should not grow for 12 months before planning
surgery)
• >35 yrs mammography is needed before surgery
• Resected tissue should be sent for HPE
• Only one time the procedure allowed
Contraindications:
• Smoking
• H/O recent radiotherapy – surgery is delayed
Complication:
• Lactation breastfeeding affected
• Nipple will have increased sensation
• Wound breakdown
• Hematoma
• Fat necrosis
Re-Implantation of cut digit / limb

Scenario:
• Cut limb case to an M.B.B.S doctor:
• Wash in clear water
• Wrap it in a sterile gauge
• Place it in a plastic bag
• Place the plastic bag in ice box
• Send him to a plastic surgeon within 6hrs
• Reimplantation by plastic surgeon

Order of anastomosis of cut limb / digit:
• B- Bone
• E- Extensor tendon
• F- Flexor tendon
• A- Artery followed by Vein
• N- Nerve
• S- Skin
EXTRA EDGE POINTS

Langer’s lines : Kraissl lines: Borges lines:
• Cosmetic lines • Lines perpendicular to • Lines formed along
identified in underlying muscle. Better the furrows when
cadavers cosmetic than Langer’s line in skin is relaxed in
living patients face

Dressing materials in surgery
• Alginate dressings: absorptive used for high drainage wounds with heavy exudates
• Foam dressing: also used for high drainage wound, not to be used in non draining wound
• Hydrocolloid dressing: used for bedsores, facilitates autolysis debridement and remove the
dead tissue, not to use in high drainage wounds
Figure: Hydrocolloid Dressings
• Hydrogel dressing: Rehydrates wound bed, not to use in high drainage wounds
• Transparent film dressing: Autolytic debridement, not to use in high drainage wounds
• VAC dressing: Negative suction of -120mm Hg, TOC for bedsores.

Figure: VAC devices

Chapter: 4 : Paediatric surgery
ABDOMINAL WALL DEFECTS
OMPHALOCELE or EXAMPHALOS GASTROSCHISIS

It is a congenital defect in anterior abdominal It is a congenital defect in the abdominal wall
wall with bowel protruding out wards with with bowel protruding out in angry looking
covering membrane (peritoneal covering) manner with no covering membrane
Umbilical cord attached to the summit of the
membrane
CVS anomalies : Septal defects seen in 20-40% It can be associated with Intestinal atresia (M/C
cause for short bowel syndrome in children)
Major Minor • Size of defect <4cm
• Defect <5cm • Defect >5cm • Immediate closure
• Small bowel • Small bowel,
protrudes Liver
• Can wait and • Difficult to
watch close abdomen
• Good prognosis wall
• Strapping • poor prognosis
• Surgical
closure
INTESTINAL ATRESIA
• Duodenal atresia is M/C Intestinal type of atresia
DUODENAL ATRESIA
Associated with
• Down’s syndrome
• Annular pancreas

• Malrotation of gut
Types
• Type I: M/C : complete atresia
• Type II: Fibrous cord separating two
ends
• Type III: In complete or partial
obstruction
• WINDSOCK DEFORMITY: Is a type of
duodenal atresia with mucosal web and
an intact muscle wall
Presentation
• 80%: Bilious vomiting
• 20%: Non Bilious vomiting, atresia is present proximal to ampulla
Treatment of choice duodeno duodenostomy
JEJUNOILEAL ATRESIA:
• 1 IN 2000 Intra uterine mesenteric ischemia
• Associated with cystic fibrosis
Types
• Type I: Mucosal web
• Type II: Fibrous cord + Intact mesentry
• Type III: Blind end with V shaped
mesenteric defect
• Type IIIB: Distal bowel with Apple peel
or Christmas tree appearance**. Distal
bowel receives blood supply from ileo
colic artery in distal way
• Type IV: Multiple Sausage shaped
atresias

Figure: type 3b- Apple peel appearance
Treatment: Resect the atresia and anastomose the normal bowel
CONGENITAL DIAPHRAGMATIC HERNIA
BOCHDALEK HERNIA: MORGAGNI HERNIA

Herniation through Bochdalek space
M/C on Lt postero lateral side
M/C content stomach

• C/F: Of congenital diaphragmatic hernia
Difficulty in breathing (bag and mask ventilation C.I)
Intubate the baby immediately
• X-ray chest: Bowel contents present in the chest
• Ryles tube: present in the chest
• Prognosis depends on: pulmonary hypoplasia
• In 24-48hrs lung expands Honey moon phase: Trans abdominal repair of the hernia
CLEFT LIP & PALATE

• Isolated cleft lip 15% (rare)
• Isolated cleft palate 40%; common in females.
• Combined cleft lip & palate 45% (m/c seen 1 in 600 births); common in male**
Figure: Types of Cleft lip and palate
Antenatal USG can detect: Cleft lip; cannot detect isolated cleft palate
Cause: Maternal exposure to drugs like
• Phenytoin
• Steroids
• Diazepam
Syndromes associated:
• M/C: PIERRE ROBIN SYNDROME** : Glossoptosis, Retrognathia &Respiratory difficulties
• Downs’s syndrome
• Treacher Collin

• Sprintzner
• Sticker’s
C/F:
• Cosmetic
• Speech problems
• Feeding problems
• Middle ear infection
Complete cleft: cleft is not attached to vomer bone

Incomplete cleft: cleft attached to vomer bone
LAHSHAL OR THALLWITZ CLASSIFICATION

LAHSHAL ( all Capital )stands for Complete cleft in order of
• Rt Lips
• Rt Alveolus
• Rt Hard palate
• Soft palate
• Lt Hard palate
• Lt Alveolus
• Lt Lips
lahSH phrase means

• Rt Side partial cleft lip, alveoli & hard palate
• Lt Side complete soft palate & Hard palate

KERNAHAN’S CLASSIFICATION: (Given numbers from 1-9 each representing a structure)
OPERATION
Timing of operation
Cleft lip and Soft palate only:
• Unilateral: 6 Months (Single surgery)
• Bilateral: 4-5Months 1st surgery; 6 Months 2nd surgery
• Only Soft palate defect: 6 Months only one surgery
Combined Soft palate & Hard palate:

• 2 operations: Soft palate operated 6Months; Hard palate 15-18Months
Combined Cleft lip + cleft soft palate + cleft hard palate:

• 2 operations:
• 1st Cleft lip & cleft soft palate operated 6Months;
• Hard palate 15-18Months
Name of surgery
Cleft lip operation Cleft soft palate Cleft hard palate
Millard Furrow’s technique Wardill & Langenbeck
Mulliken
Manchester
Rule of 10: (Old)

• 10 Wks age
• 10 lbs weight
• 10 gm% Hb

Complication after surgery
• M/C: Velopharyngeal incompetency
• Speech problem
• Hearing problem
• Oroantral fistula
• Cupid bow
Secondary problems:
• Facial growth
• Dental problems
• Hearing problems
• Speech problems
Time of operation
Urology:
• Congenital hernia : As early as possible
• Congenital hydrocele: 2 years
• Hypospadias: 6Months – 1Yr
• Undescended testis: 6 Months – 1Yr
• Phimosis: 1 – 2Yrs
Gastro surgeries
• Congenital diaphragmatic hernia: 24-48hrs
• Extra hepatic biliary atresia: <6 weeks (Kasai procedure)
• CHPS: 4 Weeks (Ramstaed procedures)
• Midgut volvulus: earlies (Ladd’s procedure)
• Umbilical hernia: 5Yrs
Head & Neck

• Cleft lip: 6 Months
• Cleft soft palate: 6 Months
• Cleft hard palate: 16 – 18 Months
• Cystic hygroma: after birth
PAEDIATRIC ONCOLOGY
• M/C cancer in childhood Leukaemia
• M/C solid tumor or 2nd M/C cancer of childhood : Brain tumor (Astrocytoma grade I or
Pilocytic Astrocytoma)

• M/C abdominal tumor or M/C extra cranial solid tumor : Neuroblastoma > Wilms tumor
• M/C malignancy in <1Yr child: Neuroblastoma
• M/C soft tissue sarcoma in children : Rhabdomyosarcoma
• M/C Renal tumor in childhood: Congenital mesoblastic nephroma > Wilms tumor
• M/C paediatric tumor producing mets: Neuroblastoma (Mets to Long bones)
NEUROBLASTOMA
Arises from sympathetic nervous system
M/C from
• Adrenal medulla (38%)
• Paravertebral 30%
• Chest 20%
• Neck
• pelvis
Neuroblastoma in abdomen: ( From adrenal medulla)

• Seen in 1-5yrs of age
• Clinical presentation as Abdominal mass or Bony metastases, Skin mets, Paralysis
• 70% will have metastases on presentation
Abdominal mass: Neuroblastoma vs Wilms tumor

Favouring Neuroblastoma:
• M/C
• Calcification
• Cross midline
• Invade spinal cord
• Extensive mets
• Elevated VMA
IVP: kidney drooping Lilly appearance

Investigation:
• Urinary VMA elevated
• Urinary Homovanillic acid elevate
• Urinary Dopamine elevated
• Urinary Nor adrenalin elevated
• Accurate diagnosis is possible with CT/MRI, take biopsy
International Neuroblastoma staging system
Treatment
• Low risk patients : Surgery alone
• Intermediate risk: Surgery +Chemo therapy
• High risk : CT + Stem cell therapy (3 Yr survival is < 30% )

Chapter 5: Oncosurgery
Part A- General aspects
Bone metastasis
• Most common site of bone involved is: Vertebra**
• After vertebra, 2nd most common site is femur > pelvis > ribs > sternum > humerus > skull
• Skull is the last common site
Tumor Lysis Syndrome

• Rapid destruction of large number of rapidly proliferating cells**
• MC associated with Burkitt’s Lymphoma, other high-grade lymphomas and Leukemias.
Pathophysiology:
• Rapid turn over of Nucleic acid – releases excess uric acid- Hyperuricemia*
• Increased release of intracellular potassium- Hyperkalemia and arrythmias
• Release of Intracellular phosphate- Hyperphosphatemia
• Phosphate combines with Calcium- Hypocalcemia
• Calcium Phosphate is deposited in renal tubules- Renal failure
• Deranged Oxidative metabolism- Lactic acidosis
Tumor Lysis Syndrome Hypercalcemia of Malignancy

Due to rapid destruction of neoplastic cells Due to Increased calcium release from bone or
due to rapid absorption by Renal tubules
Underlying Abnormalities: Underlying Problem:
• Increased secretion of PTH related
peptide

• There will be hypercalcemia on Serum
measurement
MC seen in treatment of Lymphomas and MC seen in Osteolytic secondaries**

leukemias.
Rare with Solid tumors*
Treatment: Treatment:
• Aggressive Hydration • Hydration and Dialysis
• Sodium Bicarbonate for lactic acidosis • Diuresis with Frusemide
• Allopurinol to reduce the uric acid by • Bisphosphonates ( DOC – Zolendronic
(Blocking on Hypoxanthine→ Acid)
Xanthine→ Uric Acid pathway ) • Calcitonin
• RASBURICASE- Recombinant uric • Mithramycin
oxidase – Ex vivo enzymatic • Gallium nitrate
dehydration happens • Steroids
• Hemodialysis- Renal failure
Typhilitis
• @ Neutropenic Colitis @ Necrotising Colitis @ Cecitis @ Ileocaecal syndrome
• Classically seen in Neutropenic patients after chemotherapy with cytotoxic agents.
• MC in children especially having ALL and AML
• Clinical features:
o Patient is immunosuppressed
o Fever+
o Right Lower abdominal tenderness+
o Diarrhea which is Bloody
• Diagnosis made by USG or CECT abdomen which shows thickened wall of cecum
CECT abdomen Shows Typhilitis

• Treatment:

o Most patients improve with medical treatment i.e Antibiotics
• Surgical indication:
o No improvement in 24 hours
o Perforation
Superior Vena Cava Syndrome:

• Presents with SVC obstruction features+ Severe reduction in Venous return from head and
neck and Upper limbs
• MC cause- SMALL CELL Cancer Lung and SCC lungs
• MC cause in young adults- Lymphoma**
Clinical Features:
• Neck and facial swelling
• Dyspnea
• Cough
• Hoarseness
• Tongue swelling
• Headache
• Nasal stiffness- Epistaxis
• Dizziness and syncope
• Dilated veins over chest wall and neck
• Increased Collaterals over Anterior chest wall
• Cyanosis
• Edema of face, arm and chest
Investigations:
• CECT
• Xray chest- widened Superior mediastinum and more common in right side
Treatment:
• Life threatening Complication – Tracheal obstruction
• Emergency- Surgery for superior mediastinal mass
• Treatment depends on underlying cause:
o Radiotherapy- NSCLC and Metastatic Solid Tumors
o Chemotherapy - Small cell cancer and Lymphoma
Image Based Question:

Recent AIIMS Question
CHEMOPORT DEVICE
Part B- Soft Tissue Sarcoma ( STS)

• Sarcomas are a heterogeneous group of tumors that arise predominantly from the
EMBRYONIC MESODERM, but also can originate as does the peripheral nervous system from
the ectoderm.
• Incidence:1% in adult cancers ( 7% in children’s cancers)
Most Commons in STS:

• MC Type- Liposarcoma ( Ref.Sabiston Page 762)> Leiomyosarcoma
• MC site- Extremities ( MC in Lower limb > Upper limb) > Trunk> Retroperitoneum> head and
Neck.
• MC Type of Paediatric STS- Rhabdomyosarcoma ( MC in Head and Neck)
• MC Retroperitoneal Tumor- Liposarcoma
• Most common type of STS in Extremities- MFH
• Most common type of STS in Retroperitoneum- Liposarcoma
• Most common type of STS in Viscera- GIST
Tumor Spread:
• STS grows along Facial planes and compresses the soft tissues- and hence results in Pseudo
capsules**
• MC route of spread- Hematogenous
• MC site of Distant mets- Lungs
• MC site of Distant mets in Retroperitoneal sarcoma- Liver> lungs
• Lymphatic mets is very rare
• Lymph node mets is seen in 2-10% cases only
• LN dissection is performed only in such patients with LN mets.

Histologic types with propensity for lymph nodal metastasis are (SCREAM)
• S-
• C–
• E–
• R –
• E–
• A–
• M-
Etiological Factors:
• Germline mutations:
• NF- 1 ( Chromosome 17q)
• Li Fraumeni Syndrome ( P53 mutation @ Chr. 17p)
• FAP- Desmoid Tumors ( APC gene)
• Radiation induced
• Carcinogens- Thorotrast, polyvinyl chloride, and arsenic- Especially Hepatic Angiosarcoma**
Cahan’s Criteria for Radiation induced Sarcoma:
• Different histology
• Must occur within the irradiated field
• Latency period >4 years
• Second malignancy must histo pathologically be a sarcoma
Example of Radiation induced Sarcoma is Stewart Treves syndrome- But it happens in area not
subjected to Radiotherapy as a complication of Lymphedema after RT to Cancer breast patients.
Clinical Features of STS:

• MC presentation- Painless mass**
• Size at presentation depends on the location:
o Smaller- In distal extremities
o Larger- in Proximal extremities and Retroperitoneal
Investigations:
• IOC for diagnosing- Core cut Biopsy
• IOC to assess the extent of Soft tissue Sarcoma- MRI**
• IOC to assess the extent of RP sarcoma- CECT**
STS present as Heterogenous mass in MRI and helps to delineate muscle groups, Bone, Vascular
invasion of tumor.

Treatment of STS:
• Surgery- Wide Local Excision with 2cm – we may even go beyond the Compartment
Boundaries to achieve clear margins.
• Radiotherapy- EBRT or Intensity Modulated Radiotherapy
• Chemotherapy- Doxorubicin+ Ifosfamide
Prognostic factors:
• Most important prognostic factor- GRADE**
• Most important predictor of metastasis- GRADE**
• MC cause of death in STS- Mets**
Factors predicting Better survival:

• Younger age
• Selected histologic type ( fibrosarcoma)
• Lower grade
• Smaller tumour size <5 cm
• Extremity site (** Best prognosis- Extremity STS)
Discussion of Each Type of STS
1. Rhabdomyosarcoma: ( RMS)
• MC type of Paediatric STS
• MC site- Head and Neck ( Parameningeal)> Extremity> GU tract> Trunk
• PM sites (nasopharynx/nasal cavity, the middle ear, the paranasal sinuses, and the
infratemporal fossa/pterygopalatine space) are considered as un favorable factor in RMS
• Types of Rhabdomyosarcoma:
o Embryonal Rhabdo myosarcoma (M/C type overall) 70%
o Alveolar Rhabdo myosarcoma
o Pleomorphic Rhabdo myosarcoma ( MC type in adults)

Clinical Features:
• MC presentation- Mass**
• Bimodal- 1st Peak 2-5 years; 2nd peak- 15-19 years
• MC route of spread- Hematogenous
• MC site of mets- Lungs**
Figure: Parameningeal RMS**

• Diagnostic cell- Rhabdomyoblasts ( Strap cells)
• Tumor also contains- Tadpole cells** ( White arrow in below image)
• Embryonal Type RMS:

o Embryonal type- Spindle cell variant and Sarcoma Botryoides
o In Sarcoma Botryoides- Tumor cells on HPE resemble like Tennis Racquet
Management and Prognosis:

• Unresectable tumors- Neoadjuvant Chemotherapy is given
• Positive margins on resection- Post op radiotherapy
• Embryonal variant- Favourable
• Alveolar type- Unfavourable
• Favourable primary sites: Non parameningeal( head and neck), Para testis, Orbit and Vagina
• Unfavourable sites: Extremity, Parameningeal**
2. Dermato fibro sarcoma protuberans ( DFSP)

• Low grade sarcoma
• Recurs locally
• Rarely metastasis

• MC site- Trunk( 50%) > Extremity ( 30%) > head and Neck ( 20%)
• Important DD is Keloid** or Hypertrophic Scar**
Figure: DFSP
Clinical Features:
• MC presentation- Nodular cutaneous mass
• Pattern of growth – Slow and persistent
• There is radial extension of tumor through Subcutaneous tissue
• The tumor involves both Dermis and Subcutis without penetration into EPIDERMIS**
• Lesion enlarges over many years- Protuberans name given
• Tumor associated with Satellite nodules
• CD34+
• Majority of DFSP displays the t(17;22)(q22;q13) translocation
• IOC- Incisional biopsy
• Treatment- 2-4 cm margin+ underlying Fascia
• First line treatment for advanced and unresectable tumor- Neoadjuvant therapy with
Imatinib**
3. Liposarcoma:
• M/C sites: Nape of neck, thigh, Retro peritoneum
• In the Retro peritoneum it arises from the perinephric pad of fat
• Macroscopically- Huge, soft, well circumscribed
• Histological Types- Well differentiated, Myxoid, Round cell pleomorphic Liposarcoma
Cect shows Retroperitoneal Liposarcoma
4. Malignant Fibrous Histiocytoma ( MFH):

• Old Books used to say this is Most common – Now the MC is Liposarcoma**

• Arises from fibroblastic differentiation
• M/C in Lower limbs followed by Retroperitoneum
• Intermuscular involving muscles
• Firm consistency.
• Around 5 subtypes there.
5. Synovial Sarcoma:
• Histologic hallmark of soft tissue synovial sarcoma is ‘BIPHASIC MORPHOLOGY’ of tumor cells
(Epithelial like & spindle cell)
• They do not have synoviocytes (misnomer).
• M/C around young age
• M/C arises around Knee joint (85%) and hip but <10 % are intra articular.
• Lymph nodal spread is common
6. Leiomyosarcoma:
• M/C in females
• M/C site: Uterus
• Retro peritoneum
• In Retro peritoneum it arises from the wall of Inferior vena cava.
• In intestine known as GIST* . ( Refer GIT section for GIST)
7. Angiosarcoma:
• Can occur anywhere in body
• Arises from mesenchyme of blood vessels
• H/O chronic lymphedema
• H/O chronic exposure to Arsenic, Thorotrast
• Short duration.
• Rapid increase in size
• Systemic metastasis in common
8. Kaposi Sarcoma:

• Rubbery Bluish nodules seen primarily of the extremities, but may appear anywhere on skin
and Viscera**
• MC in people of East and Africa.
• Usually multifocal rather than metastatic*
• Histologically lesions are composed of capillaries lined by atypical endothelial cells*
• Lesions are locally aggressive with intermittent periods of remission.
• Treatment: Radiation** or Combination Chemotherapy
• Surgical treatment is reserved for Intestinal or Airway obstructions only
Figure: Kaposi Sarcoma ( Multifocal)

9. AIDS related Kaposi Sarcoma:
• Seen primarily in Male homosexuals and not in IV drug abusers or Hemophiliacs*
• Lesions spread rapidly to nodes and GI and Respiratory tract are also often involved*
• AIDS- KS is associated with Herpes like virus-8 ( HHV-8) infection concurrently.
Radiotherapy and STS:

• Highly sensitive: Synovial sarcoma, Fibro sarcomas, Malignant Fibrous Histiocytomas
• Intermediate: Liposarcoma, Myxoid fibro sarcoma
• Resistant: GIST, Leiomyosarcoma, Chondrosarcoma
Part 3: Skin Cancers

• Basal cell Ca – Most common
• Squamous cell Ca- 2nd common
• Melanoma
Layers of Skin:
(Mnemonic – Cute Looking Girl Sangeetha Bijilani)

Basal Cell Cancer:
• MC in Men
• MC in Age > 40 Years
• MC site- Face ( inner canthus, Nose and upper lip along tear flow area- Tear Cancer)
• MC in White Skinned individual
• Spreads:
- Direct spread ( MC and only Mode of spread)- Rolled out edge and Rodent ulcer is
the other name.
- LN spread- Not seen as the Cells are large to enter lymphatics
- Hematogenous- Rare ( < 0.01%)
• Wedge Edge Biopsy Taken from the Tumor.
• Biopsy shows: Peripheral Palisade pattern of Cells **
Figure: Peripheral Palisading cells
• Predisposed by- UV light( Strongest), Arsenic , Coal tar and Aromatic Hydrocarbon
• Types of BCC:
- Nodular ( nodulo cystic): 90%- Usually produces ulceration**

- Superficial spreading type : 10%- Other name- Field Fire type ( Peripheral lesions
with central clearance like a burnt field)- Scaling ++ ( DD: Actinic Keratosis and
Eczema)
• Clinical Features:
- Nodular or Ulcerated lesion in Tear flow area
Figure: BCC in face
Squamous Cell cancer:

• 2nd MC
• M> F
• Arises from Malphigian/ Prickle/ Spinosum layer of skin
• Premalignant lesions:
- Bowen’s Disease: Insitu SCC of Skin/ Shaft of Penis
- Erythroplasia of Queyrat: insitu SCC of Glans Penis
- Paget’s Disease
- Leukoplakia
- Erythroplakia
- Senile keratosis
Figure Shows- Bowen and Erythroplasia of Queyrat
• Risk Factors:
- Radiotherapy
- Long standing scars or ulcers: Marjolin’s ulcer
- Sunlight

- Xeroderma pigmentosa
- Lupus vulgaris
- HPV 5 and 16
- Prolonged exposure to Irritants**
• Irritants causing cancer:
o Kang cancer-
o Kangri Cancer- Buttock Cancer in Tibetans sitting on hot pot
o Chimney Sweeper Cancer-
• Clinical features:
o Excavated edge with proliferative ulcer++
o Ulcerative or Ulceroproliferative
o Verrucous type ( Where RT is contraindicated)
• On HPE- Keratin Pearls seen++ ( Onion skin appearance in epidermis)
• Epithelial keratin pearl formation not seen in:

o Rapidly growing tumor
o Esophagus SCC
o Bladder SCC
• The grading system used is BRODER’S Grading system
• Tumor Marker for SCC- Cytokeratin CK 1 and CK 10
Treatment of BCC and SCC:

• Excision is the treatment of Choice**
• Margin given 3 dimensionally is 4-6 mm Margin for > 2cm size and 4mm margin for < 2cm
size.
• Larger tumors are given 1cm margin
• Cosmetic areas like face, Penis etc- MOH’S Micrographic surgery: serial excision by Shaving
until the tissue becomes negative.
Other modalities:
• 5FU cream

• Electro dissection
• Cryosurgery
• C02 Lasers
• Radiotherapy
Malignant Melanoma:
• 4% of skin cancer
• 79% of skin cancer deaths
• 1.4% of all cancer deaths.
Incidence in India
• Male : 0.5 / lakh
• Female : 0.2 / lakh
• Melanoma is the leading cause of death in women 20 – 40 yrs.
• m/c cancer in age group from 20-39 years- malignant melanoma.
Risk Factors:
• Sunlight
• Xeroderma pigmentosa
• Past/family history of melanoma
• Dysplatic naevi( 10% life time risk)
• Immunocompromised- HIV, cyclosporin A therapy, Hodgkin’s disease.
Classical features of Malignant Melanoma: ( ABCDE)

• A
• B
• C
• D
• E Evolution, Elevation, Enlargement
• F Funny looking
Discussion of Each types:

• Superficial spreading – Most common
• Acral lentiginous – Most common in dark skin
• Nodular – Worst prognosis
• Lentigo maligna – Best prognosis
Superficial Spreading Melanoma:

• M/C type occurring in white population
• Melanomas arising in preexisting Dysplastic naevus are usually SSM.
• M/C Sites:

Males: Trunk
Females: Lower legs and back
Nodular Melanoma:
• Second most common
• Can occur on any surface of the body, 50 – 70 yrs
• M / C site: Head, neck and trunk
• Only vertical growth, no radial spread.
• High Risk group and POOR PROGNOSIS**
Acral Lentiginous Melanoma:

• MC in Black people
• MC in white areas – Palms and Soles
• Bad prognosis
Figure: Acral Lentiginous Melanoma
Lentigo Maligna Melanoma:

• Older age individuals.
• Previously called as Hutchinson’s melanotic freckle.
• Common in face**
• Most commonly affects women than men
• Insitu variant is called lentigo maligna.
• Lowest metastatic potential
• Least common
• Least malignant
• Good prognosis
Subungual Melanoma:
• MC below the nail bed

• Hutchinson’s Sign- Pigmentation extending to the nail lateral fold from the nail bed
Amelanotic Melanoma:
• No pigmentation is seen and hence present late
Tumor markers of Melanoma:
Mode of Spread
Local spread Lymphatic spread Hematogenous spread
Vertical spread is more Nodal spread is common Brain
dangerous Nodules may be seen Lungs
MC with Nodular type • Nodules along the way of Liver
spread: Small intestine
• < 2cm from primary Skin
lesion: Satellite Nodules** Bones
• >2cm from primary lesion: MC cause of death is
In transit nodules** metastasis
Figure: Satellite and In-transit nodules
Prognostic factors:
• Depth ( most important)
• Ulceration
• Lymph node status
• Satellite lesions
• Distant mets
Based on
• Site- Lower extremities ( good)
• Sex- female( good)
• Histology- lentigo maligna(good)

Breslow Thickness Clark’s level
Based on thickness of invasion by optical Based on layer of invasion
micrometer
• Level I -Only in Epidermis
• I : Less than 0.75 mm • Level II-Into papillary dermis
• II : Between 0.76 to 1.5mm • Level III- Up to the junction.
• III : 1.51 mm to 4 mm • Level IV - Into reticular dermis
• IV : Greater than 4 mm • Level V -Extension into subcutaneous tissue
Treatment of Malignant Melanoma:

• Excision biopsy with preferred margins
• Sentinel node biopsy
• Block dissection if sentinel node is positive
• Reconstruction of defects.
Isolated Hyperthermic Limb Perfusion therapy
• For Extremity Melanoma and

Sarcomas
• The artery and Vein of the lower limb
containing the Tumor with satellite /
intransit nodules is isolated by
clamping.
• The chemotherapy ( Usually
Melphalan) is given with high
temperature as infusion and the blood
is removed and reinfused after
oxygenation only into that limb.
• Systemic toxicity is thereby avoided
Margin Excisions:
• Lesion 0-1 mm thick ( Depth)- 1cm margin
• Lesion 1-2 mm Thick- 1-2 cm margin
• Lesion 2-4 mm Thick- 2cm margin
• Lesion > 4 mm thick – 2cm margin

Chapter: 6 Cardiothoracic surgery
Topic 6a Thorax
Mediastinum parts
• Superior mediastinum (Thyroid mass, parathyroid mass, thymoma)
• Inferior mediastinum
• Anterior mediastinum
• Middle mediastinum
• Posterior mediastinum
M/C mediastinal mass Thymoma (Actual correct answer is neurogenic tumor)**
Anterior mediastinal masses

• Thymoma (M/C)
• Lymphoma
• Germ cell tumor
• Thyroid mass
• Parathyroid tumor
• Mesenchymal tumors
Middle mediastinum masses

• M/C lesion CYST (pericardial cyst, bronchogenic cyst)
• Aneurysms
• Lymph Node masses
• Ectopic pheochromocytoma

Posterior mediastinum masses
• Neurogenic tumors (M/C)
• Meningocele
• Mesenchymal tumors
• Pheochromocytoma
• Lymphoma
THYMOMA
• M/C neoplasm of thymus
• M/C location : Anterior mediastinum
• Seen in 40-60yrs age group
• It is surrounded by well defined fibrous capsule
Types of thymoma
• Lymphocytic
• Epithelial
• Mixed (M/C)
C/F:
• Usually a symptomatic, Usually detected on X-ray chest as a an incidental finding
• Dysplasia
• Dyspnoea
• SVC Syndrome
• Paraneoplastic syndrome (M/C: Myasthenia gravis)
MUSCLE related PNS Blood related PNS Orthopaedic related PNS

• Myasthenia gravis • Cytopenia • RA
• Neuro muscular • Red cell aplasia • SLE
dystrophy • Hypogammaglobulinemia • Polymyositis
• Myotonic dystrophy • Erythrocytosis • Sarcoidosis
Investigations:
• Tissue biopsy is needed to confirm thymoma (D.D Lymphoma)
• Elevated Cytokeratin is the best marker
IOC : CT scan
• On CT : Lymphoma – associated lymph node enlargement is present along with the mass
• On CT: Thymoma – well defined solitary lesion

Masoaka staging system
o I: Macroscopic well encapsulated lesion, no microscopic invasion
o II: Well defined capsule, infiltrated into fat & pleura, microscopic invasion present
o III: Macroscopic invasion into lungs, pericardium & great vessels
o IV a: Pleural & Pericardial mets
o IV b: Lympho / Hematogenous mets present
Management
• Total thymectomy performed through sternotomy for symptomatic cases
• Large thymoma >5cm Thymectomy + chemo
• Myasthenia gravis : Thymectomy + Anti cholinesterase drugs
• VATS thymectomy (Recent)
BRONCHOGENIC CYST
• Congenital lung lesion due to anomalous development of foregut or trachea bronchial tree
• It can arise in two places
• Mediastinum (M/C 85%)
• Pulmonary parenchyma (15%)
Mediastinum Pulmonary parenchyma
No trachea bronchial communication Tracheobronchial communication +
M/C location Rt lung lower lobe**
• It can rupture resulting in pneumothorax

• It can compress the lung tissue ATELECTASIS
• It can go for infection
• Risk of malignant transformation
• HEMOPTYSIS is seen If communicates with tracheobronchial tree
Treatment
• Excision of cyst with VATS method
LUNG SEQUESTRATION:
• It is a normally developed lung tissue containing bronchioles, alveoli and receiving blood
supply from aorta**
• M/C in lower lobes, Left more common than Right.
• 2 types
Intra lobar sequestration Extra lobar sequestration
Sequestration within the lung parenchyma
75% (M/C)

Has communication with tracheobronchial No communication with tracheobronchial
tree tree
It can get infection Associated with congenital diaphragmatic
Abscess hernia
haemoptysis
M/C in Lt lung
Drains 100% of its blood into pulmonary Drains blood into
vein** • Azygous vein 80%
• Pulmonary vein 20%
CHYLOTHORAX
• TG level in fluid >110mg/dL (1.2mmol/L)
• It is a complication of surgery or malignancy
Management:
• Initially managed by conservative means
• Fat free diet
• Medium chain TG
• Protein diet
• Fat free TPN
Indication for surgery:

• No improvement after 5days of conservative management
• Chyle loss > 1500ml
• Non heeling for >2 Weeks

Surgery: Ligation of thoracic duct in POIRER TRIANGLE
Boundaries of POIRIER’s TRIANGLE:

• Vertebral column
• Arch of aorta
• Lt subclavian Artery
In this triangle the thoracic duct drain into the junction of Lt Subclavian vein +Lt Internal jugular
vein
LUNG TUMORS
BENIGN MALIGNANT
• M/C : Pulmonary Hamartoma • Bronchogenic cancers
• Pulmonary Hamartoma: • Malignant mesothelioma (it arises
• M/C in males from pleura)
• X-ray: Popcorn calcification
• M/C located peripherally
BRONCHOGENIC CANCER:
• M/C primary malignant tumor in mediastinum
• M/C seen in Lung Hilum
• M/C visceral cancer
• M/C cause of death due to cancer
Risk factors:
• Smoking
• Air pollution
• Asbestos , nickel exposure
• Scars in lungs – can lead to adeno cancer
• Radiation
Mutations:

• K ras (M/C in Adeno cancer)
• Bcl 2
• Cmyc
Pathological types:
SMAL CELL CANCER (OAT CELL) NON SMALL CELL CANCER
• Adeno cancer
• SCC
• Large cell cancer
• Broncho alveolar cancer (it spreads by
air , satellite lesions are present)
• High risk of metastasis present • Less risk of metastasis
• Poor prognosis • Good prognosis
• Response to chemotherapy is excellent • No response to chemotherapy
• M/C type Adenocarcinoma
• M/C type among smokers is SCC
• Undifferentiated type is large cell cancer
Increased Paraneoplastic syndromes are Low risk of producing Paraneoplastic syndromes
present**
Usually centrally located ** Peripherally located (SCC is centrally located)**
High chances of metastasis Less risk of metastasis
• Brain
• Bone
• Liver
• Adrenal
M/C location of tumor is Right lung upper lobe**

C/F of Lung cancer:
• M/C is Cough
• Dyspnoea
• Chest pain
• Hemoptysis (Source of Hemoptysis is BRONCHIAL ARTERY)**
• Malignant pleural effusion
• Clubbing is present (Resolves after tumor excision)
• Hoarseness + (RLN involvement)
• SVC obstruction (SCC)
• Eaton lambert syndrome Seen in small cell tumors

PANCOAST TUMOR
A tumor located at the apex of lung
Causes destruction of 1st & 2nd ribs
Causes atrophy of hand muscles
Causes Horner’s syndrome
• Ptosis
• Miosis
• Anhidrosis
It is usually SCC**
SQUAMOUS CELL CANCER of lung

• M/C cancer in India : SCC
• M/C among smoking males: SCC
• Pancoast tumor is: SCC
• Usually centrally located**
• It can form cavity inside the tumor
• It has the best prognosis
• PNS: It produces ectopic PTH – Hypercalcemia, Hypophosphatemia & Clubbing**
• Treatment: surgical excision of tumor
ADENOCANCER:
• M/C type world wide
• M/C in females
• M/C peripherally located
• It produces lung to lung mets
• Good prognosis (not as good as SCC)
• NOGUCHI CLASSIFICATION is used in olden days (now TNM is used)

• PNS: DIC, Hypertrophic pulmonary osteo arthropathy & migratory
thrombophlebitis(Trousseau’s syndrome)
SMALL CELL/ OAT CELL CANCER

• Most aggressive cancer
• Worst prognosis
• Responds to CT & RT
• M/C type causing extra thoracic metastasis
• PNS M/C: produces
• Ectopic ADH – SIADH - Hyponatremia
• Ectopic ACTH – Hypocalcemia & Cushings sundrome
• Myasthenic Eaton Lamber syndrome
• Cerebellar degeneration
LARGE CELL CANCER

• PNS: Galactorrhea in females & Gynecomastia in males
Paraneoplastic syndrome (Non Metastatic Complication)

Small cell cancer Squamous cell cancer Large cell cancer Adeno carcinoma
• Excess ADH • Galactorrhea • Hypertrophic
secretion causes in females pulmonary
SIADH and • Gynecomastia osteo
hyponatremia in males arthropathy
• Ectopic ACTH • DIC
causes hypo • Migratory
kalemia and thrombophlebit
Cushing syndrome. is(Trousseau’s
• Retinal blindness syndrome)
• Myasthenic Eaton-
Lambert syndrome
• Cerebellar
degeneration
T staging of bronchogenic cancer (NEET 2020 TOPIC)

T1 Tumor size </= 3 cm
Involving lobar bronchus
Not involves main bronchus
• T1a: < 1 cm

• T1b: 1-2 cm
• T1c: 2-3 cm
T2 Tumor size 3-5 cm
• Main bronchus involved (but Carina not involved)
• Atelectasis, obstructive pneumonitis present
• It involves pleura (Visceral)
T3 Tumor size 5-7 cm
Carina not involved
It involves
• Parietal pleura
• Chest wall
• Phrenic nerve
• Parietal pericardium
T4 Tumor size >7 cm
• Satellite tumor nodules in IL lobe
• Infiltration into esophagus, trachea, heart, vertebra
Carina is involved
Non invasive investigations for lung cancer Invasive investigations
• Chest X-ray • Bronchoscopy transbronchial needle

• CT thorax: 1st investigation to be done biopsy
for suspects • Endobronchial USG and biopsy
• Assess for lung Resectability • CT guided biopsy
• Any node >2cm in mediastinum is • Chances of pneumothorax
metastatic node • Done for peripherally located tumors
• PET- CT
• Sputum cytology
Surgical methods of taking Biopsy

Mediastinoscopy: Mediastinotomy: VATS:
• Under GA a transverse incision is made • Incision is made in • Latest
over supra sterna notch 2nd ICS • Staging is
• A scope is passed through the incision • Mediastinal nodes done based
• Biopsy is taken from Sub carinal nodes biopsy can be taken on VATS
& para tracheal nodes (Lt Para aortic
• Pneumothorax & Bleeding can happen nodes biopsy can be
in this procedure taken)

Management of Lung Cancer
• Surgical excision (Best)
• Chemotherapy given only for small cell cancer (90% regression is seen)
• N2 cases: Neoadjuvant CT is advised
• Adenocancer: Oral Tyrosin Kinase Inhibitor : Geftinib**
Types of resection:
Segmentectomy and Wedge resection
• For small tumors
• If each segment is removed anatomically ligating the segmental Pulmonary artery and Vein
and bronchus it is segmental resection.
• Non anatomical resection is wedge resection
Lobectomy:
• Treatment of choice in Early Stage Lung cancer**
• Can be performed via Thoracotomy or VATS.
• Bronchus is stapled or sewn.
• One or two ICD drain left and removed later.
Pneumonectomy:
• Removal of whole lung and has highest mortality- 5-8%
• Procedure reserved for centrally placed tumor* or tumors involving Main bronchus.
• Fixation of tumour to aorta, heart or Esophagus means unresectable.
• Ligate the main Pulmonary artery, Superior and inferior Pulmonary veins and Main
bronchus divided without Stump.
• Drainage of space is important- No suction is applied. Only ICD drain kept and leave it
unclamped or unclamp it for 1 minute for every 1 hour, Slowly the fluid level within the
space rises and fills the pneumonectomy space.
Prognosis: 5 yrs survival

• SCC: 35-50%
• Adeno cancer: 25-45%
• Small cell: 5%

CHEST WALL ANOMALIES
Pectus excavatum (Figure A) Pectus carinatum (Figure B)
Disc shaped deformity Pigeon shaped deformity @ Pigeon chest
Open operation: RAVICH procedure
Minimally invasive Surgery: NUSS procedure
THORACOSCORE: (NEET 2020 TOPIC)

• It is the most widely used model to assess risk of operative mortality in thoracic surgery
• It is done preoperatively
It is based on 9 variables
Mnemonic “ASAP- Plan Doctor CME”
• Age
• Sex
• American society of anaesthesiologist score
• Performance status
• Priority of surgery
• Dyspnoea score
• Co morbidity score
• Malignant diagnosis
• Extent or duration of surgery

One liners from Thoracic Surgery:
• MC histological type overall-
• MC type in Non-smokers-
• MC type in females-
• MC type in smokers-
• MC type in India-
• MC type associated with SVC syndrome
• Peripherally located tumor-
• Noguchi Classification -
• Central Located-
• Pancoast tumor -
• Paraneoplastic Syndromes are MC with
• Worst prognosis-
• M/C site of metastasis is
• M/C endocrine organ involved is –
• Lung Ca is M/C tumor metastasizing to heart
• Brain metastasis may present with neurological deficit.
• CA lung is M/C primary for metastasis to Kidney, Esophagus, Pancreas, Spleen, Liver,
Adrenal, Brain, Skin

Image 1: Nuss Procedure done for Pectus excavatum
Image 2: Heimlich Valve used in Pneumothorax

Topic 6b: Crardiac surgery
Cardio Pulmonary Bypass Machine:

• It oxygenates blood, Remove particles, maintains temperature and circulation (Except to
Heart)
Figure: Cardio pulmonary Bypass machine*
Procedure to connect Cardio pulmonary bypass machine

• Sternotomy
• Expose
• Arterial cannulation : Ascending aorta
• Venous cannulation: purse string in Rt atrium
Machine is going to take care of entire circulation of body except myocardium.

To prevent myocardial damage:
• Infuse cardioplegic solution into Coronary artery (potassium containing fluid) it arrests the
heart in diastole and hence commonly used
• Intermittent cross clamping is performed usually heart develops Ventricular fibrillation
• In paediatric cases total circulatory arrest: myocardium can with stand ischemia for 15-
20min
CPB working complications

• Bleeding disorders
• Infections
• Air embolism
• GIT: mesenteric ischemia
• Myocardial ischemia
• Neurologic dysfunction
• Pancreatitis

• Vascular injury
• MODS
ACUTE CORONARY ISCHEMIA (M.I)

Blood supply of heart
• Lt coronary artery: it gives 2 branches Lt anterior descending artery that runs in the
anterior interventricular groove and Lt circumflex artery that runs in A.V Septum
• Rt coronary artery: it gives Rt circumflex artery that ends as Posterior descending coronary
artery in 90% and in 10% LCA gives posterior descending artery
Three vessels that supply heart:

• Lt anterior descending artery (LAD)
• Lt circumflex artery
• Posterior descending coronary artery
• M/C diseased artery: Lt Anterior Descending artery

• M/C bypassed artery: Lt Anterior Descending artery
IOC for coronary occlusion: Selective coronary angiography ( See the video in app)
CABG indications
• >50% stenosis of Lt Coronary Artery
• >70% stenosis of LAD (anterior interventricular artery)

• Triple vessel disease
• Poor ventricular function
Chronic stable angina:

• PTCA (Percutaneous Transluminal Coronary Angioplasty) > CABG
Acute coronary syndrome:
• Unstable angina: becomes asymptomatic with antianginal drugs if recurrent unstable angina
PTCA / Thrombolysis.
• CABG done after 6 weeks
Other indications:
Myocyte necrosis (VSD):
• Patient presents in 3-7days with pulmonary edema+ pansystolic murmur+ hypotension.
• Treatment : patch closure
Papillary muscle necrosis: (Mitral Regurgitation)

• Presents with pulmonary edema + pansystolic murmur.
• Treatment: Mitral valve replacement
Ventricular aneurysm:
• Can happen due to necrosis, wall of ventricle bulges out.
• Repaired after connecting the heart to Bypass machine
BYPASS OPERATION
Commonly used vessels
• Long saphenous vein
• LIMA (Lt internal mammary artery)
Long saphenous vein LIMA ( Lt internal mammary artery)

M/C used vein For LCA & LAD bypass we use only LIMA
10 years patency 60% 10 years patency is 90%
Other veins: Other arteries
• Short saphenous vein • Rt internal mammary artery
• Cephalic vein • Radial artery (Allen test is done before
taking radial artery)
Wound infection in diabetic patients

Complications of bypass operation:
• Bleeding
• Arrhythmia (M/C Sinus tachycardia)
• Neurological dysfunction
• Poor cardiac output
• Mortality 2-3%
• Wound infection
Prognosis:
• 95% living at 1 year after operation
• 90% after 5 years
• 75% after 10 years
OFF PUMP CORONARY ARTERY SURGERY: OCTUPUS DEVICE is used without Bypass machine usage

VALVE REPLACEMENTS:
TYPES OF VALVES AVAILABLE
MECHANICAL VALVE BIOLOGIAL VALVE
Can be used in any age group for any valve • Allograft from Cadavers
Available in many sizes • Autograft fom same person
• Hetero(Xeno) graft: M/C used Porcine
valves
Advantage: long durability Advantage: Turbulence is less no anticoagulant
needed
Disadvantage: Thrombogenic, hence lifelong Disadvantage: Less life expectancy
anticoagulants needed
• M/C complication using a valve is thrombus formation**

• Thrombus formation M/C in mechanical valve
• Thrombus formation M/C in Mitral valve
• Valve leaks
• Prosthetic valve endocarditis- (MC organism- Staph epidermidis) Mortality 50%
TUMORS:
• M/C cardiac tumor is metastasis**
• M/C primary tumor of heart Atrial Myxoma
• M/C organ causing metastasis is lung cancer
• The primary which has highest propensity of metastasis to heart is from Malignant Melanoma
skin**

ATRIAL MYXOMA:
It is common in 3rd to 6th decade among females
SPORADIC FAMILIAL
As a part of Carney’s complex
M/C in Lt atrium M/C found in Ventricle
Usually solitary Usually Multiple
• Clinical feature is most commonly like MS or MR

• Ventricular forms present as Obstructive features
• Tumor plop sound heard – Mid diastolic
Complication:
• Emboli like manifestation can happen if it disconnected
Investigation: 2D Echo or TEE(Trans Esophageal Echo)
Treatment: Surgical excision of myxoma

Chapter 7 : Endocrine Surgery
Topic 7A- MEN syndromes
MEN-1 ( WERMER Syndrome)

• Truncated menin protein mutation**
• Autosomal Dominant
• Male and Female= Equally affected
• Manifests from age of 5 years**
3 P’s affected
- Parathyroid Hyperplasia
- Pituitary adenoma ( Prolactinoma MC)
- Pancreas NET( Gastrinomas MC)
Clinical features:
• PHPT- 90% ( Multiglandular hyperplasia)
• 2nd MC- Pituitary NET (Gastrinoma MC in Duodenum > Pancreas)- 30-80%
• Prolactinomas ( 15-30%)
• Carcinoids in Thymus and Bronchus**
• MC cause of death in MEN 1 is from Duodenal/ Pancreatic NET or Intra thoracic Carcinoids
Hyperparathyroidism in MEN-1
• MC manifest in MEN -1
• Due to multiglandular hyperplasia**
• MC in 2nd decade*
• 1st Biochemical abnormality noted is Hypercalcemia*
• Enlargement is asymmetrical**
Treatment : 2 options:
• Total Parathyroidectomy with heterotopic implantation of one parathyroid in Brachioradialis
muscle
• Subtotal ( removal of 3 and half glands)

MEN 2 Syndrome
Hall mark – C cell Hyperplasia and Medullary cancer is always seen ( 100%)
Autosomal Dominant
RET oncogene mutation :
❑ Loss of Function: Hirschsprung disease**
❑ Gain of Function: MEN -2 Syndromes
Somatic Mutation: Thyroid Cancers
MEN 2A (Sipple Syndrome) MEN 2B

• Medullary thyroid cancer- 100%
• Pheochromocytoma- 40-50%
• Parathyroid adenoma/ hyperplasia-
20%
• Hirschsprung disease**
• Cutaneous lichen amyloidosis
Other Tumors:
• Medullary cancer- 100%
• Phaeochromocytoma- 40-50%
• MEN 2A develops PHPT – in 20% cases- Multiglandular more common
• MEN 2B never develops PHPT
• MEN- 2B develops in very young age, at infancy**
• MEN- 2B never develops Hirschsprung disease**

Familial Medullary Thyroid MEN2A MEN 2B
Cancer( FMTC) (Sipple Syndrome) (Also known as MEN 3
Syndrome)
RET oncogene RET oncogene. RET Oncogene
Exon 618 mutation* Exon 634 mutation Exon 918 mutation
Medullary cancer in MEN-2 Syndrome:

• Medullary cancer is sporadic in 75% cases and occurs in MEN syndrome as Hereditary case*
• Hereditary MTC is Multifocal, Bilateral**
• MTC will not take up RAI**
• Survival is 70% at 10 years.
• 75% have node involvement if tumor is palpable.
Phaeochromocytoma in MEN-2 Syndrome:

• Neoplasms arising from Chromaffin cells in Adrenal medulla*
• 40-50% of MEN 2A and 2B develop Pheochromocytoma.
• Age at diagnosis is 30-40 years
• Unlike Sporadic cases which may be 10% malignant and 10% Extra adrenal- these cases
associated with MEN-2 Syndrome is Benign always and will be limited to adrenal always.
• MEN-2 related cases will be Bilateral and Multifocal**
• Surgery advised recently is Adrenalectomy for the involved side only and follow up.
• Previously bilateral adrenalectomy was done which resulted in adrenal insufficiency and hence
not done nowadays.
MEN 2 Syndrome Screening and prophylactic thyroidectomy:

• 1st Degree relatives should be counselled and screened for RET oncogene mutation.
• If 918 mutation ( MEN-2B) is seen- High risk- Prophylactic thyroidectomy < 1 year
• If 634 mutation ( MEN- 2A)is seen- Low risk, Prophylactic thyroidectomy @5-6 years
MEN -4 Syndrome:
• Mutation of CDKN1B( Cyclin Dependent kinase Inhibitor) gene on Chromosome 12.
• Parathyroid adenomas
• Pituitary adenomas
• Reproductive organ tumors (Testis, Cervix)
• Renal Tumors
Topic 7B- Parathyroid

Anatomy of Parathyroid Gland:
• Superior Parathyroid – From 4th Pharyngeal pouch (Constant in position)
• Superior Parathyroid present in a Fixed position behind RLN near Zuckerkandl
• Inferior Parathyroid- From 3rd Pharyngeal pouch ( Variable in position)
• Inferior Parathyroid present anterior to RLN in inferior pole MC ; But can be highly variable
from Carotid to mediastinum
• Weight of gland- 30 gm ( Portland Brick Yellow brown color)
• PTH is 84 amino acid peptide
• Half life – 3-5 minutes
• PTH acts on Bone, Kidneys and GIT.
• Normal Calcium level: 2.2 – 2.7 mmol/litre (or) 8.5 to 10.5 mg/dl.
• Ionized calcium- 4.4 to 5.5 mg/dl
Calcium and Phosphate Homeostasis:

❑ PTH-Increased Calcium absorption & Increased Phosphate excretion from Kidney**
❑ Calcitonin- Inhibits absorption of Both Calcium and Phosphate**in kidney
❑ 1,25 Dihydroxy Vitamin D ( Calcitriol) – Absorption of Calcium and Phosphate from Kidney,
Intestines and Bones.
Hyperparathyroidism
• Primary- Due to intrinsic abnormality
• Secondary- Physiological increased secretion in response to lowered calcium
• Tertiary – Advanced form of secondary HPT in which in which autonomous secretion of PTH
occurs despite correcting underlying abnormality like renal failure and also seen in Renal
transplant cases**
Primary Hyperparathyroidism
• 5th – 6th decade, MC in females ( 3:1 ratio).
• Most are asymptomatic.
• MC presentation is Kidney stones. ( 15-20%)
• 40% patients will have Hypercalciuria**
Etiology:
• MC cause is Solitary adenoma**
• Multi gland disease (Hyperplasia)- 15% - Associated with MEN syndromes
Sporadic
Familial:
❑ MEN 1
❑ MEN 2A
❑ HPT- Jaw Tumor Syndrome

Clinical features:
• Salt and pepper Skull appearance**
Figure: Salt and pepper Skull
• Brown Tumor:
❑ Brown tumour, also known as osteitis fibrosa cystica and rarely as osteoclastoma
❑ Excess Osteoclast activity resulting in Subperiosteal bone resorption.
Figure: Brown Tumors
Bones- Stones- Abdominal Groans- Psychic Moans

❖ Others: Hypertension, LVH
❖ Muscle weakness, Fatigue
❖ Soft tissue calcifications

Hypercalcemic crisis can also happen** (When Serum Calcium> 14 mg/dl)- IVF with NS at
rate 200 ml/hour+ Start Steroids, Calcitonin, Bisphosphonates ; Do parathyroidectomy as
early possible
Diagnosis:
• Elevated Total and Ionised Calcium levels
• Increased PTH levels.
• Low serum Phosphate ( in the presence of Normal Vitamin D and Creatinine Levels)
• 24 Hour urinary calcium excretion may be normal or increased.
• Elevated alkaline phosphatase.
Localisation studies:
• Sestamibi Nuclear scan is the most accurate and reliable method to localise the adenoma**
• Parathyroid adenomas have high concentration of Oxyphilic cells with high mitochondria
content**.
• False positive can happen with Hurthle cell nodules which also have high oxyphil content.
• This can be reduced by Tc99 Pertechnetate – Subtraction images.
Other investigations:
• MIBI scan with USG showing concordant image is obtained.
• 4D CT Scanning
• MRI- Not commonly used.
• Selective Parathyroid Angiography and Venous sampling.

Surgical Management:
Guidelines for Surgical management:
Age • < 50 years
Serum Calcium • 0.25 mmol/L ( 1.0 mg/dl) above upper limit
Skeletal • BMD (Bone marrow density) by DEXA scan,
• T score -2.5 at Lumbar spine, Total Hip, Femoral
Neck or Distal 1/3rd Radius, Vertebral Fracture
Renal • Creatinine clearance- < 60 ml/min
• 24 hour Urinary calcium> 10 mmol/ dl( > 400
mL/day)
• Increased risk of stone formation by risk analysis
method
Surgical options:
• Minimally invasive Focussed Parathyroidectomy (MIP)- by an incision less than 3 cm in neck
(or)
• Bilateral Neck Exploration operation with removal of all 4 glands or 3 and half glands
Figure: Minimally invasive Parathyroidectomy

Indications for Bilateral Neck Exploration:
MIAMI Criteria
• Drop in PTH to normal range and to less than half of the maximum per operative PTH at 10
minutes appears to accurately predict the Single Gland Disease.
• If no such drop is detected suspect multiglandular disease or Hyperplasia and plan Bilateral
Cervical Neck Exploration.
Bilateral cervical Exploration:

Indications:
• Discordant images
• MEN 1
• MEN 2 Syndromes
• Lithium induced Hyperparathyroidism
• Miami criteria failed
• Multi gland disease
Procedure:
• 3 and Half glands removed with leaving back of half gland in left inferior or normal looking
gland.
Mark it with non-absorbable suture. Preferred gland to be left is Inferior Parathyroid as RLN
is posterior to it and marked with TITANIUM Clips**
• Alternately all 4 glands are removed and small pieces of parathyroid are sutured into pockets
of Brachioradialis muscle.
• Thymectomy is also advised in MEN 1 associated HPT as there is chances of Supernumery
glands on Thymus.
Newer techniques:
• MIVAP- minimally invasive Video assisted Parathyroidectomy- Cervical, Axillary, Post
auricular and Transthoracic approaches
• Robotic Technique
Post op complications:
• Permanent Hypocalcemia (Need for Vit.D and Calcium > 1 year postoperatively)- <0.5%
• Recurrent Laryngeal Nerve damage- <1%
• Persistent Hyperparathyroidism – Elevated Se. Calcium within 6 weeks of surgery
• Recurrent Hyperparathyroidism- Increase in Calcium levels after 6 months with a intervening
period of Normal Calcemia.

Medical treatment:
• Only for unfit and patients for whom Surgical treatment is contraindicated.
• Bisphosphonates
• Hormone replacement therapy (Better than SERM)
• Calcimimetics (Cinacalcet) – Amplify the sensitivity of calcium sensing to extracellular
calcium, altering the set point and thereby decreasing PTH production.
Special Cases of Hyperparathyroidism:

• Lithium induced HPT
Familial Syndromes:
• Familial Isolated HPT
• MEN 1
• MEN 2 Syndrome
• HPT – JT syndrome ( Jaw Tumor Syndrome)- Cystic Nature of Adenomas, Risk of
Parathyroid cancer is there.
• Familial Hypocalciuric Hypercalcemia ( Mutation of Calcium Receptor gene – CASR gene on
Chromosome 3)- No need of Surgical Intervention in this case. Low urinary calcium /
creatinine clearance ratio is used to diagnose.
Secondary Hyperparathyroidism
Derangement in Calcium Homeostasis with compensatory increased PTH:
• Chronic kidney Disease ( Renal HPT)
• GI malabsorption
• Vitamin D deficiencies
• Liver disease
• Lithium usage
Pathogenesis:
• Abnormalities in renal Tubular absorption of phosphate leads to Hyperphosphatemia, which
acts on Parathyroid cells and stimulates PTH secretion.
• This increased Phosphate leads to reduction of 1,25 Dihydroxy Vitamin D which acts by
reducing the intestinal absorption of calcium, also acts to increase secretion of PTH.
• Lab values shows:
o Increased Phosphate,
o Increased PTH,
o Decreased or Normal Calcium level** and
o low Vitamin D**
Investigations:
• Traditional Ostetitis Fibrosa Cystica not seen in Plain Xray

• Bone densitometry ( DEXA Scan)- Osteopenia and Osteoporosis.
• Localisation studies not needed as there is no plan of Minimally invasive surgery.
Casanova Test:
• In cases of recurrent disease after bilateral cervical exploration, when there is no active
evidence of disease in neck and a previous allograft has been kept in forearm, a selective
venous sampling for PTH from side of allografted neck or Brachial vein is useful.
• To prove there is graft hyperplasia in forearm the ratio must be greater than 20: 1
Calciphylaxis:
• Calcific uremic arteriolopathy seen in 4% patients undergoing surgery for Secondary HPT.
• There is vascular calcification and skin necrosis
• Cutaneous purpuric lesions+, Ischemic necrosis, Gangrene, Sepsis and death.
• Poor prognosis
Management of Secondary HPT:

• Renal Transplant is TOC.
Other therapies are Bridge to this:

• Replacement of Calcium and Vit D
• Phosphate Binders
• Calcimimetic drugs ( Cinacalcet)- make a set point and inhibit the stimulation of PTH
Surgical indications:
Essential components Clinical findings
• Persistently High serum level of Intact One of the below symptoms:
PTH > 500 pg/ml • Osteitis Fibrosa Cystica
• Hyperphosphatemia (Phosphate > • Subjective symptoms like Bone pain,
6mg/dl) or Hypercalcemia ( Ca>2.5 arthralgia, muscle weakness,
mmol/L or 10 mg/dl) which is irritability , pruritus and Depression
refractory to medical treatment • Ectopic calcifications
• Estimated Volume of largest gland > • Calciphylaxis
300-500 mm3 or Longitudinal axis > • Progressive reduction in bone mineral
1 cm content.
• Anemia resistant to Erythropoietin
stimulating agents
• Dilated cardiomyopathy and cardiac
failure

Surgery:
❑ Subtotal Parathyroidectomy – procedure of Choice
With 3 and half removal and half Remnant left in situ with marked non absorbable suture
Or
Parathyroid morcellated and inserted in Brachioradialis pocket.
Dramatic response is seen to surgery
Tertiary Hyperparathyroidism
Persistent Autonomous Nodule causing Hyper calcemic Hyperparathyroidism after Kidney Transplant
Biochemical analysis:
• Elevated Ionised and total Calcium
• Elevated PTH
• Reduced Phosphate
Occurs after 1 year of Transplant…
Management:
• No indication of calcimimetics.
• Definitive treatment: Subtotal parathyroidectomy or Total Parathyroidectomy with Auto
Transplantation are acceptable surgical options.
Indications of Surgery in tertiary HPT:

• Subacute Severe Hypercalcemia ( > 3 mmol/l)
• Impaired Graft function
• Nodular Hyperplasia of Parathyroid glands
• Progressive symptoms ( >2 years following Transplantation)
- Worsening bone disease ( pain/fractures/ Bone loss)
- Renal stones
- Soft tissue / vascular calcifications
Recurrent Hyperparathyroidism:
MC cause is Ectopic Parathyroid
MC site- Paraesophageal> mediastinal> Intra Thymic
Parathyroid Cancers
Incidence:

• 1% if PHPT cases.
• 0.005% of all cancers.
• H/o neck irradiation is only risk factor.
Genetic factors:
• HPT- JT syndrome.
• HRPT 2 mutation- Parafibromin inactivation.
Differential Diagnosis from PHPT adenoma

• Diagnosis one decade earlier
• Equal gender ( M:F=1:1)
• Symptomatic at presentation.
• Palpable neck mass is seen in 36-52% cases.
• Increased Calcium level
• PTH increased (5-10 times of normal range)
Immunohistochemistry:
• Downregulation of Parafibromin +ve
• Protein Gene Product ( PGP 9.5)+ve
Treatment:
• Complete removal of tumour + avoiding spillage is the Treatment of choice
Topic 7C- Adrenal Gland
Anatomy:
• Adrenal Gland Pyramidal Shape Right Side, Crescent shaped on Left Side
• 4 gm each
• Tumors arising from Chromaffin cells of Adrenal Medulla – Pheochromocytoma
• Tumors arising from Chromaffin cells Extra adrenal- Paraganglioma
Substances produced:
• Adrenal Medulla secretes- Adrenaline > NA, DA
• Zona Glomerulosa secretes Aldosterone
• Zone Fasciculata/ Reticularis secretes Cortisol and DHEA (Precursor of Androgen)

Cushing Syndrome
Clinical Features: • Hypertension

• Diabetes
• Hyper lipidemia
• Depression
• Amenorrhea
• Impotence
• Lemon on stick appearance
• Buffalo Hump

• Stria++
• Moon Facies
• Increased Hair Growth
Diurnal Variation of Cortisol:

• ACTH peaks in Early morning at 4am to 10 am… Hence Cortisol values will be high at this
time normally.
• We have to see for Diurnal Variations.
• It is not altered in “Pituitary Source of Cushing’s Disease” and lost in Adrenal Source.
High Dose Dexamethasone Test:

• It’s a routine when Steroids are injected immediately the Levels of ACTH will decrease.
• Such Decrease of ACTH by High Dose Dexamethasone is seen in “ Pituitary source of Cushing
disease” only.

Post op management:
• After unilateral adrenalectomy – the contralateral adrenal gland will be suppressed and
hence supplemental Cortisol is given.
• Opposite gland takes 1 year to recover fully.
• Before stopping Cortisol Supplements- Synacthen Test done ( ACTH Stimulation test,
Synacthen a, drug that acts like ACTH ) is given** This test confirms the normal secretion of
Cortisol by the adrenal gland.

• Conn’s Syndrome- Primary Hyperaldosteronism; Hypertension due to increased
Aldosterone**, Hypokalemia Associated. MC cause is solitary adenoma*
• Waterhouse Friderichsen Syndrome- Bilateral Adrenal Infarction seen in Meningococcal
sepsis- Rapidly fatal complication.
Adrenocortical Carcinoma:
• Rare
• Bimodal- Children and 4th decade
• F:M= 1.5:1
• MC functional
• Adrenocortical carcinoma- 60% present with Cushing Syndrome**
• Imaging: MRI >CT
• Mc Farlane Classification is used**
Treatment- ENBLOC RESECTION
• Post op- Etoposide, Doxorubicin, Cisplatin
• Hormone Excess- Ketoconazole, Mitotane are used.
Phaeochromocytoma
Catecholamine producing tumor from Adrenal medulla and Sympathetic chain.
Extra – adrenal Phaeo chromocytomas:

• MC site is Para Aortic region (75%)
• Thoracic
• Bladder
• Neck and Pelvis
“10% TUMOUR” is the other name of Pheochromocytoma:

▪ 10% extra-adrenal (closer to 15%)
▪ 10% occur in children
▪ 10% familial (closer to 20%)
▪ 10% bilateral or multiple (more if familial)
▪ 10% recur (more if extra-adrenal)
▪ 10% malignant
▪ 10% discovered incidentally
Syndromes associated with Pheochromocytoma:
o MEN 2A and 2B
o Familial Paraganglioma Syndrome
o Von Hippel Lindau Syndrome
o Sturge weber syndrome

o Neurofibromatosis 1
Features suggestive of malignancy

PASS Score- Phaeochromocytoma Adrenal Glans Scale score
• Increased Pheochromocytoma Adrenal Scale Score
• High ki- 67 Positive cells
• Vascular Invasion
• Breached Capsule
• Metastasis
Clinical features:
The five P’s:
◦ Pressure (HTN) 90% - MC manifestation
◦ Pain (Headache) 80%
◦ Perspiration 71%
◦ Palpitation 64%
◦ Pallor 42%
◦ Paroxysms (the sixth P!)-
The Classical Triad seen in >50% Cases : Pain (Headache), Perspiration, Palpitations
Hormones produced by Each site:

• Most Pheochromocytoma produce NA and Adrenaline with NA> Adrenaline*
• Extra adrenal Pheochromocytomas will secrete only Noradrenaline*
• Pheochromocytoma associated with MEN secrete only Adrenaline
• Malignant Pheochromocytoma secretes- Dopamine and Homovanillic acid(HVA)
Paroxysmal Spells:
• 10-60 minute duration
• Daily to monthly once
• Spontaneous
• Precipitated by various factors like Contrast injection, Drugs, Exercises, Micturition etc
Carney’s Triad:
* Functioning Paragangioma+ GIST+ Pulmonary Chondromas
Investigations for Phaeochromocytoma:

• Screening Investigation is 24 hours urinary VMA, Urinary Catecholamines like meta
nephrines, normetanephrines.
• Plasma metanephrines is IOC to diagnose.
• IOC to Localise the Tumor is MRI**for Adrenal, Extra Adrenal Phaeochromocytoma in
Pregnancy. (EVEN for ECTOPIC IOC is MRI)
• Iodine 123 MIBG ( met Iodo Benzyl Guanidine) scan is used only for metastatic and multiple
Extra adrenal tumors.
• But now FDG PET and DOPA PET has more sensitivity to detect mets**
Figure: Swiss Cheese Pattern on MRI in Phaeochromocytoma
Preop preparation:
• Phenoxybenzamine ( Alpha Blocker)- 20 mg to 160 mg daily until patient develops Postural
Hypotension.
• Propranolol ( Beta blockers)- for patients with tachycardia and arrythmias ( Must be started
after complete Alpha Blockade happened)
• Surgical management of Choice is Laparoscopic Adrenalectomy**
• Anaesthesia of Choice- Enflurane or Isoflurane** (Don’t use Halothane**)
Malignant Phaeochromocytoma:
• Hypertension controlled first
• Mitotane- Palliative treatment for Mets cases
• Chemotherapy-Vincristine, Cyclophosphamide and Dacarbazine

Chapter 8 – Neuro Surgery ( ELECTIVE)
Topic 8a-Basic Neuro Anatomy and Benign Topics in CNS
CSF PATHWAY
❖ CSF secreted by choroid plexus in 2 lateral ventricles
❖ CSF flows through MONRO foramen into the 3rd ventricle
❖ CSF flows down through AQUEDUCT OF SYLVIUS into the 4th ventricle
❖ CSF from 4th ventricle enters the sub arachnoid space through
o Medial opening: FORAMEN MAGENDIE
o Lateral opening: FORAMEN LUSCHKA
❖ CSF from sub arachnoid space absorbed into dural venous sinuses
❖ From dural venous sinuses into systemic circulation.
HYDROCEPHALUS
• High pressure in CSF: C/F: Headache that increases on coughing & bending. Associated with
Vomiting, Nausea+ vision problem
• Low pressure in CSF: C/F: Headache that increased on standing**

Infants: High pressure CSF
C/F:
• Bulging Fontanelles
• Papilledema
• PARINAUD SYNDROME: Dorsal midbrain compression (due to increased pressure)- Upward
gaze affected
• Results in Sunset sign
Figure: Sun Set Sign
Types of Hydrocephalus
OBSTRUCTIVE HYDROCEPHALUS COMMUNICATING HYDROCEPHALUS
Is due to compression by lesion • Is due to failure of absorption of CSF
• Inside • Post hemorrhagic
• outside • CSF infection
• Increased protein content
LP is contra indicated LP can be done
• 10-30ml removal of CSF decreases the
symptoms
Normal pressure Hydrocephalus Idiopathic Intracranial Hypertension (IIH)

• Important cause of dementia, it is seen • Also know as Benign Intracranial
in old men. Hypertension & Pseudotumor cerebri**
• Triad in Normal pressure Hydrocephalus • It rapidly progress to Blindness
o Gait disturbance • Common in young over weight females
o Incontinence Characterized by
o Cognitive decline • Head ache
Etiology : • Visual disturbance
o Denovo • Papilledema
o SAH • Cranial nerve dysfunction

o Meningitis LP : pressure >25mm Hg (High pressure)
o Head injury Reasons for IIH:
o Tumors • Sinus thrombosis
CT scan: Ventriculomegaly • Increased intra abdominal pressure in
LP: Normal Pressure obese people
Treatment:
• Weight loss
• Stop OCP usage
• Acetazolamide
• Shunt operations: prevents visual loss
o Ventriculo peritoneal shunt
o Lumbar peritoneal shunt
• Optic nerve sheath fenestration: done to
prevent visual loss
Management of Hydrocephalus:
• Hydrocephalic attack is an emergency- Rapid coma & death can happen
• Immediate external ventricular drain should be placed: through coronal suture, catheter tip is
placed near foramen of monro.
• Lumbar drain can be done for communicating hydrocephalus
Figure: External Ventricular Drain
:
Types of Internal Shunts
• Ventriculo
Peritoneal shunt
• Ventriculo plural
shunt
• Ventriculo atrial
shunt

• Ventriculo atrial
and Ventriculo
pleural Shunts
• Lumbar Peritoneal
Shunts is done in
Communicating
Hydrocephalus and
IIH
Ventriculo peritoneal Shunt:

• Starts from lateral ventricle to
abdominal cavity
• Anti siphon system is present

• Shunt valve -low/medium/high
• CSF reservoir is present in
shunt(sampling of CSF can be done)
Complications of shunt:
• Over drainage of CSF : patient develops low pressure headache on standing
• Lateral or 3rd Ventricles can collapse, leads to bleeding in ventricles, sub dural hematoma &
subdural hygroma can happen
• SLIT VENTRICLE SYNDROME:
o Seen in Children with ventricles and subarachnoid spaces are underdeveloped,
resulting in poor brain compliance.
o In these patients normal fluctuations in ICP are exaggerated so that coughing and
straining may cause symptoms of raised ICP.
o Any shunt blockage may not be evident on scan, as the ventricles fail to enlarge.

• Obstruction
• Disconnection
• Infection: Caused by Staph epidermidis
Risk factors for Infection:
o M/C seen in young patients
o Open meningo-myelocele
o Long operation time
o Increased movement of persons in and out of OT
o 75% develop in 1st month
o 15-20% needs shunt replacement in 3yrs
Treatment of Infection:
o Start IV antibiotics
o Remove the shunt & do External CSF drainage
o LP done- If protein content is Normal it indicates infection is subsided then place
a new shunt
ENDOSCOPIC VENTRICULOSTOMY
• Aqueduct stenosis: a Shunt is passed through neuro endoscope from 3rd to 4th ventricle
• Serious complication: Basilar artery/Fornix can be injured that results in permanent memory
impairment
BRAIN ABSCESS
Causes
• Infected from direct exposure (Trauma to head)
• Hematogenous infection
• 25% No cause is found
Causative organism
• If infected from Mastoiditis: Streptococci & Bacteroids
• If infected from Hematogenous route: Streptococci & Bacteroids
• Open infection (Trauma): Staph aureus & Clostridia
• Food born : Toxoplasma & Neurocysticercosis
Infections causing brain abscess in HIV patients

• Toxoplasma
• Cryptococcal
• JC virus – Multifocal Leuco Encephalopathy
• Mycobacterial

C/F:
• Low grade fever
• Seizers
• Confusion
• FND
INVESTIGATIONS:
• CRP elevated(all inflammatory markers elevated)
• Blood culture +
• IOC :CECT Brain
CECT of evolving abscess (Cerebritis stage): CECT of classical abscess: Smooth walled well
Hypodense lesion with edematous brain defined hypodense ring enhancing lesion
• Important DD is Tumor in brain

• Do an MRI to confirm the tumor
• T2 weighted on MRI Hyper intense
lesion
• Mortality is 4% in brain abscess

• If abscess ruptures into ventricles that leads Ventriculitis with mortality of 80%
Treatment: of brain abscess

• TOC: Surgical drainage of abscess with 6 weeks antibiotics
• Prophylactic anticonvulsants

Subdural abscess:
• Sinusitis, mastoiditis & meningitis can cause subdural abscess
• Frontal bone osteomyelitis (Pott’s puffy tumor) can cause subdural abscess
• Subdural abscess is present in parafalcine region that can lead to cortical veins thrombosis
with 8-12% mortality
Treatment of subdural abscess
• Drainage of abscess by + IV antibiotics
• Burr hole
• Craniectomy
• Craniotomy
• LP is contraindicated
INTRACEREBRAL HEMORRHAGE (ICH)
SUBARACHNOID HEMORRHAGE
• M/C cause : Trauma
• Spontaneous SAH
o 80% Berry aneurysm rupture
o 20% AV malformation
Perimesencephalic SAH:
• A distinct subgroup of SAH patients suffer bleeds confined to the basal cisterns anterior to the
midbrain and pons, without an underlying lesion evident on angiogram.
• Represents venous bleeding**
• Excellent prognosis
Berry aneurysm:
• Berry aneurysm that leads to SAH is seen in 10-15/lakh population
• C/F: Thunder clap headache + LOC (sudden)
Predisposing factors
• Females
• Hypertension patients
• Smokers
• Cocaine
• Family H/O berry aneurysm
• ADPKD
• Marfan syndrome
• Ehler danlos syndrome

• Fibro muscular dysplasia
Site of berry aneurysm

• M/C Anterior Communicating Artery
• 2nd common Middle Cerebral Artery
• 3rd common Posterior Cerebral Artery
• Least common : Basilar tip
Clinical features:
• 10-15% die on spot
• 1/3rd hospitalized people die
• 1/3rd develop neurological deficit
• 1/3rd Recover
Complications:
• Most common cause of death after reaching hospital- Re bleeding
• Hydrocephalus- External ventricular drain must be done.
• Vasospasm ( To be prevented by Nimodipine, Induced Hypertension or Hypervolemia)
• Terson Syndrome- Combination of SAH and Vitreous Hemorrhage ( in 10-20% cases)
World federation of neurological surgeons grading

Grade Glasgow coma scale Focal deficits
I 15 -

II 13-14 -
III 13-14 +
IV 7-12 +/-
V 3-9 +/-
• Focal deficit = dysplasia or limb weakness
CLINICAL GRADING: HUNT & HEES SCALE- Gives idea on outcome

Grade Features Outcome
1 Minimal headache+ 70% recover
Nuchal rigidity+
2 Moderate to severe headache + 70% recover
Nuchal rigidity ++
Cranial Nerve palsy +/-
3 Drowsy + Confused +FND 15% recover
4 Hemiparesis** 15% recover
+ Stupor +Decerebrate rigidity
5 Coma**+ 0% recover
Moribund
Fisher grading on SAH based on CT scan

• IOC: CT Scan : Hyper dense signal is present in sub-arachnoid space
• Xanthochromic CSF on taping (Not done in recent times)

• Cerebral angiography can be done in a stable patient
• Digital Subtraction Angiography is Gold standard investigation for aneurysm.
Management :

• Medical: Delayed Ischemic neurological deficit(3-10 Days) should be prevented ( due to
vasospasm)
• Oral Nimodipine
• TRIPLE H Therapy**
H-
H-
H-
• Surgical Clipping & Coiling of aneurysms
AV MALFORMATION
• Can bleed and cause SAH
• Seen in 10-20% cases of SAH
• Congenital in origin
• Risk of bleeding - 4% / Year
• AVM should be intervened if size is >2.5cm
• By any one technique :
o Embolisation of AVM
o Surgical resection of AVM
o Stereotactic surgical resection
SPETLER MARTIN FRADING System is used in the management of AVM**

Factors Score
Size <3 cm 1
3-6cm 2
>6cm 3
Location Eloquent 1
Non-Eloquent 0
Vein Superficial 0

Deep 1
Other causes of SAH

• HTN
• Ischemic stroke

Moya Moya Disease:
• Auto immune disease
• Internal carotid artery is obliterated
• Multiple collaterals are formed from
External carotid artery and give that
puff of smoke appearance
Treatment: Superficial temporal artery to
middle cerebral artery bypass.
Intracerebral hemorrhage:
C/F: Contra lateral hemiplegic
Mortality : 40% in 1 year
• Cause
Mainly due to HTN
Patients on Anticoagulants
Amyloid angiopathy patients
Treatment:
1.Stop anticoagulants
2.Craniotomy and evacuation of hemorrhage
can be done in fit patients
Topic 8 B- Brain Tumors

Presentation of brain tumor: TRAID

• Seizure
• Increase ICP
• FND
Syndromes associated
• Neuro Fibroma 1 : cause Astrocytoma, Schwannoma, Optic Nerve Glioma
• Neuro Fibroma 2 : causes Meningioma, Astrocytoma
• P53 mutation: Glioma
• TURCOT syndrome: Medulloblastoma
• HNPCC(Lynch 2 Syndrome): Astrocytoma
• MEN1: Pituitary adenoma
• VHL gene: Hemangioblastoma of brain
Based on location of the Tumors in various lobes: Presentation

• Pituitary tumors: Bitemporal Hemianopia
• Occipital lobe tumors: Homonymous Hemianopia
• Anterior skull base tumors (Olfactory group tumors):
o FOSTER KENNEDY SYNDROME**: Ipsilateral optic atrophy & Contralateral
Papilledema + Anosmia
• Parietal lobe tumors:
o GERSTMANN SYNDROME: Acalculia, Agraphia, Lt/Rt disorientation, Finger agnosia
• Frontal lobe tumor: Gait changes; personality changes; urinary incontinency
METASTATIC BRAIN TUMORS:

• M/C brain tumor: Mets from Lungs 40% > Breast 15% > Melanoma10% > Renal 10%

• M/C brain tumor in females Mets from Breast cancer**
• M/C brain tumor in Males/over all : Mets from Lungs cancer (Small Cell Cancer)
• Lung mets usually go to cerebral hemisphere
• Breast mets usually go to leptomeninges
• IOC for brain mets : MRI with Gadolinium Contrast
Management of brain mets:

• DOC: STEROIDS
• Single met (Up to 3) : operated
• Whole Brain RT can be given
• Stereotactic Radiosurgery can be done with Gamma knife or cyber knife
PRIMARY BRAIN TUMORS
M/C primary tumor of brain

• Children: Grade I Astrocytoma (Pilocytic)
• Adults: Grade IV Astrocytoma(Glioblastoma Multiforme)
Adults:
• 80% of tumors Supratentorial
• 20% of tumors Infratentorial
Children:
• 40% of tumors Supratentorial

• 60% of tumors Infratentorial
Brain tumors arising from Glial cells:

• Astrocytes: Astrocytoma
• Oligodendrocyte: Oligodendroglioma
• Ependymal cell: Ependymoma
Other brain tumors:

• Meningioma:
o Tumor arising from meninges
o 2nd M/C tumor
o It is the M/C extra axila tumor (Vestibular schwannoma is other axial tumor)
Other Malformations seen in brain

• Craniopharyngioma
• Dermoid cyst
Pituitary tumors
Neuro Endocrine Tumor : Medulloblastoma
ASTROCYTOMA: (Mnemonic -NINE)

Grading based on 4 criteria:

• Nuclear atypia
• Increased cellularity (mitoses)
• Necrosis
• Endothelial proliferation
4 grades
• Grade 1: Pilocytic Astrocytoma
• Grade 2: Diffuse Astrocytoma – only one criteria(Nuclear atypia)
• Grade 3: Anaplastic Astrocytoma- two criteria (Nuclear atypia+ Mitoses)
• Grade 4: Glioblastoma Multiforme – three criteria (Nuclear atypia+ Mitoses + Endothelial
proliferation or necrosis)
Grade 1 & 2 Low grade tumors / Benign tumors;
Grade 3 & 4 High grade tumors/ Malignant
ASTROCYTOMAS
Grade 1 : Pilocytic Astrocytoma
• Characterised by Mural Nodule
• No infiltration
• MC in Children.
• Best prognosis among the 4**
• MRI- IOC
• Discrete Contrast Enhancing Cystic lesion
with a MURAL NODULE**
• It is curable
Grade 2 : Diffuse Astrocytoma

• MC in Children and young adults.
• Look for P16 and CDK N2A mutation- If
present it may convert them to high grade
tumors**
• IOC is MRI
• Treatment- Surgery followed by Whole
brain RT as it diffuse
Grade 3: Anaplastic Astrocytoma
• High Grade Astrocytomas.
• Presents with Seizures, personality changes
if Frontal lobe lesion.
• MRI- irregular enhancing lesion
• Treatment- Surgery and Whole brain
Radiotherapy.

• It has infiltrating margin and hence RT is
mandatory.
• Only Cytoreductive surgery is done
Grade 4: Glioblastoma Multiforme

• MC in elderly, MC presentation is seizures.
• On HPE- Shows Tumor Necrosis, Pseudo
palisading pattern seen .
• MRI shows Ring enhancing lesion with
edema and mass effect and central necrosis.
• Surgery + Post op RT + Temozolomide is the
Chemo therapy of Choice**
Grade 4 is high grade and can extend into opposite hemisphere also and hence known as BUTTERFLY
tumors**
Figure: GBM- Butterfly shaped
OLIGODENDROGLIOMA
• Chr 19q mutation
• Calcifications + in the tumor

Figure: Calcifications in Oligodendroglioma
Histopathological examination:
• Fried egg appearance
• Chicken wire Blood vessels
• Micro calcifications
EPENDYMOMA
• C/F hydrocephalus
• Spreads via CSF
HPE:
• Cells arranged as Pseudo rosette appearance
• Treatment: Surgery + Craniospinal irradiation

MEDULLOBLASTOMA
• Neuro endocrine tumor of brain
• Associated with TURCOT Syndrome
• 3 – 4 Years children
• M/C location Infratentorial or Cerebellum
• Drop mets into the CSF is seen
• Tumor also spreads to LN, Liver & Bones
• Most radio sensitive tumor among the brain tumors
• Since it has Drop mets into CSF : Craniospinal irradiation is advised
• Chemo agents: CARMUSTINE+ VINCRYSTINE
• CHANG STAGING
o M1: CSF mets
o M2: Intracranial tumor beyond primary
o M3: tumor spreading subarachnoid space
o M4: mets outside CSF (distant metastasis)
MENINGIOMA
• Tumor arises from meninges
• Calcifications present
• Meningiomas are associated with NF1 & NF2
• M/C in females
• Progesterone receptor +ve: increased growth during pregnancy
C/F:
• Headache
• Seizures
• FND
Findings in CECT
• Calcifications +
• Dural tail +
• Sunray spicules +
• Increased vascular markings
HPE: Psammoma Bodies seen (Due to dystrophic calcification)

Good prognosis
Recurrence
Psammoma Bodies:
- Papillary cancer of Thyroid
- Papillary variant of RCC
- Serous cystadenoma Ovary
- Meningioma
- Prolactinoma
Figure: Meningioma resection
SIMPSON GRADING SYSTEM: to know the recurrence percentage

• Grade I: Dura mater and abnormal bone Removed; Recurrence < 10%
• Grade II: Dura mater is cauterized; Recurrence 15%
• Grade III : Dura mater is left as such; Recurrence 30%
• Grade IV: incomplete resection; Recurrence 80 – 100 %
• Grade V: Biopsy; Recurrence 80 – 100 %
CRANIOPHARYNGIOMA
• It arises from Rathke’s pouch
• Classical finding: Suprasellar calcification + Polyuria
• Seen in children
Features:
• Hypo pituitarism
• Diabetes insipidus

• Growth retardation
• Visual abnormality: Bitemporal Hemianopia
• Sleep alteration
Figure: Suprasellar calcification

Treatment trans sphenoidal resection
PITUITARY ADENOMA
• M/C arise in anterior lobe
• M/C associated with MEN I syndrome
• M/C cause of Hyper pituitarism is Pituitary Adenoma**
• M/C Presentation is Bitemporal Hemianopia
• They present in 3rd &4th decade of life
• Both sexes equally affected
• M/C functional pituitary adenoma Prolactinoma**- Galactorrhea and Amenorrhea in females;
Gynecomastia in Males
• IOC: MRI
• Treatment: trans sphenoidal excision**
M/C supra sellar mass

• Children Craniopharyngioma
• Adult: Pituitary adenoma
SPINAL TUMORS
• M/C tumor Mets (Intradural & extra medullary)
• M/C primary spinal tumor: Nerve sheath tumor
• M/C intra medullary tumor: Astrocytoma

NEURAL TUBE DEFECT
• It can be due to Genetic or folic acid deficiency or drugs (Trimethoprim, Phenytoin &
Phenobarbitone, Sodium valproate)
Types of defects:
• Spina bifida occulta
• Spina Bifida Apperta:
o Meningocele: Sac of meninges (Dura + Arachnoid)
o Meningomyelocele: Sac of meninges (Dura + Arachnoid) containing Spinal cord or
Nerves
Spina bifida occulta

• Congenital absence of spinous process without exposure of meninges or neural tissue
• Tuft of hair
• No neurological abnormality
• IOC: X ray

Meningocele
• Sac of meninges (Dura + Arachnoid) covered by skin
• If not covered by skin continuous CSF leak is present
• M/C location Lumbar region
• Tethering of spinal cord
• C/E Transillumination +ve, Fluctuation +ve
• X ray: Opened vertebra
Figure: Meningocele
Meningomyelocele
• Sac of meninges (Dura + Arachnoid) containing Spinal cord or Nerves
• M/C seen in lumbo sacral region
If present in lumbo sacral region :
• Bladder incontinence
• Bowel incontinence
• Paraplegia
If present in thoracic region

• Hydrocephalus +
• FND +
Associated problems in meningo myelocele:
• Hydrocephalus is 80% ( MC in Thoracic defect)
• Chiari 2 Malformation
• Bladder and Bowel Dysfunction
Treatment:
• Repair in 24 – 48 hrs (if delayed they develops CNS infection),
• Myofacial closure is advised.
• Don’t use latex gloves
• Post op 25% mortality
• Low IQ & bladder problems inspite of recovery
Chiari malformation:
Cerebellar Tonsil Herniation through Foramen
magnum >5m is Chiari malformation
Type I: Tonsil descent alone; occipital headache

aggravated on coughing & Syringomyelia,
Numbness +
Type II: Tonsil descent + Meningomyelocele;

Associated with Hydrocephalus & Syringomyelia
Dandy Walker malformation

• Cystic expansion of 4th ventricle
• Results in Cerebellar hypoplasia
C/F:
• Microcephaly
• Hydrocephalus

• Ataxia
Triad is
• Enlarged posterior fossa
• Rotation of vermis
• Hypoplasia of vermis
HERNIATION OF BRAIN
• Uncus of temporal lobe will be compressed that causes ipsilateral oculomotor nerve
compression = Fixed dilated pupil; Contralateral hemiplegia
• Kernohan notch phenomenon: Ipsilateral hemiplegia** due to corticospinal tract of opposite
side is compressed
Craniosynostosis
Craniosynostosis: is premature fusion of one or more cranial sutures, preventing growth perpendicular
to fusion
Types of Craniosynostosis:
• Scaphocephaly: Sagittal suture fuses early; Boat shaped head
• Brachycephaly : coronal suture is fuses early; Broad flat forehead
• Plagiocephaly : Unilateral lambdoid and Unilateral coronal suture fuses early; Asymmetric
head
• Trigonocephaly: Metopic suture fuses early; Pointed forehead

Epilepsy surgery:
• M/C performed surgery for epilepsy is anterior temporal lobectomy
• Complex partial seizures usually starts from temporal lobe
• Intra op grid electrode is placed area of high activity is removed (Temporal lobectomy)
• WADA test is done before performing temporal lobectomy.
• WADA TEST: used to locate which temporal lobe is dominant, inject sodium amytal into each
ICA one side at a time & check for speech and memory if impairment is seen that indicates
that side of temporal lobe is dominant

Chapter 9 - Transplantation
Topic 9a – Introduction
• August 13th – organ donation day every year
The 1st
• Kidney transplantation is done by MURRAY in 1954
• Liver transplantation is done by STARLZ in 1963
• Heart transplantation is done by BARNARD
• Pancreas transplantation is done by KELLY & LILLEHEI
Organ donation: is the process of surgical removing of organ or tissue (Graft) from one person
(Donor) and placing it into another person (Recipient) legally. It is performed by Transplant surgeon.
GRAFT (NEET 2019 TOPIC)

• Autograft:
• Isograft:
• Allograft:
• Xenograft:
Based on Placement of Graft

• Orthotopic graft placement: Graft is placed in same anatomical location Eg: Liver, Heart
• Heterotopic graft placement: Graft is placed in a non-anatomical location Eg: Kidney,
Pancreas

Before transplanting the graft HLA Matching is done ( Major Histocompatibility Complex (MHC))
• Class I MHC: we look for HLA A, B
• Class II MHC: we look for HLA DR
• HLA matching is done for antigen recognition
• HLA matching not needed for Liver and cornea**
• HLA matching is not possible for Heart because Cold ischemic time is: 3hrs**
DONAR
Types of donor
Liver donor Brain dead donor Donation after Cardiac Xenograft donor
Death ( DCD)
• Kidney They are the donor’s They are the donor’s Pigs are the ideal
• Heart who have heart beat who have no heart Heart valves are used.
and circulation+ beat and cardiac
arrest happened.
C.I for organ donation: the following persons should not donate organ
• HIV Patient
• CJ disease
• Malignancy within 5 years (Exclude SCC, BCC, Cancer in situ uterus & brain tumors)
• HBV patients
• Death due to Sepsis
Donor Matching of Blood group:

• O Group can donate to: O, A, B, AB
• A group can donate to: A, AB
• B group can donate to: B, AB
• AB group can donate to: AB
• O group is universal donor
• AB group is universal recipient
• Rh testing is not needed for organ transplantation. Only ABO and HLA matching is done.**
Brain dead donor:

• Brain not working
• Heart is still beating
In UK 2 Doctors should certify to declare as brain dead
- one should be a Consultant
- None should be a Transplant involved surgeon in the 2 doctors

Two doctors should separately examine the following in two separate occasions:
To condemn them as brain dead
• Cranial reflexes – CNS reflexes absent ( Pharyngeal, Gag reflexes etc)
• Motor response – NO Response
• No Spontaneous breathing on raising PaCO2 > 60mmHg
Donation after Cardiac Death (DCD) Donor:

Maastricht classification of DCD donor**
• Cat 1: dead on arrival at hospital
• Cat 2: dead even after attempt of resuscitation
• Cat 3: Awaited cardiac arrest after withdrawal of supports (who is not brain dead)
• Cat 4: Cardiac arrest while Brain dead
• Cat 5: Cardiac arrest in Inpatient
• Cat 3 & 4 are good donors because they have circulation in organs until death they
are controlled donors
• Cat 1, 2 & 5: Uncontrolled Donors
Donor Age group

• KIDNEY: 2yrs – no upper limit
• LIVER: No age limit
• HEART: 1 – 65 Years
• LUNGS: 5 – 65Years
• PANCREAS: 10 – 60 Years
The crisis in organ supply has required the use of extended donor criteria
Extended donor criteria for kidney: Extended donor criteria for liver:
• Age > 60 yrs
• Age 50 -59 yrs with history of 2 or
more of the following
• Death due to CVA
• Impaired kidney function (S.Creatinine >
15mg/dl)
• H/O of HTN

Process of organ extraction from Donor
On Operating Table procedure:
• The brain dead patient is taken to the OT
• Anesthetist disconnects the supports
• The moment the heart beat stops
• All the organs needed are extracted by respective surgeons simultaneously
Back Bench Procedure:

• Immediately cold ischemic solution is infused into the organ
• The organ is kept in a ice bag and taken to the recipient
Warm ischemic time is the time between the heart stops and infusion of ischemic cold solution into
the organ. It should be as less as possible <30 min
Cold Ischemic time is the time of infusion of Cold preservative solution to transplantation to the
recipient is completed and there is reperfusion of Recepient blood
Cold Ischemic Solution: m/c used is University of Wisconsin Solution. Eurocollin is another solution
University of Wisconsin Solution components
• Lactobionate: prevents cell swelling
• AdENosine: provides ENergy
• Allopurinol: it is a free radical scavenger
• Glutathione: Antioxidant
ORGAN Optimum cold ischemic time Maximum cold ischemic time

Kidney < 18 Hrs
Liver < 12 Hrs
Heart < 3 Hrs
Lungs < 3 Hrs
Pancreas < 10 Hrs
Small intestine < 4Hrs
Hyperacute rejection:
• Happens in minutes to days
• It is due to pre formed antibodies.
• It is either due to ABO incompatibility or HLA mismatching.
• Immediate Graft thrombosis followed by Gangrene of organ

Acute rejection:
• Usually happens in first 6 months
• Usually due to T cell mediated rejection
• Can be prevented by giving immune suppressants.
• Biopsy shows lymphocytic infiltration
Chronic rejection:
• Occurs after 6 months
• M/C cause of Graft failure.
• Fibrosis happening in the organ.
• It can be due to T & B lymphocytes or it can be no immune also.
Chronic rejection in
• Kidney: Glomerular sclerosis
• Liver: vanishing bile duct syndrome
• Heart: accelerated coronary artery disease
• Pancreas: acinar loss
• Lungs: obliterative bronchiolitis
Risk factors for chronic rejection in kidney (NEET SS)

• Previous episodes of acute rejection
• Poor HLA matching
• Prolonged cold ischemic time
• CMV infection
• Increased blood lipids
• Inadequate immunosuppression
Immunosuppression is given to prevent graft getting rejection

INDUCTION PHASE:
• Is started immediately after surgery
MAINTENANCE PHASE:
• Is continued for life time in many patients
Category of drugs for immune suppression drugs

• Calcineurin inhibitors: Cyclosporine, Tacrolimus
• Anti proliferative agents: Azathioprine, Mercaptopurine, Mycophenolate mofetil
• Steroids
• m ToR inhibitors (mammalian Target of Rapamycin inhibitor): Sirolimus, Everolimus

Monoclonal antibodies
• Muromonab: anti CD3 antibody
• Basiliximab: anti CD25 antibody
• Rituximab: anti CD20 antibody
M/C complication on immunosuppression- Infections:

• Infections: Recipient infection reactivation is M/C:
• CMV reactivation in 6 – 12 weeks patient presents with CMV pneumonitis
Post transplant Malignancy:

• M/C SCC > PTLD (Post Transplant Lympho proliferative disorder M/C caused EBV)
• HHV 8 Patients: Kaposi’s sarcoma
• HBV & HCV patients: HCC
• HPV : Ca cervix
Non immune mediated:

Calcineurin inhibitors:
• 1.Chronic allograft Nephropathy
• 2. NoDAT: New Onset DM after transplant happening in 30% < 2yrs)
COMPLICATION RELATED MCQS

• M/C infection : CMV
• M/C parasitic infection: Pneumocystis carinii
• Polyoma BK virus: ureteric stricture**
• M/C malignancy is SCC

Topic 9B: Organ Transplant- Individual Focus
LIVER TRANSPLANT
• M/C indication of liver transplant in adults:
• M/C indication of liver transplant in children:
• M/C metabolic disorder:
• M/C indication for emergency transplantation:
History:
• 1st liver transplant was done by: STARZL -1963
• 1st split liver transplant was done by: PICHLMAYR
• 1st live donor liver transplant was done by: TANAKA
CRITERIAS for liver transplant:

MODIFIED CHILD PUGH SCORE: Child C > B
• Bilirubin
• Albumin
• Ascites
• PT
• Encephalopathy
MELD (Model for End Liver Disease)

Logarthmic score of : C B I
MELD Score>35Priority
MELD Score<15 put under waiting list
MELD EXCEPTION: in these patients we can do transplant in a lesser score also

• HCC
• Amyloidosis
• Hepato pulmonary syndrome
• Porto pulmonary HTN

KING’S COLLEGE CRITERIA (NEET 2020 TOPIC)
Liver transplant in acute fulminant liver failure
Paracetamol induced liver failure:
• pH < 7.30 (irrespective of encephalopathy)
OR
• PT > 100sec + Serum Creatinine > 300micro mol/L + Grade 3 or 4 encephalopathy
Non Paracetamol induced liver failure:

• PT >100sec
OR
• Any 3 of the below
1. Age < 10 >40 Years
2. Aetiology: Non A/ Non B liver damage may be due to halothane or idiosyncronatic
drugs
3. 7 days of jaundice before encephalopathy developed
4. S. Bilirubin > 300 micro mol/L
5. PT > 50Sec
MILAN CRITERIA:
• Followed for HCC patients with cirrhotic liver
• Single Tumor < 5cm
• Less than 3 lesions (all 1-3 cm diameter)
• No Extra hepatic spread.
ORTHOTOPIC GRAFT HETEROTOPIC GRAFT

Diseased liver is removed & new liver is placed New liver is placed in adjacent to original liver
in the same place
M/C done Is usually followed for acute fulminant liver
failure

TYPES OF LIVER TRANSPLANT
AUXILIARY TRANSPLANT:
• Indicated for acute fulminant liver failure,
• Stop immunosuppressant drugs when the original liver recovers or can remove the
transplanted liver
• Auxiliary partial orthotopic liver transplant: part of diseased liver is removed and part of new
liver is placed in the same position
• Auxiliary heterotopic liver transplant: new liver is placed just beneath the original liver
DOMINO LIVER TRANSPLANT:

• Amyloidotic liver is removed and given to someone in need of liver and new liver is given to
amyloidotic patient. 2 patients are saved with 1 liver
SPLIT LIVER TRANSPLANT:

• Segments 5 6 7 8 will be given to adult and segment 2 3 alone is enough for children.
LIVE DONOR (can donate only to relatives):

• Segment 5 6 7 8 is taken if donating to adult;
• Segment 2 3 is taken if donation is for the paediatric patient

REDUCED LIVER TRANSPLANT:
• The retrieved liver is trimmed to suit for the body weight of the recipient (mostly to children)
STEPS IN ORTHOTOPIC LIVER TRANSPLANT

• Remove cadaveric liver along with supra hepatic IVC & Portal Triad (Portal Vein, Bile duct &
Hepatic artery)
• Recipient operation: Remove liver along with hepatic vein & part of IVC and small amount of
portal vein
Place the cadaveric liver in the donor and anastomose the structures in the following order
• 1st: IVC (supra hepatic followed by infra hepatic)
2nd: Portal vein anastomosis (May develop reperfusion syndrome: Hypotension & Bradycardia)
• 3rd: Hepatic artery
• 4th: Bile duct (End to End anastomosis)
** Bile duct anastomosis is C/I in Primary sclerosing cholangitis & Extra Hepatic Biliary Atresia
For the above 2 conditions do a Roux en Y jejuna anastomosis ( NEET SS )
Piggy Back Transplant:

• If liver alone is removed in Recipient and donor liver is removed along with IVC do PIGGY
BACK anastomosis. Advantage is blood flows throughout the process of surgery

Rejection
Hyper acute rejection Acute rejection Chronic rejection

Rare or not happens in liver Manifests as Hepatic Artery Manifests as Vanishing bile
transplant thrombosis : immediately duct (Rare)
need Re transplant
Portal vein thrombosis no Re

transplant advised
• ROTEM: Rotational thrombo

elastometry used to measure PT/INR
dynamically while transplantation is
going on.
RENAL TRANSPLANT
• M/C cause in adults: Renal failure due to Diabetic nephropathy
• M/C cause in children: Chronic glomerulonephritis
• It is always a heterotopic graft (Rt iliac fossa > Lt iliac fossa)

Types of graft:
CADAVERIC LIVE DONOR
Kidney preferred is Lt kidney b/c Lt renal vein is
longer
Donor criteria: C/I for donor:

• Age 18 – 70 Years • BMI > 40
• BMI < 35 • DM
• No caner • Malignancy
• No active sepsis • HIV +ve, sepsis
• Kidney has normal function • HTN
• ABO compatibility / HLA matching • GFR < 70, Albuminuria
• Horse shoe kidney
• Kidney stones
PROCEDURE:
• In cadaveric kidney along with the renal artery small portion of the aorta is also removed
known as Carrel patch
Ureter is anastomosed to the bladder by
• Short tunnel technique @ Lich Gregoir technique M/C done
• Long tunnel technique @ Lead Better Politano technique
Renal vein anastomosed to common iliac vein

Renal artery anastomosis: ( NEET SS)
• In cadaveric donor carrel patch is taken: do end to side wide anastomosis of carrel patch with
external iliac artery
• In live donor carrel patch is not possible: do end to end anastomosis of renal artery with
internal iliac artery. Renal artery stenosis is M/C with live donor kidney transplant**
Figure: a- Cadaveric Donor and b is Live donor

Complications of kidney transplant
Complications to live donor:
• M/C complication is urinary retention and paralytic ileus
Complications to recipient:
• Hemorrhage
• Renal vein thrombosis (1–5%)
• Renal artery thrombosis (1%)
• Renal artery stenosis (1-23%)
• Viral infections
• Bacterial infections’
• Lymphocele
• Polyoma BK virus produce multiple ureteric strictures**
Allograft dysfunction of transplanted kidney:

• BANFF classification
Risk factors for chronic rejection:

• HLA mismatch
• H/O acute rejection
• Long cold ischemic time
• CMV infection
• Increased blood lipids
• Poor compliance to immune suppression
INTESTINE TRANSPLANT
• M/C indication in adult / children: Short bowel syndrome
• M/C cause of Short bowel syndrome in adults: Acute superior mesenteric artery ischemia
• M/C cause of Short bowel syndrome in children: Gastroschisis > Midgut volvulus
Short bowel syndrome patients will be on TPN. Indications of SI transplant:

• TPN failure is the m/c indication of Small Intestine transplant
• Patient on TPN develops liver failure
• Patient on TPN develops central vein thrombosis
• Patient on TPN develops > 2 episodes of infection
• Patient on TPN develops frequent dehydration
• Single time fungal infection in central line

Small bowel can be taken from
Cadaveric donor: Live donor: Xenograft
• Isolated SB graft Last 150 – 200cm of ileum is From Pig
• Combined SB and Liver transplant taken; it is based on ileo colic
• Multi visceral transplant: SB + artery or ileo colic vein
Stomach +/- Colon
• Modified multi visceral transplant:
Liver is not included**
• Body weight of donor should be 50-75% of the recipient

• Avoid prolonged cold ischemic time
CADAVERIC SBT
• Small bowel is anastomosed with duodenum and ileum is kept as ileostomy only.
• Superior mesenteric vein is anastomosed with portal vein of the recipient
• Superior mesenteric artery is anastomosed to the infra renal aorta
Complications of SB transplant:
Rejection
• Highest chance of rejection: 70-80%
• C/F: Fever, abdomen pain and increased stool
• Do ileoscopy and biopsy to look for rejection
Graft vs Host Disease is M/C in SB transplant of all: 0-14%
New Markers for rejection: Stool Calprotectin & Stool Citrulline**
PTLD also M/C 10-20%
M/C complication overall is Bacterial infection 70-90%**
Extra edge
• Combined Liver + SB transplant has better prognosis than isolated SB transplantation alone

• M/C cause of death is infection (sepsis)
• M/C cause of graft loss is Sepsis > graft rejection
PANCREAS TRANSPLANT
• 1st done by Kelly and Lillehei
• Donor age 10 – 45 years
• Only cadaveric transplant is possible
• M/C complication following pancreas transplant is Graft Thrombosis
Types of pancreas transplant

SPK (80%) simultaneous pancreas and kidney transplant
• Has 85% 1yr graft survival rate (highest among the 3 types)
• Done in Type I (IDDM) with severe C peptide deficiency
• Type II with C peptide levels < 2ng/ml
PTA (15%): Pancreas transplant alone
PAK (5%): pancreas after kidney transplant
Contraindication for donor:

• Type I DM
• Pancreatic surgery
• Chronic pancreatic disorders
• IPMN
Procedure:
• Pancreas is retrieved including C shaped duodenum, 1 vein Superior mesenteric vein and 2
arteries superior mesenteric artery (SMA) and Splenic artery (SA).
• Y shaped graft is also taken from the cadaver (common ileac artery with internal and
external iliac arteries) anastomose the IIA with SA and EIA to SMA.
• Anastomosis of the graft can be done in 2 ways
o Enteric drainage
o Bladder drainage
Enteric drainage Bladder drainage

M/C performed
Advantage: Advantage:
it is physiological drainage Graft failure can be identified by looking
No increased infection at urinary Amylase
No UTI Early rejection can be diagnosed
Leak rate is less

Disadvantage: Disadvantage:
Leak is M/C Urethritis, UTI
Metabolic acidosis
• M/C cause of graft failure is Graft thrombus (SMV> artery); Pancreas is to removed
• M/C cause of death post transplant: CVS cause
Complication:
• Rejection
• Leak: Debridement and re anastomosis
• Bleeding (Rx Octreotide)
• Infection
• Necrosis
• Abscess
ISLETS CELL TRANSPLANT

• 8000 – 10000 islets / kg body weight is needed to make him insulin free, to get this we
need 4 donor pancreas**
• These islets is injected into the portal vein
• They live in the liver
• Complication: Bleeding and PV thrombosis
• EDMONTON Protocol** ( NEET SS)
o Steroids not to used
o IL 2 Abs are used

HEART TRANSPLANT
• Orthotopic transplant
• M/C cause for transplant is Ischemic Dilated Cardiomyopathy
• Do sternotomy and remove the heart preserve the Lt atrial Cuff, Aorta, SVC, IVC &
pulmonary arteries. Insert the donor heart and anastomose in the following order
o Left atrial cuff ( 1st)
o SVC & IVC ( 2nd)
o Aorta
o Pulmonary artery


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Section : E: Surgical Specialty Topics

Acknowledgement for this section

1. Dr. Prasanth Bylapudi, NRI institute of medical sciences, Visakapatinam, Andhrapradesh

2. Dr. Mohammed Shiyas

RRM’S SURGERY SIXER APP BASED WORK BOOK 1

Part : 1: Kidney, Ureter, Bladder and Urethra

BRODELS LINE-Avascular line on the greater curvature of the kidney

Narrow points in the ureter:

• Length of ureter - 20cm

RRM’S SURGERY SIXER APP BASED WORK BOOK 2

Category I- Simple Cyst Clear cyst

• Category IIF- <5% risk of malignancy

• Category III- biopsy is done

SPECIAL SCANS IN KIDNEY

● DMSA(Dimercapto succinic Acid)- IOC- for accessing the Morphology of kidney

RRM’S SURGERY SIXER APP BASED WORK BOOK 3

● MAG-3 (Mercapto Acetyl Triglycine Scan)- IOC FOR PUJ OBSTRUCTION**

■ Mid ureter-mimics pain like appendicitis

■ VUJ- pain radiating from loin to groin or mid thigh ( ilioinguinal

Figure: Symptoms related to Location of Stone

relieved and swelling disappears.

RRM’S SURGERY SIXER APP BASED WORK BOOK 4

Calcium Oxalate (Calcium oxalate Monohydrate and Dihydrate)

• M/c type of stone overall

• M/c stone to cause haematuria

Triple Phosphate ( Calcium , magnesium ,NH4,PO4 / Struvite )

● Only radiolucent stone

● Associated with hyperuricemia in Gout, cancer

● Indinavir (HIV patients)- Radiolucent

● Xanthine ( In Xantine Oxidase deficient patients)- Radiolucent

RRM’S SURGERY SIXER APP BASED WORK BOOK 5

Calcium oxalate monohydrate:

RRM’S SURGERY SIXER APP BASED WORK BOOK 6

RRM’S SURGERY SIXER APP BASED WORK BOOK 7

• M-Mg trisilicate ( Antacids)**

● < 5mm - No treatment needed

● Restrict : Protein, salt , oxalate diet

● Increase consumption - Calcium supplements**

● Juice - Cranberry juice** is used in management of renal stones**

Primary Bladder stone Secondary Bladder stone

RRM’S SURGERY SIXER APP BASED WORK BOOK 8

● ESWL-EXTRACORPOREAL SHOCK WAVE LITHOTRIPSY

● PCNL- PERCUTANEOUS NEPHROLITHOTOMY

(d/t pelvic brim bone hindrance))

● Absolute- pregnancy, bleeding diathesis

RRM’S SURGERY SIXER APP BASED WORK BOOK 9

● Anatomical abnormality- Calyceal Diverticulum containing Stones**

● Trans costal approach- Pleural injury and Hydrothorax can happen

● Injury to renal artery /vein/IVC**

• If this technique is not mentioned – go with PCNL**

● For mobile stone

● By retrograde method we use ureteroscopy to remove intra renal stones.

Management of Ureteric stones:

● <5mm - it will pass

● >5mm/impacted somewhere- Removed by Dormia basket technique

RRM’S SURGERY SIXER APP BASED WORK BOOK 10

● Old technique- Open Cysto lithotomy

● Latest- Transurethral Cysto lithotripsy

● Lasers used now- HO:YAG(best) Nd:YAG

Image Based question:

• The left kidney is having a Percutaneous DJ stent- for percutaneous nephrostomy**

RRM’S SURGERY SIXER APP BASED WORK BOOK 11

RENAL CELL CARCINOMA @ Grawitz Tumor @ Hypernephroma

● Juice - Cranberry juice is used in management of renal stones