Monday, May 30, 2011

CASE: Choledochal cyst type 1

12 yrs girl with h/o cholangitis 15 days back
worked up and detected to have type one choledochal cyst.

CECT:


SURGERY: CDC excision and HJ



Pt discharged on POD 6.

Wednesday, May 25, 2011

CASE: Ca Cecum with lower GI massive bleeding + GSD + LT indirect huge inguinal hernia + CA urinary bladder

57 yr male with H/O two episodes of TIA 7 Days back started on asprin. Admited under PHYSICIAN
c/o GI bleeding in the form of melena...Hb dropped to 8 from 14 in 4 days
subjected to scopy: BY GI PHYSICIAN
mass in cecum with active bleeding..
RADIOLOGIST: CECT: Detected CA CECUM, CA  BLADDER, GSD + Left Inguinal huge hernia..







CARDIOLOGIST: 2D ECHO: S/O 36 % EF

ANESTHETIST: Epidural anesthesia.

G I SURGEON: Rt hemicolectomy, cholecystectomy, preperitoneal mesh plasty.



URO SURGEON: TURBT

Discharged on POD 6... fortunately both T 1 malignancy....pt cured.....

 TEAM EFFORT.......made him go home in time .....

Saturday, May 21, 2011

CASE: CDC with ca in situ.

22 yrs male with lower CBD narrowing leading to cholangitis diagnosed in 2001
stented...bx and cytology negative..

insitu stent for 10 yrs now presented with cholangitis with stone and dilated CBD
stent, stone removed...and re stented..and Rx conservatively...

after 2 months two stents placed to dilate the lower Stricture..no e/o malignancy..
ON CECT was looking like CHOLEDOCHAL CYST ?

SURGERY: Plan: side to side bilio enteric roux en y anastomosis..
Intra op: was looking more of CDC TYPE 1  with smooth lower end tapering and dilated fusiform mid CBD..OF AROUND 3 CM..

PLAN changed and decided to remove CDC (as there are around 20% chance of development of malignancy )....AND Hepatico jejunostomy...was done....after total Excision of CDC..

Pt discharged on pod 6.

HISTOLOGY: CARCINOMA IN SITU IN CHOLEDOCHAL CYST...NO E/O INVASION...L.N. NEGATIVE....





CASE: Gall stone + CBD Stones with lower CBD Stricture

56 yr male with cholangitis
lower end bening long stricture with multiple CBD stones...ERC failed.

Open surgery and drainage: with bilioenteric anastomosis..



post operatively pt recovery was smooth and was discharged in due time..

CASE: BBS TYPE 2 ? PHB status PSRS 2008 & Open Chole in 1995

35 yrs female with h/o high spiking fever
In toxic cholangitis...
TLC : . 35K
with p/h/o open ccx in 1995 and massive bleeding at that time in Udaypur..
asymptomatic for 6-7 yrs
developed splenomegaly...and varices...and episode of cholangitis...
Diagnosed as PHB (Portal hypertensive biliopathy-  due to EHPVO) Stented and PSRS Done in SIR GANGARAM HOSPITAL IN 2007.

later stent removed,

Again developed cholangitis 2- 3 episodes before this episode..
taken up for ERCP and with great difficulty GE physician could enter CBD Beyond stricture...and place 5 fr stent..which was draining pus

DIAGNOSIS: Portal hypertensive biliopathy ? Benign biliary stricture type 2. ( ischemic stricture following Open chole- bleeding...) status PSRS status Open cholecystectomy with cholangitis

ACTION: Stenting and relief from cholangitis...nutritional build up...
SURGERY: Open hepatico jejunostomy...



pt was discharged on POD 6. Following surgery.


Tuesday, May 3, 2011

PORTAL BILIOPATHY


Bile duct obstruction due to portal biliopathy in extrahepatic portal hypertension: surgical management.

Gastrointest Endosc. 1999 Nov;50(5):646-52.


Department of Gastrointestinal Surgery, Govind Ballabh Pant Hospital, New Delhi, India.

BACKGROUND:
Varices can develop in and around the bile duct in the presence of portal hypertension, especially when it is caused by extrahepatic portal vein thrombosis. The term 'portal biliopathy' is used to describe changes in the bile duct due to these varices, which may cause bile duct obstruction. This paper reviews experience of the surgical management of patients with symptomatic portal biliopathy.
METHODS:
Nine patients with extrahepatic portal vein obstruction with symptomatic portal biliopathy. were reviewed retrospectively.
RESULTS:
Eight patients presented with jaundice, two had abdominal pain and one had recurrent cholangitis. Endoscopic retrograde cholangiography revealed abnormality of the bile duct wall, with stricture in eight patients and bile duct calculi in two. Portasystemic shunting relieved jaundice in five of seven patients, and in two a second-stage hepaticojejunostomy was required. 
Conclusion: Symptomatic biliary obstruction in patients with extrahepatic portal hypertension may be relieved by a portasystemic shunt. Rarely biliary bypass may be required and is rendered safer by previous portasystemic shunting to decompress the pericholedochal varices. A direct approach to the biliary tract without a preliminary shunt may be hazardous and is frequently unnecessary.


Biliary changes in extrahepatic portal venous obstruction: compression by collaterals or ischemic? - - - called as PORTAL HYPERTENSIVE BILIOPATHY



Department of Hepatology, Postgraduate Institute of Medical Education & Research, Government Medical College, Chandigarh, India.

Gastrointest Endosc. 1999 Nov;50(5):646-52.

Abstract
BACKGROUND:
The postulated mechanisms of biliary abnormalities in extrahepatic portal venous obstruction (EHPVO) are either extrinsic compression by collaterals or ischemic injury due to venous thrombosis. If the former hypothesis is correct, then biliary changes should revert to normal after portasystemic shunt surgery.
METHODS:
Five patients with EHPVO who underwent portasystemic shunt surgery were studied. One of these patients had obstructive jaundice due to portal cavernoma. Endoscopic retrograde cholangiography (ERC) was performed before as well as after the shunt surgery. Doppler ultrasound and splenoportovenography were obtained to confirm the diagnosis of EHPVO as well as shunt patency.
RESULTS:
All patients had biliary abnormalities on pre-shunt ERC. The post-shunt ERC showed partial reversal of biliary abnormalities in 3 patients, complete reversal in 1 patient, and no reversal in 1 patient. Smooth strictures opened after shunt surgery and proximal dilatation disappeared in most patients. The indentations and caliber irregularities disappeared after shunt surgery, whereas angulations and ectasias of biliary ducts persisted.
CONCLUSION:
Shunt surgery results in regression of some of the biliary abnormalities and relieves biliary obstruction, suggesting that mechanical compression by collaterals is the mechanism behind biliary abnormalities in EHPVO. However, some biliary changes persist after shunt surgery signifying fixed obstruction due to ischemia or fibrous scarring. Thus, the two theories are not mutually exclusive.