UROLOGY

HORSE SHOE KIDNEY

- CONGENITAL DISORDER
- LOWER POLES ARE FUSED
- ASCENT IS ARRESTED → KIDNEYS LIE LOWER DOWN IN PELVIS AT L4-L5
- ARRESTED BY IMA

CLINICAL FEATURES

- USUALLY FOUND INCIDENTALLY

- FRONT FACING PELVIS , CALYCES FACE POSTERO MEDIAL
- URETER HAS TO CROSS ISTHMUS – KINKED → STASIS → URETERIC STONE / URINARY
TRACT INFECTION

INVESTIGATION

USG ABDOMEN/ CECT ABDMEN

IV UROGRAM → KIDNEYS LOWER DOWN AND CLOSER TO EACH OTHER

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UPPER URETERS ARE MORE MEDIAL

REST OF URETERS GO ALONG NORMAL PATHWAY INTO BLADDER → FLOWER VASE URETER

MANAGEMENT

- SURVEILLENCE
- SURGERY TO TREAT COMPLICATIONS

NOTE: INCIDENCE OF WILM’S TUMOUR IS MORE IN HORSE SHOE KIDNEY

POLYCYSTIC KIDNEY DISEASE

- BOTH KIDNEYS HAVE MULTIPLE CYSTS IN PARENCHYMA

- COMPRESSION OF NORMAL NEPHRON BY CYSTS

PATHOGENESIS

- URETERIC BUD AND METANEPHRIC CAPS FUSE TOGETHER → NORMAL KIDNEY IS

FORMED
- IF FAILURE OF FUSION → POLY CYSTIC KIDNEY
- AUTOSOMAL DOMINANT PKD → ADULTS → > 30 YRS
- ARPKD → CHILDREN → < 3 YEARS, POOR PROGNOSIS

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SEQUELAE

- EARLY ONSET HYPERTESION- FIRST CLINICAL FINDING

- PROGRESSIVE END STAGE RENAL DISEASE
- STONES: OXALATE/URATE STONES
- ASSOCIATED WITH CYSTS IN OTHER LOCATIONS– LIVER / PANCREAS
- LUNG CYSTS NOT SEEN
- CARDIO-VASCULAR : MITRAL VALVE PROLAPSE , BERRY ANEURYSM

CLINICAL FEATURES

- EARLIEST : YOUNG HYPERTENSION

- B/L RENAL MASSES
- END STAGE RENAL DSEASE / CHRONIC KIDNEY DISEASE

DIAGNOSIS: IMAGING: CECT ABDOMEN

MANAGEMENT

- TREAT HYPERTENSION
- RENAL TRANSPLANT – TOC
- DEROOFING OF CYST : ROVSING’S PROCEDURE (NOT DONE ANY MORE)

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URINARY TB

- STARTS IN KIDNEYS
- DESCENDS INTO REST OF URINARY TRACT

PATHOGENESIS

- PRIMARY FOCUS IN LUNGS → HAEMATOGENOUS SPREAD

1ST SITE : GLOMERULAR VESSEL →IF POOR IMMUNITY → PAPILLARY ULCER → FIBRO CAVITARY
LESIONS → CASEATING NECROSIS → PUTTY KIDNEY (MOST OF THE KIDNEY HAS CASEOUS
NECROSIS ) → CEMENT KIDNEY

- IF GOOD IMMUNITY → CALCIFIED GRANULOMAS→ PSEUDO CALCULI

- FROM PARENCHYMA → ORGANISM SPREAD TO MINOR CALYCES – MOTH EATEN
CALYCES
- PUJ – KERR’S KINK ( INFLAMMATION AD FIBROSIS CAUSE MALFORMATION )
- BEADED URETER/LEAD PIPE URETER
- BACILLI ENTERS BLADDER NEAR THE ORIFICE → PERI ORIFICEAL EDEMA/ PALLOR
- GOLF HOLE URETERIC ORIFICE
- FIBROSIS OF BLADDER→SMALL CONTRACTED BLADDER → THIMBLE BLADDER
- PROSTATITIS
- SEMINAL VASCULITIS, EPIDIDYMITIS

C/F

- 1ST SYMPTOM : INCREASED FREQUENCY OF URINE

- CONSTITUTIONAL SYMPTOMS OF TB

INVESTIGATION

- URINE ROUTINE/MICROSCOPY → STERILE PYURIA

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 - 3 CONSECUTIVE EARLY MORNING SAMPLES OF URINE → TB GENE EXPERT , CB-NAAT
- PLAIN X RAY : KIDNEY HAS CALCIFICATIONS → PUTTY KIDNEY (IMAGE)
- IMAGING- CT UROGRAM/IVU→ MOTH EATEN CALYCES (EARLIEST FINDING), PUTTY
KIDNEY, URETERIC OBSTRUCTION, THIMBLE BLADDER(IMAGE)
- CYSTOSCOPY : GOLF HOLE URETERIC ORIFICE

TREATMENT

- ANTI TUBERCULAR THERAPY

SURGERY ONLY FOR COMPLICATIONS

- PUTTY KIDNEY : NEPHRECTOMY
- STRICTURE : STRICTUROPLASTY / RESECTION ANASTOMOSIS
- THIMBLE BLADDER : AUGMENTATION CYSTOPLASTY

TYPES OF RENAL STONES

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 TYPE MICROSCOPY RADIO-OPACITY

1.OXALATE (MULBERRY) – -DUMBELL SHAPED RADIO-OPAQUE

EARLY HAEMATURIA (MONOHYDRATE )
-ENVELOPE SHAPED
(DI-HYDRATE )

2.TRIPLE PHOSPHATE COFFIN LID APPEARANCE OPAQUE – IN INFECTED

STONE/STAGHORN URINE
CALCULI

3.URIC ACID STONE RHOMBOID RADIO- LUSCENT

4.CYSTEINE STONE HEXAGONAL OPAQUE ( SULFUR )

IOC – NC-CT KUB

TREATMENT: EMERGENCY – NSAID, ALPHA BLOCKER , FUREOSEMIDE , IV FLUIDS

ELECTIVE MANAGEMENT

1. SMALL STONE < 5mm -CAN PASS SPONTANEOUSLY

2. EXTRA CORPOREAL SHOCK WAVE LITHOTRIPSY (ESWL) – ULTRASONIC WAVES
FOCUSSED ON STONES – STONES FRAGMENTED
INDICATIONS: STONES 5mm to 20 mm IN SIZE, SOFT STONES
CONTRAINDICATIONS

i. >20mm
ii. CYSTEINE STONES – HARD STONES
iii. STONES IN LOWER CALYX

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 iv. PREGNANCY
v. COAGULOPATHY

3. PERCUTANEOUS NEPHRO-LITHOTRIPSY

INDICATIONS
i. >20 mm
ii. HARD STONES
iii. STAGHORN STONES

CONTRA INDICATIONS

- PREGNANCY, BLEEDING DISORDERS

PCNL

4. RETRO GRADE INTRA RENAL SURGERY (RIRS) / URETRO –RENOSCOPY (URS)

i. UPTO 20mm
ii. CAN BE USED IN LOWER CALYCES STONE
iii. CAN BE USED IN PREGNANCY
iv. HORSE SHOE KIDNEY STONES

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RENAL TUMOURS

MC RENAL TUMOR– RENAL CELL CARCINOMA / ADENOCARCINOMA OF KIDNEY / HYPER

NEPHROMA/ GRAWITZ TUMOUR / INTERNIST TUMOUR

RISK FACTORS

SMOKING
OBESITY
TYPES

i. CLEAR CELL – MC TYPE, A/W VON HIPPEL LINDAU SYNDROME

ii. PAPILLARY – LONG TERM DIALYSIS , PSAMOMMA BODIES
iii. CHROMOPHOBE – GOOD PROGNOSIS
iv. MEDULLARY SICKLE CELL TRAIT

PATHOLOGY:

- ARISES FROM UPPER POLE

- SURROUNDED BY GEROTA’S FASCIA
- SPREAD TO RENAL VEIN → IVC : TUMOUR EMBOLI
- HAEMATOGENOUS SPREAD -CANNON BALL METASTASIS → LUNGS

PARANEOPLASTIC SYNDROME
i. ELEVATED ESR – MC TYPE
ii. ANEMIA OF CHRONIC DISEASE
iii. POLYCYTHEMIA
iv. HYPERCALCEMIA – PTH LIKE PEPTIDES PRODUCED

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 v. LIVER DYSFUNCTION – STAUFFER SYNDROME – IN ABSENCE OF METASTASIS

C/F

i. H/O ELDERLY SMOKER MALE WITH

ii. PAINLESS PROFUSE HAEMATURIA ( CLOTS)
iii. COLICKY PAIN
iv. PALPABLE RENAL MASS

DIAGNOSIS

CECT ABDOMEN
BIOPSY: NOT NEEDED

TNM STAGING

T1 – UPTO 7 cm , T1a - < 4cm , T1b -4-7CM

T2 > 7 cm

T3 – T3a-IPSILATERAL RENAL VEIN,T3b- IVC UPTO DIAPHRAGM ,T3c- ABOVE DIAPHRAGM

T4 - BREACH OF GEROTA / IPSILATERAL ADRENAL GLAND

TREATMENT

- NOT SENSITIVE TO CHEMO/RADIATION

- T1a - <4cm – PARTIAL / NEPHRON SPARING NEPHRECTOMY
- T1b- 4-7cm – PARTIAL OR RADICAL NEPHRECTOMY
- T2/ T3 , SOME T4 – RADICAL NEPHRECTOMY
- T4/M1 – PALLIATION- IMMUNOTHERAPY

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 PROSTATE

A. ANATOMY

LOCATION
• Present just below bladder neck
SPHINCTERS
• Internal urethral sphincter: at bladder neck ,proximal
• External urethral sphincter : below prostate, more important for continence
-During TURP it may be injured, to prevent it we limit the resection up to
verumontanum.

LOBES OF PROSTATE
• 2 LATERAL LOBES
• MEDIAN LOBE
• POSTERIOR LOBE

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 • LATERAL AND MEDIAN LOBE NEAR URETHA- CAN CAUSE COMPRESSION ON
ENLARGEMENT
• POSTERIOR LOBE DOESN’T CAUSE COMPRESSION

MC NEAL ZONES
• TRANSITIONAL ZONE: BPH
• CENTRAL ZONE
• PERIPHERAL ZONE : CA PROSTATE

B. BENIGN PROSTATIC HYPERPLASIA

Adenoma in Transitional zone / central zone → BLADDER OUTLET OBSTRUCTION
CLINICAL FEATURES

• LOWER URINARY TRACT SYMPTOMS OR BLADDER OUTLET OBSTRUCTION (LUTS/BOO)

a) VOIDING SYMPTOMS : PISS
P : PRECIPITANCY/INCOMPLETE VOID(Significant post void residue>20%)
I: INTERMITTENCY – START-STOP PHENOMENA OF MICTURITION
S: STRAINING
S : STREAM IS POOR

b) STORAGE SYMPTOMS : FUNN (OCCUR EARLY)

F : INCREASED FREQUENCY
U: URGENCY
N: NOCTURIA
N: NOCTURNAL ENURESIS

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COMPLICATIONS

• ACUTE RETENTION OF URINE: EMERGENCY

• CHRONIC RETENTION OF URINE
• BILATERAL HYDRO-URETER, HYDRONEPHROSIS
• BLADDER DIVERTICULI, STONES, CYSTITIS

INVESTIGATIONS

• PER RECTAL EXAMINATION : ENLARGED PROSTATE

• S.PSA LEVELS : NORMAL <3.5
• USG PELVIS : MEASURES PROSTATE ENLARGEMENT SEVERITY+ POST VOID
RESIDUE>20 %
• IF IN DOUBT : TRUS WITH BIOPSY

• SEVERITY OF BLADDER OUTLET OBSTRUCTION (BOO) TESTS

URINE FLOW RATE (UFR):
NORMAL UFR : >15ML/sec
SIGNIFICANT BOO : < 10 mL/sec
MANAGEMENT

MEDICAL MANAGEMENT

a) 5 ALPHA REDUCTASE INHIBITOR : TESTESTERONE GETS CONVERTED TO

DIHYDROTESTESTERONE (ACTIVE FORM ) BY 5 ALPHA REDUCTASE , If we block
this by FINASTERIDE, DUTASTERIDE, WILL LEAD TO SHRINKAGE OF PROSTATE.
This takes 3-6 months to take effect

b) ALPHA 1 BLOCKERS :
• TAMSULOSIN : SELECTIVE ALPHA 1 A BLOCKER
• Relaxes the muscle of prostatic urethra

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 • Initial therapy of BPH

SURGICAL MANAGEMENT

INDICATION

• Severe Symptoms + decreased UFR(<10Ml/sec) despite medical

management: MC INDICATION FOR PROSTATECTOMY
• Any Complications:
Any Episode of RETENTION OF URINE
B/L HYDRO URETER OR HYDRO NEPHROSIS OR BLADDER STONE
SURGERIES

1) TURP –TRANS URETHRAL RESECTION OF PROSTATE (GOLD STANDARD)

• Coring out prostate from inside with cystoscope
• Enucleate till false capsule left out
• Limit of resection distally: VERUMONTENUM
• Limit of time : < 90 minutes : Irrigation of surgical field with distilled
water,can lead to dilutional hyponatremia , fluid overload , which can
lead to Pulmonary edema → TUR SYNDROME
• Management: O2 + DIURETICS + electrolyte correction
• Avoided by reducing duration of TURP < 90 mins, avoiding use of distilled
water for irrigation (use Glycine)

C. CARCINOMA PROSTATE

RISK FACTORS

M/C Malignancy in Men > 65 years

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PATHOLOGY

• Occurs in Peripheral Zone so Urethral Compression is late, hence present late with
metastasis

SPREAD

A. DIRECT SPREAD
BLADDER NECK : ABOVE

B. HEMATOGENOUS SPREAD : TO THE VERTEBRA via BATESON’S PLEXUS OF VEINS

Rarely to LUNGS

CLINICAL FEATURES

• OCCUR LATE
• EARLY DETECTION→SCREENING :ELEVATED PSA LEVELS
• Rarely BLADDER OUTLET OBSTRUCTION
• BACKACHE : due to metastasis to lumbar vertebra- Osteoblastic
metastasis

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STAGING

T1: Incidentally found after TURP / PSA levels

T1a : Foci in less than 5 %
T1b: >5%
T1c: Due to raised Se PSA
T2: Limited to prostate, within its capsule
T3 : Breach the capsule/ spread to seminal vesicles
T4 : Spread to adjacent viscera

N0-No spread to lymph nodes

N1- Regional nodes

M0-No spraed beyond regional lymph nodes

M1-Distant metastasis

INVESTIGATION

1.PSA LEVELS : Diagnostic marker

• NORMAL : <3.5
• SUSPICIOUS : 3.5-10
• MALIGNANCY : 10-35
• METASTASIS : >35

2. TRAN RECTAL USG WITH BIOPSY / TRANS PERINEAL USG WITH BIOPSY

-Confirms Adenocarcinoma
3. FOR STAGING : TNM STAGING IOC :

• MRI OF PROSTATE : LOCAL SPREAD

• CT ABDOMEN/ CT THORAX / PET SCAN : DISTANT METASTASIS

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TREATMENT

1. SURGERY
• RADICAL PROSTATECTOMY
• BLADDER TO URETHRA ANASTOMOSIS

2. RADIOTHERAPY

3. ANDROGEN ABLATION
- CHEMICAL :
LHRH ANALOGUES : GOSERELIN/ LEUPROLIDE
ANTI-ANDROGENS : FLUTAMIDE / BICALUTAMIDE
- SURGICAL
B/L ORCHIDECTOMY
4. SURVEILLENCE : if person unfit for surgery, > 70 yeaRs of age
- Early tumour
- Lowest Gleason Score : 6
- Normal PSA levels

STAGE WISE TREATMENT

• T1: SURVEILLENCE- ELDERLY / UNFIT /GOOD GLEASON

YOUNG <70 – RADICAL PROSTATECTOMY

• T2 : RADICAL PROSTATECTOMY / RADIOTHERAPY

• T3/T4 : SURGERY AVOIDED : ANDROGEN ABLATION : TO CONTROL TUMOUR

BURDEN + RADIOTHERAPY

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 URINARY BLADDER TUMOURS

RISK FACTORS

- SMOKING
- OCCUPATIONAL CANCER : BETA NAPHTHALAMINE , O-TOLUIDINE
- MC : TRANSITIONAL CELL /UROTHELIOMA
- SQUAMOUS CELL CARCINOMA OF BLADDER IF CHRONICALLY IRRITATED –
STONES , FOREIGN BODY , SCHISTOSOMIASIS
- ADENOCARCINOMA – RARE – ECTOPIA VESICAE / REMNANT URACHUS

PATHOLOGY

- EXOPHYTIC/PAPILLARY GROWTH
- TUMOR CELLS SPILL TO ADJACENT WALL- KISSING TUMORS
- CARCINOMA IN SITU- MALIGNANT CYSTITIS

SPREAD

- ANTERIOR – PELVIC WALL

- POSTERIOR : MALE : RECTUM , FEMALE : UTERUS
- HAEMATOGENOUS – LUNGS / VERTEBRAE ( BATESON’S PLEXUS )

CLINICAL FEATURES

- GROSS HAEMATURIA – AT END OF MICTURATION – TERMINAL HAEMATURIA

- WEIGHT LOSS
- METASTASIS

STAGING – CYSTOSCOPY + BIOPSY

pTa- LIMITED TO EPITHELIUM

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pT1- LAMINA PROPRIA

pT2- MUSCULARIS

pT3-PERI VESICAL TISSUE

pT4- SURROUNDING STRUCTURE

INVESTIGATION

- URINE ROUTINE – HEMATURIA

- URINARY ANTIGENS – NMP-22/BTA (NON SPECIFIC)
- IOC : CYSTOSCOPY + BIOPSY (EXCISION BIOPSY IF POSSIBLE)
- LOCAL STAGING : MRI: IOC

TUMOR BEFORE AND AFTER EXCISION

SURGERY

1. CYSTOSCOPIC EXCISION
2. RADICAL CYSTECTOMY – BLADDER / PROSTATE / LYMPH NODES + ILEAL CONDUIT (
BLADDER SUBSTITUTION )

CHEMOTHERAPY

139
 - CONTACT CHEMOTHERAPY : MITOMYCIN C / BCG
- SYSTEMIC CHEMOTHERAPY
3. RADIOTHERAPY

STAGEWISE TREATMENT

pTa - CYSTOSCOPIC EXCISION + SINGLE CYCLE CONTACT CHEMOTHERAPY

pT1/ HIGH GRADE pTa→ CYSTOSCOPIC EXCISION + REAPEAT CYSTOSCOPY (AFTER 2-6 WEEKS ) +
CONTACT CHEMOTHERAPY

-MUSCLE INAVDING TUMOUR – RADICAL CYSTECTOMY + ILEAL CONDUIT + ADJUVANT -

CHEMOTHERAPY

- TUMOUR INVADING SURROUNDING STRUCTURES – PALLIATIVE THERAPY

BLADDER RUPTURE

PATHOPHYSIOLOGY

- INJURY TO LOWER ABDOMEN / PUBIS + DISTENDED BLADDER AT TIME OF

INJURY

TYPES

- INTRA PERITONEAL BLADDER RUPTURE : INJURY TO LOWER ABDOMEN ,

TEAR AT FUNDUS → URINE GOES INTO INTRA PERITONEAL CAVITY →
CHEMICAL PEROTINITIS
- EXTRA PERITONEAL BLADDER RUPTURE – INJURY TO PUBIS → LATERAL
WALL TEARS → URINE LEAKS IN THE PER VESICAL SPACE (CAVE OF RETZIUS) ,

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 LIMITED BY PELVIC DIAPHRAGM → SPREADS ALONG ANTERIOR ABDOMINAL
WALL – MELENEY’S SYNERGESTIC GANGRENE

CLINICAL FEATURES

- H/O BLOW TO LOWER ABDOMEN / PUBIS

- NOT ABLE TO PASS URINE SINCE TIME OF INJURY
- NOT PALPABLE BLADDER (SINCE ITS RUPTURED)
- NO BLOOD SEEN AT URETHREAL MEATUS

TO CONFIRM – INSERT A FOLEY’S AND INJECT CONTRAST IN BLADDER→

ASCENDING CYSTOGRAM
i. LEAK OF CONTRAST IN PERITONEAL CAVITY→ – INTRA PERITONEAL
RUPTURE → LAPAROTOMY → DRAIN URINE → SUTURE TEAR AND
PERFORM SUPRA PUBIC CYSTOSTOMY

ii. LEAK OF CONTRAST FROM LATERAL WALL→ EXTRA PERITONEAL

RUPTURE → SURGICAL REPAIR IS DIFFICULT → LEAVE FOLEYS IN
PLACE FOR 8-10 DAYS → BLADDER CONSTRICTS → TEAR AREA
COMES CLOSER → TEAR HEALS SPONTANEOUSLY → CONFIRM LATER

141
 WITH REPEAT ASCENDING CYSTOGRAM→ IF NORMAL, REMOVE
FOLEYS

URETHRAL RUPTURE

PARTS

• PROSTATIC URETHRA +MEMBRANOUS URETHRA : POSTERIOR URETHRA

• BULBOUS URETHRA+ PENILE URETHRA : ANTERIOR URETHRA

PATHOLOGY

• Bladder should be Non Distended at time of injury

• Injury to Lower Abdomen, Pelvis or Perineum

TYPES OF RUPTURE

1. BLOW TO PELVIS/PUBIS :
• Leading to posterior urethral rupture
• Urine will leak above Levator Ani/Pelvic Floor : In Cave of Retzius
→ ascend along the Anterior Abdominal wall

2. PERINEAL INJURY
• AKA FALL ASTRIDE INJURY/ VERTICAL INJURY : h/o perineum
striking against a vertical object (fall on scaffold)
• Force to Bulbous urethra : this gets crushed against pubis
bone → ANTERIOR/BULBOUS URETHRAL RUPTURE
• BUTTERFLY SHAPED HEMATOMA seen in perineum
• Urine leaks in Superficial perineal pouch → Tracks in Skin and
Subcutaneous planes of Penis and Scrotum

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 PRESENTATION OF RUPTURE

• Pelvis/Perineum Injury
• Unable to pass urine
• BLOOD AT URETHRAL MEATUS
1. INJURY TO PUBIS →Post. Rupture : Ant. Abdominal Wall
swelling ,Floating prostate on P/R
examination(VERMOOTEN SIGN)
2) PERINEAL INJURY →Ant. Rupture : Perineal Hematoma , Swelling of Scrotum and Penis

Common finding in both types of rupture: Bladder will be distended and palpable

CONFIRMATION OF DIAGNOSIS: Foley’s is contra-indicated. Insert tip of Foleys at urethral

meatus and inject contrast (ascending urethrogram) and take X ray (Image below)

143
 ASCENDING URETHROGRAM

POSTERIOR RUPTURE ANTERIOR RUPTURE

SUPRA PUBIC CYSTOSTOMY SUPRA PUBIC CYSTOSTOMY

STRICTURE

ELECTIVE STRICTURE REPAIR (AFTER 2 TO 3 MONTHS)

CARCINOMA PENIS

- SQUAMOUS CELL CARCINOMA

RISK FACTORS AND PRE MALIGNANCY : ALL Ps

• PLAKIA: LEUKOPLAKIA
• PLASIA : ERYTHROPLASIA OF QUERAT/BOWENS DISEASE/PENILE INTRA EPITHELIAL
NEOPLASM
• PLAQUE:PENILE PLAQUES/ PEYRONIES DISEASE
• PAPILLOMA VIRUS : HPV16,18
• POOR HYGIENE /POOR CLEANING OF PENIS
• PROTECTED IF CHILDHOOD CIRCUMCISION is done : NEONATAL CIRCUMCISION IS BEST
• SMOKING

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PATHOLOGY

- MC SITE : GLANS / PREPUCE

• SPREAD
I. Along penis (glans to shaft)
II. Urethra
III. Lymph node mets
a) Sup. Inguinal nodes : SENTINEL NODES
b) Deep Inguinal nodes
c) Iliac Lymph nodes :Femoral Artery erosion
IV. Hematogenous metastasis is rare :Lungs

CLINICAL FEATURES

• H/o Smoking
• Caulifllower/ Exophytic growth at Glans with discharge
• Palpable Inguinal Lymph nodes

INVESTIGATION

• For confirmation- Wedge BIOPSY : Squamous cell Ca

• If Inguinal LN + : FNAC of node
• Metastasis : CECT

145
MANAGEMENT

Based on location of tumour:

• ON GLANS/Prepuce : EXCISION with 2 CM MARGIN : PARTIAL PENECTOMY

• SHAFT : TOTAL PENECTOMY +PERINEAL URETHROSTOMY

NOTE: FOR LOW GRADE TUMOUR : MOHS MICROGRAPHIC EXCISION can be done

INGUINAL NODES :

• IF PALPABLE before surgery→PREOPERATIVE FNAC : IF MALIGNACY +

: ILIO INGUINAL BLOCK DISSECTION (same time as penectomy)

• If PALPABLE before surgery → FNAC shows BENIGN : 3 Weeks of

Antibiotics after penectomy : If doesn’t resolve : Mets missed on
FNAC : ILIO INGUINAL BLOCK DISSECTION (later)

• NO PALPABLE NODES preoperatively: INTRA-OP SENTINEL LN BIOPSY

and decide

FOURNIER’S GANGRENE

- Synergistic gangrene of scrotum and perineum. A type of necrotising fasciitis.

RISK FACTORS

- LOW IMMUNITY , UNCONTROLLED DIABETES

- H/O TRAUMA/boil/trivial injury

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PATHOGENESIS

- Organisms enter skin and subcut. → obliterative end arteritis→ Infective Gangrene
- Polymicrobial inflammation (Aerobes + anerobes)

CLINICAL FEATURES

- Fever
- Scrotal/perineal wound with dirty foul smelling discharge

- Dehydrated/septicaemia/shock

TREATMENT

- IV Fluids+ Antibiotics
- Debridement of gangrene (Testes are normal and spared)
- Repeated debridement after 24-48 hours may be needed
- Hyperbaric Oxygen therapy may be beneficial
- If both scrotal sacs r excised, testes are entirely exposed- “Shameful exposure of testis”

147
 CARCINOMA TESTES

RISK FACTOR- Undescended testis

TYPES

1. GERM CELL TUMOUR

- SEMINOMA (MC)
- TERATOMA
- CHORIOCARCINOMA
- YOLK SAC TUMOUR

2. STROMAL TUMOUR
- LEYDIG CELLS tumor, Sertoli Cell tumor

3. LYMPHOMA / MELANOMA

CYSTIC SPACES/ VARIEGATED → SEMINOMA

TERATOMA

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SPREAD

- LOCAL : DOESN’T SPREAD TO SCROTUM – BUT IF BIOPSY DONE THEN CAN SPREAD TO
SCROTUM , DON’T DO BIOPSY

- LN metastasis:

ABDOMINAL NODES → PARA AORTIC

INGUINAL LN METS → UNCOMMON, seen if scrotal spread

- HAEMATOGENOUS -LUNGS – CANNON BALL METASTASIS (MC in CHORIOCARCINOMA)

CLINICAL FEATURES

- YOUNG MAN IN 20s WITH PAINLESS TESTICULAR MASS / ABDOMINAL LN MASS (PARA
AORTIC LN )

INVESTIGATION

1. TUMOUR MARKERS
- Beta HCG- CHORIOCARCINOMA
- Placental alkaline phosphatase (PLAP)- SEMINOMA
- AFP- YOLK SAC TUMOUR
- LDH – TUMOUR BURDEN

2. USG TESTIS – will confirm the mass

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 3. INGUINAL EXPLORATION → DELIVER TESTIS → TAKE A PIECE OF MASS → FROZEN
SECTION (CHEVASSUS’S MANEUVER) → IF MALIGNANCY + → HIGH INGUINAL
ORCHIDECTOMY → STAGING ( CECT THORX + ABDOMEN – METASTASIS )

IF BENIGN → REPOSIT THE TESTIS

STAGING

I – ONLY IN TESTIS , NO METS

II – LN METS +

III- HEMATOGENOUS METS OR LN METS WITH ELEVATED TUMOUR MARKERS

Seminoma NSGCT

Stage 1 - EARLY Radio therapy/single cycle Single cycle chemo

chemo
Stage 2,3 – ADVANCED Adjuvant chemo Adjuvant chemo
[Bleomycin, etoposide, Bleomycin,etoposide;platinum
platinum]
Lymph node residue Retroperitoneal LN dissection SAME AS SEMINOMA
despite chemo [RPLND]

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 BREAST

CARCINOMA BREAST

RISK FACTORS

• Increased estrogen exposure

• Early menarche (<12 years)/late menopause (>55 years)
• Nulliparity /Late age of 1st birth (>35 years)
• Hormone replacement therapy
• OCP pills – negligible risk
• Obesity
• Prior chest radiation
• Alcoholism
• Smoking – Negligible risk
• Breast feeding (>1 year) – protective

FAMILIAL BREAST CANCERS

- SPORADIC BREAST CANCER – More common than familial

- Familial cancers occur due to known mutations which run in families
- Known mutations – BRCA 1 and BRCA 2
- BRCA – 1 – lifetime risk of developing breast cancer – 50-80%
Lifetime risk of developing ovarian cancer – 40%
- BRCA 2 – associated with male breast cancer
Life time risk of breast cancer – 50-60%
Lifetime risk of ovarian cancer – 20-25%
More associated with male breast cancer and Cancer prostate
- BRCA 1 and BRCA 2 associated with triple negative breast cancer (ER-ve,PR-ve,HER2-ve)

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PREMALIGANANT LESIONS

1. Highest risk lesion – DCIS/LCIS – 8-10 fold

2. Atypical ductal hyperplasia and lobular hyperplasia –4-5 fold
3. Complex fibro-adenoma :increases risk 2-3 fold

PATHOLOGY

• Location – upper outer quadrant -MC

• Least common site :Lower inner quadrant

Microscopically

• In-situ – DCIS, Paget’s disease of nipple

• Invasive – ductal or lobular – Not otherwise specified
• Medullary carcinoma
• Tubular variant – Good prognosis
• Inflammatory carcinoma – worst prognosis

MOLECULAR SUBTYPES

- Immunohistochemistry – ER/PR/HER 2 neu receptor , and Ki 67 activity

1. Luminal A
- ER/PR positive
- HER 2 negative
- Ki 67 negative

2. Luminal B
- ER/PR positive
- HER 2 negative

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 - Ki 67 positive

3. Triple negative breast cancer

- ER/PR/HER 2 negative
- Ki 67 positive

4. Her 2 enriched
- ER/PR negative
- HER 2 positive
- Ki67 positive

SPREAD

1. LOCALLY

-Cooper’s ligament/ skin/lactiferous ducts / P. Major or chest wall

2. Lymph nodes metastasis-axillary – I-II-III →infra-clavicular →supraclavicular

I: Anterior, Lateral, posterior groups

II: Central /Inter-pectoral group
III: Apical group
Can go to Internal mammary nodes too if tumor in inner quadrants of breast
3. Hematogenous

- Most common to bone – lumbar> femur>thoracic>neck

- Lung metastasis

- Brain –via leptomeninges

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CLINICAL FEATURES

- Presents as lump in breast, with or without bloody discharge from nipple

1. COOPER’S LIGAMENT INVOLVEMENT

- Dimpling – single cooper’s ligament is infiltrated.
- Puckering – multiple cooper’s ligaments are infiltrated

2. LACTIFEROUS DUCT invasion→ Nipple retraction

3. SUBDERMAL LYMPHATICS invasion →Peau – D – orange
4. Axillary Lymph node palpated
5. Supra clavicular nodes palpable

STAGING

p-PATHOLOGICAL

c-CLINICAL

y- AFTER NEO ADJUVANT CHEMO THERAPY

TNM staging – CLINICAL EXAMINATTION + IMAGING

T – tumor size

Tis- IN SITU – DCIS, PAGET DISEASE

154
T1 – <= 2cm

T2 - > 2cm -5cm

T3 - > 5cm

T4a – Invasion of chest wall (does not include pectoralis major)

4b – Skin invasion (ulcer /peau d orange/ satellite nodules)

* Cancer en cuirasse – multiple tumors in skin of chest + arm + shoulder

4c- a+b

4d – inflammatory breast cancer

N1 – Ipsilateral mobile axillary nodes

N2a – Ipsilateral fixed axillary nodes

N2b – Internal mammary nodes

N3a – Ipsilateral infra clavicular

N3b – 2a+2b

N3c- Ipsilateral supra clavicular

Any C/L – Metastatic disease-M1

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INVESTIGATIONS

Triple assessment -Diagnostic accuracy -99.9%

1. History+ Examination
2. Imaging
3. Tissue diagnosis

Imaging

Mammogram

X ray of breast, low radiation x ray (equal to 4 chest x rays) -0.1 rad/cGy

2 views – cranio-caudal +medio-lateral views

Danger findings

a. microcalcification

b. irregular borders/spiculations

c. wide halo

BIRADS SCORE

Breast imaging reporting and data system

Score 0 – film improper

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 1- No lesion
2- Benign
3- Probably benign
4- Suspicious
5- Suggestive
6- Biopsy proven

BIRADS 1 &2 – no risk , continue screening as per norm

BIRADS 3 – probably benign , 6 month follow up
BIRADS 4 – suspicious – 2-95% risk- biopsy
BIRADS 5 – suggestive - >= 95% - biopsy plus management
BIRADS 6 – biopsy proven – like malignancy

4a – low risk – 2-10 % chance of malignancy

4b – medium risk – 11-50 % chance of malignancy
4c – high risk – 51- 95% chance of malignancy

Indications of mammogram
• Breast lump in woman of age > 40 years
• If age is < 40 years and has lump in breast – sonomammogram
• Screening - US guidelines – annual mammogram > 40 years
• UK guidelines - > 50 years – 2-3 yearly

MRI breast

• BRCA +ve- Early screening -Start from 30 years

• Can be done when scar recurrence is suspected post surgery
• In women with breast implants with new onset lump

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Tissue diagnosis
1. FNAC – 21-23 G – cells are seen , cannot differentiate between In-situ/ Invasive

2. Core biopsy/ trucut biopsy – IOC

Malignancy – staging – FNAC of axillary lymph nodes

CT thorax / CT abdomen
PET scan

TREATMENT
In most cases, multimodal treatment is needed
Surgery

Modified radical mastectomy / MRM

- Removal of skin with nipple areolar complex with entire breast + pectoral fascia +
axillary LN I,II + III
- Spared are pectoralis major/ribs (removed in radical mastectomy)

- Structures preserved are

- A – axillary vein
- B – Bells’ nerve

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 - C – Cephalic vein
- D- dorsal (thoracodorsal) nerve + vessels

TYPES OF MRM
Patey’s - excision of pectoralis minor along with apical node
Scanlon – divide Pectoralis minor and remove apical node
Auchincloss – leave pectoralis minor intact- apical nodes may or may not be removed

Breast conservative therapy (BCT)

1. Wide local excision (>1cm gross margin)
2. Sentinel lymph node biopsy (or axillary LN clearance)
3. Adjuvant radiotherapy

Sentinel lymph node biopsy

• Peri-tumor infiltration of dye ( isosulfian blue) + Tc 99 with albumin → this dye will enter
the lymphatics of tumor and from there it goes to the axillary node
• Incision on axilla – identification of sentinel node by blue colored node or gamma
camera- these are removed and sent for frozen section – report will be either no
metastasis or metastasis
• If report says metastasis , all the axillary lymph nodes are removed
• If no metastasis- close axilla
• If already lymphadenopathy present pre-operatively→Axillary lymph node clearance is
done without SLNB

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C/I of BCT
- Pregnancy ,previous chest radiotherapy
- Connective tissue disorder – SLE , RA
- Wide local excision is not possible – multi-centric tumors/tumor close to the NAC/ large
tumor in size/ diffuse microcalcification

Chemotherapy / immunotherapy
- Can be given prior to surgery – neoadjuvant chemotherapy
- After surgery – adjuvant chemotherapy
Types
CEF – cyclophosphamide/epirubicin/5FU
CAF – cyclophosphamide/Adriamycin / 5FU
TAXANES– Paclitaxel, Docetaxel
HER 2 neu +ve cancer -Transtuzumab

- Indications
• All tumors > 1cm will need adjuvant chemotherapy
• 0.5 cm tumor with bad histology – poorly differentiated or triple negative breast cancer
• Locally advanced breast cancer (neoadjuvant)

160
NOTE
Good prognostic early breast cancer: ER/PR +ve HER2neu -ve
We do GENETIC PROFILE
- Oncotype Dx / Mammaprint → If low risk tumor → may avoid chemotherapy

Radiotherapy
Indications
1. BCT
2. LABC
3. Early breast cancer with bad prognostic factors (poorly differentiated/Lympho-vascular
invasion etc.)

Hormonal therapy
Indication -ER/PR positive
1. SERM – Tamoxifen is given in premenopausal age group
Increased risk of cancer endometrium and DVT
2. Aromatase inhibitors – anastrazole / letrozole – in post-menopausal only

Stage wise treatment

Stage I/II: EARLY BREAST CANCER – T1N1/T2N1/T1N2/T2Mo/T3Mo– BCT/MRM – SURGERY 1st

→Chemotherapy →Radiotherapy (if indicated) → Hormonal therapy if ER/PR positive

Stage III: LABC – T3N1/ ANY T4, Any N2: Neoadjuvant chemotherapy → MRM → Chemotherapy
and Radiotherapy in all cases →Hormonal therapy if ER/PR positive

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Stage IV: Metastatic cancer – M1 disease: Palliative care by radiotherapy
/chemotherapy/Hormonal therapy

PHYLLOIDES TUMOR

- Also called cystosarcoma phylloides / serocystic disease of Brodie

- Pathology – arises from epithelium and stroma of the breast

- C/F
• Presents at age >40 years
• Huge breast lump ,No lymph node mets
• Does not infiltrate the skin - no fixity to skin /NAC
• Skin ulceration due to pressure necrosis may be seen
• Usually benign tumor, suspect malignancy if there are > 10 mitosis/high power
field
• ON BIOPSY – cystic spaces are seen in leaf like pattern
• DIAGNOSIS - Triple assessment
• Treatment – Wide local excision(> 2cm margin ) / simple mastectomy -No
lymphadenectomy required

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BREAST ABSCESS

- Seen in – Lactating women- early phase/ late phase

- Infectious agent – Staph Aureus
- Begins with Mastitis (Redness)→ may progress to formation of pus pockets→ Abscess
- USG –Mastitis /Pus (abscess)
- In Non lactating/elderly – Rule out Inflammatory Carcinoma

TREATMENT

Mastitis alone – antibiotic – cloxacillin

Abscess –

Small - < 3cm/30ml – aspiration under USG guidance +antibiotics

Large - > 3cm /> 30ml – Suction catheter drainage +Antibiotics

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 THYROID

ANATOMY

• ANTERIOR MOST– SKIN OF NECK → PLATYSMA → SUPERFICIAL FASCIA →STRAP

MUSCLES FUSE IN MIDLINE of neck
• Behind the strap muscles lies the thyroid enclosed in pre-tracheal fascia
• PRE TRACHEAL FASCIA gets CONDENSED posteriorly → LIGAMENT OF BERRY
• POSTERIOR RELATIONS OF THYROID → TRACHEA → OESOPHAGUS → THEN LATERALLY
CAROTID SHEATH
• BEAHR’S TRIANGLE : CCA , Inferior thyroid artery, RLN – HELPS LOCALISE RLN AS THE
ANTERIOR BOUNDARY

• MC NERVE INJURY : EXTERNAL LARYNGEAL BRANCH OF SUPERIOR LARYNGEAL NERVE

• MC SITE OF RLN INJURY – BERRY’S LIGAMENT

• AVOIDED BY USING BIPOLAR CAUTERY AND NERVE MONITORING

164
 Right RLN

Left RLN

BLOOD SUPPLY

- SUPERIOR THYROID ARTERY FROM External Carotid Artery

- INFERIOR THYROID ARTERY FROM THYROCERVICAL TRUNK

GOITRE

• Enlargement of thyroid
• May be associated with hypothyroidism/hyperthyroidism or euthyroid
• May or not be a functional abnormality
• 3 types
- Diffuse goitre
- Multinodular goitre
- Solitary thyroid nodule

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Diffuse goitre

EUTHYROID / HYPERTHYROID / HYPOTHYROID

May occur due to physiological changes

- Increased demand during puberty, pregnancy , serious illness

(Physiolological goiter)
- associated with autoimmune hypothyroidism – Hashimotos
thyroiditis
- In grave disease – diffuse goitre + hyperthyroidism

Multinodular goiter (MNG)

-Complication of long standing diffuse goitre

-Function of the gland initially normal

-Long standing MNG(20-30%) – some nodules autonomous, secondary thyrotoxicosis

Solitary thyroid nodule

-One nodule in a part which may be – cyst or tumor

-Nodule may become autonomous leading to hyperthyroidism (toxic nodule)

CLINICAL FEATURES

o Of swelling – moves up on deglutition

166
o May compress the Trachea – dyspnea , Esophagus – dysphagia, RLN – hoarseness of
voice/ stridor, CCA- syncope

RETROSTERNAL GOITRE
Usually an external of goiter from neck into mediastinum (sub-sternal)
Blood supply comes from neck vessels
Excised by neck incision – only if causing problems – sternotomy not required
Pemberton sign – marker of retrosternal goitre
Raise hands → congestion of face → SVC compression

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 HYPOTHYROIDISM HYPERTHYROIDISM
Weight gain, poor appetite Weight loss despite good appetite
Cold intolerance Heat intolerance
Cold/dry extremities Warm/moist extremities
Eyes signs of Graves
Tremors over fingers/tongue
Delayed relaxation of ankle jerk DTR exaggerated

INVESTIGATIONS

1. History and examination

2. Thyroid function tests – TSH,FT3,FT4
3. Imaging –
- USG Neck – Work horse imaging- Diffuse/ Multinodular//Solitary nodular goitre
- With USG NECK → FNAC can be done

- Radioactive iodine uptake study /Thyroid scan /Iodine scan

I 123/I 131/Tc99m given in form of tablet or IV, gamma camera used
I123- preferred, short half-life – 8-10 hours
I131- long half-life– 8-10 days
Normal uptake – appears warm
Increased uptake – hot nodule (5% risk of malignancy)
Decreased uptake – cold nodule(20% risk of malignancy)

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Indications for scan

- HYPERTHYROIDISM with nodularity

- Post thyroidectomy in carcinoma thyroid to look for recurrence or metastasis
- Ectopic thyroid

CT/MRI neck– For local staging / Retrosternal goitre

4. Tissue diagnosis

Only FNAC – USG guided FNAC

- Core biopsy /TRUCUT biopsy contraindicated

Only done in two cases

- Differentiate Anaplastic carcinoma from Riedel’s Thyroiditis

- Thyroid Lymphoma

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TREATMENT – SURGERY TYPES AND INDICATIONS

Indications

- Compressive symptoms
- Cosmetsis
- Carcinoma

Thyroid surgery

1. Hemi-thyroidectomy/total lobectomy – affected lobe + isthmus removed- Least invasive

surgery BENIGN / SINGLE LOBE disorders of thyroid

2. Subtotal thyroidectomy – both lobes + isthmus removed

Leave behind – rim of tissue (8g) on each side – protect B/L RLN

3. Near total thyroidectomy – both lobes +isthmus removed

Preserved – rim of tissue on 1 side
Aka DUNHILL PROCEDURE

4. Total thyroidectomy – all visible thyroid tissue – SURGERY OF ALL B/L THYROID DISEASES
OR MALIGNANT THYROID

Non surgical

1. Medical management
- Hypothyroidism – Thyroxine
- Hyperthyroidism – Carbimazole/PTU

2. Radio active iodine ablation – I131 → Half life – 8 to 12 days

Hyperthyroidism – graves disease

170
 Recurrence of malignancies/Metastasis > total thyroidectomy

C/I – pregnancy, lactation, graves ophthalmopathy, young age

COMPLICATIONS OF THYROIDECTOMY

1. RLN injury –
- U/L – hoarseness – usually transient
- B/L – stridor
- To prevent –use intra-op nerve monitors
Intra op injury identified– suture the cut ends
If gap is more – suture ends to ansa cervicalis

2. Post OP haemorrhage – Reactionary haemorrhage due to Superior thyroid artery

bleed→ Haematoma→ Tracheal compression → Breathlessness
Shift to OT - ET intubation → Remove sutures – skin/subcutaneous/deep fascia→
Drain hematoma- attain haemostasis

3. Hypoparathyroidism
- Ischemia of parathyroids >> Accidental removal
- Happens when Inferior thyroid artery is ligated away from glands
- Presents 2-5 days post OP – peri-oral tingling/ carpo-pedal spasm – check Calcium
and PTH levels
- Treatment – Mild - supplement with oral calcium
Severe – IV calcium

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PAPILLARY CARCINOMA

-MC THYROID CANCER overall

-Most common in iodine sufficient areas

RISK FACTORS

-Low dose neck radiation

-Thyroglossal duct cyst

PATHOLOGY

- Nuclei are clear – Orphan Annie eyed nuclei

- Dystrophic calcification called as Psammoma bodies
- Psammoma bodies are seen in – P – papillary renal cell cancer
S – serous cystadenoma of ovary
M – meningioma
- Multi-centric – involves both lobes
- LN metastasis– Level VI (DELPHIAN LN)

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TREATMENT

• Total thyroidectomy + level 6 lymph node clearance

• Micropapillary carcinoma is < 1cm – treatment of choice is surveillance – serum
thyroglobulin / USG neck
• Tumor marker for papillary and follicular cancer is serum thyroglobulin

FOLLICULAR CARCINOMA

Risk factors
-MC thyroid cancer in places where there is endemic goitre
-Long standing multi-nodular goitre
Pathology
Solitary thyroid nodule
FNAC – cannot differentiate benign vs malignant

MALIGNANT IF
-Capsular /vascular invasion is seen (image)
- FNAC – thy3- cannot differentiate benign from malignant

SPREAD
Hematogenous metastasis is common to bones→ thoracic vertebrae/skull

Treatment

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 • If solitary nodule →Hemi thyroidectomy (Affected lobe and isthmus removed )→
Intra-op frozen section
• If frozen section shows benign – leave it as hemi thyroidectomy is adequate
• If frozen section shoes malignant – do total thyroidectomy

NOTE: No lymph node clearance is needed

• Hurthle cell variant of follicular Ca – more aggressive

High risk scores for both PAPILLARY AND FOLLICULAR CARCINOMA

• A – age > 40 years

• M – metastasis
• E – extra-thyroid extension
• S – size > 4cm

• Age
• G - Grade
• E – extraintestinal extension
• S – size > 4cm

MEDULLARY CANCER

- Arises from C cells/para-follicular cells→ Calcitonin producing

- Either sporadic (80-90%) / familial is seen in MEN 2 syndromes- 2A and 2B

Clinical features

- Goitre
- Diarrhoea (<30%)

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Diagnosis

• TFT normal, USG will show thyroid mass

• FNAC: Amyloid stroma is present microscopically
• LN metastasis and hematogenous metastasis is common

Treatment
• Total thyroidectomy +level 6 clearance + Ipsilateral/ bilateral MRND
• If medullary thyroid carcinoma is a part of MEN 2A or MEN 2B, do prophylactic
total thyroidectomy (<5 years for MEN 2A, < 1 year for MEN 2B)

ANAPLASTIC

- Most Aggressive malignancy in man

-
- Undifferentiated and seen after the age of 60 years
Pathological
- Locally invasive
- Bizarre/multinucleate cells
Clinical features
• Rapidly growing neck mass
• Diagnosis – woody hard goitre on palpation
• Core biopsy is done to rule out Rieldel’s thyroiditis from anaplastic carcinoma
• Poor prognosis
• Palliative chemotherapy/radiotherapy + tracheostomy

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HASHIMOTOS THYROIDITIS /CHRONIC LYMPHOCYTIC THYROIDITIS

Pathology

- Part of auto immune spectrum of disorders

- Antibodies – Anti TPO(seen in 80%), Anti TG ( 60%)
- These antibodies will go and attack the gland , there will be transient hyperthyroidism
followed by hypothyroidism due to destruction of thyroid

Investigations

• TFT – increased TSH

• Anti TPO, Anti-Tg antibodies
• Histopathology – Lymphocytic infiltration , Hurthle cells (image)

NOTE: INCREASED RISK OFLYMPHOMA AND PAPILLARY THYROID CARCINOMA

Treatment

-Thyroxine supplements

-Surgery (TOTAL THYROIDECTOMY ) is not needed – only when compression features are
present or malignant transformation is present

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PRIMARY HYPER PARATHYROIDISM

ETIOLOGIES

• ADENOMA/HYPERPLASIA:
i. PTH SECRETING ADENOMA: MC cause
ii. MULTI GLANDULAR HYPERPLASIA: In MEN SYNDROME

BIOCHEMICAL CHANGES

PRIMARY HYPER PTH:

a. ↑PTH: ↑ S.CALCIUM (HYPERCALCEMIA)
b. Inc/normal URINARY CALCIUM
c. INC. URINARY EXCRETION OF PHOSPHATE
d. INCREASE IN BONY ALKALINE PHOSPHATASE

CLINICAL FEATURES

- INCIDENTAL (MC)- HYPERCALCEMIA

- If symptomatic:
1. RENAL STONES
2. BONY PAIN – OSTEOPENIA / CYSTS / pathological fractures
3. ABDOMINAL GROANS – PEPTIC ULCER
4. FATIGUE OF MUSCLES
5. PSYCHIATRIC PROBLEMS – MOANS

177
INVESTIGATIONS

• BIOCHEMICAL ANALYSIS:
a. INCREASE IN PTH AND SERUM CALCIUM
b. INCREASE IN ALKALINE PHOSPHATE
c. INCREASE IN URINARY PHOSPHATE
• ADENOMA VS MULTIGLANDULAR DISEASE
a. USG: If all 4 glands enlarged then MG disease, If one enlarged then
Adenoma
b. In case of one gland enlargement, localising study done TO KNOW
WHICH GLAND HAS ADENOMA: SESTAMIBI SCAN – IOC

c. X RAY – RADIAL SIDE OSTEOPENIA/ OSTEOPOROSIS→ 2ND OR 3RD FINGER

– MIDDLE PHALYNX
- BROWN TUMOURS
- BONY CYST

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 d. SESTAMIBI SCAN

i. Goes to actively metabolic tissues in neck

ii. Due to tumour, delayed excretion of sestamibi
iii. At 15 mins : Present in every tissue in neck
iv. At 2 hours : Gone from all the tissues except the affected
(inferior) parathyroids (image)

Treatment:

A. Medical Management – LOW RISK PATIENT

Indication: NO COMPLICATIONS, NO SYMPTOMS

• BISPHOSPHONATES
• TAMOXIFEN/SERM
• CALCIMIMETICS

B.SURGICAL MANAGEMENT:

Indications: Symptomatic/ Osteoporosis /Inc. Urinary loss of Calcium (At Risk )

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1. MINIMALLY INVASIVE PARATHYROIDECTOMY:

- Removal of affected parathyroid containing the adenoma by small neck incision

- To avoid accidental removal of normal parathyroid (leaving behind the adenoma), we do

MIAMI CRITERIA

- MIAMI CRITERIA: Fall of >50 % of Serum PTH levels after 10 mins of removal of PTH gland

- If it doesn’t fall, hunt for adenoma again

2. TOTAL PARATHYROIDECTOMY:

-Done for multi-glandular HYPERPLASIA

- No localisation needed as all 4 glands are removed

- B/L EXPLORATION OF NECK and excise the parathyroids

- Re-implant some pieces of the gland in left brachio-radialis muscle (not in neck because graft
may undergo hyperplasia and it’s easier to remove from forearm instead of neck)

* If patient has recurrence, check PTH levels in brachial vein, compare to that in neck:
CASANOVA TEST

3. 3 and a half PARATHYROIDECTOMY: Done for multi-glandular disease

- 3 glands removed entirely, ½ Gland left behind and 1/2 sent for frozen section to confirm its
PTH gland

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MEN SYNDROME

- MULTIPLE ENDOCRINE NEOPLASIA SYNDROMES

- FAMILIAL, occur at younger age
- Autosomal Dominant
- MORE AGGRESSIVE THAN SPORADIC CANCER

MEN 1 syndrome: Due to mutation in MEN 1 gene coding for MENIN PROTEIN

P: PARATHYROID TUMOURS : M/C : 80 %-90 % : MG HYPERPLASIA

P: PITUITARTY TUMOURS : Non functional or Functional (Functional :Prolactioma : C/F :

Galactorrhoea)

P: PANCREATIC TUMOURS : Non-functional OR Functional : IF FUNCTIONAL THEN

GASTRINOMA(DUODENAL ) >INSULINOMA

MEN 4 syndrome : CYCLIN DEPENDENT KINASE MUTN. : Rest same as MEN 1

For Multi-glandular HYPERPLASIA : TOTAL PARATHYROIDECTOMY +THYMECTOMY

MEN 2 SYNDROME

RET MUTATION :

I) MEDULLARY THYROID CARCINOMA (90-100%)

II) PHEOCHROMOCYTOMA (10-60%)

• SUBTYPES : MEN2A and MEN2B/3

• MEN2A:
- MTC

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 - PHEOCHROMOCYTOMA
- PARATHYROID TUMOUR →MULTIGLANDULAR HYPERPLASIA

• MEN 2B/3 :MARFANOID HABITUS, MUCOSAL NEUROMAS , MEGACOLON

/HIRSCHPRUNG
• IF MEN 2A MUTATION – PROPHYLACTIC TOTAL THYROIDECTOMY – 5 YRS
• IF MEN 2B MUTATION – PROPHYLACTIC TOTAL THYROIDECTOMY –1 YR

ARTERIAL AND VENOUS DISORDERS

PERIPHERAL ARTERIAL OCCLUSIVE DISEASE:

• Arterial narrowing :Chronic occlusion

• Occlusion of any of the arteries except coronary and cerebral artery

ETIOLOGIES

• ATHEROSCLEROSIS (mc)
• BUERGER'S DISEASE/THROMBOANGITIS OBLITERANS: Male, young, SMOKERS
• VASCULITIS
• DRUGS like Ergots for migraine

182
 • RAYNAUD'S DISEASE
SITES OF OCCLUSION

1. ABDOMINAL AORTA
2. COMMON ILIAC
3. EXTERNAL ILIAC
4. SUP. FEMORAL
5. POPLITEAL ART.
6. ANT. TIBIAL
7. POST. TIBIAL NOTE: ACUTE LIMB ISCHAEMIA NOT A PART OF PVD
8. ANT. TIBIAL
9. PERINEAL ART.

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CLINICAL FEATURES

• Occlusion to any of these arteries : Part distal to Occlusion: Ischaemia : Intermittent

claudication
• Intermittent claudication-Pain on exercising muscle
• Gets relieved on rest
• Within 5 minutes of rest: Symptom gets relieved

• AORTO ILIAC BLOCK : B/L GLUTEAL CLAUDICATION, IMPOTENCE →LERICHE’S

SYNDROME
• EXT. ILIAC/UPPER PART OF COMMON ILIAC block: U/L THIGH MUSCLES claudication
• SUP. FEMORAL block: CALF MUSCLES claudication (MC site of LL PVD)
• POPLITEAL /ATA/PTA : claudication in LOWER CALF/FOOT

• Rest pain : Ischaemia of nerves

• Ischaemic ulcers / Arterial ulcers – at tips of toes/shin/above malleoli
• Gangrene : Dry gangrene (Image) : Clear line of demarcation separating viable from non
viable
• Weak/absent peripheral pulsation

184
INVESTIGATIONS

• IOC: ARTERIAL DUPLEX SCAN/ DOPPLER (Image):

1st B MODE is done→ THEN DOPPLER DONE
GIVES DIECTION OF FLOW, ALSO TELLS SITE AND SEVERITY OF OCCLUSION,
COLLATERALS
• ANKLE BRACHIAL PESSURE INDEX (ABPI): SBP IN ANKLE/ SBP IN ARM
• ABPI: NORMAL > 0.9
0.5-0.9: SIGNIFICANT ISCHAEMIA
<0.4: CRITICAL LIMB ISCHAEMIA
• FOR EVERY DROP IN O.1 IN ABPI : 10% INCREASE IN MORTALITY

185
 • ABPI: GIVES PROGNOSTIC INFORMATION

IF ABDOMINAL AORTIC OCCLUSION: NOT SEEN WELL ON DOPPLER

- ANGIOGRAM
1. CT/ MR ANGIOGRAM
2. CONVENTIONAL ANGIOGRAM/digital subtraction angiogram (DSA) : ONLY DONE IF
INTERVENTION IS PLANNED

MANAGEMENT

1. MEDICAL MANAGEMENT
- BLOOD THINNERS : ASPIRIN WITH OR WITHOUT CLOPIDOGREL
- STATINS : ALWAYS GIVEN : EVEN IF LIPID PROFILES NORMAL
- RAYNAUD’S DISEASE : Calcium Channel Blockers : FOR VASOSPASM
- STOP SMOKING

2. CRITICAL LIMB THREATENING ISCHAEMIA:

186
- COMPLICATIONS : GANGRENE , ULCER
- ABPI <0.4: RISK OF LIMB LOSS
HERE REVASCULARISATION IS DONE

- ANGIOPLASTY
I. BALLOON DILATION→STENT (image)
II. OPEN Sx → BYPASS
PREFERRED GRAFT
FOR
LOWER LIMB : GREAT SAPHENOUS VEIN
ABDOMINAL AORTIC: DACRON GRAFT

187
ABDOMINAL AORTIC ANEURYSM

RISK FACTORS

- MC LOCATION : INTRA CRANIAL

- MC EXTRA CRANIAL : INFRA RENAL ABDOMINAL AORTA
- MC PERIPHERAL ANEURYSM : POPLITEAL ARTERY

CLINICAL FEATURES

- USUALLY ASYMPTOMATIC
- ANY SYMPTOM—BAD SIGN → SIGN OF IMPENDING RUPTURE
- LUMP IN ABDOMEN IF VERY THIN PATIENT
- BACK PAIN

INVESTIGATION

- SCREENING/ SURVEILENCE: USG ABDOMEN

- IOC : CECT ABDOMEN

188
TREATMENT

• TREAT IF HIGH CHANCE OF RUPTURE : WHEN DIAMETER IS> 55mm

• Symptomatic aneurysm of any size- repair
• IF DIAMETER > 10 mm / year : TREAT IT
• IF LESS THAN 55 mm : PERIODIC SURVEILLENCE

1. OPEN REPAIR:LAPAROTOMY →GRAFT REPAIR: IN YOUNG PATIENTS

2. ENDO VASCULAR ANEURYSM REPAIR (EVAR): IN ELDERLY/ UNFIT PATIENT

*POPLITEAL ANEURYSM: RISK OF RUPTURE if >20mm → Repair

VARICOSE VEINS

They are dilated > 3mm, elongated, tortuous superficial venous due to reflux of blood.

ETIOLOGY:

- CONGENITAL
- PROLONGED STANDING
- DVT
- OBESTY
- INC. ABD. PRESSURE

PATHOLOGY

- VEINS <1mm: THREAD VEINS/PIN VEINS/SPIDER VEINS/TELANGIECTASIAS

- 1-3mm : RETICULAR VEINS/VARICES
- >3 mm : VARICOSE VEINS

189
COMPLICATIONS

1. EDEMA
2. SKIN CHANGES
- PIGMENTATION: HEMOSIDERIN DEPOSITS
- ECZEMA/DERMATITIS
- LIPODERMASCLEROSIS
- VENOUS ULCER : ABOVE MED. MALLEOLUS : GAITER’S AREA : SHALLOW ULCER
- ATROPHY BLANCHE

ECZEMA

VENOUS ULCER

190
 ATROPHIE BLANCHE

CLINICAL FEATURES AND CEAP

C1 : PRECURSORS : THREAD VEIN / RETICULAR VEINS

C2 : VARICOSE VEIN> 3mm

C3 : EDEMA

C4a: PIGMENTATION/ ECZEMA

C4b: LIPODERMA SCLEROSIS/ATROPHY BLANCHE

C4c:CORONA PHLEBECTICA

C5 : HEALED ULCER

C6 : ACTIVE ULCER

a- ASYMPTOMATIC

s- SYMPTOMATIC

r- RECURRENT

191
E-ETIOLOGY

Ep-PRIMARY

Es- SECONDRY

Ec-CONGENITAL

En- NO CAUSE

A – ANATOMY

As- SUPERFICIAL

Ad-DEEP VEINS

Ap-PERFORATOR VEINS

192
PATHOLOGY

Po-OBSRUCTION

Pr-REFLUX

INVESTIGATION

- TO IDENTIFY SITE OF REFLUX / INCOMPETENCE

1. To localise GREAT SAPHENOUS VEIN:

- SAPHENOUS EYE: Between 2 FASCIAS lies the GSV (Image)

- SAPHENOUS FASCIA ON TOP, DEEP FASCIA BELOW

193
2. To localise SAPHENO FEMORAL JUNCTION→ MICKEY MOUSE SIGN: GSV +Femoral Vein +

Femoral artery

- REFLUX SEEN ON DOPPLER , FLOW OF BLOOD FROM DEEP TO SUPERFICIAL VEIN

- DEMONSTRABLE REFLUX

TREATMENT

1. CONSERVATIVE Mx
- CALF EXERCISES
- LIMB ELEVATION
- COMPRESSION STOCKINGS : ONLY SYMPTOMATIC RELIEF , NO IMPROVEMENT IN THE
SEVERITY OF DISEASE, NO PREVENTIVE ROLE EITHER

194
 STOCKINGS GRADE of compression

I—14-17 mmHg

II- 18-24mmHg

III-25-35mmHg -ULCER

2. SURGICAL MANAGEMENT
- IF SEVERE SYMPTOMS,NOT IMPROVING WTH STOCKINGS
- COSMESS
- COMPLICATIONS : ECZEMA, ULCERATIONS

A. ENDO VENOUS LASER ABLATION

- DONE FOR SAPHENO FEMORAL JUNCTION INCOMPETENCE
- UNDER LOCAL ANESTHESIA : TUMESCENT ANESTHESIA
- A LASER PROBE is passed in the vein under USG guidance
- ABLATE the vein from within

195
B. RADIO FREQUENCY ABLATION- similar to EVLA
C. FOAM SCLEROTHERAPY

-SCLEROSANT: POLIDOCANOL/SODIUM TETRADACYL

- MIXING IT WITH AIR WITH 3 WAY CANNULA (ration 1:4)
- TESSARY TECHNIQUE OF CREATION OF FOAM
-INJECT IN VEIN → CHEMICAL INFLAMMMATION AND FIBROSIS
- ONLY USED FOR A SHORT SEGMENT,USUALLY RETICULAR VEINS OR RECURRENT
VARICOSITIES AFTER TREATMENT

D. OPEN SURGERY
-TRENDELENBURG PROCEDURE
- LIGATE THE TERMINAL TRIBUTARIES OF GSV
- FLUSH LIGATION OF GSV AT SAPHENO-FEMORAL JUNCTION

- PUT A METALLIC PROBE AND STRIP THE GSV

- COULD INJURE THE SAPHENOUS NERVE
- TO PREVENT THIS : DON’T STRIP BELOW THE KNEE

196
 GENERAL SURGERY

ORAL MALIGNANCIES

RISK FACTORS
• RULE OF S
S : SMOKING / TOBACCO/BETEL QUID
S: SPIRITS/ALCOHOL
S: SPICY FOOD
S: SEPSIS / POOR ORAL HYGIENE /HPV
S: SHARP TOOTH / IRRITATING DENTURES :
S: SQUAMOUS CELL CARCINOMA
PRE MALIGNANT LESIONS

LEUKPLAKIA

• White patch
• Can’t be rubbed off
• No pathological character
• BIOPSY : Parakeratosis/Hyperkeratosis

197
ERYTHROPLAKIA

• RED VELVETY PATCH

• CANT BE RUBBED OFF
• CANT BE CHARACTERISED PATHOLOGICALLY
• MORE MALIGNANT
• ALWAYS DO BIOPSY AND DECIDE
• DYSPLASIA VERY FREQUENT

SPECKLED LEUKOERYTHROPLAKIA

• MAXIMUM MALIGNANT POTENTIAL

• ALWAYS EXCISE/ RFA

VERRUCOUS LEUKOPLAKIA

- HIGH MALIGNANT POTENTIAL

TREATMENT

1. LEUKOPLAKIA – BIOPSY – NO DYSPLASIA- OBSERVATION AND SURVEILLENCE

2. ERYTHROPLAKIA- BIOPSY – DYSPLASIA- RADIO FREQUENCY ABLATION
3. SPECKLED LEUKO ERYTHROPLAKIA – RFA/ EXCISION

198
PATHOLOGY

THEORY OF FIELD CANCERISATION

• Oral cavity lining exposed to the same carcinogens → so malignancy can happen
throughout the oral mucosa→ if found at one site , other sites are at risk too :
Synchronous/ Metachronous lesions

SITES

• WORLD WIDE : TONGUE > FLOOR OF MOUTH

• INDIA- GINGIVO-BUCCAL SULCUS / BUCCAL MUCOSA
• Typically Ulcerative tumours,solid or infiltrative tumours

CLINICAL FEATURES

• ULCERO PROLIFERATIVE TUMOUR

• EDGES EVERTED
• LN METS TO CERVICAL NODES (I TO V)
• 1st GOES to level Ia or Ib
• HAEMATOGENOUS METS RARE

INVESTIGATION

• WEDGE BIOPSY → taken from the EDGE – HAS MAXIMUM PROLIFERATION

• STAGING: MRI OF ORAL CAVITY AND NECK >CT SCAN
• DISTANT METS : PET SCAN : Rarely required

TREATMENT

- TOC :SURGERY

199
 - IF ELDERLY / UNFIT FOR SURGERY- RADIOTHERAPY

SCC AT BUCCAL MUCOSA/ TONGUE/ FLOOR OF MOUTH

• WIDE LOCAL EXCISION ( 1 CM MARGIN)

• NECK NODES
A. NO ENLARGED NODES : SENTINEL LYMPH NODE BIOPSY
-IF METS on SLNB: NECK NODE DISSECTION
-IF NO NODAL METS on SLNB: ELECTIVE NODE DISSECTION (Level I TO
Level III removed)

B. IF ENLARGED LN + pre-operatively : MODIFIED RADICAL NECK

DISSECTION
• RECONSTRUCTION : Using FLAPS

I. LOCAL FLAP

- ABBE FLAP (image): LOWER LIP TISSUE used → TURN IT AROUND → FILL UP DEFECT IN UPPER
LIP

200
II. DISTANT FLAP

a) PEDICLED : Pectoralis Major myo-cutaneous flap (PMMC )→ WORK HORSE FLAP OF

HEAD AND NECK RECONSTRUCTION
b) FREE : RADIAL FREE FOREARM FLAP- fascio-cutaneous (RFFF)
FREE FIBULA FLAP- osseomyocutaneous (FFF)

NECK DISSECTIONS

• RADICAL NECK DISSECCTION : (CRILE’S RADICAL NECK DISSECTION): Remove level I to V

nodes + SUBMANDIBULAR GLAND + TAIL OF PAROTID + SCM+ Spinal Accessary Nerve
(SAN) + INT JUGULAR VEIN (IJV)
• MODIFIED RADICAL NECK DISSECTION: Same as radical neck dissection but SCM + SAN +
INT JUGULAR VEIN SPARED
• SELECTIVE NECK DISSSECTION : Less than I to V level of nodes removed
Example: 1. Supra-omohyoid neck dissection: Level I to III are removed
2. Lateral neck dissection: Level II to IV are removed
3. Postero-lateral neck dissection: Level II to V are removed

201
 SALIVARY GLANDS

ANATOMY

CLASSIFICATION

• MAJOR SALIVARY GLAND : ALL ARE PAIRED

i. Parotid
ii. Submandibular
iii. Sublingual
• MINOR SALIVARY GLAND : >800 in number
• MC SALIVARY TUMOUR – PLEOMORPHIC ADENOMA

PLEOMORPHIC ADENOMA

PATHOLOGY

• Benign Tumour
• Glandular and Stromal elements
• Aka MIXED SALIVARY GLAND TUMOUR
• Malignant transformation rarely : Sudden increase in size of tumour-
MALIGNANCY EX PLEOMORPHIC ADENOMA
• MC SITE : Superficial Lobe of parotid

CLINICAL FEATURES of parotid pleomorphic adenoma

• Swelling that lifts ear Lobule, Obliterates RETRO MANDIBULAR GROOVE

• Mobility in antero-posterior direction, but Immobile vertically = CURTAIN’S SIGN
• Variable Consistency
• Usually arises from superficial lobe
• Facial Nerve Involvement is rare unless malignant
• If Involving Deep Lobe : can cause compression of Tonsillar Pillars :Intra Oral
Swelling seen

202
INVESTIGATION

- IMAGING: USG PAROTID : SITE OF SWELLING

MRI : If you’re suspecting malignancy

- Tissue Dx : FNAC -CONFIRMS DIAGNOSIS

- TRUCUT Biopsy is contraindicated because that spills the cells in the tract aand makes
the recurrence high

Pleomorphic adenoma on histopathology

203
TREATMENT

SURGICAL EXCISION

A.SUPERFICIAL PAROTIDECTOMY

-Remove entire superficial lobe and leave deep lobe

-IDENTIFY THE FACIAL NERVE : Seperates the Superficial And Deep lobe (In front of Facial nerve
is the Superfical Lobe)

LANDMARKS

TRAGAL POINTER:Pointing towards facial nerve inferiorly (Facial nerve is below)

POSTERIOR BELLY OF DIGASTRIC: Facial Nerve lies above this

Tympano mastoid suture

Retrograde dissection

Stylo mastoid foramen : Rarely used

HOW TO AVOID ACCIDENTAL INJURY

- Identify the nerve before cutting the gland

204
 - Use Bipolar energy source

B.WIDE LOCAL EXCISION / EXCISION WITH A MARGIN / EXTRA CAPSULAR EXCISION

- Remove the tumour with a little margin

- Ensure Pseudopodia is also removed
- Lesser complications

COMPLICATIONS OF PAROTIDECTOMY

1. NERVE INJURY

- FACIAL NERVE or its BRANCHES ,MC Marginal Mandibular Nerve

- Greater Auricular Nerve : Anesthesia at Shaving area or Ear Pinna

- AURICULOTEMPORAL NERVE : FREY’S SYNDROME

2. SALIVARY FISTULA : Rare

*FREY’S SYNDROME /GUSTATORY SWEATING /AURICULOTEMPORAL SYNDROME

205
 • Secretomotor Nerves come from Auriculotemporal neve : Post Ganglionic
Parasympathetic
• GUSTATORY SWEATING → Abnormal regenertion of parasympatheic fibres of
Auriculo temporal nerve (which unite with sweat fibres of face)
• Dx : MINORS IODINE STARCH TEST (image)
-Paint half of the Face with Iodine and Spray the starch
- Give patient a lemon to suck on: The starch and Iodine will cause
staining
• Rx :
i. ANTI PERSPIRANT
ii. BOTOX INJECTION
iii. TYMPANIC NEURECTOMY(JACOBSON’S PROCEDURE)

*AVOIDED by Extra capsular excision , Sternocleidomastoid flap

206
SUBMANDIBULAR GLAND SIALOLITHIASIS

PATHOLOGY

• Thick secretions in submandibular gland, drainage is antigravity-

highest risk of stones seen
• Calcium Phosphate stone : Radio-opaque : Seen on X RAY

CLINICAL FEATURES

• After every meal : Patient gets a Swelling + Pain : Swelling subsides in

one to two hours : MEAL TIME SYNDROME
• Swelling at ANGLE OF MOUTH / JAW / MANDIBLE
• See /Feel the stone if it is in the inta-oral part of the duct

207
DIAGNOSIS

• ORAL X RAY/ USG/ CECT OF GLAND : Confirms the diagnosis

• DUCTOGRAPHY : Gold standard

TREATMENT

• <4 mm : ENDOSCOPIC REMOVAL WITH DORMIA BASKET

• >4 mm: LITHOTRIPSY or INCISION on duct AND REMOVAL
• Removal of Submaandibular gland not necessary
• Nerves injured in SUBMANDIBULAR Sx : LINGUAL, HYPOGLOSSAL , MARGINAL
MANDIBULAR NERVE

208
ULCERS: Break in continuity of skin/mucous membrane

TYPES OF ULCERS

BASED ON
1. ETIOLGY
2. EDGE

209
ETIOLOGY OF ULCER

1. ISCHAEMIC ULCER : PVD

2. TROPHIC ULCER : NEUROPATHIC
3. VARICOSE VEIN/DVT
4. INFECTION : TB
5. MALIGNANCIES : SCC/ BASAL CELL CA

TROPHIC ULCER/NEUROPATHIC ULCER

Occur due to neuropathy- motor/sensory/autonomic

LOCATION: SOLE/PLANTAR ASPECT OF FOOT

PUNCHED OUT ULCER, SURROUNDING CALLOSITY

WEIGHT BEARING AREAS

Occur due to: 1. CHANGE IN ARCHITECTURE OF FOOT

(MOTOR COMPONENT)

2. LOSS OF SENSATION

3. REDUCED SWEATING

210
DIABETIC FOOT TRIAD

1. NEUROPATHY : SENSORY + MOTOR +AUTONOMIC

2. ISCHAEMIA : MICROANGIOPATHY
3. LOCAL SEPSIS

ISCHAEMIC ULCER

• AT DISTAL TOES / DORSUM OF FOOT

• DEEP ULCERS
• NAILS APPEAR WEAK /BRITTLE
• HAIR IS PARSE
• SURROUNDING AREA SHOWS
FEATURES OF ISCHAEMIA :
GANGRENE / ISCHAEMIA AT EDGE
OF ULCER
• H/O SMOKING , INTERMITTENT
CLAUDICATION
VENOUS ULCER

• ABOVE MEDIAL MALLEOLUS /

GAITER’S AREA
• SHALLOW ULCER
• ASSOCIATED WITH OTHER
FEATURES OF VARICOSE VEIN :
PIGMENTATION/ DERMATITIS

211
PRESSURE SORE / BED SORE / DECUBITUS ULCER / PRESSURE INJURY

PATHOLOGY

• Seen in areas of sustained pressure : Ischaemia : Reduction of nutrition in that area →

ULCERATION
• Bed ridden patients : Hemiplegia/ Paraplegia

LOCATIONS

ISCHIUM > GREATER TROCHANTER > SACRUM / AREA OVERLYING SACRUM

PREVENTION

• FREQUENT CHANGE IN POSITION : 2 HOURLY

• AIR BEDS / AIR MATTRESS / WATER BEDS USEFUL

STAGES

I: NON BLANCHING ERYTHEMA WITH INTACT SKIN

II : PARTIAL THICKNESS SKIN LOSS ( SOME SKIN INTACT )

212
 III : FULL THICKNESS SKIN LOSS ( SUBCUT. FAT SEEN)

IV : SUBCUT. LOSS ( DEEP FASCIA/MUSCLES / BONES/ TENDONS SEEN )

MANAGEMENT

• OFF LOADING : AIR MATTRESS / WATER BED

• COVER THE PRESSURE SORE : FASCIA LATA FLAP / NEGATIVE PRESSURE WOUND
THERAPY ( VAC DRESSING )

GANGRENE

• CELL DEATH : VISIBLE / MACROSCOPIC

• WITH SUPERADDED PUTREFACTION

213
TYPES

• DRY GANGRENE : CHRONIC ISCHAEMIA

• WET GANGRENE : ACUTE ISCHAEMIA WITH OR WITHOUT INFECTION

DRY GANGRENE

• DRY AND SHRIVILLED LOOKING GANGRENOUS PART

• LINE OF DEMARCATION + : SEPERATES VIABLE FROM NON VIABLE PART

214
WET GANGRENE

• SWOLLEN
• EDEMATOUS
• FOUL SMELLING DISCHARGE
• ASSOCIATED INFECTION

NECROTOSING FASCITIS / SYNERGISTIC GANGRENE

-INFLAMMATION OF SUB CUTANEOUS TISSUE + FASCIA BY DANGEROUS ORGANISMS

- CAN LEAD TO SYNERGESTIC GANGRENE – SEEN IN POOR IMMUNITY

- TRIVIAL TRAUMA TO ABDOMEN/LOWER LIMB

- FROM site of BREACH , COMMENSALS ENTER THE SUBCUT. PLANE

- CAUSES FLORID/ FULMINANT INFECTIOUS GANGRENE
- OBLITERATIVE END ARTERITIS: SKIN + SUBCUT. +DEEP FASCIA (FASCITIS )+ MUSCLES
(MYOSITIS)

TYPES

1. FOURNIER’S GANGRENE → SCROTUM

2. MELENEY’S GANGRENE ON ABDOMEN
215
 CLINICAL FEATURES

- SICK patient (SEPTICEMIA)

- WOUND with discharge with features of gangrene

TREATMENT

• RADIACAL WIDE DEBRIDEMENT : Repeat every 24-48 hours

• Give IV ANTIBIOTICS + IV FLUIDS
• Some benefit of HYPERBARIC O2 THERAPY

TOTAL PARENTERAL NUTRITION

- Provision of NUTRITIONAL REQUIRMENT DIRECTLY INTO A VEIN, BYPASSING GIT

INDICATION

1. PROLONGED NIL BY MOUTH > 5 days

2. GIT UNAVAILIBILITY→ FOLLOWING MASSIVE BOWEL RESECTION ( SHORT BOWEL
SYNDROME )/ GIT DISEASED / PROLONGED PARALYTIC ILEUS

216
CENTRAL VENOUS CATHETER for providing TPN

• IJV : MC USED
• SUBCLAVIAN – BEST
• KEPT FOR 5-7 DAYS
• TIP OF CATHETER AT
LOWER 3rd OF SVC /
CAVO ATRIAL
JUNCTION

TRIPLE LUMEN CANNULA→ CENTRAL

VEIN for TPN

217
 TPN BAG

- 1-2 L of fluid
- Contents: DEXTROSE+ AMINO
ACIDS + LIPIDS (SCFA/MCFA)
- 1000-2000 CALORIES
- VITAMINS / MINERALS
- NO FIBRES

COMPLICATIONS OF TPN

1.TUBE / LINE RELATED

-MC : CATHETER LINE SEPSIS

2. TECHNIQUE

- MC : PNEUMOTHORAX

- AIR EMBOLISM

3. FEEDS

- DEFICIENCIES : VITAMINS/ ELECTROLYTES

- EXCESS : FLUID OVER LOAD / HYPER GLYCEMIA / LIPIDEMIA / HYPER AMINO ACIDEMIA

- TPN INDUCED CHOLESTASIS : TO AVOID THIS, FAT FREE TPN could be used

4. RE FEEDING SYNDROME: If patient is CHRONICALLY STARVED → And SUDDEN CALORIES

given (TPN > ENTERIC )→ UPREGULATION OF biochemical CYCLES → UTILISATION OF

218
PHOSPHATE TO PRODUCE ATP → HYPOPHOSPHATEMIA , ALSO LOW Mg, K , Ca → CNS AND CVS
complications → DEATH

TO AVOID THIS, GRADUAL introduction of feeds should be done in chronically starved patients

INTESTINAL ATRESIA

- MC : DUODENAL > JEJUNAL > ILEAL

CLINICAL FEATURES

• Neonatal Intestinal Obstruction

• Bilious Vomitting at birth

D/D

- Meconium ileus
- Midgut Volvulus
- Hirschprung disease

1st stabilise → X RAY ABDOMEN OF CHILD

TYPES

• TYPE I : WEB LIKE ATRESIA

• TYPE II : MISSING SEGMENT,CORD LIKE ATRESIA
• TYPE III : MESENTERIC DEFECTS (APPLE PEEL APPEARANCE)
• TYPE IV : MULTIPLE ATRESIA : STRING OF SAUSAGES

219
 TYPE III : APPLE PEEL

TYPE IV : SAUSAGE
LIKE/MULTIPLE DEFECTS

INVESTIGATION

1. : XRAY ABD : Tells level of obstruction

220
 DUODENAL ATRESIA : DOUBLE BUBBLE APP.

A/W DOWNS SYND. AND ANNULAR

PANCREAS

Sx-DUODENODUODENOSTOMY

JEJUNAL ATRESIA : TRIPLE BUBBLE APP.

Sx- RESECTION AND ANASTOMOSIS

2. CECT ABDOMEN : CONFIRMS THE Dx

TREATMENT : RESECTION AND ANAASTOMOSIS

221
ABDOMINAL WALL DEFECTs

GASTROSCHISIS

GASTROSCHISIS

• RIGHT PARA UMBLICAL DEFECT

• UNCOVERED INTESTINE PROTRUDING
• NO PERITONEUM COVERING
• IN YOUNG MOTHERS/teenage pregnancies
• ISOLATED DISEASE, other abnormalities are rare
• Management: IF SMALL DEFECT : REDUCE CONTENT : CLOSE DEFECT
• LARGE DEFECT : COVER INTESTINE WITH A SILO,AS EDEMA DECREASES, PLAN A
RECONSTRUCTION LATER

222
 OMPHALOCELE

EXOMPHALUS/ OMPHALOCELE

• UMBILICAL DEFECT (Like an UMBILICAL HERNIA)

• INTESTINAL PROTRUSION : COVERED BY 3 LAYERS : PERITONEUM, WHARTONS
JELLY , AMNION
• ASSOCIATED ABNORMMALITIES : CVS > MUSCULOSKELETAL
• Rx : UNDER ANESTHESIA : REPOSIT CONTENT : CLOSE DEFECT

• IF DEFECT >5 CM OR LIVER PROTRUDING : EXOMPHOLUS MAJOR

- STAGED OR PLANNED RECONSTRUCTION

- WAIT → GRANULATION TISSUE TO DEPOSIT →SCAR WILL FORM → BEHAVE LIKE
HERNIA → HERNIA REPAIR (LATER )
- MANAGE ASSOCIATED DEFECTS

223
CONGENITAL DIAPHRAGMATIC HERNIA

TYPES

• RIGHT ANTERIOR DEFECT : MORGAGNI HERNIA

• LEFT POSTERIOR DEFECT : BOCHDALEK HERNIA : M/C TYPE OF CONGENITAL
DIAPHRAGMATIC HERNIA

224
CLINICAL FEATURES

• SCAPHOID ABDOMEN
• HYPOXIA DUE OF PULMONARY HYPOPLASIA
• AUSCULTATION : GURGLING SOUNDS IN CHEST (DUE TO HERNIATED BOWEL)

INVESTIGATION

• NG TUBE TIP SEEN IN CHEST ON XRAY (IMAGE)

• CT THORAX +ABDOMEN

MANAGEMENT

• INITIALLY : ET INTUBATION+MECH. VENTILATION

• AVOID BAG AND MASK VENTILATION

• DELAYED SURGERY : TIMING OF REPAIR : AFTER 24 OR 48 HOURS : AFTER CHILD

IS STABLE

225
 • Sx: LAPAROTOMY/THORACOTOMY WITH REDUCTION OF CONTENTS, AND
CLOSURE OF DIAPHRAGMATIC DEFECT

HERNIA

TYPES

CONGENITAL INGUINAL (PATENT PROCESSUS VAGINALIS) OR UMBILICAL

PRESENTATION OF CONGENITAL INGUINAL HERNIA

• AT BIRTH OR WITHIN FIRST FEW YEARS OF LIFE DEPENDING ON THE SIZE OF THE
HERNIA
• INGUINO SCROTAL SWELLING
• REDUCED ON LYING DOWN
• MORE PROMINENT WHEN CHILD CRIES
• PALPABLE SPERMATIC CORD THICKENING MAY BE THE ONLY FINDING IN SOME CASES

DIAGNOSIS

• USG GROIN

TREATMENT

• HERNIOTOMY PROMPTLY /ELECTIVE REPAIR

CONGENITAL UMBILICAL HERNIA

• OCCURS DUE TO PATENT UMBILICAL TUBE

• SMALL DEFECT : WAIT AND WATCH
• DEFECT CAN SPONTANEOUSLY CLOSURE UPTO THE AGE OF 4 YEARS

• IF DOESN’T RESOLVE UPTO 4 YEARS , SURGICAL REPAIR : PREVIOUSLY K/A MASSTERLY

INACTIVITY

226
 • IF LARGE → ELECTIVE HERNIA REPAIR

ORGAN TRANSPLANT

GRAFTS

TYPES OF GRAFTS

• ALLOGRAFT
-Graft from same species , best person to receive it from is an identical twin
• XENOGRAFT
-Graft from other species
• ORTHOTOPIC GRAFT : LIVER/ HEART /LUNG TRANPLANTS
- Implanted in the normal anatomical site
• HETEROTOPIC GRAFT:KIDNEY TRANSPLANT , PANCREATIC TRANSPLANT
-Placed at alternative site

TYPES OF DONORS

- LIVING DONOR
- Ideal
- Renal transplant , Lobe of the liver (Pediatric liver transplant)

- DBD- DECEASED BRAIN DEAD

- After brain stem death
- After severe head injuries, massive intracranial hemorrhages

227
 - BRAIN STEM DEATH CRITERIA
• CIRCULATION WORKING
• RESPIRATION NOT WORKING
• NO CRANIEAL NERVE REFLEXES SEEN
• NO MOTOR RESPONSE
• POSITIVE APNEA TEST

- DCD : DECEASED CARDIAC DEATH

MAASTRICHT CLASSIFICATION

TYPE III, TYPE IV → CONTROLLED

NOTE : BEST DONOR : LIVING DONOR > DBD >DCD

ORGAN HARVEST AND PRESERVATION

• UNDER ANESTHESIA THORACOTOMY +LAPROTOMY IN OT AFTER CONSNT FROM

FAMILY MEMBERS
• START RESECTING ORGANS FOR HARVEST
• FLUSHED WITH CHEMICALS (PLEGIC SOLUTIONS): WARM ISCHAEMIA STOPS→ ORGANS
ENTER LOW METABOLIC STATE (COLD ISCHEMIA STARTS)

SOLUTIONS:
- UNIVERSITY OF WISCONSIN OR EURO COLLIN SOLUTIONS
- RICH IN K+ AND LOW IN NA +
- CONTAIN HIGH MOLECULAR WEIGHT : MANNITOL
- CONTAIN BUFFERS : BICARBONATE AND PHOSPHATE
- SLOW DOWN THE DECAY OF DONOR ORGAN AND METABOLIC PROCESS

228
 - STARTS COLD ISCHAEMIA TIME
COLD ISCHAEMIA TIME
• KIDNEY : LONGEST : 15 -18 HRS
• HEART/BOWEL/LUNGS : SHORTEST : 3-5 HRS

WARM ISCHAEMIA TIME

• Should be kept as low as possible

• Stop it by pledgic solution
• Longer the warm ischemia time, poorer is
graft survival

GRAFT REJECTIONS AND HLA

• ABO :Blood group antigens : Present on all cells

• HLA : Human leucocyte antigens
- Unique to every individual
- Except identical twins :They have the same HLA
- Coded from MHC on Chromosome 6
- HLA CLASS I : A, B,C : ALL NUCLEATED CELLS
- HLA CLASS II: DP/ DQ/DR
- We match HLA A , HLA B , HLA DR (MOST IMP )
- IF MISMATCH→ CELL MEDIATED REJECTION

TYPES OF REJECTIONS

• HYPERACUTE REJECTION:
- Due to PREFORMED ANTI BODIES like ABO MISMATCH
- Manifests within few minutes of transplant→ Intraoperative diagnosis ,
irreversible
NOTE: LIVER IS RESISTANT TO HYPERACUTE REJECTION

229
 • ACUTE REJECTION
- Manifests within 3-6 months
- Cell mediated response, due to HLA mismatch
- HPE :Lymphocytic destructions and infiltrates
- All organs susceptible
- Controlled by immunosuppression

• CHRONIC REJECTION
- Manifests after 6 months
- Risk factors: h/o acute rejection, EBV INFECTION, Long ischaemia type,
dyslipidemia
- Liver resistant to it
- HPE : Myointimal fibrosis
- MC TYPE OF REJECTION
- Most difficult to treat
- MC reason for graft failure

IMMUNOSUPPRESSION

To avoid acute or chronic rejections

- INDUCTION PHASE : STEROIDS +ANTI CD25

- MAINTAINANCE PHASE
1. CALCINEURIN INHIBITORS : CYCLOSPORIN , TACROLIMUS : IL 2 PATHWAY OF T
LYMPHOCYTES
2. mTOR INHIBITORS : SIROLIMUS /EVEROLIMUS
3. ANTI PROLIFERATIVE DRUGS : AZATHIOPRINE

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 COMPLICATIONS of immunosuppression
1. Increased risk of infection
- CMV Infection : PNEUMONITIS / ENCEPHALITIS
- PNEUMOCYSTITIS JIROVECI

2. CANCER due to immunosuppression: Squamous cell carcinoma

Post-transplant Lympho-proliferative Disorders (PTLD)

RENAL TRANSPLANT

- LIVING DONOR TRANSPLANT or DBD/DCD

INDICATIONS

End stage renal disease due to

- CHR. GLOMERULONEPHRITIS
- DIABETIC NEPHROPATHY

TECHNIQUE

- HETEROTOPIC→ NEW KIDNEY PLACED IN THE RIGHTT/LEFT ILIAC FOSSA IN RETRO

PERITONEUM

- NATIVE KIDNEYS USUALLY INTACT

EXCEPTIONS
i. RENAL SEPSIS
ii. VERY LARGE KIDNEYS (PCKD )

- USG ABDOMEN : 3 KIDNEYS

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- ANASTOMOSIS
A. LIVING DONOR TRANSPLANT
-RENAL ARTERY TO INTERNAL ILIAC ARTERY OF RECIPIENT
- RENAL VEIN TO EXT. ILIAC VEN/ INT. ILIAC VEIN OF RECIPIENT
- URETER IMPLANTED DIRECTLY INTO BLADDER : SUB MUCOSAL TUNNEL

B. FROM DECEASED DONOR

- CHIP/ RIM OF ABDOMINAL AORTA ALONG WITH RENAL ARTERY : CARREL’S PATCH
- THIS PERMITS END TO SIDE ANASTOMOSIS OF RENAL ATERY TO EXT. ILIAC ARTERY OF
RECIPIENT

C. PEDIATRIC
- NEW KIDNEY PLACED IN THE PELVIS.

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