5th Year Surgery Final Answers

1. Complications of cholelithiasis. The effects and complications of gallstones.

Clinical forms obstructive jaundice. Mirizzys syndrome.
The effects and complications of gallstones.
(i)
-

In the gallbladder:
Silent stones
Chronic cholecystitis
Acute cholecystitis
Mucocele/Hydrops of the gallbladder

(ii)
In the bile ducts:
- Obstructive jaundice
- Acute cholangitis
(iii)
In the pancreas and the intestine:
- Acute pancreatitis
- Acute intestinal obstruction
Clinical forms of obstructive jaundice.
5 Clinical Forms:
1. Icteric-pain form Most often clinical form. Characterized by pain, fever,
vomiting and jaundice. Pain appears suddenly in right hypochondriac region and
irradiates to shoulder. Usually it is a very severe colicky-type pain, especially if
the stone is localized in papilla of Vater. The fever in this clinical form isnt so
long and disappears when pain resolves. Jaundice is the most constant sign. It
appears 12-24 hours from the beginning of the attack. Its development is slow. In
cases of floating bile stones, the jaundice becomes intermittent.
2. Icteric-pancreatic form This clinical form is met in cases of impactive stones in
papilla of Vater. The main signs jaundice and acute pancreatitis. The biliopancreatic reflux and pancreatic juice congestion lead to acute pancreatitis.
3. Icteric-cholecystical form This clinical form is characterized by acute
cholecystitis and obstructive jaundice combination. The signs of acute
cholecystitis are prevalent. Sometimes this cholecystitis has enzyme genesis due
to presence of pancreato-gallbladder reflux in cases of papilla of Vater
obstruction.
4. Icteric-painless form This clinical form is characterized by pain syndrome
absence, that is meeting with malignant jaundice as well. The jaundice appears
alowly, on background of satisfactory general patient condition. Sometimes
accompanied by mild to moderate fever. The frequency of this form is about 4.15.9% only, but it a more difficult form for differential diagnosis.

5. Icteric-septic form Quick development of suppurative cholangitis is the basis of

this clinical form. It is the most severe of all forms and carries a mortality rate of
about 37.8%. It can lead to sepsis. The severe development of this disease is in
consequence of suppurative bile break into blood flow. First clinical picture of
this form was described by Charcot in 1877 as 3 main signs (pain in right
hypochondrial region, fever till 38-39 degrees Celsius with shaking chills,
jaundice). This clinical form can lead to bacterial shock, acute liver and kidney
insufficiency.
Mirizzys syndrome.
- The stone ulcerating through into the common duct. (Bailey and Loves)

This is the complication of bile stones disease, which is characterized by

presence of bilio-bile fistula between the gallbladder and the common bile
duct due to decubitus of their walls.
There are no specific clinical signs of this complication. Usually it
manifests by obstructive jaundice due to very large stone.
Pre-operative diagnosis can be established by direct methods of contrast
examination of bile system only. We suspect this disease if a large stone is
found in the bile tree by US.
Surgical correction includes some types of the CBD plastics. Sometimes
the fistula can be formed between the GB and the duodenum or the
intestinum. So it is possible that the stone migrates into the bowel with its
obstruction Bouvere disease. Correction by surgical mode only.

2. Diagnostic-treatment algorithm of in a case of acute cholecystitis.

Ultrasound: (To define changes in GB wall, its content, and surrounding tissues)
There are 4 forms:
(i)
Acute cholecystitis without wall destruction (indication for conservative
therapy).
(ii)
Acute destructive cholecystitis without extra-GB complications (indication for
non-invasive surgery, laparoscopic treatment).
(iii)
Acute destructive cholecystitis accompanied with local complications
abscesses, infiltrative masses. (same treatment as (ii))
(iv)
Acute destructive cholecystitis accompanied with general complications,
peritonitis. (Absolute indication for urgent traditional surgical procedures).

To add to the traditional conservative therapy, there are some methods of invasive
sonography which are:
Transhepatic punctural lavage of the GB or
Transskinal transhepatic microcholecystostomia.

1. Invasive sonography
2. Nasogastral aspiration and intravenous fluid therapy
3. Analgesics
4. Antibiotics
5. Subsequent management - most often cholecystectomy has been performed during 2-3
days after the acute attack has resolved.

Harrisons:
It should be noted that acute symptoms will resolve in 70% of patients.
No oral intake!
Nasogastric suction, IV fluids and electrolytes, analgesics (meperidine, NSAIDS),
antibiotics (ureidopenicillins, ampicillin sulbactam, 3rd generation cephalosporins,
and anaerobic coverage (if suspicion of presence of gangrenous or
emphysematous cholecystitis) should be added.
Consider combination with aminoglycosides in DM patient or others with signs of
Gram-negative sepsis.
Time of surgery depends on patient stabilization and should be performed as soon
as feasible.
Farquharsons:
In view of calculous-acute cholecystitis (which is less dangerous than acalculous
cholecystitis. Acalculous variety is rapidly progressive, leading often to gangrene
of GB wall. Early surgery indicated!), the management is initially conservative in
anticipation of ~70% patients the condition will settle later allowing elective
cholecystectomy.
Early confirmation of diagnosis by US scan or by IV cholangiography (provided
liver function is okay) should be undertaken in the 1st 24 hours.
Improvement of patients condition will allow reintroduction of oral intake at 48
hours, discontinuation of antibiotics at 7 days, discharge from hospital at 7-10
days and appointment for elective cholecystectomy in 8-12 weeks time.
Indications to abandon conservative regime include:
1. Failure to improve after 48 hours therapy.
2. Development of a tender enlarging mass in the right hypochondrium.
3. Development of rigors.
4. Features of general peritonitis (uncommon).
Early surgery policy, with proviso that it is undertaken by a surgeon with
considerable experience in surgery of biliary tract.
Cholecystectomy with per-operative cholangiography is the procedure of choice.
Cholecystostomy is indicated in difficult patients ( if initial policy has failed ie.)
and indicated if surgeon is inexperienced.

According to Bailey and Loves:

The standard conservative regime applies.
Ultrasonography is performed to ensure no local complications have occurred,
normal bile duct size and no stones.
Conservative treatment is abandoned if the pain and tenderness increase, in this
case, a percutaneous cholecystectomy performed by the radiologist under US
control will rapidly relieve symptoms.
Subsequent cholecystectomy required.
Conclusion: Basically, you resolve the inflammation to cut out the GB later on.
Always conservative first, followed by surgery, providing there are No complications.
Key words: Conservative, cholecystectomy.

3. Treatment of acute cholecystitis, using modern minimal-invasive technologies.

1. Laparoscopic cholecystectomy (Bailey and Loves)
Anesthetized patient is placed on operating table and a pneumoperitoneum is
created.
4 ports are placed in abdomen (usually at umbilicus and epigastrium) with two
5-mm ports laterally.
The triangle of Calot is laid widely open by dividing the peritoneum on the
posterior and on the anterior aspect.
The cystic duct is carefully defined, as is the cystic artery, which is divided.
Once triangle of Calot has been laid widely open, the cystic duct and cystic artery
is clipped and divided.
The GB is then removed from its bed and once free, removed from the umbilicus.
Advantages:
- Rapid speed of recovery. 80% patients discharged within 24 hours.
- Lesser cosmetic defects.
2. Minicholecystectomy
Performed through a 5 cm transverse incision at subcostal region using special
instruments and a stabilized ring retractor for exposure.
Advantages:
- Small incision enables rapid recovery.
In case of gall stones:
1. Ultrasonic shock wave lithotripsy (USWL) or (ESWL)

Extracorporeal shock-wave lithotripsy (ESWL) disrupts/shatters gallstones and

allows debris to pass into bile ducts and beyond.
Suitable only if there are 1-3 gallstones in functioning GB.

2. Percutaneous cholecystolithotomy
A puncture is made in the GB under US control.
The track is dilated and a tube is inserted. I dont know the name of the tube.
A nephroscope is passed into the GB and the stones are removed.
This procedure is suitable for:
(i)
Those who had a percutaneous cholecystectomy.
(ii)
Those who are unsuitable for cholecystectomy due to stenosis/sclerosis?
(iii)
Those who wish to retain their GB. Or would u rather have it in a jar by your
bed at night? *happy grin* Do Gallbladder ghosts exist?

4. Acute cholangitis etiological condition, clinical features, diagnosis. Step-by-step

treatment.
Etiological condition.
Cholangitis means a state of inflammation of the bile ducts but the main site of
infection are the radicles of the biliary tree within the liver.
Causes As a result of obstruction of the common bile duct by a gallstone or
stricture or in mucoviscidosis. Also in suppurative cholangitis, like pyelophlebitis
may be followed by formation of multiple liver abscesses.
Stasis or obstruction of bile in the CBD is due to following causes:
Pancreatic cancer
Cholangiocarcinoma
Porta hepatis tumors or metastasis
Strictures or stenosis
Endoscopic manipulation of CBD IBD (inflammatory bowel disease)
Choledochocele
Sclerosing cholangitis (from biliary sclerosis)
Ascaris lumbricoides infection.
Congestion of bile bacterial infection of bile tree (directly from the gut,
lymphatics or vascular supply)
Most common bacterias: E.coli, Klebsiella, Enterobacter, Enterococcus,
Streptococcus.

Clinical features.
1. Pay attention to Charcots triad! (fever, jaundice and RUQ pain).

2. Fever, chills, rigors.

3. Acholic or hypocholic stools.
4. Mild hepatomegaly, jaundice.
5. Change of mental status.
6. Pruritis
7. Sepsis
8. Hypotension
9. Tachycardia
10. In severe cases of hypotension septic shock and peritonitis. But unusual.
Diagnosis.
1. Laboratory studies:
- Blood picture: Leukocytosis with left shift or leucopenia if patient is septic.
- Blood culture: May show polymicrobial infection.
- Urine analysis usually normal
- Biochemical evaluation: Elevation in serum bilirubin, alkaline phosphatase,
aminotransferases. Amylase elevated in 15% cases.

- Imaging studies:
Diagnosis usually made by cholangiography either pre-operatively by endoscopic
retrograde cholangiopancreatography (ERCP) or intraoperatively at the time of
cholecystectomy.
Ultrasonography may reveal dilated bile ducts but is not sensitive for detecting
common duct stones.
Percutaneous cholangiography images.
CT scan.
Step-by-step treatment.
Cholangitis is treated like acute cholecystitis: no oral intake, hydration and analgesia
are the mainstays. Stones removed surgically or endoscopically.

1.
2.
3.
4.
5.
6.

Degree of urgency of treatment depends on severity.

Important points are:
(i)
Resuscitation.
(ii)
Diagnosis.
(iii)
Treatment.
Assessment of ABCs: Make access to IV, Oxygen, ECG monitoring, Send labs
when IV is placed.
In hypotensive patients, admin of volume resuscitation.
Nasogastric tube may be helpful for patients who are vomiting. (Nil per os)
Endoscopic decompression of bile tree.
Antibiotics.
Medical therapy , consider elective surgery in patients who show improvement.

7. Patients with deterioration do ERCP and sphincterotomy or percuatneous

drainage.
Laparoscopic cholecystectomy and ERCP have decreased the need for
choledocholithotomy and T-tube drainage of the bile ducts.
Endoscopic biliary sphincterotomy followed by spontaneous passage or stone
extraction is the treatment of choice esp. in elderly or high-risk patients.
Pre-operative ERCP is indicated in gallstone patients with:
1. History of jaundice or pancreatitis.
2. Abnormal LFT
3. US evidence of dilated CBD or stones in the duct.

5. Pancreatic cancer. Etiological conditions, clinical picture. Clinical classification.

Instrumental diagnosis. Principles of treatment.
Etiological conditions.
Etiology of pancreatic cancer and other tumors of peripapillary zone are:
- DM
- Gallstones disease
- Chronic pancreatitis
- Smoking
- Surplus content of meat and animal fats in food
- Drinking of strong alcohol
- Caffeine
- Presence of congenital predisposition to cancer
- Chemical agents and irradiation take part in appearance of pancreatic tumor too.
It is known that in Japan after transformation of the Japan mode of life into West
once ( when Japanese started using meat-rich food, smoking a lot ) the mortality for
pancreatic cancer increased.
It was proved that the increase of pancreatic cancer risk by 27% was due to cigarette
smoking and 11% due to daily meat-rich foods. Combinative influence of both these
factors led to risk increase of pancreatic cancer by 2XX.
Among food factors, the most carcinogenic significance belongs to animal fats. A lot of
authors report about the increase of pancreatic cancer in 5.4 X due to constant strong
alcohol using.

The interrelation between pancreatic cancer and chronic pancreatitis is the most
debatable. The cancer may be considered as a complication of chronic pancreatitis, but
maybe the development of chronic pancreatitis on background of primary pancreatic
cancer maybe possible too. It is becoming more interesting, because among 14% patients
with pancreatic cancer had a first clinical manifestation of acute pancreatitis. And among
5% of patients with acute pancreatitis are developing on background of pancreatic tumor.
Clinical picture.
Classic clinical features are jaundice, abdominal pain and weight loss.
Clinical picture of pancreatic tumors depends on their localization and spreading.
Among early symptoms is the pain syndrome. It is characterized by the epigastric
region site with irradiation to the back.
Weight loss.
Anemia.
General malaise.
The 2nd group of tumor symptoms include the signs of common bile duct
impassibility and main pancreatic duct compression, partial displacement of the
stomach and the duodenum.
In general, it is possible to separate the 2 main clinical forms:
The 1st with syndrome of obstructive jaundice. The jaundice is the cause of
patient address to doctor.
The 2nd Pain syndrome prevalence accompanied with signs of cancer intoxication
and weight loss.
** The 1st clinical form is more characterized for ductal adenocarcinoma of the
pancreatic head. The 2nd clinical is observed in cases of pancreatic cancer of the body
or tail. The jaundice is the sign of late cancer development of the pancreas.
Clinical classification.
1st stage Cancer is < 3cm. No metastasis.
2nd stage Cancer is > 3 cm, but doesnt grow out of pancreas.
3rd stage
a. Infiltrative growing of the cancer into nearest tissues, the duodenum, common bile
duct, GB, the portal wall.
b. cancer metastasis in regional lymphatic nodes.
4th stage distant cancer metastasis presence.
Endocrinal pancreatic cancer most oftenly develops from duct epithelium. The endocrinal
pancreatic tumor growing can be node or diffuse. The node-form of carcinoid is more
characterized for high and middle differentiated pancreatic tumors, diffuse form for
lower differentiated carcinoids.

Carcinoids of the pancreas take place in the body or tail, they can be plural, and their
sizes arent > 3-6 cm. These tumors as a rule have round form with thick capsule.
All carcinoids of pancreas can be divided into 3 hroups:
(i)
Ortoendocrinal tumors The tumors which are secreting the enzymes are
characterized for normal endocrinal cells of this localization.
Insulinoma/glucagonoma.
(ii)
Paraendrocrinal tumors The tumors which are secreting the enzymes are and
arent for normal endocrinal cells of this localization.
Gastrinoma/corticotropinoma/melanocytostimulative tumors.
(iii)
Polyendocrinal tumors The tumors with cells which are secreting several
different enzymes. It is the most often carcinoid type of the pancreas about
78%.
All pancreatic carcinoids according to their morphological structure must be described as
malignant tumors. But they are characterized by lower malignant degree with benign
clinical development. All types of carcinoids can give regional and distant metastasis in
the liver, lungs, bones, skin.
Neoplasms originating in region of ampulla of Vater are categorized as periampullary
tumors. Clinically, radiographically, intraoperatively and pathologically it is often
difficult to accurately differentiate cancer of the head of pancreas from 3 other
periampullary neoplasms ampullary carcinoma, duodenal cancer, carcinoma of the
common bile duct. Approximately 85% of these tumors arise from the pancreatic head.
Instrumental diagnosis.
There are 5 questions to answer. Are you ready?
1.
2.
3.
4.
5.

Is there tumor of the pancreas?

Is this tumor malignant?
Where is the localization?
What is the clinical stage?
Are there any complications?

The most difficult task is Question no. 1.

In general, the correct diagnosis of pancreatic tumor may be created by US
examination (73.3%) and CT-scanning (85.7%).
US and CT scanning are more effective in cases of pancreatic head tumors.
In patients with distal pancreatic cancers, the sensitivity of US examination is
46.2% and by CT is 76.2% only.
The only effective diagnostic measure in cases of periampullary cancer is
endoscopy. Its sensitivity is about 96.3%.
In cases of pancreatic head cancer, the RPCG gives possibility to diagnose the
disease basing on main pancreatic duct image. Its diagnostic value is about 89%.
In 85.7%, the diagnosis can be created by angiography.
Angiography is especially indicated for differential diagnosis between benign and
malignant pancreatic tumors.

Very important diagnostic information can be reached by direct cholangiography

due to transhepatic access under US control.
- The most valuable differential diagnostic method of pancreatic cancer is the
attention paid to define carbohydrate antigen /CA-19-9/.
- The punctinal transkinnal biopsy using special needles is more traumatic. This
method however gives the possibility to obtain tissue column with 1.5-2 mm in
diameter for histological examination.
Morphological dates about pathology can also be found out as well.
Complications such as bleeding, necrotic pancreatitis and external pancreatic
fistula may occur.
- So instead of punctional biopsy, the aspiration method can be used.
Needles with small diameter (0.7-1.0 mm) are used.
During aspiration, cultures of pancreatic cells are obtained for cytological
examination.
This method is realized under US or CT control.
NB: The aspiration method is not able to answer about histological structure of the
pancreatic tumor, but it can verify the malignant character of the tumor.
Principles of treatment.
The only radical method of treatment of pancreatic tumors is surgical operation. In
cases of pancreatic cancer of the head, the pancreato-duodenal resection, Whipple
procedure or total pancreatoduodenectomy. Distal pancreatic rsection can be used
only in some forms of pancreatic cancer of the tail.
Only in cases of duodenum cancer in critically ill patients is it possible to use the
conventional-radical operations, such as transduodenal papillectomy/Makocha
procedure and duodenectomy.
In cases of pancreatic cancers some radical procedures are used (8.4%) and palliative
(76.9%). Palliative operations can have the following aims:
Disappearance of jaundice
Disappearance of duodenal impassability
Disappearance pain syndrome
Including pancreatic enzymes into digestive process
Disappearance os side effects from metastasis.
-

Bile recurrence into digestive tract may be realized by traditional biliodigestive

anastomosis and by transskinal transhepatic procedures under US and CT control.
Transskinal transhepatic stent-procedures increases patients life to 6 months,
more than the average life-time of patient with 4th stage cancer.
In stable somatic patients with 4th stage of pancreatic tumors, some variants of
biliodigestive anastomosis by traditional modes gives a life-time of 1 year.
Duodenal impassability is being reduced by GIT anastomosis.

In severe pain syndrome, pancreatic tumors may be connected with acute HT in

the main pancreatic duct due to its pressing. Indication for longitudinal
pancreatojejenum anastomosis creation appear.
Pain relief procedures cannot be achieved by traditional surgical procedures. In
this case, cryodestroying of pancreatic cancer can be used.
This doesnt give the patient increase of life-time but quality of life will be better.

Conservative therapy of pancreatic cancer:

Lower respectability and bad results of palliative surgical procedures are the initial
point for working up to the question of conservative management of pancreatic
cancer.
Chemotherapy.
- Not an independent mode of pancreatic cancer management.
- Monotherapy of cytostatics isnt > 15%.
- In cases of the use polychemotherapy in traditional method:
FAMC ( ftoruracylum+adriamycinum+metotrecsat+cyclofosfanum ) FAM or CMF
gives the positive results of 40%. But of course it leads to partial destroying of the
tumor and increases patient life-time for 3-8 months.
Radical therapy.
- This treatment method involves distant gamma-therapy, brake radiations and
intertissue radioactive therapy with ir192.
- Combination of chemotherapy and radical therapy ( combinative management ),
including radical surgical operation yields more positive results.
- Average survival rate after radical surgical management is 11 months. In
combinative treatment 20 months.
- 2-years survival rate in cases of surgical management is only 9%, 5 years 4.5%.
- In cases of combinative therapy 2 years survival rate 68%, 5 years 14.3%.
- One of the modern directions are hormonotherapy.
This is based on presence of estrogenic receptors in adenocarcinoma or
cystadenocarcinoma.
So some positive results can be reached by use of anti-estrogenic therapy by
tamoxyfenum. It was showed that the average life-time is 7 months, and in control
group 3 months only.
NB The main and most important mode of treatment of pancreatic cancer is the
surgical method, so the main task is possible early finding of initial cancer stages,
then radical management would be possible.

6. Postcholecystectomical syndrome. Definition of the idea. Its causes. Clinical

groups of it.
Definition of the idea.
Strictly speaking, the term postcholecystectomical syndrome (PCHS) means functional
changes of pancreato-biliary area after cholecystectomy only. But historically under this
term, it means all pathological conditions with pain syndrome after cholecystectomy
Its causes. Clinical groups of it.
Today all pathological conditions after cholecystectomy are divided into 4 groups:
1. The lesions of bile ducts and papilla of Vater.
2. The diseases of liver and pancreas.
3. The duodenal diseases.
4. The diseases of other organs.
Elaboration of each clinical group will take place as follows:
1. THE LESIONS OF BILE DUCTS AND PAPILLA OF VATER.
It is the most important group among causes of PCHS. It includes in itself
choledocholithiasis with frequency about 2-65.5%. The GB is the main place of
stones formation and duct stones have the same origin as well. For primary stones
formation in the bile duct the presence of following factors are necessary:
inflammation, bile congestion, high lithogenic activity of the bile. The over-looked
stones have the same structure as the GB ones. Primary duct stones are friable,
looking like the duct mould. Long time silent period between the 1st surgical
procedure and stones relapse isnt a strict diagnosis criterion. Sometimes bile stones
firm on sutures or other foreign substances.
In clinical picture of cholelithiasis, the pain syndrome is constant and can be
accompanied by fever and jaundice. BUT if bile tree stones arent obstructive, the
jaundice may be absent, intermittent or for a short time. Dark urine appears only after
pain attack.
(i)
The papilla of Vater stenosis.
Primary PV stenosis was named the disease of Del-Valle-Donovan. Primary PV
stenosis is rare, about 0.17%-13% of all operations on bile ducts. Diagnosis of
primary stenosis can be created by exclusion mode only.
Secondary stenosis has posttraumatic genesis, most often due to stones migration
through the papilla of Vater.
(ii)
The insufficiency of papilla of Vater.
This syndrome was described by Mallet-Guy in 1941. The basis of this syndrome lies
in the absence of PV block up function due to dystrophical changes. As the real cause

of PCHS, PV insufficiency 5%. Clinical picture of this syndrome has no specific

signs. There is pain syndrome on upper region of abdomen and dyspeptical lesions.
(iii)
The long stump of the cystic duct.
It is thought that pain relapse after surgical procedures such as cholecystectomy
connects with keeping of the disease cause. This concerns the cases of GB keeping or
long cystic duct stump preservation, esp if there are bile stones in it. However not all
patients suffer from pain syndrome relapse after cholecystectomy, the long stump in
some cases may be the cause of PCHS. The long cystic duct stump has more clinical
significance in cases of accompanying bile HT.
(iv)
The bile duct stenosis.
The stenosis is caused by direct intraoperativ damages to the bile tree, 1dt of all due
to some difficulties of CBD, cystic duct and cystic artery verification. Classical
morphological structure of the hepatoduodenal ligament is meeting in 50% only. A
surgeon must not use any hemostatic forceps to cut and ligate any structures on the
area before being fully confident of all morphological elements in the operative
wound.
The 2nd bile duct stenosis causes are inflammatory changes. Duct inflammation can be
caused by stones, drainage tube, and decubitus after their using. The duct stricture
may be caused by primary sclerotic changes, so called Delbe disease. Most common
in males aged 20-40 yrs. Morphological picture of it includes periportal tissue
reaction with lymphoid infiltration of bile duct walls and periductal fibrosis.
In the clinical picture of CBD strictures, signs of bile congestion are prevalent. There
is obstructive jaundice, fever, spastic pain in right hypochondrial region.
(v)
The cysts of the CBD.
The cystic dilatation of the bile tree is the congenital defect of bile ducts
development. There is probably neonatal occlusion of the hepatic artery branches in
the base of pathology. It leads to trophic lesions of the ducts walls with their cyst
transformation. Frequency of the pathology is so called Carroli disease about
0.11%.
There are 2 clinical forms of the pathology:
The isolated congenital dilation of intrahepatic bile tree.
The same pathology accompanied with congenital hepatic fibrosis.
The clinical picture of the disease includes in itself the bile congestion signs and
intermittent cholangitis.
(vi)
Bile duct tumors.
Tumors of bile tree contribute to about 2.3-4.7% as a cause of PCHS. The pathology
may be overlooked during the primary operation. Bile ducts cancer is characterized
by slow-growing and late distant metastasis.
In the clinical picture, the signs of obstructive jaundice and cancer intoxication are
prevalent.

2. THE DISEASES OF LIVER AND PANCREAS.

Inflammatory liver and pancreas disease are interconnected with each other. The
degree of expression of parenchymal changes depend on few factors, first of all the
duration of bile duct disease, its site. If lesions have been resolved, it will lead to
relieving of parenchymal changes as well. However, primary diseases of liver and
pancreas may have the same clinical picture as in bile tree disease. So these changes
can be accompanied by pain syndrome after cholecystectomy and be interpreted as
PCHS.
(i)
Acute hepatitis.
Among different forms of acute hepatitis, the most important role belongs to viral Bhepatitis. The patients after some invasive procedures/injections/operations are
attributed to the risk group of this disease. B-hepatitis incubatory period is about 180
days.
(ii)
Chronic pancreatitis.
Some early changes in pancreas on background of bile stone disease are reversible, if
surgical procedure has been performed in time. But in cases of indurative
transformation of the pancreas, chronic pancreatitis begins to develop as an
independent disease with its own clinical picture with periods of acute attacks and
remissions. This leads to compression of the CBD and the duodenum with bile
passage lesions. ~ 31.2-65% of patients after cholecystectomy have some clinical
manifestations of chronic pancreatitis. In 70-85% cases, chronic pancreatitis is
connected with lesions of secret passage in pancreatic duct due to stones, cysts,
inflammation. This pancreatitis is called secondary. Clinical manifestations of the
disease usually appear in first half year after cholecystectomy. The pain syndrome is
accompanied by vomiting. There are signs of intra/extrasecretory insufficiency of the
pancreas.
3. THE DUODENAL DISEASES.
In patients with bile tree diseases, 72.5-98.5% experience changes of the duodenum.
The motor-evacuative changes of the duodenum were known and may be considered
as one of the 1st cases of the bile congestion and stone formation. If these changes
have become irreversible, they are keeping the GB removing (huh?!).
So it Can be the real cause of pain relapse after primary surgical procedure.
Chronic duodenal impassability can be divided into functional and organic. The latter
is connected with aorto-mesenterial compression. Its frequency is about 0.09-0.5%.
Another cause of organic duodenal impassability is the high fixation of the
duodenaojejunal flexure, most often due to scary changes (boo!). At the beginning of
this variant of duodenal impassability, there are no specific clinical signs, so the
primary diagnosis can be incorrect cholecystitis, pancreatitis.

(i)
Diverticulum of the duodenum.
Diverticuli are most oftenly located on the medial wall of duodenum. The muscular
membrane is weak here, because of ducts and vesseoles in this area. 60% of
duondenal diverticulums form near papilla of Vater. The diverticuli of this
localization are divided into para and perivatery.
Inflammation is one of the commonest complication of diverticulum. It leads to bile
and pancreatic juice passage lesions.
Inflammation becomes the base of the papilla Vatery stenosis. Bleeding, ulceration,
perforation and malignization can complicate duodenal diverticuli. If diverticulum
hasnt been fooun dout during primary surgical procedure, it becomes the real cause
of PCHS.
Clinical picture is same as in duodenal ulcer. Obstructive jaundice can also appear.
NB In light of the already many details of this question and in order not scare too
many readers away, for those who are still brave enough and wish to add diagnostic
and surgical procedures information(s) to these clinical groups may kindly do so by
referring to Question 7. Have fun!

7. Preoperative & intraoperative diagnostic methods for postcholecystectomical

syndrome exposure. Kinds of surgical procedures.
Pathological
condition
1. Choledocholithiasis

2. Stenosis of papilla of
Vater
3. Insufficiency of PV

Diagnostic method
- Intraoperative examination
palpation bouginage
- US examination
- RPCG
- X-ray
- Transfistular
cholangiography/cholangioscopy.
- Transhepatic cholangiography
- Debit manometry
- Visual examination of PV by
endoscopy or RPCG.
- X-ray and barium suspension
reflux from duodenum into bile

Surgical procedure
- Transpapillotomycholedodocholithoextraction.
- Transfistular or
transhepatic litho
extraction and stone
destruction by ESWL.
- Open surgical procedure.
Endoscopic papillotomy
No proven well-known

tree.
- Fibroduodenoscopy.
- US
- RPCG
- Direct contrast methods of bile
tree researching due to antegrade
transhepatic access.
- US scanning
- RPCG
- Transhepatic cholangiography

surgical procedure.

6. Cyst of CBD

- US

- Open surgical
management.
- Biliodigestive
anastomoses cration.

7. Acute/Chronic
hepatitis

- Epidemiological anamnesis.
- Lab tests transaminase level,
Australian antigen.
- US scanning
- CT scan
- RPCG
- X-ray
- Endoscopy
- Angiography
- X-ray with baric suspension.
- Endoscopy
- In cases of arterio-mesenterial
impassability, angiography is
necessary.

4. Long stump of cystic

duct

5. Stenosis of bile duct

8. Chronic duodenal
impassability
(functional and organic)
9. Diverticulum of
duodenum

Surgical procedure
remal of stump
accompanied with bile HT
correction.
- Bouginage and dilatation
through transhepatic
access.
- Surgical procedures are
in 2 groups (restorative
and reconstructive).
Restorations: same for
recreation of natural
normal bile passage into
duodenum. (Eg. resection
of CBD stricture with its
plastic)
Reconstructions: To
presuppose the formation
of abnormal way for bile
passage. Includes different
types of biliodigestive
anastomoses.

Surgical correction
Biliodigestive
anastomoses.

Preoperative:
ERCP:
Positive Endoscopic sphincterotomy with CBD clearance if successful
laparoscopic cholecystectomy, unsuccessful open cholecystectomy with CBD.
Negative Laparoscopic cholecystectomy
Suspected intraoperatively:
Cholangiogram Positive ERCP (laparoscopic CBDE/open CBD exploration.
Negative Complex laparoscopic cholecystectomy
Diseases of duodenum:
1. Motor evacuatory changes first cause of bile congestion and how formation (xray and barium)
2. Diverticulum of duodenum mostly on the medial wall can be complicated with
inflammation, bleeding, perforation.
8. Overlook of bile stones
1) Def:
- stones formation in the bile duct, the stones are friable, looking like duct mould.
2) clinical features:
- the patient may be asymptomatic but usually has bouts of pain, the pain syndrome
is constant, jaundice and fever but if the bile tree stones arent obstructive, the
jaundice may be absent or short time and intermittent
- the patient is often ill and feels unwell
- the term cholangitis is given to the triad of pain, jaundice and fevers sometimes
known as Charcots triad
- tenderness in the epigastrium and the right hypochondrium
3) diagnosis
- ultrasound scanning(can see dilatations of bile ducts, finding the obstruction site),
liver function tests, liver biopsy if the ducts are not dilated and MRI or ERCP will
demarcate the nature of the obstruction, x-ray pictures can see as filling defects
- cholangioscopy by transpapillary or transhepatic access
4) treatment
- patient may be ill. Pus may be present within the biliary tree and liver abscesses
may be developing. Full supportive measures are required with rehydration,
attention to clotting, exclusion of diabetes and starting the appropriate antibiotics.

Endoscopic papillotomy is the preferred 1st technique with a sphincterotomy,

removal of the stones using a Dormia basket or the placement of a stent if stone
removal is not possible. If this technique fails, percutaneous transhepatic
cholangiography can be performed to provide drainage and subsequent
percutaneous choledochoscopy
Surgery in the form of choledochoscopy
Transpapillary choledocholitoextraction, transfistular or transhepatic
litoextraction with accompany with stone destroying the destroying can be
reached by ESWL procedure

9. Differential diagnosis of jaundice syndrome.

INDICES
BILIRUBIN
Unconjugated
Conjugated
Cholesterol
Bile acids
Urobiliin
Urine colour
Stercobilin
Feces colour
CHOLAEMIC
SYNDROME

ACHOLAEMIC
SYNDROME
ENZYMES

US

FGDS

OBSTRUCTIVE
JAUNDICE

HEPATOCELLULAR
JAUNDICE
BLOOD

Increased or norm.
Increased
Very increased
Increased or norm.
Increased
Increased or norm
Increased
Increased
URINE
Presence
Presence
Dark
Dark
FECES
Norm
Slightly increased
Pale
Slightly dark
CLINICS
- Itching
- Sleepiness
- Bradycardia
Only slightly
- Decreased BP
expressed.
- Hemorrhagic
diathesis
- Steatorrhea
Absent
- Constipation
Alkaline
Elevated
phosphatase from
aminotransferases.
epithelial cells of
small ducts.
-

Dilation of the
bile duct above
the obstruction.
- Visible calculi.
Infiltration of papilla of
Vater.

Maybe signs of
hepatic inflammation.
None

HEMOLYTIC
JAUNDICE
Very increased
Increased
Norm
Norm
Norm
Norm
Increased
Dark

Absent
Absent

None
Splenomegaly

None

ERCP
PTC

Filling defect in biliary

system.
Dilated

None

None

Contraindicated.

KEY WORDS:
FGDS: Fibrogastroduodenoscopy
ERCP: Endoscopic retrograde cholagiopancreatography
PTC: Percutaneous transhepatic cholangiography
INDICES
Unconjugated bilirubin
Conjugated bilirubin
Cholesterol
Bile acids
Bile salts
Urobilin
Urobilinogen
Colour
Stercobilin
Colour
CHOLAEMIC
SYNDROME
ACHOLAEMIC
SYNDROME
ALKALINE
PHOSPHATASE
US

FGDS

OBSTRUCTIVE
JAUNDICE
BLOOD
Increased/Norm
Very increased
Increased
Increased
URINE
+
+
Dark
FECES
Decreased
Clay
- Itching
- Sleepiness
- Bradycardia
- Decreased BP.
- Steatorrhea
- Constipation
Increased 10-12 X.
-

ERCP

Dilation of bile duct

above the
obstruction.
Visible calculi.
Maybe infiltration
of papilla of Vater.
Stenosis, impacted
stones.
Filling defect.
Calculi, bulging of

PARENCHYMAL
JAUNDICE
Increased
Increased, later decreased
Increased
Increased
+
Increased in early phase,
later decreased
Dark
Decreased
Light colour
-

Same but less

expressed.
+ Hemorrhagic
diathesis.

Increased 2-3 X.

No obstruction or
infiltration.

PTC

bile ducts.
Dilated

Contraindicated

10. Chronic pancreatitis. Definition. Classification according morphology & clinical

forms. Etiology and pathogenesis. Modern methods of chronic pancreatitis
diagnosis.
Definition.
Chronic pancreatitis is not an independent disease, it is a phase condition, a continued
result of acute pancreatitis.
Chronic pancreatitis is a chronic relapsing process which includes in itself episodes of
acute oedema and necrosis of the pancreas, outside of which development of pancreatic
sclerosis and parenchyma atrophy are presented.
According to Bailey and Loves: Chronic pancreatitis is defined as a continuing
inflammatory disease of the pancreas characterized by irreversible morphological change
typically causing pain and/or permanent loss of function.
Classification according morphology & clinical forms.
Morphological:
- Alcohol pancreatitis ( I think )
- Chronic indurative pancreatitis
- Chronic pseudocyst pancreatitis
- Chronic pseudocalculous pancreatitis
Clinical forms:
(i)
Chronic relapsing pancreatitis It is the most spread clinical form. It can be a
consequence of acute pancreatitis. Intermittent acute attacks are characterized
for this clinical form. The attack is described as pain crisis. The crisis is
accompanied by increased level of pancreatic enzymes in the blood and urine,
sometimes jaundice. During acute attacks, not only does pancreatic edema
occur but necrotic pancreatitis can appear as well. However, in patients with
long time anamnesis of chronic pancreatitis, necrotic changes are rare. It is
explained by atrophy of functional active gland cells and their transformation
into fibrous tissue.
(ii)
Chronic painful pancreatitis In this case, a pain syndrome is constant. The
pain is a dull ache-y type pain, gnawing in character. In anamnesis of patients,
pancreonecrosis quite often occurs. Besides pain syndrome, there is also
weight loss and dyspeptical complaints. Dyspeptical?! There are 2 things
Russians are good at, drinking vodka and making up words that sound really
odd.
(iii)
Latent pancreatitis This variant is sometimes described as painless. But it IS
NOT true because Some pain Does take place. Firstly, functional lesions of
the pancreas take place.

(iv)

Pseudotumorose pancreatitis Stable obstructive jaundice is the most

important clinical sign of this form. SO the clinical picture of this form is
usually associated with cases of pancreatic cancer. But in patients with chronic
pancreatitis, the jaundice is accompanied by pain syndrome and there are
manifestations of extra-secretory and intra-secretory insufficiencies. Correct
diagnosis is difficult before and during surgical procedure. A long time of
medical supervision gives possibility of correct diagnosis.
(v)
Chronic cholecystopancreatitis Independently on presence/absence of
gallstones, pancreatitis may be relapsing, painful or latent.
Etiology and pathogenesis.
Etiology:
We follow the Hollander etiological classification
(i)
Main factors:
Gallstone disease
Alcoholism
Post-operative pancreatitis
Endoscopical procedures on bile and pancreatic ducts
Abdominal trauma.
(ii)
Seldom factors:
Endocrinal diseases
Pregnancy
Drugs pancreatitis
Immunological and allergological factors
Neurogenic pancreatitis
Congenital pancreatitis
(iii)
Shock and acidosis caused pancreatitis:
- 1 of the most important etiological factor of pancreatitis gallstones.
- In cases of > 5 years disease presence, chronic pancreatitis can be found in 35%
of patients.
Pathogenesis:
3 Main Mechanisms:
(i)
Increase level of protein
(ii)
Dysfunction of duodenum, Oddi sphincter stimulation of secretion.
(iii)
Obstruction of Versunckel duct
-

Also decrease of inhibitorsactivation of enzyme in ductautodigestion.

Abnormalities in juice production, in juice: H20, HCO3-, protein, lipase, trypsin,
amylase.
Intrapancreatic enzyme activity precipitation of protein in duct plug
formation calcification ductal obstruction ductal HT pancreatic
damage.
Abnormal drainage of lymphpancreatic edemadisbalance between
enzyme/liquid productionautodigestion.

Hereditary cases genetic abnormalities of cationic trypsinogen and its

inhibitory protein leads to unopposed trypsin activity in pancreas.

- Pathogenesis of alcohol chronic pancreatitis:

1. Hyperstimulation of external secretory function of the pancreas.
2. Retention of pancreatic duct with intraductal pressure increase due to protein
precipitation in it.
Modern methods of chronic pancreatitis diagnosis.
Instrumental method:
(i)
US edematous, fibrosis, cysts. But in meteorism, difficult to see pancreas
because inflated bowel covers it. This method gives possibility to expose one
of the 3 variants of chronic pancreatitis:
1. Secondary; accompanied with bile stones disease
2. Pancreatitis; complicated by cysts
3. Primary pancreatitis without pancreatic cysts.
(ii)
Valuable diagnostic info may be received by X-ray examination.
- In cases of stones pancreatitis, they may be found.
- There is possibility to expose increase of pancreatic masses.
(iii)
(iv)
(v)
(vi)

Prime investigation is either an MRI or CT scan, which will show outline of

the gland, main area of damage and the possibilities of for surgical correction.
An MR cholangiogram will show presence of biliary obstruction.
An MR pancreatogram the state of pancreatic duct.
ERCP or percutaneous pancreatography can elucidate anatomy of the duct and
whole organ morphology , determine type of operation required if operative
intervention is indicated.

11. Chronic pancreatitis definition. Indications for surgical treatment. Treatment

mode choice.
Definition.
Chronic pancreatitis is not an independent disease, it is a phase condition, a continued
result of acute pancreatitis.
Chronic pancreatitis is a chronic relapsing process which includes in itself episodes of
acute oedema and necrosis of the pancreas, outside of which development of pancreatic
sclerosis and parenchyma atrophy are presented.

According to Bailey and Loves: Chronic pancreatitis is defined as a continuing

inflammatory disease of the pancreas characterized by irreversible morphological change
typically causing pain and/or permanent loss of function.
Indications for surgical treatment.
1.
2.
3.
4.
5.
6.

Intractable pain is the cardinal indication for operation.

Formation of a pseudocyst or abscess.
Obstructive jaundice.
Bleeding.
Duodenal obstruction.
Splenic vein thrombosis ( with left-sided portal HT, hypersplenism and bleeding
gastric/esophageal varices )
7. Pancreatic ascites or fistula formation.
8. Signs of pancreatogenic stenosis of the CBD and the duodenum or segmental
portal HT.
Indications for surgical operation on bile ducts are:
1. Cholangiogenic pancreatitis where lesions of CBD, PV and GB are the causes
of secondary changes of the pancreas.
2. Primary pancreatitis of alcoholic etiology and development of tubular stenosis of
intrapancreatic part of CBD. In case of complications, the indications are
pseudocysts, pancreatic fistulas, late suppurative complications.
Treatment mode choice.
Surgical correction should be targeted to the following:
1. Pain relieving
2. Pancreatic complications management
3. Preservation of pancreatic function.
All operations are divided into 5 groups:
1.
Operations on adjoining organs.
Operations on bile ducts and papilla of Vater.
Operations on digestive organs.
2.
Direct surgical procedures on pancreas:
pancreas resection
internal drain procedures of pancreatic ducts and cysts
pancreatic duct occlusion
external drain procedures of pancreatic ducts and cysts
3.
Palliative operations:

Surgical procedures on nerves system

Cryodestroying of the pancreas

4.
Endoscopic procedures on the pancreas and its ducts.
5.
Closed surgical operations under US and CT control.
In case of pancreatitis due to duodenal impassability:
Dissection ileic ligament, duodenointestinal anastomosis, antrumactomy,
vagotomy.
Direct surgical procedures on pancreas:
Distal resection.
Near total pancreatomy.
Sectoral pancreatomy.
Pancreatoduodenal resection (Whipple procedure)
Total pancreatoduodenectomy
Internal drain procedures:
1. Dissection to plastic of main pancreatic duct openly.
2. Longitudinal pancreatointestinectomy by Preston I, II or terminal
pancreatointestinectomy by Du Vale.
Main pancreatic duct occlusion The exception of exocrinal pan secretion leads to
pain disappearance.
This is used in severe fibrous lesions of pancreas.

12. Pancreatic cysts. Classification. Clinical picture, diagnostic methods. Treatment

of uncomplicated pseoducysts.
Classification.
The Howard classification of pancreatic cysts is the most spread in practice:
1.
A.

True cysts with mucous epithelium:

Congenital
The single or plural cysts in the pancreas only.
The pancreatic cysts accompanied with cyst formations in other organs/Landau
disease.
The fibrocystose of the pancreas.
Dermoid cysts.

B.

Acquired cysts
Retentional cysts/cyst dilatation of the pancreatic ducts
Parasitogenic cysts
Tumorous cysts malignant, benign.

2.
A.
B.

C.

Pseudocysts without mucosal epithelium:

Inflammatory due to acute or chronic pancreatitis
Posttraumatic:
due to accident
due to any surgical procedures
Unknown genesis:

The subdivision of pancreatic cysts into true and false is conditional. It has
become known that the primary retentional true cysts receive signs of pseudocysts
due to necrotic or inflammatory changes. From another side, the wall of post
necrotic acquired pancreatic cysts can be covered by epithelium. Besides it was
proven that the possibility of presence of both epithelium and scary changes on
cystic wall at the same time. Separation of true and false pancreatic cysts isnt so
strict.

Subdivisions:
1. Extrapancreatic pseudocysts. They are post necrotic big size cysts. They can be
posttraumatic too. Their walls are formed and may be considered as
parapancreatic leaks or suppurative fluid. They may occupy a lot of room.
2. Intrapancreatic pseudocysts. They have been formed due to attack of relapse
pancreatitis. The cysts arent big-sized, usually connected with the pancreatic
ducts and localized in head of pancreas.
3. The cyst dilatation of the pancreatic ducts/hydrops. Most often in cases of alcohol
pancreatitis.
4. Retentional cysts the rarest sort of pancreas cyst lesions. Localized in distal part
of pancreas, have thick walls. Usually appear due to chronic pancreatitis.
5. The plural thick wall cysts They can be isolated or accompanied with the same
ones in other organs. There are usually no doubts in congenital genesis of the
disease.
6. The cystic tumors of the pancreas.
Clinical picture, diagnostic methods.
Clinical picture: (syndromes)
1. Pain syndrome Connected with compression of surrounding tissues and organs
by the cysts or its distension due to inflammation, bleeding into it. Additional
significance in pain syndrome appearance pancreatic juice hypertension has due
to direct pressing of the main pancreatic duct by the cyst, especially if it is
localized in head of pancreas.

2. The clinical syndrome of extracrinal insufficiency Characterized by weight loss,

diarrhea. This syndrome is not specific for pancreatic cysts, but IS important for
diagnosis of chronic pancreatitis which is the background of pancreatic cyst
formation.
3. The syndrome of endocrinal insufficiency This syndrome is characterized for
chronic pancreatitis as well and is being showed by DM or decrease sugar
tolerance test.
4. The syndrome of bile congestation This sign appears in cases of pancreatic cysts
of head with compression of common bile duct compression.
5. The syndrome of duodenal impassability.
6. The syndrome of segmental portal HT.
Diagnostic methods:
1. US-scanning: Imaging shows pancreatic cysts as cavity sign. It is the lower
acoustic density zone.
2. Ripe pancreatic cysts have correct round form with sharp regular borders and
homogenous contents. The density of cyst capsule is more than surrounding
tissue. In cases of unripe pancreatic cysts, the capsule isnt sharp, their contents
are not homogenous, there are debris, flakes.
3. US not only gives the possibility to diagnose pancreatic cysts, but also to find
complications such as obstructive jaundice signs of which are bile tree
dilatation, GB enlargement. If cyst displaces surrounding organs (stomach and
duodenum) it can lead to acute/chronic duodenal impassability. By US, it will be
imaged as stomach distension with changed peristalsis.
4. RARELY do cysts press the main pancreatic duct with its dilatation in distal part
of the pancreas. But I guess Ill just mention it anyway to make everyones lives a
little harder. What is life if not a challenge? This duct can be confidently found
by US. The minimal cyst size can be found to be 10-15 mm. Difficulties can be in
initial period of their formation due to the inflammatory debris presence in it.
Needle biopsy under US control is important for differential diagnosis of benign
and malignant pancreatic cysts.
5. CT-scanning: This cavity thing is the most important sign in CT-scanning. CT
rules, it not only determines presence of cavity, but also researches localization
and peculiarities of its structure. Contents of cavities have very low density so CT
can find them confidently.
6. Angiography: So pancreatic cysts have a stable, constant angiographic picture.
Large cysts lead to displacement of visceral arteries till celiac trunk. In addition,
there are vasselloss areas in the pancreas. This method can be recommended for
topical diagnosis of large formations suspected to be going out from pancreas.
7. X-Ray examination: Can only give indirect signs of volume lesion of the pancreas
without differential diagnosis between pancreatic cyst, chronic pseudotumorous
pancreatitis and tumor.

Treatment of uncomplicated pseudocysts.

- Pseudocsyts are common after pancreatitis but most disappear spontaneously
unless larger than 5 cm.
- Ultrasound is an excellent method of confirming diagnosis of an abscess.
- If possible, drainage should be delayed to allow the pseudocyst wall to thicken
and mature, but undue delay should be avoided in case further complications
ensue.
- There are 4 stages of cysts formation:
(i)
1st stage ( duration 1.5 months ): The cyst hasnt yet formed from destructive
cavity in omental bursa. There are indications for conservative therapy of
acute pancreatitis only.
(ii)
2nd stage ( 2-3 months after cyst formation ): Cyst walls are presented by
friable granular tissue. Operation is not indicated except for any cases
presenting complications. In those cases, suppurative inflammation, pain
pressing syndrome external drain procedure should be used only.
(iii)
3rd stage ( 3 motnhs-1 year ): Cyst wall is durable. There are possibilities for
traditional external or internal drain procedures.
(iv)
4th stage ( > 1 year ): In this stage, there are clear borders of cyst and
surrounding tissues. Cystectomy or some sorts of internal drainage procedure
can be used.

13. Complications of pancreatic cysts. Clinical features, diagnosis, treatment modes.

Complications include:
(i)
Rupture of cysts.
(ii)
Infection of cysts.
(iii)
GIT bleeding.
(iv)
Peritonitis
Clinical features:
1. Pain due to compression of surrounding organs. Also due to pressure of bile
juice by compression of CBD.
2. Signs of exocrine insufficiency weight loss, diarrhea.
3. Signs of endocrine insufficiency DM.
4. Bile congestion.
5. Duodenal impassability signs.
6. Portal HT ( segmental )
7. Signs of intoxication in case of suppurative inflammation.
8. Epigastric swelling.
Diagnosis:
1. US
2. CT scan

3.
4.
5.
6.

Angiography
X-Ray with barium meal
Blood test
Urine test

Treatment modes:
1. Drainage + Antibiotics + Low fat diet.
2. If infected: percutaneous catheter drainage. PCD is contraindicated in:
- Patients who cannot manage a catheter at home.
- Patients with strictures of the main pancreatic duct.
- Patients with cysts containing blood or solid material.
3. Endoscopic drainage transpapillary ( via ERCP ), transmural.
Cyst communication = pancreatic duct.
4. Internal drainage is the procedure of choice.
Additional:
Complications of treatment:
1. If there are signs of bleeding:
- Sudden increase f abdominal pain
- Drop in hematocrit
- Change in vital signs.
- Reaction: emergency surgery or angiography with embolization of bleeding walls.
- Do not perform a percutaneous or endoscopic drainage procedure if there is
suspected bleeding.
2. Infection:
- Increase WBC, fever.
- Reaction: urgent drainage and antibiotics.
3. GIT obstruction:
- Nausea, vomiting.
- Reaction: urgent drainage
4.
-

Rupture:
GIT bleeding
Peritonitis or even
Death

14. Ileofemoral thrombophlebitis. Clinical picture. Diagnosis. Differential diagnosis.

Treatment. Blue and white phlegmasia definition.
Clinical picture.

Swelling extending from foot to inguinal fold.

Bursting of pain in the calf muscle and groin.
Redness.

Low-grade pyrexia.
Skin cyanosis.
Colour of limb varying from pale to cyanotic.
Palpation of the femoral vein tenderness.
Later: dilated superficial veins.

History:
1. Subjects with clinically predicting factors for DVT in lower limb (like immobility) from
any cause; old age, obesity, magnitude of injury or operative procedures, MI, HF,
previous episodes of venous thromboembolism, varicose veins and drugs like estrogens.
2. Onset sudden/spontaneous particularly subjects on oral contraceptives following injury,
operation or some prolonged illness.
SYMPTOMS:
(i)
Bursting pain or tightness in affected lower extremity (particularly calf) especially
during sitting, walking, standing.
(ii)
Swelling of affected calf or whole leg difficulty in walking.
(iii)
Unexplained pyrexia and rapid pulse towards end of 1 st post-operative week.
LOCAL FEATURES:
1. Swollen leg.
2. Slight edema around ankle (thrombosis confined to calf).
3. Iliofemoral venous thrombosis of the thigh, lower leg or even groin.
4. Both legs, perhaps even buttocks, abdominal wall and genitalia with distended collateral
veins over abdomen and thorax even with bilateral varicosis in inferior vena cava
obstruction.
5. Calf muscles (turgid due to thrombosed vein) are swollen, woody (induration), and tender
(Moses sign).
6. Tenderness over involved veins (posterior tibial and peroneal vein) with venous
distension of the involved part.
7. Homans sign: pain in calf during dorsiflexion of foot.
8. Finger firmly pressed on Achilles in the midline at its insertion into the calcaneum is
drawn up towards the muscles belly of the calf eliciting tenderness at site of where
thrombosis passes over. (pay attention! Commonest site of thrombosis is usually the
soleus just above its junction with the tendo Achilles in the midline)
9. A large painful swollen and pale limb due to severe edema is called WHITE LEG or
MILK LEG (occlusion of a length of deep femoral vein + associated lymphangitis) or
phlegmasia alba dolens.
10. Large swollen, congested and blue limb or BLUE LEG is due to extensive DVT of the
iliac and pelvic veins phlegmasia caerula dolens. In this condition, either venous
gangrene or areas of infarction may threaten part of or the whole limb.
11. Varicosity of veins.
12. Skin changes like pigmentation, eczema
Diagnosis.
1. Full case history and clinical examination should be taken.
2. Clinical examination carried out with patient standing will reveal ankle swelling, skin
discolouration, eczematous changes, presence of varicosities, presence of saphena varix.
3. Examination of peripheral pulses should be carried out.

4. By use of a tourniquet, (Brodie-Trendelenburg test) information can be obtained about

the position of incompetent valves, for example, incompetence of the saphenofemoral
junction, a midthigh perforator or a saphenopopliteal valve incompetence.
5. Doppler ultrasonography Now the minimum level of investigation required before
treating a venous disease. A Doppler flow probe can be used to exclude arterial disease
and to determine patency of a vein. A bidirectional flow probe can be used to detect
venous reflux.
6. Photoplethysmography Technique which measures the amount of blood in the skin.
7. Strain gauge plethysmography Measures volume changes in the leg in response to a
tourniquet applied around the thigh. Provides useful info on venous outflow and can be
used to diagnose iliofemoral venous thrombosis.
8. Duplex imaging Involves use of B-mode US and a coupled Doppler probe. Allows
direct visualization of the veins and provides functional as well as anatomical info.
9. Venography Including cavogram, if necessary. For direct visualization of the veins with
contrast material. Accurate but has disadvantages of being invasive, expensive and risky.
Differential diagnosis.
POINTS
1. Major cause
2. Size
3. Size of primary thrombus
4. Size of propagated clot
5. Clinical features

6. Embolism

THROMBOPHLEBITIS
Inflammation of superficial
vein as in varicose vein or in
vein cannulated for infusion.
Any superficial vein

PHLEBOTHROMBOSIS
Stasis (non-inflammatory)

Larger, depending upon the

extent of involvement of veins
Usually none, short and wellanchored if present.
Signs of acute inflammation
(local and general) with a
painful cord-like inflamed and

Smaller

Rare, as the thrombus is

adherent to intima, except in
infective cases Pyaemic.

Deep veins

Long and often poorly

attached.
Silent, painless, very
overlooked. Unexplained
fever or tachycardia at the end
of the 1st post-operative week.
Common and massive but
sterile.

Cellulitis
Pulmoary embolism
Septic thrombophlebitis
Superficial thrombophlebitis

Other problems to be considered:

- Achilles tendonitis
- Arterial insufficiency
- Arthritis
- Asymmetric peripheral edema secondary to CHF, liver disease, renal failure,
nephrotic syndrome.
- Cellulitis, lymphangitis
- Extrinsic compression of the vein secondary to tumor, hematoma or abscess.

Hematoma
Lymphedema
Muscle of soft tissue injury
Neurogenic pain
Postphlebitic syndrome
Prolonged immobilization or limb paralysis
Ruptured Baker cyst
Stress fractures or other bony lesions
Superficial thrombophlebitis
Varicose veins.

Treatment.
1. Conservative measures:
(i)
Elevation
(ii)
Elastic stocking
(iii)
Massage as described under lymphedema
(iv)
Anticoagulant therapy Heparin IV for 7-10 days followed by warfarin orally for 3
months.
(v)
Analgesics
(vi)
Fibrinolytic therapy Streptokinase or urokinase may cause severe bleeding at site of
operation if used in about 10 days after operation.
(vii)
If fever persists, blood culture should be taken and antibiotics should be given in fear
of septicemia/pyaemia.
(viii) Patients with extensive thrombosis are often very anemic and urgent blood
transfusion should be considered.
2. Operative measure (should conservative fail):
(i)
Thrombectomy If presence evidence of venous gangrene.
(ii)
Venous interruption may be called for extension of life-threatening thrombus.
(iii)
Palma operation Iliac vein obstruction is bypassed by long saphenous vein of the
good leg. The vein is rerouted across the pubis through a subcutaneous tunnel and
anstomosed to a vein below the iliac vein obstruction.
Femoral and iliac venous thrombectomy.
Femoral vein ligation
The access and dissection are identical to those for iliac thrombectomy, with which ligation
may be combined. Femoral thrombus may be removed above the profunda vein by the
techniques described above, and distal thrombus is then prevented from embolizing by
ligation of the femoral vein below the confluence with the profunda vein. Ligation may be
used as the sole maneuver if thrombus is present only below profunda origin.
Caval clipping or placation
Carefully dissect free and snare and segment of vena cava between 2 pairs of lumbar
veins using a combo of sharp and blunt dissections.
Place a plastic Miles-DeWeese clip around the vena cava and hold it closed with a silk
ligature as shown.
Alternatively pass 3 or 4 mattress sutures across the vena cava from front to back and tie
them down.

Both techniques convert the vena cava into a number of small channels which prevent
large emboli from reaching the lungs.

Insertion of umbrella filter

Both the Mobin-Uddin and Greenfield-Kimway umbrella filters may be inserted into the
inferior vena cava via a venoiomy in the internal jugular vein under LA.
Blue and white phlegmasia definition.
A large painful swollen and pale limb due to severe edema is called WHITE LEG or
MILK LEG (occlusion of a length of deep femoral vein + associated lymphangitis) or
phlegmasia alba dolens.
A large swollen congested and blue limb or blue leg due to extensive DVT of the iliac
and pelvic veins is called phlegmasia caerulea dolens. In this condition, either venous
gangrene or areas of infarction may threaten part of or whole of limb.

15. Varicous disease idea definition. Etiology and pathogenesis. Classification.

Clinical picture according to stages. Diagnosis/name the methods. Differential
diagnosis.
Idea definition.
Varicose disease is the kind of chronic venous insufficiency and its characterized by
present of sacciformis venous dilations of superficial and deep veins with haemodynamic
damages and vines congestion in lower limbs.
Etiology and pathogenesis.
In base of varicose disease congenital disbalance between elastin and collagen in vascular
wall lies. Because of, the vascular wall becomes disresistant to normal intravenous blood
pressure and it leads to vein dilation.
Second factor of varicous disease congenital or acquired valves insufficiency is. Only on
background of congenital venous incompetence venous hypertension and retrograde
blood flow are leading to varicous disease.
Valves incompetence can be anatomical and functional. The last sort of it is developing
due to venous dilation in valve area.
Most of all pathological venous dilation of lower limbs appears due to retrograde blood
flow. Deep veins are defended by fascies and muscles, so their dilation is even. In

superficial veins subskinal fatty tissue cant defend them equal, so varicies are appearing.
Pathomorphological changes in varicous veins are defined as phlebosclerosis.
Classification.
1. According to etiology Primary or idiopathic
Secondary
2. According to clinical stages
compensation,
decompensative without trophic lesions
decompensative with trophic changes.
3. According to clinical forms of the disease.
Ascending and descending.

Clinical picture according to stages.

There are 3 stages of the disease: compensation, decompensative without trophic lesions
and decompensative with trophic changes.
In compensative stage there are two levels. The first - varicous disease without varicose
transformation. In this case patients complain to some pain in region of typical
communicating veins localization, they fell discomfort in legs after working day. But
there are no any varicies and oedema.
Second level of compensative stage is characterized by varicies presence without any
other clinical manifestations. And only cosmetic problems have leaded patients to doctor.
In stage of decompensation without trophic changes patients have such complications, as
varicies presence, transitional leg oedema after working day, night cruralgia.
In stage of decompensation with trophic changes pigment areas and trophic ulcers
appear, first of all, in lower leg one/third.
Besides tree stages of varicose disease there are two clinical forms of the disease. They
are ascending and descending.

Diagnosis/name the methods.

Diagnosis of varicose disease is based on patients complaints and results of general

examination.

Anamnesis of the disease must include in itself the following:

when did first symptoms appear ?
in what region they did appear ?
what is their dynamic ?
has patient ever had thrombophlebitis ?
has patient ever had any venous diseases before ?
General examination should be realized in standing patient position and include in itself
both lower limbs, abdominal wall and chest examination. Skin color, trophic changes
presence and varicies localization are exposed. General examinations includes some
functional tests. But now its importance has increased due to wide spread phlebography.
There are two sorts of phlebography - proximal and distal. Proximal phlebography gives
information about valves competence in main lower limbs veins.
Distal - is necessary for finding incompetent communicating veins and deep veins
passability.
Besides X-Ray examination great importance is belonged to US- examination. It gives
possibility to find not only subskinal and deep lower extremities veins, but
communicating veins and their valves.
Among all patients with varicous disease there is group with clinical syndrome of
functional deep veins incompetence.
It consists of:
Early beginning and quick development of the disease
Pain and leg oedema after physical efforts
Trophic changes presence
Disseminative or untypical varicous transformation of subskinal veins.
Lesions of short subskinal vein
Muscular part volume increase of the leg

Differential diagnosis.
1. Acute arterial impassability, platypodia, osteochondrosis varices is absent,
increase fatigability of lower limbs, some pain syndrome in exception any other
causes of it. These symptoms occurs only in varices too
2. Subskinal veins dilation in cases of congenital venous diseases and
postthrombotic disease.
3. Postthrombotic disease correct diagnosis may be created on base of anamnesis
and distal phlebography.

16. Complications of varicous disease. Clinical picture. Treatment. Indications for

surgical treatment. Kinds of surgical procedures.
-superficial thrombophlebitis
-bleeding from varicose
-ulcers
Clinical picture.
superficial thrombophlebitis
Pigmentation and induration of superficial veins
Tenderness,pain,redness,swelling,increase local temperature
Overlying skin inflamed.
Patient may have constitutional disturbance with pyrexia and malaise.
Secondary bacterial infection may occasionally complicate the thrombosis.
bleeding from varicose
painless spontaneous rupture of Veins
continious bleeding through sup V and communicating incompetent V
ulcers present on areas of medial malleolus in the back ground of lipodermatosclerosis
and pigmentation of skin
Treatment.
superficial thrombophlebitis
local anticoagulant
NSAID
Anelgetics
Physiotherapy
Elevation of extremity
Bed rest
bleeding from varicose
patient laid recumbent with the leg elevated & pressure bandage is applied.
subsequent to emergency-- varicose vein treated by operation.
compression over bleeding
suturing of bleeding vein & communicating incompetence vein.

ulcers
application of cream or zing gelatin bandage
elastic bandage
leg levation
surgical skin grafting
suturing of underlying perforated vein CID if deep V impassibility is present
Indications for surgical treatment.
superficial thrombophlebitis
in thrombosis spread beyond proximal 1/3 of greater saphenous V surgery
bleeding from varicose

ulcers subcompensated + decomensative stage

complication of vericouse v
symptomatic cases
cosmetic reasons
Kinds of surgical procedures.
- trophic ulcers.
Main purposes of surgical treatment are following:
1* Removal of up and down veno-venous shunts. Its realized by ligation of
junctions between femoral vein and long scaphen vein, so as the once between
short scaphen vein and popliteal. Second part of the purpose reaching is
obligative ligation of incompetent communicating veins.
2* Ablation of varicose transformed subskinal veins.
3* Surgical correction of deep veins valves incompetence.
Troianov-Trendelenburg procedure- long scaphen vein opening and its 3-5 main
branches.
Incompetent communicating veins- local skin incisions by Narat and Cocett procedures.
In patients with a lot of incompetent communicating veins and severe manifestations of
chronic venous insuff- Linton-Felder procedure, includes neartotal ablation of
communicating veins on leg through subfascial posterior longitudinal incision.

The second principle -by removing of main subskinal veins by special olive-end probe
device, by Babcok. Some varices are ligating through small additional incisions by
Narat. Some can be sewed by vertical sutures by Clapp or Sokolov.
The third principle of treatment has been being reached by different surgical procedures
on deep veins by relative valves incompetence relieving. These are extra-, intra- and
extra-intra vascular modes of correction. The last type is more effective. Reached results
are being controlled by retrograde phlebography.

17. Varicous disease idea definition. Muscle-venous pump of leg definition,

structure. Physiology of venous outflow from the lower limbs.
Varicous disease - -idea definition.
Varicose disease is the kind of chronic venous insufficiency and its characterized by present
of sacciformis venous dilations of superficial and deep veins with haemodinamic damages
and vines congestation in lower limbs.
Muscle-venous pump of leg definition, structure.
Lower limb venous haemodinamics has sharp changes, which are depended from body
position and muscular function condition. In reclining position of patient hydrostatic
resistance for venous blood outflow is absent. There isnt muscular pump function. So, in
this condition venous blood outflow volume and velocity become.
In cases of muscular activity their blood supply increases in 8-10 times. In walking, increase
of blood flow volume in main vein of lower limb is because of blood arriving from muscles.
Venous sinusoides of gastrocnemius and soleus muscles, as blood chambers, in muscular
contraction phase become empty. A large blood volume is going into main vein of lower
limb.
First blood portion, which has come from muscular veins, is creating some retrograde flow
and local venous hypertension. Valves are closing due to it.
General intravenous pressure includes in itself static pressure, dynamic pressure and
hydrostatic once. The hydrostatic pressure is determinated as a weight of blood column under

measuring level. So, hydrostatic pressure is more in foot veins then in femoral once in
standing patient position.
Static pressure is determinated due to vessels and muscles tonus, microcircularitive pressure.
Dynamic portion of intravenous pressure is more important . Its determined by kinetic
energy of blood jet, going from lateral anastomosis, first of all.
Venous blood outflow is continual and in relaxing condition venous valves are opened. They
are closing due to retrograde blood flow only. Its realized in cases of quick muscular
constriction, quick standing up, tussis, Valsalva test.
Valves in small veins are protecting microcicularity region from retrograde blood flow and
dynamic venous hypertension. Increase of blood flow velocity in main vein is accompanied
with pressure decreasing in it And this connection is direct. This peculiarity has positive
influence to venous outflow from tissue veins.
Foot has two sorts of venous pumps. Muscular pump, of cause, isnt so important that once
in leg, and compressive pump. Compressive pump is realized by periodical plantar veins
compression. In physiological conditions by walking and running the increase of blood flow
volume is presented in main limb veins as in subskinal veins. And if the increase of main
veins blood flow is depending on muscular pump of leg or femur, the blood flow increase
in short and long scaphen veins are providing by muscular and compressive foot pump. This
outflow ways are presented the shunts from foot veins to popliteal and femoral veins and in
normal condition, they prevent venous hypertension in foot veins.
The Venous (calf-muscles) PumpVenous blood from the lower limb is returned to the
heart by pumping action of call muscles within strong fascial cover. Contraction of the
muscles within strict confines of the encircling deep fascia (venous or calf-muscle pump)
squcey.e the blood and its flow is directed to heart by unidirectional strategic valves. During
momentary phase (diastolic phase of calf pump) blood flows from the superficial venous
system to the deep venous syslcm via the perforating veins under the guidance of valves.
Physiology of venous outflow from the lower limbs.
The venous system of the lower limb can be conveniently classified into three groups
The superficial veins, external to deep fascia and therefore, unsupported

The deep veins deep to deep fascia and

Communicating (Perforating) system of veins connecting the superficial and

deep veins.

The superficial venous system consists of i) Dorsal venous arch lying beyond the heads of
the metatarsals. ii) Lone saphenous veinsFormed at the medial end of the dorsal venous
arch, ascends up the high and finally through the saphenous opening to empty into the
femoral vein. At this end, the long saphenous vein receives the following tributaries :
superficial external iliac, superficial epigastric and superficial external pudendal. The
saphenofemoral junction is always guarded by a valve.
iii) Short saphenous veinFormed at the lateral end of the dorsal venous arch, passes
upwards behind the lateral malleolus to reach the midline of the calf (accompanied by sural
nerve) to open into the popliteal vein. The short saphendpopliteal junction is also guarded by
a valve.
Deep venous system : This high pressure system accompanying the main arteries lies deep to
deep fascia and is well supported by powerful muscles (muscle or calf pump). Deep venous
system consists of the following veins : (i) Posterior tibial vein (lateral+medial plantar veins)
which joins the (ii) Anterior tibial veins (upward continuation of the venae comitantes of the
dorsalis pedis artery) to form (iii) Popliteal vein at the lower border of the popliteus muscle.
It courses up from the opening in the adductor magnus as femoral vein to run up as the
external iliac vein as it passes under the inguinal ligament. Valves in the deep venous system
help to direct the blood flow upwards towards the heart.
Communicating or perforating veins: The perforating veins pass through the deep fascial
layer at numerous anatomical sites in the foot, leg and thigh to connect the superficial and
deep venous systems. The junctions between the superficial and deep venous systems are
guarded by unidirectional strategic valves (see below). Constant medial perforating veins
(lateral perforators being inconstant) are situated behind the medial border of tibia at 5 cm..
10 cm. and 15 cm. above the medial malleolus. This area is susceptible to venous
hypertension and development of venous ulcers.
Functional valve mechanismValvular mechanism is situated at the level of deep fascia.
The valves (veillike bicuspid valve) in the perforating veins permit unidirectional flow of
blood from the superficial to deep venous system. Valves are generally located just proximal
to the entry of a tributary. The retrograde How of blood from the high pressure deep veins to

the low pressure superficial veins is prevented by this valvular mechanism. Normally, this
one-way flow mechanism is guided by valves which are kept closed by the pressure of the
muscles against the deep fascia and a pinch cock mechanism at the deep fascial opening.

18.Muscle-venous pump of leg disorders in a cause of varicous disease. Pathology of

venous outflow from the lower limbs.
All the major leg vv have valves that prevent bld flowing away from the heart. As the calf
mm contract the deep vv within are squeezed and emptied, the bld passing upward,
dineched towards the heart by the non return valves.
As the mm relaxes bld flows in from the superficial system via perforations as well as
from more distal segment of the v only to be pumped upward again by the next
contraction of the calf mm which are thus acting as a pump

Pathology of venous outflow from the limbs:

1. insufficiency of values firstly appears in deep vv
2. bld flows retrograde when standing due to hydrostatic P
3. this P 1st inc in deep V-cause insufficiencies valve C, inc bp in sinusoid, insuff of
valve B
4. bld enters superficial vv standing P transmitted from deep v to sup v
further causes insuff of valve A+congest in
supv
5.bld congest in sup v both in relaxation & in contraction of mm varicous appears.

19. Varicous disease idea definition. Phlebography and US examination,

indications, contraindications, complications and diagnostic possibilities.
Varicous disease idea definition.
Varicose disease is the kind of chronic venous insufficiency and its characterized by present of
sacciformis venous dilations of superficial and deep veins with haemodynamic damages and
vines congestion in lower limbs.
Phlebography and US examination, indications, contraindications, complications and
diagnostic possibilities.
Phlebography.
- There are 2 sorts of phlebography distal and proximal.
- PROXIMAL(DESCENDING) phlebography gives info about valvular competence in
main lower limbs veins.
Procedure:
Cannula is inserted in the femoral vein and contrast material is injected while patient is
standing
Compress above cannula and inject contrast Valsa va maneuver.
There is incompetence if DV below compression contrast moves downward (check
patency of veins).
Contraindications Thrombophlebitis suspicion, allergy to contrast material.
Indications Varices seen superficially, ulcers, hyperpigmentation.
- DISTAL/ASCENDING phlebography necessary for finding incompetent
communicating veins and DV passability. A foot vein is cannulated and a narrow
tourniquet placed just above malleoli to direct blood flow into DV. Contrast is then
injected to outline veins.
Possibilities Anatomic info of veins, patency of veins, to find incompetence of
communicating veins.
US examination.
- To detect arterial disease and patency of veins.
- Gives possibility to find not only subskinal and deep lower extremities veins, but
communicating veins and their valves.
- Indications All patients with DV to detect source, all patientsdiagnosed to confirm
source.
- Duplex US High resolution B-mode US imaging + Doppler US obtain image of
veins and measure flow in veins (anastomosed and functional images).
- Possibility dignosis:
Patency of DV and thrombus localization.
Blood flow through SV and DV valves.
Valvular function and venous reflux (origin).
Patient stands, vein is imaged compress calf to produce forward flow blue in colour
map, release.
Incompetent valve Retrograde flow Red flow map
Indication:

 Patient with recurrent varices history.

Any patient with skin changes to detect causes.
Patient history of suggestive previous venous thrombosis.

20. Main principles of varicous disease surgical treatment. The use and purpose of
conservative therapy and sclerosurgery in a cause of varicous disease.
Main principles of varicous disease surgical treatment.
For today the most effective mode of varicous disease management surgical is. But, it
should remember, that there isnt finally method for radical correction of the disease,
because of its, first of all, congenital disease. So, the main aim of all kinds of varicous
disease management is complications prevention, first of all - trophic ulcers.
Main purposes of surgical treatment are following:
Removal of up and down veno-venous shunts. Its realized by ligation of
junctions between femoral vein and long scaphen vein, so as the once between
short scaphen vein and popliteal. Second part of the purpose reaching is
obligative ligation of incompetent communicating veins.
Ablation of varicose transformed subskinal veins.
Surgical correction of deep veins valves incompetence.
1. LIGATION OF SAPHENOUS POPLITEAL JUNCTION (SPJ) AND
SAPHENOUS FEMORAL JUNCTION (SFJ) AND ABLATION OF
INCOMPETENT COMMUNICATING VEINS (REMOVAL OF VENOUS
SHUNTS): The first principle can has been reached by Troianov-Trendelenburg
procedure. It includes long scaphen vein opening and its 3-5 main branches.
Incompetent communicating veins are removing through local skin incisions by
Narat and Cocett procedures. In patients with a lot of incompetent communicating
veins and severe manifestations of chronic venous insufficiency Linton-Felder
procedure is indicated. It includes neartotal ablation of communicating veins on
leg through subfascial posterior longitudinal incision.
2. REMOVAL OF VARICOSE TRANSFORMED SUPERFICIAL VEINS: The
second principle is realized by removing of main subskinal veins by special
olive-end probe device, was invented by Babcok. Some varicies are ligating

through small additional incisions by Narat. Some of them can be sewed by

vertical sutures by Clapp or Sokolov.
3. SURGICAL CORRECTION OF DV VALVULAR INCOMPETENCE: The third
principle of treatment has been being reached by different surgical procedures on
deep veins by relative valves incompetence relieving. There are extra-, intra- and
extra-intra vascular modes of correction. The last type is more effective. Reached
results are being controlled by retrograde phlebography.
In cases of decompensive varicous disease with trophic ulcers some modes of posterior
tibial veins resection or occlusion may be applied. The sense of it is contained in ablation
of retrograde blood flow from deep leg veins into small vessels in trophic changes area.
The use and purpose of conservative therapy and sclerosurgery in a cause of
varicous disease.
1.Conservative
1) Elevation
2) Elastic stocking
3) Massage
4) Anticoagulant therapyHeparin I.V. for 7-10 days followed by warfarin orally tor 3
months
5) Analgesics
6) Fibrinolytic therapy e.g. streptokinase or urokinase may cause serious bleeding at the
site of operation if used in about 10 days after operation.
7) If fever persists, blood culture should be performed and antibiotics given for fear of
septicaemia & pyaemia
8) Patients with extensive thrombosis are often very anaemic and urgent blood
transfusion should be considered.
Conservative treatment of varicous disease has additional importance only. Among them
there are the use of elastic compressive bandage and sclerotherapy. Elastic bandage can
be realized by special bandages and stocking. Elastic bandage traditionally is using in
postoperative period.

For treatment of trophic leg ulcers zinc-gelatin dressing is using. This dressing improves
skin blood supply due to vent effect stimulation. During muscles contraction skin venous
rate is pressed between muscles and dressing and is empty. During muscle relaxation
dressing pressure is decreasing and skin veins begin to be filled up from microcirculative
area. It leads to increase arterial blood supply of the skin and relieves blood congestition
in ulcer area.
For today it is rational to use combined mode for varicous disease treatment - surgical
and sclerotherapy. This may may be accompanied with dissection and ligation of varicous
subskinal veins by Narat, Clapp, Sokolov.
The main shot-coming of sclerosing therapy is unstable results and early recurrence of
phlebectasia. As an independent management mode it can be used in small patient groups
with initial signs of varicous disease and in cases of critical-ill patients.
21. Postthrombotic disease idea definition, pathology of venous outflow from
the lower limbs according disease stage.
Postthrombotic disease idea definition.
Postthrombotic disease is the most severe clinical form of chronic venous insufficiency.
The disease is wide-spread and leads to stable invalidism.
The term postthrombotic disease was proposed by Saveliev, and its determining
pathological condition, which has developed after acute thrombophlebitis or
phlebothrombosis in vein cava inferior system, including its subkidney part, iliac veins
and main deep veins of lower extremities.
Pathology of venous outflow from the lower limbs according disease stage.
There are 3 stages:
Clinical form can be determined by general examination. In 1 stage of sclerotic form of
postthrombotic disease there are no pathological superficial veins dilations. In 2 and 3
stages varicous changes appear, but they arent so severe and localize in region of
incompetent communicating veins. Main subskinal veins havent varices. But indurative

process in fat tissue and skin hyperpigmentation on leg are more severe, then in cases of
varicose form.
In sclerotic form testaceous fibrosis may be in lower one third of leg. There are no
oedemas here due to severe tissue induration, but it localizes some upper.
In cases of varicose form of postthrombotic disease varicous transformation of subskinal
veins are expressed. There are all signs of varicous disease, but they are redoubled by
severe blood outflow lesions in deep veins.
In first stage edema of fat tissue puts on a mask of varicose dilation. But in second stage
this dilation is more severe.
Its very important, that limb edema after acute DVT is the most important sign of
postthrombotic disease.
Morphologically 1 stage of postthrombotic disease conforms to stage of deep veins
occlusion. Recanalization finishing means transformation of 1 stage into 2 once.
Clinically, beginning of the 2 stage is conformed to presence of trophic changes - tissues
hyperpigmentation and induration in leg lower one third. This changes are conditioned by
retrograde blood flow in deep veins.
In 3 stage trophic ulcers appear. Peculiarities of venous blood outflow are the same, as
in 2 stage. But spreading of indurative cellulitis areas are accompanied with lymph
insufficiency. So, 3-d stage of postthrombotic disease is named chronic lympho-venous
insufficiency.
Besides clinical forms and stages of postthrombotic disease venous outflow condition
determination is very important. They are subcompensation and decompensation.
Obviously there are no direct accordance between disease stages and venous outflow
condition. First stage of the disease conforms to deep veins occlusion, so venous outflow
lesions are the most severe. But in 2 and 3 stages after reconalization of deep veins blood
outflow improves. Clinically its manefistated by oedema decrease. And trophic changes
in it are connected not so with venous congestition, but with retrograde blood flow.

Usually, in 1 stage patients fell themself badly, disease manifestations are more
painful, then in 2 stage, when trophic changes appear. Postthrombotic disease heaviness
is characterized by venous outflow condition.
Besides clinical forms, disease stages and venous outflow condition, sort and
localization of venous lesions are distinguished. The lesions includes occlusion, total and
partial reconalization. According using classification diagnosis can be following, for
example, postthrombotic disease of right lower extremity, sclerotic form, 2 stage, partial
reconalization of left iliac vein, occlusion of left femoral vein, reconalization of leg deep
veins, decompensative condition of venous blood outflow.

22. Likeness and differences between varicous disease & postthrombotic disease in:
a) etiology,
PTD- pathological condition, which has developed after acute thrombophlebitis or
phlebothrombosis in vein cava inferior system
Acute deep venous thrombosis in limbs leads to postthrombotic disease in 90-96%
VARICOUS (etio & path)-Primary1. genetic predisposition- congenital disbalance between elastin and collagen vascular
wall becomes resistant to normal blood pressure to vein dilation.
congenital or acquired valves insufficiency. venous incompetence venous hypertension
retrograde blood flow varicous disease.
Secondary-deep V thrombosis resulting in shunting of blood through incompetent
perforates to the superficial system.
Valves incompetence can be anatomical and functional.
all pathological venous dilation of lower limbs appears due to retrograde blood flow.
Deep veins are defended by fascies and muscles, so their dilation is even. In superficial
veins subskinal fatty tissue cannt defend them equal, so varicies are appearing.
Pathomorphological changes in varicous veins are definited as phlebosclerosis
b) pathogenesis,
PTD- Mech 1. Due to venous occlusion severe blood hypertension appears lower it.
It leads not only to main deep vein dilation, but to muscular once too. Due to venous
hypertension collateral blood out flow ways are opening.

Mech 2. Acute venous thrombosis transforms into stable occlusion or changed by

recanalization of the vein.
Mech 3.Thrombosis and recanalization lead to venous valves destroying and
retrograde blood flow appears.
Mech 4. Retrograde blood flow promotes pathological changes in leg soft tissues,
microcirculative bad and veins dilation.
Capillary permeability inc for bld proteins and dec for 02 supply. Arterial-venous shunts
become active. Colloid-osmotic intertissue P is inc, due to proteins and electrolytes
coming out with tissue oedema appearance.
Stable occlusion appears more often in the general iliac vein and the superficial femoral
vein due to rich rate presence for collateral blood outflow in this areas.
Valves destroying is realized due to two mechanisms
1. direct damage during thromb reconalization and
2. indirect - due to vein dilation. It leads to relative valve insufficiency, thromb
recanalization to absolute once.
c) morphology,
PTD-direct damage to venous wall+valves ,thrombi,strictures venous wall sclerosis. Less
venous dialation more tropic changes.
Vericouse-no damage to anatomic venous structure more venous dialation less tropic
change
d) blood outflow disorders,

LikenessesBoth are chronic venous insufficiency caused by venous valvular incompetence +

retrograde bld flow.
Varicous dilatation of superficial v + tropic changes of skin + subcutaneous tissue.

23. Postthrombotic disease. Indications for surgical treatment, the principles and
ways of treatment.
Indications for surgical treatment.

In 1st stage of sclerotic form of postthrombotic disease there are no pathological

superficial veins dilations.

In 2 and 3 stages varicous changes appear, but they arent so severe and localize
in region of incompetent communicating veins. Main subskinal veins havent
varices. But indurative process in fat tissue and skin hyperpigmentation on leg
are more severe, then in cases of varicose form.

In sclerotic form testaceous fibrose may be in lower one third of leg. There is no
oedema here due to severe tissue induration, but it localizes some upper.

In cases of varicose form of postthrombotic disease varicous transformation of

subskinal veins are expressed. There are all signs of varicous disease, but they are
redouble by severe blood outflow lesions in deep veins.

In first stage oedema of fat tissue puts on a mask of varicose dilation. But in
second stage this dilation is more severe.

Its very important, that limb oedema after acute deep venous thrombosis is the
most important sign of postthrombotic disease.

Morphologicaly 1st stage of postthrombotic disease conforms to stage of deep

veins occlusion. Recanalization finishing means transformation of 1 stage into 2
once. Clinically, beginning of the 2 stage is conformed to presence of trophic
changes - tissues hyperpigmentation and induration in leg lower one third. These
changes are conditioned by retrograde blood flow in deep veins.

In 3 stage trophic ulcers appear. Peculiarities of venous blood outflow are the
same, as in 2 stage. But spreading of indurative cellulitis areas are accompanied
with lymph insufficiency. So, 3-d stage of postthrombotic disease is named
chronic lympho-venous insufficiency.

Besides clinical forms and stages of postthrombotic disease venous outflow condition
determination is very important. They are subcompensation and decompensation.
The 2nd and 3rd stage of both sclerotic and varicous are indication for restorative and +
reconstructive procedures.
The principles & the ways of treatment.
The main principle of surgical management of postthrombotic disease includes venous
outflow correction by restorative and reconstructive procedures. And, at last place - the
use of subskinal veins ablations and ligations of perforating veins.

Among reconstructive surgical procedures Palm-Esperon and Thayer-Warren:

Palm-Esperon procedure includes creation of venous bypass between iliac veins due to
the long scaphen vein. Venous blood from ill extremity is shunting into iliac vein of
another side.
Thayer-Warren procedure includes artificial anastomosis creation between long
scaphen vein and femoral or popliteal veins on the same side.

24. Postthrombotic disease determination of the idea. Clinical classification

according to forms and stages. Relation between disease stage and blood outflow
condition.
Determination of the idea.
Postthrombotic disease is the most severe clinical form of chronic venous insufficiency.
A pathological condition, which has developed after acute thrombophlebitis or
phlebothrombosis in vein cava inferior system
Acute deep venous thrombosis in limbs leads to postthrombotic disease in 90-96%
Clinical classification according forms and stages.
There are two clinical forms of postthrombotic disease - varicose and sclerotic once.
Clinical form can be determined by general examination.
In 1 stage of sclerotic form of postthrombotic disease there are no pathological
superficial veins dilations.
In 2 and 3 stages varicous changes appear, but they arent so severe and localize in region
of incompetent communicating veins. Main subskinal veins havent varicies. But
indurative process in fat tissue and skin hyperpigmentation on leg are more severe, then
in cases of varicose form.
In sclerotic form testaceous fibrose may be in lower one third of leg. There are no
oedema here due to severe tissue induration, but it localizes some upper.
In cases of varicose form of postthrombotic disease varicous transformation of
subskinal veins are expressed. There are all signs of varicous disease, but they are
redouble by severe blood outflow lesions in deep veins.
In first stage oedema of fat tissue puts on a mask of varicose dilation. But in second
stage this dilation is more severe.
Its very important, that limb oedema after acute deep venous thrombosis is the most
important sign of postthrombotic disease.

Morphologicaly 1 stage of postthrombotic disease conforms to stage of deep veins

occlusion. And recanalization finishing means transformation of 1 stage into 2 once.
Clinically, beginning of the 2 stage is conformed to presence of trophic changes - tissues
hyperpigmentation and induration in leg lower one third. This changes are conditioned by
retrograde blood flow in deep veins.
In 3 stage trophic ulcers appear. Peculiarities of venous blood outflow are the same, as
in 2 stage. But spreading of indurative cellulitis areas are accompanied with lymph
insufficiency. So, 3-d stage of postthrombotic disease is named chronic lympho-venous
insufficiency.

Besides clinical forms and stages of postthrombotic disease venous outflow condition
determination is very important. They are subcompensation and decompensation.
Relation between disease stage and blood outflow condition.

25. Postthrombotic disease. Determination of the idea. Pathogenesis. Clinical picture

according to disease stage. Differential diagnosis.
Determination of the idea.
Postthrombotic disease is the most severe clinical form of chronic venous insufficiency.
pathological condition, which has developed after acute thrombophlebitis or
phlebothrombosis in vein cava inferior system
Acute deep venous thrombosis in limbs leads to postthrombotic disease in 90-96%.
Pathogenesis.
Mech 1. Due to venous occlusion severe blood hypertension appears lower it. It
leads not only to main deep vein dilation, but to muscular once too. Due to venous
hypertension collateral blood out flow ways are opening.

Mech 2. Acute venous thrombosis transforms into stable occlusion or changed by

recanalization of the vein.

Mech 3.Thrombosis and recanalization lead to venous valves destroying and

retrograde blood flow appears.

Mech 4. Retrograde blood flow promotes pathological changes in leg soft tissues,
microcirculative bad and veins dilation.
Capillary permeability increases for blood proteins and decrease for oxygen supply.
Arterial-venous shunts become active. Colloid-osmotic intertissue pressure is increased,
due to proteins and electrolytes coming out with tissue oedema appearance.
Stable occlusion appears more often in the general iliac vein and the superficial femoral
vein due to rich rate presence for collateral blood outflow in this areas.
Valves destroying is realized due to two mechanisms
-

direct damage during thromb reconalization and

indirect - due to vein dilation. It leads to relative valve insufficiency, thromb

recanalization to absolute once.

Clinical picture includes in itself increase of fatigability, leg pain, edema, subskinal veins
dilations, recurrence of acute thrombosis. Later, skin hyperpigmentation, fat tissue
induration and trophic ulcers appear.
Clinical picture according disease stage.
Clinical form can be determined by general examination.
In 1 stage of sclerotic form of postthrombotic disease there are no pathological
superficial veins dilations.
In 2 and 3 stages varicous changes appear, but they arent so severe and localize in region
of incompetent communicating veins. Main subskinal veins havent varicies. But
indurative process in fat tissue and skin hyperpigmentation on leg are more severe, then
in cases of varicose form.
In sclerotic form testaceous fibrose may be in lower one third of leg. There are no
oedema here due to severe tissue induration, but it localizes some upper.
In cases of varicose form of postthrombotic disease varicous transformation of
subskinal veins are expressed. There are all signs of varicous disease, but they are
redouble by severe blood outflow lesions in deep veins.
In first stage oedema of fat tissue puts on a mask of varicose dilation. But in second
stage this dilation is more severe.

Its very important, that limb oedema after acute deep venous thrombosis is the most
important sign of postthrombotic disease.
Morphologicaly 1 stage of postthrombotic disease conforms to stage of deep veins
occlusion. And recanalization finishing means transformation of 1 stage into 2 once.
Clinically, beginning of the 2 stage is conformed to presence of trophic changes - tissues
hyperpigmentation and induration in leg lower one third. This changes are conditioned by
retrograde blood flow in deep veins.
In 3 stage trophic ulcers appear. Peculiarities of venous blood outflow are the same, as
in 2 stage. But spreading of indurative cellulitis areas are accompanied with lymph
insufficiency. So, 3-d stage of postthrombotic disease is named chronic lympho-venous
insufficiency.
Besides clinical forms and stages of postthrombotic disease venous outflow condition
determination is very important. They are subcompensation and decompensation.
Differential diagnosis.
With varicous.
26. Likeness and differences between varicous disease & postthrombotic disease in
treatment.
PTD- The main principle of surgical management of postthrombotic disease includes
venous outflow correction by restorative and reconstructive procedures. And, at last place
- the use of subskinal veins ablations and ligations of perforating veins.
Among reconstructive surgical procedures Palm-Esperon and Thayer-Warren

Palm-Esperon procedure includes creation of venous bypass between iliac veins

due to the long scaphen vein. Venous blood from ill extremity is shunting into
iliac vein of another side.
Thayer-Warren procedure includes artificial anastomosis creation between long
scaphen vein and femoral or popliteal veins on the same side.

Varicose- For today the most effective mode of varicous disease management surgical is.
But, it should remember, that there isnt finally method for radical correction of the
disease, because of its, first of all, congenital disease. So, the main aim of all kinds of
varicous disease management is complications prevention, first of all - trophic ulcers.
Main purposes of surgical treatment are following:
Removal of up and down veno-venous shunts. Its realized by ligation of
junctions between femoral vein and long scaphen vein, so as the once between
short scaphen vein and popliteal. Second part of the purpose reaching is
obligative ligation of incompetent communicating veins.

 Ablation of varicose transformed subskinal veins.

Surgical correction of deep veins valves incompetence.
The first principle can has been reached by Troianov-Trendelenburg procedure. Its
including long scaphen vein opening and its 3-5 main branches.
Incompetent communicating veins are removing through local skin incisions by Narat
and Cocett procedures. In patients with a lot of incompetent communicating veins and
severe manifestations of chronic venous insufficiency Linton-Felder procedure is
indicated. It includes neartotal ablation of communicating veins on leg through
subfascial posterior longitudinal incision.
The second principle is realized by removing of main subskinal veins by special
olive-end probe device, was invented by Babcok. Some varicies are ligating through
small additional incisions by Narat. Some of them can be sewed by vertical sutures by
Clapp or Sokolov.
The third principle of treatment has been being reached by different surgical
procedures on deep veins by relative valves incompetence relieving. There are extra-,
intra- and extra-intra vascular modes of correction. The last type is more effective.
Reached results are being controlled by retrograde phlebography.
In cases of decompensive varicous disease with trophic ulcers some modes of
posterior tibial veins resection or occlusion may be applied. The sense of it is contained
in ablation of retrograde blood flow from deep leg veins into small vessels in trophic
changes area.
Conservative treatment of varicous disease has additional importance only. Among
them there are the use of elastic compressive bandage and sclerotherapy. Elastic bandage
can be realized by special bandages and stocking. Elastic bandage traditionally is using in
postoperative period.
For treatment of trophic leg ulcers zinc-gelatin dressing is using. This dressing
improves skin blood supply due to vent effect stimulation. During muscles contraction
skin venous rate is pressed between muscles and dressing and is empty. During muscle
relaxation dressing pressure is decreasing and skin veins begin to be filled up from

microcirculative area. It leads to increase arterial blood supply of the skin and relieves
blood congestition in ulcer area.
For today it is rational to use combined mode for varicous disease treatment - surgical
and sclerotherapy. This may may be accompanied with dissection and ligation of varicous
subskinal veins by Narat, Clapp, Sokolov.
The main shot-coming of sclerosing therapy is unstable results and early recurrence
of phlebectasia. As an independent management mode it can be used in small patient
groups with initial signs of varicous disease and in cases of critical-ill patients.

27. Cancer of the lung. Classification, etiology. Pathological anatomy, stages of

the disease. Differential diagnosis between central and peripheral lung
cancer.
Classification:
Clinical classification of CL (prof. Savitsky, 1957)
1. Central CL (endobronchial, peribronchial, branching)
2. Peripheric CL (spherical, pneumonic, cancer of apex pulmonis -Pancost's, cavitary
form of cancer...)
3. Atypical forme of cancer of
the lung (mediastinal, miliary)
Histological types:
1. squamous cell carcinoma: (high differentiation, medium differentiation, poor differentiation)
2. adenocarcinoma: (acinar adenocarcinoma; papillary adenocarcinoma; solid
adenocarcinoma with mucus formation; bronchioloalveolar carcinoma)
3. small-cell carcinoma;
4. large-cell carcinoma;
5. other types
Etiology:
- Smoking
- Genetic predisposition
- Asbestos
- Metals (Arsenic and arsenic compounds,chromate,trivalent and hexavalent
chromium)
- Hydrocarbons
- Radiation
Pathological anatomy:
Pathogenetically, ciliary function of the bronchial surface epithelial cells and, thus, the
self-cleaning function of the bronchial mucosa is disturbed by various toxins, mainly the
gas phase of tobacco smoking. The subsequent loss of the natural protective properties of

the bronchial mucosa and chronic irritation cause a transformation of the bronchial
surface epithelium with squamous metaplasia.
Morphological findings in bronchial preneoplasia, i.e. dysplasia with epithelial atypia
extending to carcinoma in situ and invasive carcinoma, are suggestive of a multistep
process of carcinogenesis
Stages of the disease:
4 major distinct phases have been identified:
1) initiation;
2) promotion;
3) conversion;
4) progression.
The initiation phase is described as an early, rapid and largely irreversible change in a
permanently altered cell. Tumour initiation begins through mutation of genetic material
following exposure to carcinogens.
Promotion of carcinogenesis is a more gradual process, during which an initiated cell
acquires more and more malignant characteristics. This complex phase of carcinogenesis,
involving a variety of cellular changes, is thought to last decades in humans. The two
final stages of carcinogenesis are conversion and progression. In contrast to initiation and
promotion, which have been studied extensively in experimental animals, much less is
known about tumour conversion and tumour progression, although these are the aspects
of carcinogenesis that most concern clinicians. In both of these processes genetic changes
are involved.
Differential diagnosis between central & peripheral lung cancer:

Central
1. acc to clinics
cough (dryinitially)
hemoptysis
chest pain
intoxication synd.
Headache
Anorexia
Asthenia
2. acc to mec Of dise dvlp
bronchial obstruction
obst. Emphysema
atelectasis
cancerous pneumonitis
sund of intra thoracic inflformation of abscess
3. acc to diagnosis
fibrobonchoscopical Dx
-take biopsy
-fluid aspiration
-cytological investigation
CXR lat& straight view
-nodule like fom
-infiltrative/atelectasis
CT scan
Investigation of
sputum+pleual fluid
Trans thoracic tumor punctue
Radionucleide method
Surgical method
Punctue biopsy of lymph
nodes
laparoscopy

Perephral
Chest pain
Sympt of germination & m
Horners synd
Aphonia
Strokes collar synd

Tumor germination(other organ +

m)
Relatively slow gowth of tumor
Affection of sub segmental + low
bronchi
Flurography examination
X-ray
Percutaneous biopsy

28. Central lung cancer. Clinical picture. Diagnosis. Differential diagnosis. The
importance of special examination methods in the diagnosis of central lung cancer.
Clinical picture.
1. Central CL (endobronchial, peribronchial, branching):
- Endobronchial
- Exofitic type quick start, infringement of movement of sputum, tussis
(sometimes with blood), pains, developing of atelectasis.

Endofitic type later beginning of disease. The main symptoms: tussis, sputum
(with blood). Almost similar to exofitic type.
Peribronchial
Nodal rise of temperature, 36.8-37.5
Furcal (the tumoral node is absent) sputum with blood, clinic of the chronic
pneumonia. Difficult diagnosis.

Diagnosis.
The cardinal imaging signs of central tumor are collapse/consolidation of the lung beyond
the tumor and the presence of hilar enlargement; signs which may be seen in isolation or
in conjunction with one another. Obstruction of a major bronchus often leads to a
combination of atelectasis and retention of secretions with consequent pulmonary
opacity, but collateral air drift may partially or completely prevent these pose-obstructive
changes. Secondary infections beyond the obstruction may occur. The following features
suggest that pneumonia is secondary to an obstructing neoplasm:
1. The shape of the collapsed or consolidated lobe may be altered because of the
bulk of the underlying tumor. In cases with lobar collapse, the fissure in the region
of the mass is unable to move it in the usual manner and therefore the fissure
appears bulged (golden S sign). This sign indicates that the collapse is the
result of an underlying mass and that the mass will be amenable to bronchoscopic
biopsy.
2. The presence of pneumonia in a patient in the cancer age group, confined to one
lobe (or more lobes if there is common bronchus supplying these lobes) that
persists unchanged > 3 weeks.
Differential diagnosis.

The importance of special examination methods in the diagnosis of central lung

cancer.

30. Peripheral lung cancer

Clinical pic
-fever
-cough with sputum
-chest pain in de side of the tumour
-weight loss
-malaise
-bone pain dt spreading

-pancoast brachial n humeral pain

-atrophy of shoulder n distal part
-horner ptoasis n miosis
-right laryngeal nerve palsy
-hoarseness

Diagnosis
1.Sputum cytology
-With the ready availability of fibreoptic bronchoscopy, reliance on sputum cytology has
diminished.
-it is useful, particularly in patients unsuitable for fibreoptic bronchoscopy, such as those
with a recent myocardial infarct or very poor lung function.
-The best specimens are obtained from a 'deep cough' early in the morning. Specimens
collected 1-4 h after bronchoscopy and on the following morning can produce a positive
yield even if the bronchoscopy is normal.
2.Bronchoscopy
-

bronchoscopy has a role in staging the disease, and an extended role in the deciding
the therapeutic choice.

It is convenient to perform, safe, and well-tolerated by the patient. The requirement

of only minimal sedation makes it acceptable as an out-patient procedure

The major advantage of the flexible scope is its ability to reach more peripheral
bronchi

Contraindications to the procedure are few and include: hypoxaemia refractory to

supplemental oxygen; intractable bleeding diathesis; severe pulmonary
hypertension; cardiovascular instability; and acute hyper -capnia.

Fibreoptic bronchoscopy may be performed safely in the presence of superior vena

caval obstruction.

3.Transbronchial biopsy
4.Transbronchial needle aspiration
-

It involves the insertion of a metal needle into the tissue to be sam pled, and whilst
suction is applied, the needle is moved back and forti to obtain an aspirate for
cytological examination.

5.Bronchoalveolar lavage

-The main role of bronchoalveolar lavage (BAL) in patients with lung cancer is the
diagnosis of opportunistic infections in patients undergoing chemotherapy.

Differential diagnosis
1.retrosternal thyroid aneurysm of aorta
2.thymic tumor n cysts
3.cardiomegaly
4.hodgins n nonhodgins

Indications n contraindications for surgical treatment

Indications:
-pt can compensate life after pulmonectomy or S1lobectomy or S11 lobectomy
Contraindications:
1. extensive ipsilateral lymph nodes
2. malignant pleural effusion
3. involvement of tracheal carina
4. SVC syndrome
5. recurrent laryngeal/phrenic nerve paralysis
6. involvement of main pulm artery

operation strategies

incisions r posterolateral n ant thoracotomy

posterolateral thoracotomy is route of choice,providing wide visualization both of
ant n post hilar regions n the mediastinum
de ant incision has de advantage of speed in opening n closing de chest n is more
muscle sparing but provides oly limited exposure to post hilar
structures,consequently impairing complete lymhadenopathy.

Sleeve resections of bronchial n vascular tree r difficult to perform frm dis

incision.
It is mainly performed for diagnostic open lung biopsy n may also use in
treatment of benign lesions.
Median sterotomy leads to less postoperative pain,but has not been routinely
accepted for lung carcinomas.
It requires very elaborate preparatory procedures,especially for resection of left
lower lobe n in particularly in elderly pts,who r present with enlarged left
ventricle as compression of heart may cause arrhytmias.
Plastic surgery of left bronchial tree is not feasible via access.
Median sternotomy is import in de surgical approach to pulm metastasis.

31. Acute lung abscesses. Definition of the idea. Classification. Etiology and
pathogenesis. Clinical picture. Diagnosis.
Definition of the idea.
Lung abscess: A localized cavity with pus, resulting from necrosis of lung tissue, with
surrounding pneumonitis.
A lung abscess may be putrid (due to anaerobic bacteria) or nonputrid (due to anaerobes
or aerobes). "Gangrene of the lung" denotes a similar though more diffuse and extensive
process in which necrosis predominates.
Classification.
Acc Etiology:
1 Bacterial (Aerobic , Anaerobic, Mixed)
2. Not bacterial (The elementary organisms , Fungus)
Acc Pathogenesis
1. Bronchogenic (With aspiration ,With obtiration, Metapneumonic)
2. Hematogenous (embolic).
3 Traumatic
4. Lymphogenous.
5. Contact.
Acc Localization:
1.Central
2 Peripheric (cortical , subpleural)
Acc Spreading:
1. Singular.
2. Multiple(Unilateral, Bilaterial)
Acc Character of the clinical features
1. Acute
2. Chronic:( In phase of the remission, In phase of the exacerbation)
Acc Connection with the bronchus:
1. It is not drained.
2. It is drained:( There is enough, There is not enough)
Acc Complications:
Empyema of the pleura

Bleeding.
Defeat of another mild
Phlegmon of the thoracal wall.
Bacterial shock
Sepsis

Etiology and pathogenesis.

Lung abscesses are usually due to infected material from the upper airway aspirated when
a patient is unconscious or obtunded from alcohol, other drugs, CNS disease, general
anesthesia, coma, or excessive sedation. The causative organisms are usually
anaerobes. Lung abscesses are often associated with periodontal disease, in which
anaerobes are prevalent. Bacteria cultured from lung abscesses include common and
nasopharyngeal flora, particularly anaerobes, and less often, aerobic bacteria or fungi.
Bronchogenic carcinoma is an occasional underlying cause in older smokers.
Pneumonia due to Klebsiella pneumoniae (Friedlnder's bacillus), Staphylococcus
aureus, Actinomyces israelii, -hemolytic streptococcus, Streptococcus milleri (and
other aerobic or microaerophilic streptococci), Legionella sp, or Haemophilus
influenzae is sometimes complicated by abscess formation. Lung abscess in the
compromised host is usually due to Nocardia sp, Cryptococcus sp, Aspergillus sp,
Phycomycetes sp, atypical mycobacteria (primarily Mycobacterium aviumintracellulare or M. kansasii), or gram-negative bacilli. Blastomycosis, histoplasmosis,
and coccidioidomycosis may also cause acute or chronic lung abscesses. Less common
causes of lung abscess include septic pulmonary emboli, secondary infection of
pulmonary infarcts, and direct extension of amebic or bacterial abscesses from the
liver through the diaphragm into the lower lobe of the lung.
Single lung abscesses are most common. Multiple abscesses usually are unilateral; they
may develop simultaneously or spread from a single focus. In abscesses due to
aspiration, the superior segment of a lower lobe and the posterior segment of an upper
lobe are affected most often. A solitary abscess secondary to bronchial obstruction or
to an infected embolus starts as necrosis of a major portion of the affected
bronchopulmonary segment. The base of the segment is usually next to the chest wall,
and the pleural space in the area is often obliterated by inflammatory adhesions.
Embolic spread of infection, most often due to S. aureus with tricuspid endocarditis in
IV drug abusers, has become more common and is usually characterized by multiple
lung lesions in noncontiguous sites. Suppurative venous thrombophlebitis due to
aerobic or anaerobic bacteria may also cause embolic lung abscesses.
An abscess usually ruptures into a bronchus, and its contents are expectorated, leaving a
cavity filled with fluid and air. Occasionally, an abscess ruptures into the pleural
cavity, resulting in an empyema, sometimes with bronchopleural fistula. Similarly, the
rupture of a large abscess into a bronchus or vigorous attempts at drainage may cause
widespread bronchial dissemination of pus with diffuse pneumonia and a condition
resembling adult respiratory distress syndrome.
Clinical picture.
There are two periods of development this disease.
The first period - before break of pus in the bronchi.

Signs:
Body temperature about 40 C
Stethalgias on the side of defeat
Backlog of the struck side in the act of respiration
Morbidity at the palpation of the struck side
The second period The second period begins after break of an abscess in bronchus (draining bronchus).
Signs:
Fast downstroke of temperature (37,5-38 C)
A plenty of the sputum. The sputum is parted on three layers
1. Bottom Layer - pus
2. Average Layer - serous liquid
3. Top Layer - foam.
Sometimes there is the impurity of blood.
Onset may be acute or insidious. Early symptoms are often those of pneumonia, ie,
malaise, anorexia, sputum-producing cough, sweats, and fever. Severe prostration and
a temperature of 39.4 C (103 F) or higher may be present. Fever, anorexia,
weakness, and debility are sometimes minimal if the infection is limited or indolent.
Unless the abscess is completely walled off, the sputum is purulent and may be bloodstreaked. An abscess may not be suspected until it perforates a bronchus, when a large
amount of purulent sputum, putrid or not, may be expectorated over a few hours or
several days. The sputum may contain gangrenous lung tissue. A putrid (penetrating
and foul) odor is diagnostic of anaerobic bacterial causation. Putrid sputum occurs in
30 to 50% of all patients with lung abscess, but about 40% of patients with abscesses
due to anaerobes do not have a putrid sputum, so its absence does not exclude this
diagnosis. Chest pain, if present, usually indicates pleural involvement.
Physical signs include a small area of dullness, indicating localized pneumonic
consolidation, and usually suppressed (rather than bronchial) breath sounds. Fine or
medium moist crackles may be present. If the cavity is large there may be tympany
and amphoric breath sounds.
If the abscess becomes chronic, weight loss, anemia, and hypertrophic pulmonary
osteoarthropathy may occur. Physical examination of the chest may be negative in the
chronic phase, but rales and rhonchi are usually present.
Diagnosis.
Methods of Diagnostics:
- Chest Imaging
conventional chest x-ray
CT with or without contrast or high-resolution techniques
angiography of the pulmonary or bronchial circulation using contrast materials or
digital subtraction
ultrasonography
radionuclide scanning
MRI.

- Diagnostic thoracentesis
- Thoracoscopy
- Bronchoscopy
- Ancillary procedures:
Bronchoalveolar lavage
Transbronchial lung biopsy
Submucosal and transbronchial needle aspiration
- Percutaneous Transthoracic Needle Aspiration
- Thoracotomy
- Tracheal Aspiration
Chest x-rays early in the course may show a segmental or lobar consolidation, which
sometimes becomes globular as pus distends it.
After an abscess ruptures into a bronchus, a cavity with a fluid level appears on x-ray. If
chest x-rays suggest an underlying tumor or foreign body or if the presentation is
atypical, CT scanning may provide better anatomic definition.
Sputum should be examined by smear and culture for bacteria, fungi, and mycobacteria.
Expectorated sputum is not appropriate because the mouth normally contains anaerobic
organisms that contaminate the specimen during passage through the upper airways. The
attribution of disease to anaerobes usually requires a specimen obtained by transtracheal
aspiration, transthoracic aspiration, or fiberoptic bronchoscopy with a protected brush and
quantitative cultures, but these procedures are not performed often. Such invasive
procedures should be reserved for cases that have an atypical presentation or that are
unresponsive to antibiotics; however, once antibiotics are initiated, there is no reliable
method for obtaining specimens useful for bacterial culture. Bronchoscopy is
unnecessary if response to antibiotics is adequate and if a foreign body or tumor is not
suspected.

32. Acute lung abscesses - the modes of minimal-invasive surgical treatment.

Results.
Postural drainage may be a helpful adjunct, but it may also cause spillage of infection
into other bronchi with extension of the infection or acute obstruction. If the patient is
weak or paralyzed, tracheostomy and suctioning may be necessary. Rarely does
bronchoscopic aspiration help facilitate drainage. Surgical drainage is rarely necessary
because lesions usually respond to antibiotics. Patients with large cavities who do not
respond to drugs may be candidates for percutaneous drainage; patients with empyema
require it.

Pulmonary resection is the procedure of choice for an abscess resistant to drugs,

particularly if bronchogenic carcinoma is suspected. Lobectomy is the most common
procedure; segmental resection usually suffices for small lesions. Pneumonectomy may
be necessary for multiple abscesses or pulmonary gangrene refractory to medical
management. The mortality rate after pneumonectomy is 5 to 10%; after lesser resections,
it is much lower.
Antibiotics should be started as soon as sputum and blood have been collected for culture
and sensitivity. The preferred drug is clindamycin, initially 600 mg IV tid, then 300 mg
po qid. An alternative regimen is IV penicillin G 2 to 10 million U/day, followed by oral
penicillin V 500 to 750 mg qid. Antibiotics are changed to oral when the patient is
afebrile and subjectively improved. Some authorities prefer to combine penicillin with
oral metronidazole 500 mg qid. If a gram-negative organism, S. aureus, or other aerobic
pathogen is implicated, the antibiotic chosen depends on the results of sensitivity tests.
Treatment should be continued until the pneumonitis has resolved and the cavity has
disappeared, leaving only a small stable residual lesion, a thin-walled cyst, or clear lung
fields. Resolution usually requires several weeks or months of treatment, much of which
is given as oral antibiotics on an outpatient basis.
Results of acute abscess of the lung:
1. whole recovery- formation of limited pneumosclerosis
2. clinical recovery- formation of dry cavity
3. clinical improvement
4. transition to chronical form
5. death of the patient.
33. Differential diagnosis of acute lung abscesses. Treatment.
Lesions that simulate bacterial lung abscess include cavitating bronchogenic carcinoma,
bronchiectasis, empyema secondary to a bronchopleural fistula, TB, coccidioidomycosis
and other mycotic lung infections, infected pulmonary bulla or air cyst, pulmonary
sequestration, silicotic nodule with central necrosis, subphrenic or hepatic (amebic or
hydatid) abscess with perforation into a bronchus, and Wegener's granulomatosis.
Repeated clinical evaluation and the procedures described above can usually differentiate
these disorders from simple lung abscess.
Prognosis and Treatment:

Prompt, complete healing of a lung abscess depends on adequate antibiotic treatment.

Most patients recover without surgery.
Antibiotics should be started as soon as sputum and blood have been collected for culture
and sensitivity. The preferred drug is clindamycin, initially 600 mg IV tid, then 300 mg
po qid. An alternative regimen is IV penicillin G 2 to 10 million U/day, followed by oral
penicillin V 500 to 750 mg qid. Antibiotics are changed to oral when the patient is
afebrile and subjectively improved. Some authorities prefer to combine penicillin with
oral metronidazole 500 mg qid. If a gram-negative organism, S. aureus, or other aerobic
pathogen is implicated, the antibiotic chosen depends on the results of sensitivity tests.
Treatment should be continued until the pneumonitis has resolved and the cavity has
disappeared, leaving only a small stable residual lesion, a thin-walled cyst, or clear lung
fields. Resolution usually requires several weeks or months of treatment, much of which
is given as oral antibiotics on an outpatient basis.
Postural drainage may be a helpful adjunct, but it may also cause spillage of infection
into other bronchi with extension of the infection or acute obstruction. If the patient is
weak or paralyzed, tracheostomy and suctioning may be necessary. Rarely, bronchoscopic
aspiration may help facilitate drainage. Surgical drainage is rarely necessary because
lesions usually respond to antibiotics. Patients with large cavities who do not respond to
drugs may be candidates for percutaneous drainage; patients with empyema require it.
Pulmonary resection is the procedure of choice for an abscess resistant to drugs,
particularly if bronchogenic carcinoma is suspected. Lobectomy is the most common
procedure; segmental resection usually suffices for small lesions. Pneumonectomy may
be necessary for multiple abscesses or pulmonary gangrene refractory to medical
management. The mortality rate after pneumonectomy is 5 to 10%; after lesser resections,
it is much lower.
34. Lung gangrene. Definition of the idea. Clinical picture. Diagnosis. Treatment.
Definition of the idea.
Gangrene is pyo-putrefactive decomposition of lungs tissue without tendency to
limitation
(G).
G - is putrefactive necrosis of lobe or the whole lung without legible limitation with
tendency to spreading and hard state of the patient.
Clinical picture.
1. clinics of pneumonia with signs of inflammation
2. Clinics of necrosis and lysis: foul smell hemoptysis
3. Signs of intoxication
Diagnosis.
- case history
- clinical data
- fistulograph
- diagnostic pucture, biopsy
- examination of purulen discharge on microflora, sensibility to antibiotics, cytology.

- Chest Imaging:
conventional chest x-rays
CT with or without contrast or high-resolution techniques
angiography of the pulmonary or bronchial circulation using contrast materials or
digital subtraction
ultrasonography
radionuclide scanning
MRI.
- Diagnostic thoracentesis
- Thoracoscopy
- Bronchoscopy
- Ancillary procedures:
Bronchoalveolar lavage
Transbronchial lung biopsy
Submucosal and transbronchial needle aspiration
- Percutaneous Transthoracic Needle Aspiration
- Thoracotomy
Treatment.
1. Drainage and complex lavement of abscesses and TBD.
2. Complex antibiotic therapy registrating sensibility of the flora.
3. Correction of homeostasis and immunodeficiency.
4. Method of treatment choosing of abscess of the lung is complex therapy with
methods of menor surgery, forsed surgical management (hemorrhage).
5. Method of gangrene of the lung treatment is resection of the lung or
pulmonectomy after intensive preparing to operation for 7-10 days.
6. Methods of drainage of purulent cavities :
1) transthoracal transtrochar according to Monaldi
2) according to Seldiner
3) with the help of pasker
4) with the help of fibronehoscopy
5) postural drain
6) with cathetertrocar
7. Methods of lavement of purulent cavity:
1) drainage
2) flowing-aspiratious lavement with antiseptics
3) administration of proteolytic enzymes (terridecaze, cathaline)
4) treatment of cavity with ultrasonic complex lasertherapy( intravenous,
intracavitary, epicutaneous ) .
8. Correction of homeostasis and immunodeficiency.
Intravenous infusion of hemodesis , reopolyglucine, glucose, Ringer's , protein
preparations with vitamins, and medicines, which improve microcirculation (trenthal
curantil)
9. Immunoprotectors- levamisolum, tymosinum, decaris, Natrii
hypochloritum.

35. Chronic lung abscesses. Definition of the idea. Classification. Transformation

causes of acute lung abscesses into chronic ones. Clinical picture. Diagnosis.
Treatment.
Definition of the idea.
Pulmonary abscess which is not completed in two months (light weeks) is named
chronical. If during acute pulmonary abscess the main morphologic sign is
cavity with pus, walls of which consist from pulmonary tissue, during chronical abscess
they are formed with connective tissue.
Forming of connective capsula may be noted to the end of sixth-eighth week from the
beginning of the disease. Pulmonary tissue around destruction cavity also concentrates.
Pyogenic processin abscess cavity and complined inflammatory process in surrounding
parenchyma mutually support each other. Gradually purrulent infiltration of surrounding
pulmonary tissue is taring place.
Classification.
Etiology:
Aerobic
Anaerobic
Mixed
2. Not bacterial
The elementary organisms
Funguses
Pathogenesis
1. Bronchogenic
With aspiration
With obtiration
Metapneumonic
2. Hematogenous (embolic).
3 Traumatic
4. Lymphogenous.
5. Contact.
Localization:
1 Central
2 Peripheric
cortical
subpleural
Spreading:
Singular.
Multiple
Unilateral
Bilaterial
Character of the clinical features
Acute

Chronic:
In phase of the remission
In phase of the exacerbation
Connection with the bronchus:
1. It is not drained.
2. It is drained:
There is enough
There is not enough
Complications:
Empyema of the pleura
Bleeding.
Defeat of another mild
Phlegmon of the thoracal wall.
Bacterial shock
Sepsis
Transformation causes of acute abscesses into chronic ones.
There are some important components of chronic pyogenic process in the lungs:
1. noneffective drainage
2. perypherical secondary bronchiectasis
3. changings in pulmonary tissue like sclerosis, deformation of bronchi
These are the causes promoting transformation of acute abcsesse into chronic:
1. unsatisfactory out floor of pus from cavity;
2. sequesters in abscess cavity;
3. height pressure in the cavity;
4. forming of pleural commisures in defeated segments zone in lungs, which
prevent early lung collapse and obliteration of cavity;
5. epithelization of cavity
Clinical picture.
The disease usually flows with alternation of aggravation and remission. The most
constant symptom is tussis with purulent sputum. Quantity of sputum grows in
aggravation period. During abundant expectoration the organism loses much protein, and
it leads to inanition
The main complaint of patients with chronic abscess:
asthenia (weakness)
bad appetite
sleeplessness
pain in thorax.
unpleasant smell from the mouth
edematous face
chement of ribs
falling behind of the "sick" half of thorax during breathing;
fingers looking like "drum sticks" (may be seen in 85-95% of cases)

 deformation of nail plates like "watch glass".

Symptomatology found during physical examination of thorax is variable, it depends
upon localization of defeated zone, phase of disease flow, availability of changes in
pleural cavity.
In blood count - leucocytosis, deviation to the left, anemia, hypoproteinemia.
Spirography - lowering of vital capacity. There are dystrophic changes in liver, heart.
Diagnosis.
Lab Studies:
A complete white blood cell count with differential may reveal leukocytosis and a
left shift.
Obtain sputum for Gram stain, culture, and sensitivity.
If tuberculosis is suspected, acid-fast bacilli stain and mycobacterial culture is
requested.
Blood culture may be helpful in establishing the etiology.
Obtain sputum for ova and parasite whenever a parasitic cause for lung abscess is
suspected.
Imaging Studies:

Chest radiograph
o A typical chest radiographic appearance of a lung abscess is an irregularly
shaped cavity with an air-fluid level inside. Lung abscesses as a result of
aspiration most frequently occur in the posterior segments of the upper
lobes or the superior segments of the lower lobes.
o The wall thickness of a lung abscess progresses from thick to thin and
from ill-defined to well-circumscribed as the surrounding lung infection
resolves. The cavity wall can be smooth or ragged but is less commonly
nodular, which raises the possibility of cavitating carcinoma.
o The extent of the air-fluid level within a lung abscess is often the same in
posteroanterior or lateral views. The abscess may extend to the pleural
surface, in which case it forms acute angles with the pleural surface.
o Anaerobic infection may be suggested by cavitation within a dense
segmental consolidation in the dependent lung zones.
o Lung infection with a virulent organism results in more widespread tissue
necrosis, which facilitates progression of underlying infection to
pulmonary gangrene.
o Up to one third of lung abscesses may be accompanied by an empyema.
CT scan
o CT scan of the lung may help visualize the anatomy better than the chest
radiograph. It is very useful in identification of concomitant empyema or
lung infarction.
o On CT scan, an abscess often is a rounded radiolucent lesion with a thick
wall and ill-defined irregular margins.
o The vessels and bronchi are not displaced by the lesion as they are by an
empyema.

o
o

The lung abscess is located within the parenchyma compared to loculated

empyema, which may be difficult to distinguish on chest radiograph.
The lesion forms acute angles with the pleural surface chest wall.

Procedures:
To obtain an uncontaminated specimen, transtracheal aspirate or transthoracic
needle aspirate are the techniques employed in lung abscess.
Although transtracheal aspirate and transthoracic needle aspiration may provide
microbiologic diagnosis, obtaining pleural fluid and blood cultures in patients
with lung abscess is easier.
Flexible fiberoptic bronchoscopy is performed to exclude bronchogenic
carcinoma whenever bronchial obstruction is suspected. Bronchoscopy using a
protected brush to obtain a specimen uncontaminated by the upper airway or
quantitative culture of organisms from the bronchoalveolar lavage fluid has been
advocated to establish bacteriologic diagnosis in lung abscess. However, the
experience with this technique in diagnosis of anaerobic lung infections is limited
and the diagnostic yield is uncertain. Furthermore, risk of spillage of infected
material into the uninvolved areas of lung exists.
Histologic Findings: Lung abscesses begin as small zones of necrosis developing within
the consolidated segments in pneumonia. These areas may coalesce to form single or
multiple areas of suppuration, which are referred to as lung abscesses. If antibiotics
interrupt the natural history at an early stage, the healing results in no residual changes.
When the progressive inflammation erodes into the adjacent bronchi, the contents of the
abscess are expectorated as malodorous sputum. Subsequently, fibrosis occurs, which
causes a dense scar and separates the abscess. The abscess may still occur, and spillage of
pus into the bronchial tree may disseminate the infection
Treatment.
Absolute depositions to operation are repeated pulmonary hemorrhage, quickly growing
intoxication. Only radical operation is effective (resection of lobe of the lung or
pulmonectomy). Majority of patients, who had lobectomy, recover their capacity for
work in three four months after operation. After pulmonectomy in first six month
patients are transferred to invalidism.

Antibiotic therapy
o Standard treatment of an anaerobic lung infection is clindamycin (600 mg
IV q8h followed by 150-300 mg PO qid).
o This regimen has been shown to be superior over parenteral penicillin in
published trials. Several anaerobes may produce beta-lactamase (eg,
various species of Bacteroides and Fusobacterium) and therefore develop
resistance to penicillin.
o Although metronidazole is an effective drug against anaerobic bacteria,
the experience with metronidazole in treating lung abscess has been rather
disappointing because these infections are generally polymicrobial. A
failure rate of 50% has been reported.
o In hospitalized patients who have aspirated and developed a lung abscess,
antibiotic therapy should include coverage against S aureus and
Enterobacter and Pseudomonas species.

Cefoxitin is a second-generation cephalosporin that has gram-positive,

gram-negative, and anaerobic coverage. This agent may be used when a
polymicrobial infection is suspected as cause of lung abscess.
Duration of therapy
o Most clinicians prescribe antibiotic therapy generally for 4-6 weeks.
o Antibiotic treatment should be continued until the chest radiograph has
shown either the resolution of lung abscess or the presence of a small
stable lesion.
o The rationale for extended treatment maintains that risk of relapse exists
with a shorter antibiotic regimen.
o

36. Bronchiectatic disease. Definition of the idea. Classification. Etiology and

pathogenesis. Clinical picture according to the disease stages. Diagnosis. Differential
diagnosis. Treatment.
Definition of the idea:
Irreversible focal bronchial dilation, usually accompanied by chronic infection and
associated with diverse conditions, some congenital or hereditary. Bronchiectasis may be
focal and limited to a single segment or lobe of the lung, or it may be widespread and
affect multiple lobes in one or both lungs.
Classification:
1. unilateral, bilateral, total damage.
2. cylindrical,saccular and mixed bronhiectasis
3. anatomic localization (number of the lobe, etc)
4. with or without complications
Bronchiectasis can be classified as cylindrical, cystic or varicose:
(i)

In cylindrical bronchiectasis, bronchi have a uniform caliber. They have

parallel walls and do not taper.

(ii)

Cystic/saccular bronchiectasis is a severe form of bronchiectasis. Involved

bronchi are cyst-like in appearance and extend to the pleural surface. Air-fluid
levels are commonly present.

(iii)

Varicose bronchiectasis relatively uncommon. Bronchi have a beaded

appearance with a dilated bronchus and interspersed sites of relative
narrowing.

CLINICO-ANATOMICAL CLASSIFICATION:
1. The first stage cylindrical bronchiectasis, are localized in basal segments of
lungs, unilateral damage. Bronchi have a uniform caliber, they do not taper and have
parallel walls. Treatment conservative.
2. The second stage cylindrical and saccular bronhiectasis, unilateral damage.
Treatment conservative and surgical treatment (segmentectomy, lobectomy,
pulmonectomy- if there are no contraindications)
3. the third stage saccular, bilateral bronhiectasis. Symptomatic conservative
treatment.
Etiology and pathogenesis.
1. Congenital bronchiectasis is a rare condition in which the lung periphery fails to
develop, resulting in cystic dilation of developed bronchi.
2. Acquired bronchiectasis results from:
(1) direct bronchial wall destruction--due to infection, inhalation of noxious
chemicals, immunologic reactions, or vascular abnormalities that interfere with
bronchial nutrition--or
(2) mechanical alterations--due to atelectasis or loss of parenchymal volume with
increased traction on the walls of airways, leading to bronchial dilation and secondary
infection.
3. Bacterial endotoxins and proteases; proteases derived from circulating or
pulmonary inflammatory cells; superoxide radicals; and antigen-antibody complexes
may mediate bronchial wall damage.
Amounts of functionally active neutrophil elastase, cathepsin G, and neutrophil matrix
metalloproteinase MMP-8 found in bronchoalveolar lavage fluid increase with the
severity of disease in moderate to severe bronchiectasis. Furthermore, the antiproteases
-antitrypsin and antichymotrypsin may be proteolytically or oxidatively cleaved into

lower molecular weight forms, which provide less protection against enzymatic
destruction of extracellular matrix. Detection of proinflammatory cytokines interleukin-1
(IL-1 ), IL-8, and tumor necrosis factor-alpha in sputum and demonstration of
chemokine and cytokine bronchial cell interactions have led to the hypothesis that such
interactions activation of certain inflammatory cells modulate ongoing
inflammation, (a cardinal feature of bronchiectasis).
Nitric oxide, which affects the immune response, cell signaling, and plasma exudation at
inflammatory sites, may help perpetuate the inflammatory response in bronchiectasis.
Exhaled nitric oxide is increased in patients with bronchiectasis compared with normal
subjects and bronchiectatic patients taking inhaled corticosteroids.
4. Conditions commonly leading to bronchiectasis are severe pneumonia (especially
when complicating measles, pertussis, or certain adenovirus infections in children);
necrotizing pulmonary infections due to Klebsiella sp, staphylococci, influenza virus,
fungi, mycobacteria, and, rarely, mycoplasmas; and bronchial obstruction from any
cause (eg, foreign body, enlarged lymph nodes, mucus inspissation, lung cancer, or
other lung tumor).
5. Miscellaneous chronic fibrosing lung diseases (eg, those following aspiration
pneumonia or inhalation of injurious gases or particles--eg, silica, talc, or
bakelite) also predispose to bronchiectasis.
6. Immunologic deficiencies, including AIDS, and various other acquired,
congenital, and hereditary abnormalities that increase host susceptibility to
infection or impair respiratory defenses are less common but important
predisposing factors. Although incidence and mortality have decreased with the
widespread use of antibiotics and immunizations in children, bronchiectasis as a
manifestation of cystic fibrosis is still common.
7. Bronchiectasis, along with situs inversus and sinusitis, is a feature of Kartagener's
syndrome, a subgroup of the primary ciliary dyskinesia (PCD) syndromes. In
these syndromes, structural or functional abnormalities in ciliary organelles result

in defective mucociliary clearance that leads to suppurative bronchial infections

and bronchiectasis as well as chronic rhinitis, serous otitis media, male sterility,
corneal abnormalities, sinus headaches, and a poor sense of smell.
8. An unusual pattern of bronchiectasis occurs in allergic bronchopulmonary
mycosis (An allergic reaction to Aspergillus fumigatus occurring in asthmatic
patients as eosinophilic pneumonia): The reported association of bronchiectasis
with probable or possible autoimmune diseases, such as rheumatoid arthritis,
Sjgren's syndrome, Hashimoto's thyroiditis, and ulcerative colitis, has not been
satisfactorily explained.
Clinical picture according to the disease stages. (Not segregated into stages, sorry
people. Pandai pandai ko estimate)
Most patients have chronic cough and sputum production--the most characteristic and
common symptoms--but occasionally, a patient is asymptomatic. These symptoms often
begin insidiously, usually after a respiratory infection, and tend to worsen gradually over
a period of years. Severe pneumonia with incomplete clearing of symptoms and residual
persistent cough and sputum production is a common mode of onset. As the condition
progresses, the cough tends to become more productive. Typically, it occurs regularly in
the morning on arising, late in the afternoon, and on retiring; many patients are relatively
free of cough during the intervening hours. Sputum usually is similar to that of bronchitis
and is not characteristic. Less commonly, in long-standing cases, sputum is abundant and
may separate into three layers: frothy at the top, greenish and turbid in the middle, and
thick with pus at the bottom. Hemoptysis from erosion of capillaries, but sometimes from
anastomoses between the bronchial and pulmonary arterial systems, is common and may
be the first and only complaint. Recurrent fever or pleuritic pain, with or without visible
pneumonia, is also common; investigation of such symptoms may lead to the diagnosis of
bronchiectasis. Wheezing, shortness of breath and other manifestations of respiratory
insufficiency, and cor pulmonale (Heart failure (congestive heart failure): Symptomatic
myocardial dysfunction resulting in a characteristic pattern of hemodynamic, renal, and

neurohormonal responses) may occur in advanced cases with associated chronic

bronchitis and emphysema.
Physical findings are nonspecific, but persistent crackles over any part of the lungs
suggest bronchiectasis. Signs of airflow obstruction (decreased breath sounds, prolonged
expiration, or wheezing) tend to be more pronounced in smokers than in nonsmokers.
Finger clubbing sometimes occurs with extensive disease and persistent chronic infection
(Measuring finger clubbing. The ratio of the anteroposterior diameter of the finger at
the nail bed (a-b) to that at the distal interphalangeal joint (c-d) is a simple measurement
of finger clubbing. It can be obtained readily and reproducibly with calipers. If the ratio is
> 1, clubbing is present. Clubbing is also characterized by loss of the normal angle at the
nail bed).

Diagnosis.
Bronchiectasis must be suspected in anyone with the above symptoms and signs.
1. Standard chest x-rays may show increased bronchovascular markings from
peribronchial fibrosis and intrabronchial secretions, crowding from an atelectatic
lung, tram lines (parallel lines outlining dilated bronchi due to peribronchial

inflammation and fibrosis), areas of honeycombing, or cystic areas with or

without fluid levels, but occasionally x-rays are normal.
2. High-resolution CT (HRCT) of the chest (1- to 2-mm cuts) has largely replaced
bronchography. With 10-mm collimation, dilation of small bronchi may be
missed, but the better resolution of HRCT provides results comparable or
preferable to bronchography. Its widespread use indicates that bronchiectasis is
probably more common than can be diagnosed by clinical findings and standard
x-rays alone.

Characteristic CT findings are dilated airways, indicated by tram lines, by a signet

ring appearance with a luminal diameter > 1.5 times that of the adjacent vessel in
cross section, or by grapelike clusters in more severely affected areas. These
dilated medium-sized bronchi may extend almost to the pleura because of the
destruction of lung parenchyma. Thickening of the bronchial walls, obstruction of
airways (evidenced by opacification--eg, from a mucus plug--or by air trapping),
and, sometimes, consolidation are other findings.

Helical CT may be considered for surgical candidates because at least one study
has shown it to be superior to HRCT in identifying the extent of bronchiectasis
and distribution within a given segment, but the additional radiation exposure has
prevented it from supplanting HRCT for general use. HRCT may be performed
with or without contrast; the precise protocol is tailored to the patient's clinical
situation. Excessive secretions or blood in the bronchial tree or acute
bronchopneumonia can lead to misinterpretation. Sputum cultures, bronchial
washings, serologic studies for fungal antigen or antibodies, and even biopsy of
appropriate tissue (but not highly vascular bronchiectatic airways) may be
indicated.

3. When disease is unilateral or of recent onset, fiberoptic bronchoscopy is indicated

to rule out tumor, foreign body, or other localized endobronchial abnormality.
HRCT is often performed first to provide maximum information to the

bronchoscopist in advance, but bronchoscopy is usually still necessary for precise

pathologic diagnosis.
4. Immunoglobulin (Ig) deficiencies may be identified by serum Ig measurements. If
serum protein electrophoresis detects low -globulin levels, serum IgG, IgA, and
IgM should be measured. Even when total levels of IgG or IgA are normal, some
IgG subclass deficiencies have been associated with sinopulmonary infections;
IgG subclasses should be measured in patients with unexplained bronchiectasis.
-Antitrypsin ( 1-antiprotease inhibitor) deficiency, which is occasionally

associated with bronchiectasis, may be suspected when

-globulin is low and

may be confirmed by phenotyping with crossed immunoelectrophoresis.

5. Blood and sputum eosinophilia are often present.
Differential diagnosis.
(i)
Alpha-1-Antitrypsin deficiency
(ii)
Asthma
(iii)
Bronchitis
(iv)
Chronic bronchitis
(v)
COPD
(vi)
Emphysema
(vii) Empyema, Pleuropulmonary
(viii) GORD
(ix)
Pneumonia, aspiration
(x)
Pneumonia, bacterial
(xi)
TB
Treatment.
1.

Treatment is directed against infections, secretions, airway obstruction, and

complications (eg, hemoptysis, hypoxemia, respiratory failure, cor pulmonale).
Treatment of infection includes antibiotics, bronchodilators, and physical therapy
to promote bronchial drainage. Sputum usually contains gram-positive and gramnegative

microorganisms

(eg,

Streptococcus

pneumoniae,

Haemophilus

influenzae, Staphylococcus aureus, Moraxella [Branhamella] catarrhalis,

Pseudomonas sp); anaerobes commonly inhabit bronchiectatic cysts.

2.

A broad-spectrum antibiotic (eg, ampicillin 250 to 500 mg po q 6 h for adults or

50 to 100 mg/kg/day in divided doses q 6 to 8 h for children, with a maximum
dose of 2 to 3 g/day for large children; amoxicillin 250 to 500 mg po q 8 h for
adults or 40 mg/kg/day in divided doses for children; or, only for adults,
tetracycline 250 to 500 mg po q 6 h) is often used until the sputum is nonpurulent
and less voluminous, about 1 to 2 wk. Trimethoprim-sulfamethoxazole (TMPSMX) 320/1600 mg po q 12 h for 14 days can also reduce sputum volume and
eliminate pathogens; for children, TMP-SMX 6/30 to 12/60 mg/kg/day is given
in divided doses q 12 h, depending on the size of the child and severity of the
infection.

3.

Tetracycline or trimethoprim can inhibit increased airway absorption of sodium

in vitro and might have a double benefit in a disease such as cystic fibrosis, in
which enhanced sodium absorption in the airways is believed to contribute to
inspissated secretions. A newer macrolide, such as clarithromycin or
azithromycin, or a 2nd-generation cephalosporin is another possible choice.
Antibiotics should be repeated at the first sign of recurring infection (eg,
increased volume or purulence of sputum). If infection recurs often, prolonged
chemoprophylaxis with ampicillin, amoxicillin, or tetracycline may be tried but
is generally disappointing. In severe cases, high-dose amoxicillin (3 g po bid) is
reported to achieve higher serum and sputum concentrations than do equal doses
of ampicillin.

4.

Prophylactic or suppressive antimicrobial regimens can reduce the bacterial load

(associated with purulence and destructive elastase activity in some), but there is
no consensus about long-term continuous versus intermittent therapy or about
specific regimens. With short-term therapy (1 to 2 wk), purulence and elastase
activity rapidly return to pretreatment levels. One goal is to prevent development
of resistant microorganisms and conditions favoring Pseudomonas sp, which is
particularly difficult to eradicate. Regimens include an oral antibiotic for 7 to 10
days each mo, 7 to 10 days of treatment alternating with equal rest periods,
continuous long-term treatment with a reduced dose, or high doses of an

antibiotic (such as amoxicillin) for 3 to 6 mo. A fluoroquinolone, such as

ciprofloxacin 500 to 750 mg po bid, may be effective and can be given longterm, but resistance frequently develops after one or two treatment cycles. In
severe cases, aerosol or IV regimens may be needed, but resistance is always a
problem. Alternating drugs may help avoid early resistance and persistence of
pneumococci, which tends to occur with ciprofloxacin.
5.

For bronchopneumonia or serious respiratory infection, parenteral antibiotics-chosen on the basis of Gram stain, cultures, and sensitivity studies--are indicated.
Cefuroxime 750 mg IV tid for 48 to 72 h followed by cefuroxime axetil 500 mg
po bid for 5 days is as effective as amoxicillin 1.2 g IV tid with clavulanic acid
followed by amoxicillin 625 mg po tid. Amoxicillin penetrates lung secretions,
especially in the presence of active inflammation, but some local inactivation
may occur, correlating with -lactamase levels. For broader coverage to include
Mycoplasma, Legionella, and Pseudomonas sp, a macrolide plus a 3rdgeneration cephalosporin (such as ceftazidime or cefoperazone) plus an
aminoglycoside can be used, or piperacillin or azlocillin with an aminoglycoside
can be used when Pseudomonas predominates.

6.

MAIC commonly colonizes the lungs of patients with bronchiectasis, so

treatment is reserved for patients with strongly suspected or proven disease. An
empirical multidrug regimen for MAIC may include clarithromycin 500 mg po
bid, ethambutol 25 mg/kg po daily, clofazimine 200 mg po daily, and
streptomycin 10 to 12 mg/kg/day IM or amikacin 12 to 15 mg/kg IM three times
a week for 1 to 2 mo, followed by clarithromycin 750 mg po daily, ethambutol 15
mg/kg po daily, and clofazimine 50 to 100 mg po daily for 3 to 24 mo, usually
given until cultures are negative for 12 mo. Basing therapy on drug susceptibility
testing, however, is important.

7.

Patients with bronchiectasis should avoid cigarette smoke and other irritants and
refrain from using sedatives or antitussives.

8.

Postural drainage, clapping, and vibration performed regularly may facilitate

sputum clearance in some patients.

9.

Diffuse chronic bronchitis, often accompanying bronchiectasis, should be treated

accordingly.

-Agonists, theophylline, and corticosteroids may decrease airflow

obstruction, facilitate ciliary clearance, and reduce inflammation. I

10. f asthma or allergic bronchopulmonary aspergillosis is also present,
corticosteroids may be especially beneficial in reducing inflammation, and in
young children, who are most susceptible to fungal sensitization, they may
enhance fungal elimination. Itraconazole 200 to 400 mg/day po reduces the
corticosteroid requirements, reduces serum IgE, and improves airflow rates in a
small number of patients with allergic bronchopulmonary aspergillosis, but
antifungal drugs are usually reserved for invasive Aspergillus infection.
11. Other drugs--such as the mucolytic N-acetylcysteine and recombinant human
deoxyribonuclease (rhDNase), which breaks down DNA in purulent sputum-may benefit selected patients but have no proven benefit in bronchiectasis.
NSAIDs, such as indomethacin, have been tried experimentally. Despite mild
reduction in sputum volume and changes in peripheral neutrophil function,
sputum elastase and myeloperoxidase levels were not reduced, and viable
bacterial load was not altered in bronchial secretions.
12. Chronic hypoxemia should be treated with O 2. Respiratory failure and cor
pulmonale should be treated as in other patients with chronic obstructive airway
disorders. Intubation and mechanical ventilation should, if possible, be avoided,
because the ability to cough is lost and the risk of inadequately evacuating
secretions by suctioning alone and of promoting further infection is enhanced.
13. Lung transplantation can be performed in patients with advanced cystic fibrosis
and bronchiectasis. Double lung transplantation is usually the procedure of
choice.

14. Surgical resection is rarely necessary but should be considered when

conservative management yields to recurrent pneumonia, disabling bronchial
infections, or frequent hemoptysis and the disease is sufficiently localized and
stable. For massive pulmonary hemorrhage, emergency resection or embolization
of the bleeding vessel (usually a bronchial artery) can be lifesaving.

37. Inflammative pleura diseases. Classification. Acute suppurative/purulent

pleurisy. Definition of the idea. Clinical picture. Diagnosis.
Classification.
Exudate
Purulent
Putrefactive
Microflora
Nonspecific (a staphylococcus, diplococcus)
Specific (tubercular, fungoid)
Mixed
Prevalence of process
Free (total, subtotal, small)
Circumscribed (parietal, intralobal, basal, apical, mediastinal, multichamber)
Acute suppurative /purulent/ pleurisy.
Inflammation of pleura. Direct entry of all infections. Agent of irritating substance
pleural space via blood or lymph, parietal pleura injury by trauma.
Rib fracture pleura becomes edematous and congested. Pleural exudates develops
from an outpouring of fluid rich in plasma protein from damaged capillaries.
Definition of the idea.
Inflammation of the pleura, usually producing an exudative pleural effusion and stabbing
chest pain worsened by respiration and cough.
Clinical picture.
Fever
Cough
Chills
Shortness of breath
Weight loss
Poor appetite
Sharp chest pain with breathing. Pain can limit the movement on the side of the
chest with Pleurisy.
Rapid shallow breaths
Inability to take a deep breath due to chest pain

Diagnosis.
Pleurisy is readily diagnosed when characteristic pleuritic pain occurs. A pleural friction
rub is pathognomonic. Pleurisy that produces referred abdominal pain is usually
differentiated from acute inflammatory abdominal disease by x-ray and clinical evidence
of a respiratory process; absence of nausea, vomiting, and disturbed bowel function;
marked aggravation of pain by deep breathing or coughing; shallow rapid breathing; and
a tendency toward relief of pain by pressure on the chest wall or abdomen. Intercostal
neuritis may be confused with pleurisy, but the pain is rarely related to respiration and
there is no friction rub. With herpetic neuritis, development of the characteristic skin
eruption is diagnostic. MI, spontaneous pneumothorax, pericarditis, and chest wall
lesions may simulate pleurisy. A pleural friction rub may be confused with the friction
rub of pericarditis (pericardial rub), which is heard best over the left border of the
sternum in the third and fourth interspaces, is characteristically a to-and-fro sound
synchronous with the heartbeat, and is not influenced significantly by respiration.
Chest x-rays are of limited value in diagnosing fibrinous pleurisy. The pleural lesion
causes no shadow, but an associated pulmonary or chest wall lesion may. The presence of
a pleural effusion, generally small, confirms the presence of acute pleurisy.
Differential diagnosis.

Congestive heart failure

Nephrotic syndrome

Cirrhosis

Hypoalbuminemia

Urinothorax

Peritoneal dialysis

Atelectasis (early)

Infection
(Bacterial, viral fungal, tuberculosis, or parasitic)

Malignancy

Connective tissue disease

Chylothorax

Hemothorax

Pancreatitis

Postcardiotomy syndrome

Drug-induced (eg, by amiodarone)

Esophageal rupture

Uremia

Subdiaphragmatic abscess

Pulmonary embolism

Asbestos exposure

Atelectasis (chronic)

Treatment.
Treat underlying disorder
Rest
Oxygen, if levels are low
Aspirin and other NSAIDs (e.g., Ibuprofen, Indocin, etc.) are effective in reducing
the inflammation, fever, and pain.
Painkillers such as codeine can help.
In severe pain, a nerve block is performed using a numbing agent (e.g.,
Xylocaine) that is injected into the nerves between the ribs for temporary relief of
pain.
Therapeutic Thoracentesis is done to remove the effusion, which helps breathing.
Adequate bronchial drainage must be provided to prevent pneumonia
Antibiotics and bronchodilators should be considered for treatment of associated
bronchitis
38. Chronic pleura empyema. Definition of the idea. Transformation causes of acute
pleura empyema into chronic. Clinical picture. Diagnosis. Differential diagnosis.
Treatment.
Definition of the idea.
Empyema is a condition in which pus and fluid from infected tissue collects in a body
cavity. Empyema is most often used to refer to collections of pus in the space around the
lungs (pleural cavity), but sometimes refers to similar collections in the gall bladder or
the pelvic cavity. Empyema in the pleural cavity is sometimes called empyema thoracis,
or empyema of the chest.
Transformation causes of acute pleura empyema into chronic one.

I 1.prescence of large broncho pleural fistula which pevent the lung from expansion and
cause constant contamination of pleura.
2. Extensive destruction of the lung tissue with development of lage sequester
3. Multi chamber empyema
4. Decease of the immunological response on infection
II 1. Inadequate exudates and air removing from pleural cavity during curative puncture
and drainage
2. Inadequate antibacterial therapy without information about microflora type and its
sensitivity to antibiotic.
3. Presence of residual cavity after treatment and inadequate lung expansion.
4. Early wide thoracotomy which prevent the pleural cavity from hermatization.
Clinical picture.
History: The patient's history may reveal the following findings:
Many patients give a history of a recent diagnosis and treatment for pneumonia.
A recent history of penetrating chest trauma should raise clinical suspicion for
empyema.
Patients report a cough productive of bloody sputum that frequently has a fetid
odor or offensive appearance.
Fever
Shortness of breath
Anorexia, weight loss
Night sweats
Pleuritic chest pain
Physical: The physical examination may reveal the following findings:
Temperature frequently elevated but usually not greater than 102F
Tachypnea
Rales
Rhonchi
Egophony
Tubular breath sounds
Decreased breath sounds
Dullness to percussion
Diagnosis.
Lab Studies:

A CBC with differential may reveal a leukocytosis and a left shift.

Collect sputum for Gram staining, culturing, and sensitivity testing.

If tuberculosis is suspected, acid-fast bacilli testing should be ordered.

Blood culturing

Imaging Studies:

Perform chest radiography to diagnose and differentiate pneumonia, pulmonary

abscess, and empyema. Distinction of these conditions is important because lung
abscesses and pneumonia require medical treatment, while empyema frequently
requires definitive surgical therapy.

On the chest radiograph, a lung abscess appears as a solitary cavitary area with an
air-fluid level, which typically is present in a dependent portion of the lung.

A surrounding patchy area of infiltrate aids in differentiating a pulmonary abscess

from a cavitary lung cancer.

On the chest radiograph, findings that suggest empyema, as opposed to lung

abscess, include extension of the air-fluid level to the chest wall, extension of the
air-fluid level across fissure lines, and a tapering border of the air-fluid collection.

The costophrenic angle should be closely inspected on the chest radiograph to

assess the presence of fluid that suggests effusion or empyema.

On the chest radiograph obtained with the patient upright, blunting of the
costophrenic angle occurs when approximately 175 mL of fluid accumulates.

A lateral chest decubitus radiograph, obtained with the patient on his or her side,
reveals whether the pleural fluid is mobile and forms layers or whether it is
loculated.

If the chest radiograph does not adequately distinguish between lung abscess and
empyema (versus mass or tumor), CT of the chest or ultrasonography will be
required.

Other Tests:

Pulse oximetry - To assess oxygenation

ABG analysis - To assess respiratory adequacy

Transtracheal aspiration for culturing - If sputum findings are nondiagnostic

Procedures:

If a pleural effusion is present, a diagnostic thoracentesis should be performed,

and the fluid should be analyzed for pH, lactate dehydrogenase, and glucose
levels; specific gravity; and cell count with differential.

Gram staining, cultures, and acid-fast bacillus and sensitivity tests should also be
ordered.

The fluid should be sent for cytology if cancer is suspected.

The following findings are suggestive of an empyema or a parapneumonic

effusion, which resolves only with a chest tube:
o

Grossly purulent pleural fluid

pH less than 7.2

WBC greater than 50,000 cells/mm3 (or polymorphonuclear leukocyte

count of 1,000 IU/dL)

Glucose less than 60 mg/dL

Lactate dehydrogenase level greater than 1,000 IU/mL

Differential diagnosis.
1. cancer of the lung
2. tuberculesis of the lungs
3.

suppurated cysts of the lungs

4. echinococcus
5. actinomycosis
6.

abscess of the lung

7.

gangrene of he lung

Treatment.
Main aims of complex conservative treatment:
1. drainage and washing of purulent cavity
2. conducting antibacterial therapy,taking into consideration type of agent of a disease
and its sensity to antibiotics
3. Aim is smoothing out collabing lung
4. correction (normalisation) of homeostasis and immunodeficit.
Drainage is made with the help of trochar in the point, defined be-forehand (during
auscultation, percussion, X-ray finding) and first of all we made pleural puncture.
Very often we put two drains - in maximum point and eboser to thebottom of empyema
cavity. After in empyema cavity is fractionally washed with antiseptic solutions. We also
use proteolytic ferments (ter-rilytin, terredecaza, catalytin) to accelerate rejection of
necrotictissues and pus making liquid.
We may get transdrain intracavital treatment of empyema walls withlazer or ultrasonics.

Antibiotics (two-three types) are injected intra venous to abscesscavity with ultrasonic
inhalations, endobronchial during fibrobronc-hoscopy, or with the help of intratissual
electrophoresis.
During it day dose intravenosus antibiotic is injected into vein,and above the
inflammation focus electrodes are put and they influencewith constant (halvanic clerect)
current during sixty minutes ( prof.Alechseev). In difficult cases antibiotics are
injected endolymphati-cally.
To smooth out collabing lungs we use transdrain vacuum-aspiration,breathing with
increased pressure on expiration (rubber bag, tube under water), breathing gymnastics.
Providing infussion therapy we pay special attention to organism detoxication and
recovery of protein deficiency.
Curability of chronical EC is possible only with surgical way.
The most effective operation is tatae resection of emphyema cavity pleurectomy with
lung decortication. This operation leads to smoothing out the lung and improves
breathing function. It is made in one moment and has no hard deformation of chest.
If it is necessary, pleurectomy is combined with lobectomy (during collabing lung
abscess, broncho-pleural fistula).
If patient is hard or elderly, to liquidate empyema and residual cavity surgents use staged
thoracoplasty (Shade, Lymberg).
39. Pyopneumothorax. Causes. Acute, mild and latent forms. Total and local
pyopneumothorax. Peculiarities of their development and clinical picture. Diagnosis.
Treatment.
Causes.
- Rupture of peripheral lung abscess into pleural cavity.
- Lung gangrene:
Primary: Penetrating wounds of thorax.
Secondary: Due to purulent process transition from thoracic wall to lung,
pericardium, subdiaphragmatic space (due to pneumonitis, abscess, cavernous or
suppurating cyst, destructive tumor, pericarditis, mediastinitis).
Acute, mild and latent forms.
Acute form:
It occurs as a result of rupture of suppurative destructive lung focus into pleural
cavity (acute abscess + lung gangrene w/o adhesions)
Perforation occurs as a rule at the time of intensive coughing and is characterized
by a sudden sharp chest pain pt. leans forward to decrease dyspnea.
Cough, severe dyspnea, pallor of skin with sticky sweat.
Skin and mucosal cyanosis.
BP decrease (0-40 mm Hg) and tachycardia.
Objectively:
- Decrease mobility of affected lung.
- Enlarged intercostal spaces.
- Percussion: Band box sound + dull sound.
- Auscultation: amphoric respiration

Complicated by cardiorespiratory failure + shock.

If as a result of gangrene symptoms will aggravate.
If as a result of acute abscess destructive process in lung decreases and when
pus is removed from pleural cavity symptoms improve.
Mild form:
Often perforate at a small peripheral lung abscess localized pyopneumothorax.
Clinicals: Thoracic pain, dyspnea + cough, intoxication signs, pus with purulent
sputum.
This type is a localized process.
Latent/suppressed form:
Rupture of small abscess into a limited part of pleural cavity (limited by
adhesions).
In case of chronic purulent lung disease, rupture of bronchiectatic.
No clinics, no symptoms.
Clinicals: General condition of patient doesnt change, dyspnea, cough with
sputum.

Total and local pyopneumothorax.

-According to the degree of collapse of the lung, pyopneu can be total or local
-Total the lung collapse is greatly expressed and symptoms are more aggressive.
-Local-lung collapse is limited and symptoms are less expressed.
Peculiarities of their development and clinical picture.
Pyopneumothorax is due to rupture of lung abscess into pleural cavity, due to trauma
(blunt/open).
Diagnosis.
X-Ray:
- Horizontal level of fluid in pleural cavity.
- Collapse of lung
- Tomography (?)
Labs:
- Blood Leukocytosis shift to the left, increased ESR and CRP.
- Anemia, dysproteinemia (Decrease albumin)
Treatment.
1. 2 drainages:
(i)
2nd IC space for air evacuation
(ii)
Lower for pus evacuation

2. Surgical:
- Lobectomy (if collapsing lung abscess, bronchopleural fistula)
- Thoracoplasty.

Differ Answer

Pyopneumothorax.
a) Causes.
-primary develops after penetrating wounds of thorax (chest)
-secondary is a result of purulent process transition from thoracic wall, lung,
pericardium, mediastinum,subdiaphragmatic space. In such case bacis primary diseases
are
pneumonitis abscess,
cavern or suppurating cust in lungs,
decomposing tunor,
costal osteomyelitis,
pericarditis,
mediastinitis.
-very seldom secondary begins with metastatic way (hematogenic of lymphogenic)
during
angina,
acute appendicitis,
hematogenic osteomyelitis,
sepsis.
-Pyopneumothorax is also one of the most hard compications of different intrathoracal
operations, especially in lungs and esophagus.
-breaking of pulmonary abscess into pleural cavity can cause pneumothorax

b) Acute, mild & latent forms.

-According to the severity of clinical picture pyopnumothorax is divided into
acute , mild , and latent type.
-in the acute form more complaints
-in the mild form -less complaints
-in the latent form no complaints n pt is asymptomatic.

c) Total & local pyopneumothorax.

-According to the degree of collapse of the lung, pyopneu can be total or local
-Total the lung collapse is greatly expressed and symptoms are more aggressive.
-Local-lung collapse is limited and symptoms are less expressed.

d) Peculiarities of their development & clinical picture.

Acute
-Develops in case of burst of supurative or destructive lung focus in to free plural
cavity.
-Most often it can appear in case of acute abscess and lung gangrene, when there
are no adhesions in the plural cavity, as a rule perforation of abscess occurs while
hard cough and characterized by
sudden sharp chest pain,
cough ,
severe dyspnoea ,
skin pallor ,
sticky sweat , skin
mucous cyanosis,
decreased Bp, 50-70 mmhg,
tachycardia
-Acute pneumothorax appears in case of presence of tension pnumothorax,

increase in dyspnoea forces the patient to sit leaning forward and resting
on bed edge,
affected part of thorax participate in respiration less intensive. I
ntercostals gaps are enlarged ,
band box resonance is determined ,
whole percussion and emphoric respiration is marked during
auscultation.
-Occasionally cardio respiratory failure or shock are developed so intensive that only
urgent surgical operation can save the patient.
-If acute pyopnumothorax is acute abscess complication , it means that the after the
abscess burst into plural cavity destructive process in lung decrease and after pus
removal from plural cavity improvement starts.
Mild
-Develops after penetration into plural cavity of a small peripheral lung abscess ,
patient complains of
increased thoracic pain ,
dyspnoea ,
cough,
increased body temp,
other symptoms of intoxication.
-Process is localized in the place of abscess because as a rule there is no connection
with large bronchus, and in this case air enters plural cavity in small volume .This
process leads to localized pneumothorax.

Suppressed
-Suppressed type develops in small abscess burst into adhesions limited part of
plural cavity.
-It can be frequently found in case of chronic purulent lung disease abscess of
brochiectatic perforation of the purulent focus can occur in imperceptible for the
patient..
-General condition of the patient usually doesnt change , this type of
pneumothorax is frequently diagnosed only in case of x ray examination, when
horizontal fluid level in plural cavity and collapse of lung part is determined
e) Diagnosis.
1.Clinical picture characterized with:
flank pain
dyspnea
temperature increase to 38- 39 degree celsius
evening temperature higher than in the morning on two-three

degrees.
2. blood analysis:Leucocytosis develops in blood ( 20-30 10 9/l )
3.X-ray:
-During roentgenologic examination on the empyema side we define intensive
darkening, mediastinum displace to the opposite (healthy) side.
4.puncture:
-During pleural cavity puncture we get pus, in which during bacterial
examination unspecific or specific microbic flora may be found.
f) Treatment.
Main aims of complex conservative treatment:
1.drainage and washing of purulent cavity
2.conducting antibacterial therapy,taking into consideration type of agent of a
disease and its sensity to antibiotics
3.smoothing out collapsing lung
4.correction(normalizaation) of homeostasis and immunodeficit.
-Drainage is made with the help of trochar in the point, defined beforehand (during
auscultation, percussion, X-ray finding) and first of all we made pleural puncture.
-Very often we put two drains- in maximum point and eboser to the
bottom of empyema cavity.
-After in empyema cavity is fractionally washed with antiseptic solutions.
-can use proteolytic ferments (terrilytin, terredecaza, catalytin) to accelerate
rejection of necrotic tissues and pus making liquid.
-Antibiotics (two-three types) are injected intra venous to abscess cavity with
ultrasonic inhalations, endobronchial during fibrobronchoscopy, or with the help
of intratissual electrophoresis.
-To smooth out collapsing lungs we use transdrain vacuum-aspiration,
breathing with increased pressure on expiration (rubber bag, tube under water),
breathing exercises.
-infusion therapy
-The most effective operation is resection of emphyema cavity pleurectomy
-If itis necessary, pleurectomy is combined with lobectomy (during collapsing lung
abscess, broncho-pleural fistula).
-thoracoplasty
40. Acute subcutaneous thrombophlebitis. Classification. Etiology and pathogenesis.
Principles of treatment. Indications for surgical treatment.
Classification.
Traumatic thrombophlebitis

Thrombophlebitis in a varicose vein

Thrombophlebitis as the result of an infection
Migratory thrombophlebitis
Thrombophlebitis of the superficial veins of the breast and the anterior chest wall
(Mondor disease
(1) Varicose vein (as complication),
(2) latrogenic (Cannulated vein for infusion),
(3) Vascular diseaseBuerger's polyarteritis,
(4) Idiopatheic,
(5) Spontaneous Polycythaemia. Bronchus, pancreas, stomach and lymphoma
(thrombophlebitis visural migrans).
Etiology & pathogenesis.
(1) Varicose vein (as complication),
(2) latrogenic (Cannulated vein for infusion),
(3) Vascular diseaseBuerger's polyarteritis,
(4) Idiopatheic,
(5) Spontaneous Polycythaemia. Bronchus, pancreas, stomach and lymphoma
(thrombophlebitis visural migrans

AIDS (lupus anticoagulant),Antithrombin III deficiency

Burns
Catheters (indwelling venous infusion catheters)
Chemotherapy
Congestive heart failure
Drug abuse (intravenous [IV] drugs)
Drug-induced lupus anticoagulant
DVT in the past
Estrogen replacements (high dose only)
Fibrinogen abnormality
Fractures
Heparin-associated thrombocytopenia
Homocystinuria
Immobilization
Malignancy
Myocardial infarction
Obesity
Old age
Oral contraceptives
PE in the past
Polycythemia
Postoperative
Postpartum period
Pregnancy
Systemic lupus erythematosus

Thrombocytosis
Trauma
Ulcerative colitis
Varicose veins
Venography
Venous pacemakers
Venous stasis
Pathophysiology: Although the etiology frequently is obscure, superficial venous
thrombosis most often is associated with one of the components of the Virchow triad, ie,
intimal damage (which can result from trauma, infection, or inflammation), stasis, or
changes in the blood constituents (presumably causing changes in coagulability).
Although superficial thrombophlebitis usually occurs in the lower extremities, it also has
been described in the penis and the breast (Mondor disease). Superficial thrombophlebitis
also occurs anywhere medical interventions occur, such as in the arm or neck (external
jugular vein) from intravenous catheters.

Principles of treatment.
Medical Care: The treatment of superficial venous thrombosis depends on its etiology,
extent, and symptoms. Duplex scanning gives an accurate appraisal of the extent of
disease and thus allows determining more rational therapy.
For the superficial, localized, mildly tender area of thrombophlebitis that occurs
in a varicose vein, treatment with mild analgesics, such as aspirin, and the use of
some type of elastic support usually are sufficient. Patients are encouraged to
continue their usual daily activities. If extensive varicosities are present or if
symptoms persist, phlebectomy of the involved segment may be indicated.
More severe thrombophlebitis, as indicated by the degree of pain and redness and
the extent of the abnormality, should be treated by bedrest with elevation of the
extremity and the application of massive, hot, wet compresses. The latter measure
seems to be more effective when a large, bulky dressing, including a blanket and
plastic sheeting followed by hot water bottles, is used, taking care to avoid
burning the patient. The immobilization probably is as beneficial as the moist
heat. Long-leg heavy-gauge elastic stockings or multiple elastic (Ace) bandages
are indicated when the patient becomes ambulatory.
With persistence or spread of the process, the thrombophlebitic vein should be
excised. This is especially true for the greater saphenous vein if the process
extends upward toward the femoral vein in the groin.
If the thrombophlebitis is associated with a cannula or a catheter, the device
should be immediately removed and cultured. If the patient is septic, appropriate
antibiotics should be given. If suppurative thrombophlebitis is suspected,
immediate and complete excision of all of the involved veins is indicated. The
wound may be left packed open for secondary closure or skin grafting at a later
date. The use of appropriate systemic antibiotics always is indicated.
If the suppurative process involves one of the deep veins, aggressive antimicrobial
and anticoagulant therapy are necessary.
The most aggressive treatment is necessary for patients with superficial phlebitis
involving the greater saphenous vein above the knee, because greater saphenous

phlebitis often ascends to pass through the saphenofemoral junction at the groin
and into the deep venous system.
o These patients are treated as outpatients with full-dose anticoagulation
using subcutaneous LMWH.
o Antibiotics should be used whenever the phlebitis involves the proximal
thigh.
o Nonsteroidal anti-inflammatory agents, gradient compression hose,
increased ambulation, and early repeat examination are also essential.
Indications for surgical treatment.
41. Cancer of the esophagus. Classification. Diagnosis. Treatment/general principles.
Classification.
TNM classification:
TABLE 37-9 -- Stage Grouping of Esophageal Cancer
Stage 0

T0N0
T is N 0 M0

Stage I

T 1 N 0 M0

Stage II

IIA T 2 N0 M 0
T 3 N 0 M0
IIB T 1 N 1 M0
T 2 N 1 M0

Stage III

T 3 N 1 M0
T 4 any N M 0

Stage IV

any T any N M 1

T: PRIMARY TUMOR
T 0 No evidence of a primary tumor
T is Carcinoma in situ (high-grade dysplasia)
T 1 Tumor invading the lamina propria, muscularis mucosae, or submucosa but not breaching the
boundary between submucosa and muscularis propria
T 2 Tumor invading muscularis propria but not breaching the boundary between muscularis
propria and periesophageal tissue
T 3 Tumor invading periesophageal tissue but not adjacent structures
T 4 Tumor invading adjacent structures

N: REGIONAL LYMPH NODES

N 0 No regional lymph node metastasis
N 1 Regional lymph node metastasis
M: DISTANT METASTASIS
M 0 No distant metastasis
M 1 Distant metastasis

Also:
According to histology
(I)
Epithelial:
1. Squamous cell carcinoma
Well-differentiated
Moderately differentiated
Poorly differentiated
2. Adenocarcinoma
Adenocanthoma
Adenoid cystic carcinoma
Mucoepidermoid carcinoma
3. Adenosquamous carcinoma
4. Carcinoid
5. Undifferentiated carcinoma
(II)
Non-epithelial
1. Leiomyosarcoma
2. Rhabdomyosarcoma
3. Malignant melanoma
(III)
Microscopically
1. Mucous
2. Infiltrative
3. Nodular
Diagnosis.
Based on complaints, clinical features:
CLINICS:
1. Local dysphagia, odynophagia, regurgitation.
2. Common weight loss, loss of appetite

3. Complications dysphonia, diaphragmatic paralysis, trachoesophageal fistula,

superior vena cava syndrome, malignant pleural effusion/ascites, bone pain,
Hornets syndrome.
Lab studies:
BLOOD:
Anemia.
IMAGING:

Barium swallow masses in lumen.

Esophagogastroduodenoscopy visualization and biopsy.

Endoscopic US to find depth of penetration and involvement of lymph nodes.

Abdominal and chest CT check for lung metastasis or other metastases.

Bronchoscopy - to exclude invasion of trachea.

Bone scan for metastasis.

Laparoscopy and thoracoscopy to see tumor.

Positron emission tomography scanning can show hypermetabolic foci and disease
activity.

Below are the elaborations for imaging studies:

COMPUTED TOMOGRAPHY
CT scanning of the chest and upper abdomen is standard and permits evaluation of the esophageal
wall thickness (should normally not exceed 5 mm), assessment of direct mediastinal invasion by
the tumor, and the presence of regional lymphadenopathy and/or pulmonary, liver, adrenal, and
distant nodal metastases. CT enables one to accurately detect distant metastases (M stage),
especially in the liver, [73] [133] and to evaluate adjacent organ (T 4 ) invasion, especially
tracheobronchial.
ENDOSCOPIC ULTRASOUND
Endoscopic ultrasound is the method of choice to determine depth of tumor invasion and regional
nodal disease and involvement of adjacent structures, with an overall accuracy to 92%. For
patients in whom the probe can be positioned within the esophageal lumen involved by tumor,
endoscopic ultrasound has an 86% accuracy in defining involved mediastinal lymph nodes. [100]
Impassible stenosis has been reported in 25 to 43% of patients with cancer.

A significant error associated with endoscopic ultrasound T staging is to overstage 7 to 11% of

early disease. [146] [158] Diagnostic accuracy ranges from 84 to 92%, with increasing accuracy
directly correlated with increasing T stage [146] [161] (about 85% accuracy for T 1 to more than 95%
for T 4 disease). A learning curve is involved with using endoscopic ultrasound to stage
esophageal tumors. [134]
T 1 and T 2 masses are located within the esophageal wall, whereas T 3 and T 4 masses invade the
muscularis (extraesophageal). Because the muscularis propria is only millimeters thick, staging
errors can result in misclassification of the tumor (intraesophageal versus extraesophageal) and
may lead to errors in treatment choice. Irregular tumor border and interrupted muscularis propria
( subjective criteria to discriminate T 2 and T 3 disease) are inaccurate; however, overall mass
thickness and extraluminal mass thickness ( objective measurements of mass thickness) are
highly accurate. [15Accurately detecting T 4 disease recognizes patients with advanced disease and
precludes them from unnecessary surgical intervention while reducing associated morbidity and
costs. The Japan Esophageal Oncology Group [105] has assessed the accuracy of preoperative
staging of resectable esophageal cancer, using esophagography, esophagoscopy, and percutaneous
and endoscopic ultrasonography. Overall, the accuracy of stage grouping was 56%.
Endoscopic ultrasound tends to understage lymph nodes, with an accuracy ranging from 50 to
88% for N stage. [163] Sensitivity decreases as distance increases from the esophageal wall. The
rising incidence in distal and gastroesophageal junction adenocarcinoma increases the need for
accurately staging celiac lymph nodes. [133] The sensitivity and specificity of endoscopic
ultrasound for determining the presence or absence of malignant celiac nodes are 72 and 97%,
respectively, with a decrease in sensitivity for nodal metastases smaller than 1 cm in diameter.
Advances in endoscopically guided fine-needle aspiration allow direct cytologic evaluation of
lymph nodes or masses within 5 cm of the esophagus (Fig. 37-33).
Ultrasonic miniprobes enable safe passage through high-grade malignant strictures and achieve
both higher accuracy rates for T staging and similar rates for N staging. [87]
POSITRON EMISSION TOMOGRAPHY
The PET scan is a more expensive technique that appears to increase the recognition of distant
metastasis. [86] The main advantage of PET is that it does not rely on anatomic or structural
distortion for detecting malignancy. PET produces whole-body images in three dimensions, but
without anatomic resolution, to assess both metastatic spread and primary disease. The best
technology, although not widely available, for detection of distant metastases is PET. PET is 88%
sensitive, 93% specific, and 71 to 91% accurate for identifying distant metastasis. [44] [86] Overall,
PET can identify distant metastases and results in upstaging of approximately 20% of patients
who have no distant metastases detected with conventional staging. [80] The accuracy, sensitivity,
and specificity of PET for detecting distant metastases are 90% or better. [86] PET has a 48 to 76%
accuracy in detecting nodal involvement.
[44] [85]

The disadvantages of PET scanning : PET is a low-resolution functional technique based

on increased cellular metabolism and not on anatomic changes, the level of tumor invasion (T
stage) is not reliably predicted. Although PET scan is more reliable than CT alone for identifying
metastatic disease, the functional advantages of PET and the structural advantages of CT combine
to enhance the detection rate for metastasis to 80 to 90% accuracy. If the tumor is anatomically
evident, but metabolically inactive, it will be detected by CT. If it shows increased glycolysis, but
no anatomic abnormalities, it will be detected by PET.
MAGNETIC RESONANCE IMAGING

Additional studies such as MRI to evaluate mediastinal structures, bone and brain scans to detect
metastatic disease, and staging mediastinoscopy are not performed routinely unless these tests are
indicated by specific symptoms or findings. MRI can accurately detect T 4 and metastatic disease,
especially disease involving the liver. [127] Comparing CT with MRI, the sensitivity and specificity
for metastatic detection are almost equal; however, CT scans cost less and are more readily
available than MRI scans. Bronchoscopy is imperative for esophageal carcinomas, which are in
proximity to the trachea or main stem bronchi (i.e., upper-third and middle-third tumors), because
endoscopic evidence of invasion of the airway precludes a safe esophagectomy. Video-assisted
thoracoscopy and laparoscopy can provide direct access to thoracic or celiac lymph nodes for
biopsy or fine-needle aspiration. Major disadvantages of thoracoscopic or laparoscopic staging
are the requirements for general anesthesia, a double-lumen endotracheal tube, several access
ports, a 2 to 3-hour procedure, and a 2 to 3-day hospital stay with all associated costs and risks.
THORACOSCOPY AND MINIMALLY INVASIVE STAGING
Video-assisted thoracoscopy to stage esophageal cancer has been shown to be highly accurate,
although invasive, in evaluating nodal status. Thoracoscopy allows visualization of the entire
thoracic cavity and esophagus from the thoracic inlet to the diaphragmatic hiatus, for biopsy of
lymph nodes as well as for visualization of the extent of local involvement. [77] Thoracoscopy can
also visualize metastatic disease involving nearby or adjacent structures, such as the trachea,
azygos vein, aorta, pericardium, and diaphragm. A right-sided thoracoscopy is most commonly
performed so the esophagus can be viewed and manipulated without interference from the aorta.
A left-sided thoracoscopy is used when the patient has suspicious left-sided nodal findings,
especially aortopulmonary window nodes, from prior noninvasive radiologic techniques. [74]
Celiac nodal involvement is common in patients with esophageal cancer, up to 46%, and also
predicts a poor prognosis. [43] To overcome this limitation of thoracoscopy, laparoscopy has been
added as a complementary technique.
Laparoscopy is useful in evaluation and biopsy of the celiac axis, the surface of the peritoneal
cavity, the esophagogastric junction, and the liver. [75] As a result, laparoscopy is routinely used to
complement thoracoscopy, to provide a method for accurate minimally invasive staging.
Laparoscopy is more sensitive than CT and ultrasound in the diagnosis of nodal and peritoneal
metastases. Laparoscopic ultrasound can visualize nodes as small as 3 mm in diameter with
resolution comparable to that of endoscopic ultrasound potentially to improve overall TNM
staging accuracy.
Treatment/general principles.
Curative efforts include surgery, chemotherapy, radiation, or a combination of these techniques;
however, no treatment modality alone has proved superior. Current trials have focused on
radiation and chemotherapy with or without resection. In the past, palliative techniques were
advocated because of the poor long-term survival rates of patients with esophageal carcinoma.
Palliation affords the patient the ability to swallow (at least saliva) and perhaps to resume a
normal life for 9 to 12 months. After the initial evaluation for staging, the physician can assess
whether palliative or curative approaches are indicated.
Treatment:
1. Stage I surgical resection
2. Stage II surgical resection and chemotherapy, radiation. Maybe subsequent surgery.
3. Stage III Chemo and radiotherapy. Subsequent surgery, surgical resection of T3 lesions.
4. Stage IV Radiation, intraluminal intubation and dilation. Intraluminal brachytherapy.

Nst:YAG laser endoluminal tumor destruction and electrocoagulation.

Chemotherapy.

42. Cancer of esophagus. Ways of treatment.

Treatment:
Curative efforts include surgery, chemotherapy, radiation, or a combination of these
techniques; however, despite multitudes of clinical trials and retrospective reviews, no
treatment modality alone has proved superior. Current trials have focused on radiation and
chemotherapy with or without resection. Therapy for esophageal carcinoma is influenced by
the knowledge that in most of these patients, local tumor invasion or distant metastatic
disease precludes cure. In fact, 85 to 95% of patients have lymph node involvement at the
time of surgical resection. Fewer than 10% of patients with lymph node involvement survive
for 5 years. In the past, palliative techniques were advocated because of the poor long-term
survival rates of patients with esophageal carcinoma. Palliation affords the patient the ability
to swallow (at least saliva) and perhaps to resume a normal life for 9 to 12 months. After the
initial evaluation for staging, the physician can assess whether palliative or curative
approaches are indicated.
PALLIATIVE TREATMENT:
Palliation is appropriate when patients are too debilitated to undergo surgery or have a tumor
that is unresectable because of extensive invasion of vital structures, recurrence of resected or
irradiated tumor, and/or metastases. Most of these patients have complete or partial
obstruction of the esophagus resulting from the tumor, and swallowing is painful or
impossible. The goal of palliation is to use the most effective and least invasive means
possible to relieve dysphagia and discomfort, to support nutrition, and to limit
hospitalization. Palliation includes dilatation, intubation, photodynamic therapy, radiotherapy
with or without chemotherapy, surgery, and/or laser therapy. None of these methods have
proven superior.
Dilatation:
Dilatation of malignant strictures to palliate dysphagia and to allow endoscopic ultrasound
evaluation is associated with a 2 to 3% risk of esophageal wall rupture or bleeding.
Unfortunately, relief is measured only in weeks. Patients with high-grade malignant strictures
more likely present with advanced disease. Similarly, 91% of patients with an obstructing
tumor precluding passage of an endoscope have stage III to IV disease.
Stenting:
The purpose of a stent is to bridge the obstruction in the esophagus to allow luminal patency
primarily for control of saliva and secondarily for nutrition. Flexible, self-expanding stents
are constructed of two layers of superalloy monofilament wire with a layer of silicon between
them. The silicon sandwiched between the layers delays tumor ingrowth through the holes in
the wire mesh. After administration of local or general anesthesia, the stricture is dilated to 42
to 45 French, the lesion is identified, and the expandable covered stent is inserted under
fluoroscopic or endoscopic control. Once the stent is inserted and expanded, the ends flange
out to anchor to the wall of the esophagus. Patients note chest discomfort initially because of

the stretching of the stricture. The insertion of self-expanding metal stents does not preclude
further treatment with chemotherapy or radiation.
The average survival after palliative intubation for esophageal carcinoma is less than 6
months. Intraesophageal tube may permit oral alimentation for the several months of
remaining life.
Photodynamic Therapy:
For photodynamic therapy, a photosensitizer such as dihematoporphyrin ether, is given
intravenously and after 2 or 3 days is retained in the tumor in a much higher concentration
than in healthy tissue. Then, a low-power laser system that produces red light is delivered to
the tumor by a flexible endoscope. The photosensitizer absorbs the red light and produces
oxygen radicals to destroy the tumor. Two to 3 days after photodynamic therapy,
esophagoscopy is repeated, and the necrotic tumor tissue is removed, often monthly.
Complications can include development of fistulas and aspiration. Edema of the hands and
face and sensitivity to sunlight after this therapy are common complaints. Photodynamic
therapy has high 5-year survival rates (62% in patients with Stage I tumors), and some
patients with Stage I tumors have experienced a complete response. This form of therapy can
be used in conjunction with chemotherapy and can be repeated indefinitely.
Radiation Therapy:
External-beam radiation relieves dysphagia in approximately 80% of the patients who
undergo therapy. In half of the patients, tumor regrowth occurs 6 months after radiation
therapy has been completed.
Intracavitary radiation does not affect the radiosensitive adjacent structures such as the lungs
and spinal cord that may be affected with external-beam therapy. Dysphagia-free survival can
last up to 12 months in 25 to 40% of patients. Complications are uncommon and include
fibrotic strictures, which can be effectively managed with dilatation.
Laser Therapy:
Endoscopic laser therapy similarly improves dysphagia, but multiple treatments are required,
and long-term benefit is seldom achieved. The goal of this procedure is to produce necrosis
of the tumor with high-power (80 to 120 watts) and short-power durations of approximately 1
second (range, less than 1 to 2 seconds) without administering general anesthesia. Treatments
to re-establish luminal patency are required on average every 4 weeks (range, 3 to 10 weeks).
Morbidity and mortality risks with laser therapy are relatively low (less than 5%).
Complications include esophageal perforation, bacterial infection, abdominal distention, and
either massive or acute hemorrhage.
Surgical Palliation:
In the past, a palliative surgical bypass with interposed stomach or colon was used when a
tumor was unresectable in a patient with severe dysphagia or when a tracheoesophageal
fistula occurred. Complications from this procedure included wound sepsis and anastomotic
leaks. The operative mortality was 11 to 40%. Postoperative death rates were much higher in
patients with cervical fistulas. Overall, of those patients returning home after surgery, most

(75%) were able to eat a full diet. Nevertheless, postoperative survival was only 1.5 to 14
months, with a mean survival of 3 to 6 months.
An endothoracic endoesophageal pull-through operation consists of stripping the esophagus
of its mucosal layer and tumor and using the muscular tube of the esophagus as a sleeve
through which the stomach is pulled. Normal swallowing and normal diet are achieved in
almost 80% of the patients. Operative mortality rates are approximately 15%, and morbidity
rates approach 25%. Complications include anastomotic and respiratory conditions.
CURATIVE TREATMENT:
If an esophagectomy is indicated, three major technical approaches are available:
(1) a transthoracic esophagectomy,
(2) transhiatal esophagectomy without a thoracotomy, and
(3) an en bloc radial esophagectomy. Although no consensus has been formed on the
preferred technique, transthoracic esophagectomy is preferred by most thoracic surgeons.
Transthoracic Esophagectomy:
Transthoracic esophagectomy is still preferred by most thoracic surgeons because it allows
complete lymph node dissection under direct vision, complete resection of tumor mass and
adjacent tissue, and complete staging of the tumor.
The traditional surgical approach to distal esophageal carcinoma has been a left-sided
thoracoabdominal incision. The distal esophagus, proximal stomach, and adjacent lymph
node-bearing tissues are resected, and an intrathoracic esophagogastric anastomosis is
performed.
For higher thoracic esophageal tumors, a thoracoabdominal incision or separate thoracic and
abdominal incisions are used, and a high intrathoracic esophagogastric anastomosis is
performed. Unfortunately, a combined thoracic and abdominal operation in a debilitated
patient may lead to respiratory insufficiency, resulting from postoperative incisional pain and
an inability to breath deeply, that requires prolonged mechanical ventilatory assistance and
often causes death. Disruption of an intrathoracic esophageal anastomosis results in
mediastinitis and sepsis, fatal in 50% of the patients. An additional disadvantage of the
intrathoracic esophageal anastomosis is inadequate long-term relief of dysphagia either
because of anastomotic suture-line tumor recurrence or because of the development of reflux
esophagitis above the anastomosis. Finally, intrathoracic esophagogastric anastomoses are
almost invariably associated with the development of reflux esophagitis, which follows
disruption of the LES mechanism. The operative mortality varies significantly, ranging from
as high as 14% to as low as 2.2%.
The posterior lateral thoracotomy incision is made (on the right, the fifth intercostal space is
entered, and on the left, the sixth to seventh). Then, an upper midline laparotomy and, if the
tumor is in the upper third, a left neck incision are made. The lung and pleural space are
examined for any evidence of metastatic disease.

The inferior pulmonary ligament is divided to the inferior pulmonary vein. The tumor area is
then examined for any evidence of direct invasion of any vital or unresectable mediastinal
structures. The esophagus, periesophageal lymphatics, and adjacent pleura are resected,
preferably en bloc. The paratracheal lymph nodes are also removed. Great care is taken to
avoid any damage to the recurrent laryngeal nerve, to avoid hoarseness. The azygos vein and
the thoracic duct are resected along with the primary specimen. The opposing pleura is not
resected unless it appears to be invaded with tumor. If dissection of the esophagus at the
thoracic inlet has been adequate, the esophagus should be easily mobilized from the anterior
longitudinal ligament of the spine. The esophagus is then transected 5 to 8 cm from the UES,
yet a sufficient distance away from the primary tumor, at least 5 cm but usually 10 cm, to
avoid skip metastases or longitudinal lymphatic spread. The esophagogastric anastomosis
may be performed in a single layer or a double layer, or with an end-to-end stapling device or
end-to-side stapling system.
The most direct route for the conduit of reconstruction (stomach, colon, roux-en-Y loop of
jejunum) is the posterior mediastinum in the prevertebral space created by the resected
esophagus. Some investigators have advocated placing the neoesophagus in a substernal
position to reduce the likelihood of a local recurrence that causes obstruction. For distal-third
tumors that are located at the esophageal hiatus and the diaphragm, a left thoracotomy alone
allows a sufficient amount of diaphragm to be resected with the specimen to achieve a
negative margin. A cephalad transection site is then chosen approximately 10 cm above the
most superior portion of the esophageal tumor. The gastric margin is approximately 5 cm
from the lowest portion. The remaining stomach is then pulled up into the retromediastinum,
and an anastomosis is performed (end-to-end or end-to-side anastomosis) using either a
single-layer or a two-layered hand-sewn anastomosis or stapling devices.
A total thoracic esophagectomy is similar, but plans include removal of the entire esophagus
to maximize the resection margin. This procedure begins with a laparotomy, as do all
esophagectomies, to mobilize the conduit of choice. A right-sided thoracotomy is then made,
and the esophagus is resected from a 5-cm gastric margin at the cardia to within 2 to 3 cm of
the UES. The conduit, whether it be the stomach or the colon, is placed either retrosternally
or in the original esophageal bed, and a cervical anastomosis is performed.
En Bloc Esophagectomy:
Because many patients present with metastases to regional lymph nodes as well as to the
surrounding tissue and organs, a more radical resection, the en bloc esophagectomy, has been
advocated by a few thoracic surgeons. An envelope of normal tissue is removed along with
the spleen, celiac nodes, posterior pericardium, azygos vein, thoracic duct, and adjacent
diaphragm. With this aggressive surgery, operative mortality ranges from 5.1 to 11%, not
significantly different from other approaches. The two major complications are similar to
transhiatal and transthoracic esophagectomy: anastomotic leak and respiratory complications.
With the en bloc technique, 5-year survival rate is 40 to 55% for patients with Stage I
adenocarcinoma confined to the esophageal wall. In adenocarcinoma, increased incidence of
regional lymph node metastases has been reported with increasing depth of invasion of the
primary tumor. Lymph nodes are involved in 80% of patients with muscular invasion. Some
surgeons advocate a three-field dissection (bilateral cervical, mediastinal, and abdominal)
followed by esophagectomy for patients with locally advanced carcinoma of the thoracic

esophagus in the presence of lymph node metastasis; 5-year survival is 42% and up to 54% in
patients with fewer than four positive nodes.
Transhiatal Esophagectomy:
Because of the risks associated with the more radical transthoracic or en bloc
esophagectomies and the overall low survival rate of patients with esophageal carcinomas,
transhiatal esophagectomy without thoracotomy was proposed. In this operation, regardless
of the level of the tumor, the entire thoracic esophagus is resected and replaced, whenever
possible, with the stomach anastomosed to the remaining cervical esophagus above the level
of the clavicles.
Advocates of transhiatal esophagectomy report a low operative mortality of 2 to 8% and a
low anastomotic leak rate of 5 to 7.9%. However, other studies of this operation reported a
higher anastomotic leak rate of 26%, with similar patient morbidity and mortality compared
with transthoracic and en bloc esophagectomy. In performing a transhiatal esophagectomy,
the surgeon removes accessible cervical, intrathoracic, and intra-abdominal lymph nodes for
staging, but a complete en bloc resection of adjacent lymph node-bearing tissue is not
accomplished. The advantages of this approach are as follows:
(1) a thoracotomy is avoided, thus minimizing the physiologic insult of the operation;
(2) an intrathoracic esophageal anatomosis is avoided, and if a cervical leak does occur, it is
more easily managed and rarely causes mediastinitis or fatal complications;
(3) no intra-abdominal or intrathoracic gastrointestinal suture lines are present; and
(4) clinically significant gastroesophageal reflux seldom occurs after a cervical
esophagogastric anastomosis.
Contraindications to the transhiatal approach include evidence of tumor invasion of the
pericardium, aorta, and/or tracheobronchial tree.
Some early and late complications associated with the transhiatial approach are wound
infection, anastomotic leak, respiratory complications, pneumothorax, recurrent laryngeal
nerve injury, esophageal stricture, and delayed gastric emptying.
The transhiatal esophagectomy is performed through an upper-midline abdominal and
cervical incision without thoracotomy; therefore, the thoracic esophagus is resected through
the diaphragmatic hiatus and the neck. The stomach is mobilized by dividing the left gastric
and left gastroepiploic vessels, and the right gastric and the right gastroepiploic arcades are
preserved. Pyloromyotomy and feeding jejunostomy are performed routinely. The entire
thoracic esophagus from the level of the clavicles to the cardia is resected, while one
carefully monitors intra-arterial blood pressure to avoid prolonged hypotension from cardiac
displacement during the transhiatal esophageal dissection. The surgical stapler is used to
fashion a gastric tube from the greater curvature while still preserving its entire length. The
stomach is mobilized through the posterior mediastinum in the original esophageal bed and is
anastomosed (hand sewn or stapled) to the cervical esophagus. The normal stomach readily
reaches to the neck in every patient. For distal-third esophageal tumors localized to the
cardia, the high lesser curvature of the stomach is resected 4 to 6 cm beyond the gross tumor,
to preserve that point on the high greater curvature that reaches cephalad to the neck for the
cervical esophagogastric anastomosis. Even relatively large intrathoracic esophageal
carcinomas are resectable through the enlarged hiatus. For tumors of the upper-thoracic

esophagus, the addition of a partial upper sternal split facilitates dissection of the esophagus
from the trachea under direct vision.
Thoracoscopic Esophagectomy:
Several authors have reported the use of video-assisted thoracoscopy or laparoscopy in
performing esophagectomy.Thoracoscopic esophagectomy has three stages. The first is the
thoracoscopic dissection of the thoracic esophagus. The second is the laparoscopic
mobilization of the intended gastric conduit, and the third is the cervical anastomosis.
Major causes of complications include respiratory disorders, anastomotic leak, and laryngeal
nerve injury. Some investigators have concluded that, at this early stage, this procedure has
no advantage over open surgical procedures.
Reconstruction After Esophagectomy:
After a portion of the esophagus is removed, or after complete esophagectomy, a conduit
must be established for alimentary continuity. The stomach, colon, and jejunum have all been
successfully used as esophageal substitutes, but the stomach appears to be the conduit of
choice because of ease in mobilization and its ample vascular supply. A higher incidence of
mortality is noted with the use of the colon because of the necessity for three anastomoses
(coloesophagostomy, colojejunostomy, and colocolostomy). The colon is used if the patient
has undergone a partial or total gastrectomy previously or if tumor involves the stomach .
Jejunal loops can also be used, but their limited vascular supply restricts mobility.
Anastomosis can be performed in the chest just below the arch of the aorta (intrathoracic
anastomosis), or a cervical anastomosis can be made in the neck, depending on the choice of
reconstruction. Mechanical staplers continue to improve, and leak rates are decreasing.
Leakage is more likely to occur in patients who are malnourished, in those who have had
preoperative radiation therapy, and in those who have tension at the anastomosis. A leak most
frequently occurs within 10 days of the surgical procedures, often at the time of the first
contrast swallow examination. Patients with a leak may also present with signs of sepsis or
increased drainage output from previously placed chest tubes and drains. For a cervical
anastomotic leak, a conservative approach is advised. The drainage can be controlled by
opening the cervical incision to create a cervical fistula. With adequate drainage, the leak
usually spontaneously closes within 1 to 2 weeks and mortality is rare. Nutritional support is
maintained by an enteral feeding tube. Approximately half of the patients who have an
anastomotic leak develop a stricture relieved by serial esophageal dilatation. For small leaks
that are well drained, the patient may be managed with antibiotics, nutritional support, and
close observation. Leaks from an anastomosis in the mediastinum are significantly more
serious, with mortality rates of 20 to 40%. For an intrathoracic anastomotic leak, in most
cases, reoperation should be performed. The anastomosis should be inspected. If repair seems
feasible, it may be attempted. Usually, however, the safest option is to take down the
anastomosis and mobilize the remaining esophagus out of the chest through a cervical
incision for construction of an anterior thoracic end-esophagostomy. Devitalized stomach is
resected, and the remaining stomach is returned to the abdominal cavity. A decompressing
gastrostomy is performed. The pleural cavity and mediastinum should be debrided,
thoroughly irrigated, and adequately drained. Future reconstruction with a colon interposition
remains an option.

Laryngopharyngectomy for cervicothoracic tumors and concomitant transhiatal

esophagectomy without thoracotomy provide the maximum distal esophageal margin beyond
the tumor and permit restoration of continuity of the alimentary tract. However, a colon
interposition is the best means of restoring alimentary continuity in this situation, as
regurgitation after a pharyngogastric anastomosis gives a less satisfactory functional result.
Radiation Therapy:
The goals of preoperative radiation therapy are to reduce the tumor size, to control the
amount of local spread of the tumor before surgery, and to reduce the risk of tumor spread at
the time of surgical manipulation. Preoperative radiation therapy does not significantly
improve 5-year survival after surgery. The goal of postoperative radiation therapy is to
destroy residual malignant cells after surgical resection, especially if positive tumor margins
are discovered after resection. Despite improvement in local recurrence, no improvement in
survival has been realized.
Chemotherapy:
Chemotherapy as a single modality in the treatment of esophageal cancer is the least effective
strategy. Although radiographic improvement can be seen in up to one-half of patients, two or
three cycles (6 to 12 weeks) of chemotherapy are required, relief of dysphasia is slow and/or
incomplete, and survival is anecdotal. Unfortunately, no reliable method exists to identify
"responders" before therapy is begun. Chemotherapy is used preoperatively alone or in
combination with radiation therapy to treat micrometastases and to reduce the size of the
tumor to improve resectability rate. Moreover, if surgery is not appropriate, chemotherapy is
used with radiation therapy for palliation and possibly to improve survival. Chemotherapy is
typically given in a combination of two or more drugs.

43. Benign diseases of the oesophagus. Classification. Modern methods of the

oesophagus examination.
Classification.
Classification of Benign Esophageal Tumors:
I. Epithelial tumors
A. Papillomas
B. Polyps
C. Adenomas
D. Cysts
II. Nonepithelial tumors
A. Myomas
1. Leiomyomas
2. Fibromyomas

3. Lipomyomas
4. Fibromas
B. Vascular tumors
1. Hemangiomas
2. Lymphangiomas
C. Mesenchymal and other tumors
1. Reticuloendothelial tumors
2. Lipomas
3. Myxofibromas
4. Giant cell tumors
5. Neurofibromas
6. Osteochondromas
III. Heterotopic tumors
A. Gastric mucosal tumors
B. Melanoblastic tumors
C. Sebaceous gland tumors
D. Granular cell myoblastomas
E. Pancreatic gland tumors
F. Thyroid nodules
Modern methods of the oesophagus examination.
(Baileys and Love)
Radiography:
Very useful for demonstrating narrowing, space-occupying lesions, anatomical
distortion or abnormal motility.
An adequate barium swallow takes time to do. It may be helpful to give a solid
bolus (bread or marshmallow) if a motility disorder is suspected.
Video-recording is also useful to provide subsequent delay and detailed analysis.
It should be stressed that barium radiology is very inaccurate in the diagnosis of
GORD (gastro-oesophageal reflux disease) UNLESS the reflux is gross.
Plain radiographs will show opaque foreign bodies.
Cross-sectional imaging by CT scanning is now an essential investigation in the
assessment of neoplasms of the esophagus.

Endoscopy:
Necessary for investigation of most oesophageal conditions.
It is required to view the inside of the oesophagus and the esophagogastric
junction to obtain a biopsy or cytology specimen for removal of foreign bodies
and to dilate strictures.
Traditionally 2 types of instrument available:
(i)
Rigid oesophagoscope
(ii)
Flexible video-endoscope
Rigid oesophagoscopy:
This is now virtually obsolete, some surgeons still cling to this traditional
method. I wonder WHICH surgeons from WHICH cold country would CLING to
this.
Most commonly used instrument: Negus oesophagoscope.
A newer variety Earlam oesophagoscope.
Passage of a rigid oesophagoscope requires skill and is relatively safe in hands of
an expert. There is however, risk of perforation.
Most foreign bodies may be removed with a flexible gastroscope and an over-tube
to protect the oesophagus, but some may prefer the irgid instrument and large
grasping forceps for a large foreign body such as dentures ( Fig. 61.9) he he. Page
993.
Dilatation of oesophageal strictures has been undertaken for many years with the
rigid instrument and the classic Chevalier jacksons carrot-shaped bougie.
Video-endoscopy:
The flexible video-gastroduodenoscope has many advantages.
- GA is not required.
- Examinations can be done on an out-patient basis.
- Quality of magnified image is superb. Superbe. Magnifique.
- Much safer to pass.
As a matter of routine, the stomach and duodenum are examined as well.
If stricture is encountered, it may be dilated to allow complete inspection of the
upper GIT, but this should be handled with clinical common sense.
Endoscopic ultrasonography complements computerized tomography (CT)
scanning for assessment of tumor stage.
- It gives very detailed images of the oesophageal wall and of lymph nodes close to
the oesophagus.
- Some endoscopes allow fine-needle aspiration samples of lymph nodes to be
taken.
Remember: Endoscopy is essential!
THERAPEUTIC PROCEDURES: (in relation to examining as well. Dilatation of
strictures and laser therapy are palliative/radical procedures, not included)
Oesophageal manometry:

Widely used to diagnose oesophageal motility disorders.

Recordings are made by passing a multilumen catheter with 3-8 recording orifices
at different levels down the oesophagus and into the stomach.
The catheter channels are perfused with water by a low compliance
pneumohydraulic pump for accurate measurement of rapid pressure changes.
The catheter is withdrawn progressively up the oesophagus and recordings are
taken at intervals of 0.5-1 cm to measure length and pressure of LOS and to assess
motility in body of oesophagus during swallowing.

24-hour pH recording:
Prolonged measurement of oesophageal pH is now the most accurate method of
examining GORD.
A small distal pH probe is passed into the distal oesophagus and positioned 5 cm
above the upper margin of the LOS.
The probe is then connected to a miniature digital recorder that is owrn on a belt.
20-24 hour recording period is usual and the pH recording is analysed by an
automated computer program using DeMeesters criteria.

44. Cardiospasm (achalasia) of the esophagus. Definition of the idea. Clinical

picture. Diagnosis. Differential diagnosis. Treatment.
Definition of the idea.
Achalasia ( Greek failure of relaxation )
- Its a disease characterized by progressive dilation of the esophagus due to loss of
the smooth muscle ganglion cells of the Auerbach myenteric plexus.
- Usually occurs in severe stress, major physical trauma, drastic weight reduction,
Chagas disease, varicella zoster.
Clinical picture.
Classis triad: dysphagia + regurgitation + weight loss.
- In early stages, patient will feel a sticky sensation at the level of the xiphoid area
after food. Patients eat slowly with a lot of water, may twist upper torso or walk
around to force food down.
- Dysphagia to liquids Solids form a bolus and by gravity, when they touch the
contracted segment, the sphincter may partially open up and there is no dysphagia
for solids. Dysphagia for liquids is the important feature and it results in
regurgitation Oesophageal pseudovomiting.
- Regurgitation and aspiration becomes life-threatening. Regurgitated food is not
acidic.
- As esophagus dilates, foul-smelling stagnant intraesophageal content regurgitation
occurs.
- Malnourishment, ill health, dehydration follows
- Complications:

Aspiration pneumonia
Lung abscess
Bronchiectasis
Dyspnea due to compression of bronchi
Malignancy

Diagnosis.
The basic methods of cardiac achalasia are X-ray examination, esophagoscopy,
esophagotomography, pharmocologic test.
1. Radiography picture changes to see progression.
- Typically: A double mediastinal stripe throughout the length of the chest.
- Fundic air bubble is absent because of stasis of fluid in the esophagus, the air
occupies a higher position than the fundus.
Ba esophagram Mild uniform dilatation with a smooth tapering below
cucumber esophagus pencil tip deformity in stages and massive dilatation,
tortuosity and a sigmoid shape in later stages.
Retained food may be seen.
Typical BIRD BEAK taper of gastroesophageal junction.
2. Manometry: failure of lower esophageal sphincter to relax with swallowing.
- Conractions descreases later, absent or weak.
- Admin of vagomimetics (bethanecol) increases intraesophageal pressures.
3. Esophagoscopy can show severity of esophagitis +/- cancer. Distal esophageal
stricture (due to gastroesophageal reflux). Esophagitis severe edema, red-purple
colour, marked friability.
4. Endoscopic US Subepithelial tumor. Can be used to inject botulinum toxin as
treatment.
5. Gastroscopy Gives impression as if one is entering into a cave filled with dirty
necrotic fluid due to stasis which splashes out with each heart beat and with each
respiratory movement. Gastroscopy also done to rule out proximal malignancy.
Differential diagnosis.
DIFFERENTIAL DIAGNOSIS :
1. with cancer of esophagus. Decisive importance esophagoscopy has, together with
puncture biopsy;
2. benign tumors of esophagus (leumyoma...)
3. peptic esophagitis (very often combined with sliding hiatus hernia)
4. esophagus strictura after burn
5. esophageus diverticulum
Feature

Achalasia

Diffuse esophageal spasm

Dysphagia
Pain
Barium esophagogram
Motility

Rare
Rare
Abnormal dilated, Birdbeak taper.
Non-relaxing lower
esophageal sphincter,
absent/weak contractions on
swallowing.

Common
Common
Cork screw esophagus
Hypertonic simultaneous
multiphasic contraction
after swallowing.

More to be considered: classified version

1. Causes from the outside:
- Thyroid swellings
- Cardiomegaly
- Aortic aneurysm
- Mediastinal nodes: TB, lymphoma, secondaries.
- Rolling hiatus hernia (paraesophageal hernia)
- Alveolar abscess (retropharyngeal abscess)
2.
-

Causes in wall of esophagus:

Esophageal stricture: Corrosive acid poisoning, TB stricture.
Cancer of esophagus
Esophagus diverticulum
Muscular spasm: plummer Vinson and Achalasia Cardia
Tetanus: due to spasm.

3. Causes in lumen of esophagus:

- Foreign body: dentures, coins, marbles, old socks (he he. Joking)
Treatment.
CLASSIFICATION ( professor B.V.Petrovsky 1970)
4 stages are distinguished:
1st stage - funtional, uncontinous cardiospasm, widening of esophagus is absent;
2nd stage- stable cardiospasm with unexpressed widening of esophagus;
3rd stage- cicatrical changings in muscular layers of cardia with expressed widening of
esophagus;
4th stage- evidently expressed cardiostenosis with esophagus dilatation, with its Scrook, esophagitis.
The 1st/2nd stages - conservative therapy fractional feeding, food must be
mechanically and thermically sparing, per os nitroglycerine.
Electrophoresis with novocain, giathermy on cardia field.
The basic method of CA treatment is cardiodilatation with means forced
distention and partial tearing of low third of E and C.
Cardiodilatation may be done in any disease stage.
Contraindication to cardiodilatation are - varicosis of esophagus, acute
esophagitis, flood diseases.

The most widespread cardiodilatator is pneumatic. It consists of tube-probe.

Pressure in system is made by pear and is controlled by manometer at first 180200 mm Hg during next procedures maximum pressure is 300 the time of
procedure is about 1 min, break between them are 2-4 days.
In nearest time after cardiodilatation exellent and good results are marked by
95% of patients, however after some years 37% patients have relapse, which
demands repeating of treatment course.

NESSECITY OF OPERATIVE TREATMENT:

1.
2.
3.
4.

impossiblity of cardiodilatation
absence of effect after cardiodilatation
esophagus breakage during cardiodilatation
the fourth stage of disease with S-like dilatation esophagus

15-20% of patients are subjected to surgical treatment.

The most oftenly used operation is extramucosus cardiomyotomy
according to Heller.
If during it fundus of the stomach is hemed to the place of muscles
dissection such operation is called Heller's-Suvorova's; if rag is from
diaphragma-Heller's-Petrovsky's.
During the 4th stage of disease esophagofundoanastomosis is put
exterpation of esophagus with its plasty from small or large intestine is
done.

ALSO:
Conservative: sublingual NG, long-acting nitrates, Ca-channel blockers to dilate
smooth muscles.
Intrasphincteric botulinum through flexible esphagoscope inhibits release of
Ach from nerve endings relaxation of sphincter.
Passage of weighted mercury bougee (boogie) down to LES relieves dysphagia
for days to weeks only.
Most widely used Disruption of circular layers of muscle fibers of LES. 2 ways:
(i)
Forceful dilatation pneumatic or hydrostatic.
(ii)
Esophagomyotomy
Forceful dilatation Gruntzig type balloon is positioned under fibroscopy at LES
and inflated to 300 tors in 15 seconds, can be repeated 2nd time if no positive results.
Esophagomyotomy Open(thoracicapproach) or video-assisted
(laparoscopically/thermoscopically.
A longitudinal incision is made 7-10 cm from level of inferior mesenteric vein down
through LES into 3-5 cm into the stomach.
Consider these 2 as well: heller and plummer.

1. Hellers Cardiomyotomy
With left thoracoabdominal incision, esophagus and stomach are completely
mobilized.
The contracted segment is felt between fingers.
A long incision is made through the lower end of esophagus carried over to the
stomach and muscles are cut till the mucosa bulges out dysphagia is relieved.
10% of patients develop reflux esophagitis treat conservatively.
2. Plummers Hydrostatic bag
After dilating the contracted segment, hydrostatic bag is distended to a transverse
diameter of 5 cm.
It ruptures the circular muscle fibers.

45. Chemical burns and scarring stenosis of the esophagus. Etiology and
pathogenesis. Clinical picture in acute period. First aid and treating principles in
this period. Early and late bouginage.
Etiology and pathogenesis.
High in children under 5 yrs (< 75%) and late adolescents suicide attempts.
Chemical agents are dyes, acids, household bleaches.
Burns can occur in oropharynx, larynx, stomach, intestine and severity of injury depends
on character, quantity, concentration and time of exposure.
- In acid ingestion, esophagus can escape injury because of relative resistance of
squamous epithelium. But it accumulates in the stomach due to pylorospasm
destroys antrum.
- In alkali ingestion, there is pylorospasm spasm of stomach alkali back into
esophagus cricopharyngeal muscle spasm to stomach (forms a SEESAW)
leading to both stomach and esophageal burns.
Burns can be:
(i)
Superficial mucosal erythema, edema, blisters and small isolated ulcers.
(ii)
Deep circumferential ulcerations, full thickness.
Injury most often occurs in cricopharyngeal narrowing, aortal and left bronchus
narrowing, LES.
Clinical picture in acute period.
- Oral pain
- Drooling
- Excessive salivation
- Inability to swallow or drink
- Erythema/edema and blistering of the lips, tongue, oropharynx, face, hands and
neck can occur.
- Substernal discomfort mediastinal perforation, abdominal discomfort
peritoneal perforation.
- Hoarseness, stridor, dyspnea due to laryngeal edema/trauma.

Hemoptysis, hematemesis, fever.

First aid and treating principles in this period.

1. Lavage with neutralizing sltn or water (1% KMNO2 or soda). Alkaline solutions
with a pH lower than 11.5 are considered relatively safe, but those with a
pH exceeding this level possess a proportionately increasing potential for
injury.
Take note: Treatment of these patients by administration of antidotes is
probably ineffective because the corrosive action is largely completed within
seconds.
2. Never induce vomiting.
Take note: Ipecac-induced vomiting poses a threat of compounding the
original injury by re-exposing tissues to the offending agent.
3. Early endoscopy and The only exceptions to proceeding are instances in
which esophageal or gastric perforation or impending airway obstruction
is suspected.
4. Give patient 0.5% solution novocaine per os.
5. Detoxification
6. Antishock therapy
7. After 2 dys lavage again.
8. After 5-7 days eat (If not possible, do gastrostoma)
9. Early bouginage and corticosteroids.
Early and late bouginage:
- Used to prevent and treat stenosis.
Early bouginage.
It is performed early for several weeks every other day for 2-3 weeks and finally
once a week for months.
Dilation must be initiated only after re-epitheliazation of esophagus (6 weeks after
injury).
Late bouginage.
Usually done for late complications like Barretts syndrome, dysplasia, late
strictures.
Dilatation by bouginage should be continued for as long as progressive
improvement can be achieved.

46. Diverticula of the oesophagus. Classification. Diagnosis. Treatment.

Classification.
Esophageal diverticula are epithelial-lined mucosal pouches that protrude from
the esophageal lumen. Almost all are acquired, occur in adults, and are

CLASSIFIED according to their site of occurrence , wall thickness , and

mechanism of formation .
Diverticula commonly occur at three distinct sites :
1) pharyngoesophageal (Zenkers) diverticula occur at the junction of the
pharynx and esophagus,
2) parabronchial (midesophageal) diverticula occur near the tracheal
bifurcation, and
3) epiphrenic (supradiaphragmatic) diverticula arise from the distal 10 cm of
esophagus.
According to wall thickness :
1) A true diverticulum contains all layers of the normal esophageal wall,
including mucosa, submucosa, and muscle, whereas a
2) false diverticulum consists primarily of mucosa and submucosa.
According to mechanism of formation :
1) Pulsion diverticula (pharyngoesophageal and epiphrenic) are false
diverticula that arise because elevated intraluminal pressure forces the
mucosa and submucosa to herniate through the esophageal musculature.
Abnormally elevated intraluminal pressure, secondary to an esophageal
motility disorder or distal obstruction, is responsible for the mucosal
herniation through the muscle of the esophagus.
2) Traction diverticula (parabronchial) are true diverticula resulting from
external inflammatory reactions in adjacent mediastinal lymph nodes that
adhere to the esophagus and that pull the entire wall toward these lesions
as they heal and contract. Almost all diverticula of the body of the
esophagus are of the pulsion variety caused by an underlying motility
abnormality. [38 ]
Diagnosis:
The barium esophagogram is characteristic. The manometric or motility
abnormalities associated with diverticula are varied and frequently do not fit
the pattern of a known motility disorder.
1) Pharyngoesophageal (Zenker's) Diverticula:
- Manometry of the UES shows incoordination during swallowing,
with pharyngeal contraction occurring after cricopharyngeal closure
and resting pressures lower than in control subjects.
- Zenker's diverticula are usually asymptomatic initially and are only
discovered during a routine radiographic evaluation. An air-fluid
level in the diverticulum can be detected on a plain film during
chest or cervical studies.
- Endoscopic assessment and biopsy are necessary when mass defects
or ulcers are seen on a barium esophagram. Safe endoscopy
requires prior recognition of the diverticulum.
2) Midesophageal Diverticula:
- A barium esophagram is the most effective diagnostic test for
midesophageal diverticula. Midesophageal diverticula are often

wide mouthed, more common on the right side, and most often
singular.
- CT or MRI may be indicated in patients with concerns about
malignancy.
- Manometrically, these patients may have achalasia, diffuse
esophageal spasm, or other nonspecific esophageal motor disorders.
The dysmotility can be classified as normal, achalasia-like,
scleroderma-like, or nonspecific. Endoscopy is often required to
pass the manometry catheter into the stomach, particularly if an
epiphrenic diverticulum is also present.
3) Epiphrenic Diverticula:
- A barium esophagogram best detects the presence of epiphrenic
diverticula and often characterizes the underlying motility disorder.
- Although epiphrenic diverticula are readily detected with a barium
esophagogram, motility studies are necessary to rule out an
underlying diffuse motor disorder.
Treatment:
Treatment of patients with diverticula is designed to relieve dysphagia, to
palliate chest pain, and to protect against pulmonary soilage caused by chronic
aspiration of regurgitated esophageal contents. Surgical therapy must address the
motor disorder; therefore, esophagomyotomy of the abnormally functioning
muscle identified by manometric examination is essential. If the myotomy
crosses the LES, a nonobstructive antireflux procedure such as a partial
fundoplication is usually performed to protect against the development of
iatrogenic reflux.
1) Pharyngoesophageal (Zenker's) Diverticula:
- The most popular current surgical approach to the incoordinated
UES is cervical esophagomyotomy and resection of the
diverticulum performed through an oblique left cervical incision
that parallels the anterior border of the sternocleidomastoid muscle
or a transverse cervical incision centered over the cricoid cartilage.
- The sternocleidomastoid muscle and carotid sheath and its contents
are retracted laterally, and the thyroid and the trachea are retracted
medially. The inferior thyroid artery is identified and is divided.
The diverticulum is located beneath this vessel.
- With a 40-French bougie within the esophagus, the pouch is
dissected to its base, and an extramucosal esophagomyotomy is
performed in both directions from the base of the pouch
(7 to 10 cm) to ensure that all cricopharyngeal muscle fibers are
divide. Most pouches between 1 and 2 cm in diameter blend into the
exposed mucosa and submucosa after the cervical esophagomyotomy.
- Some surgeons terminate the operation at this point without
resecting the diverticulum, regardless of its size. Most surgeons
advocate excising larger pouches by using a surgical stapler.

Diverticulopexy (mobilizing the pouch, inverting it, and suspending

it from adjacent tissues so the mouth is dependent) combined with a
cricopharyngeal myotomy is an alternative.
Endoscopic division of the common wall between the diverticulum
and the esophagus (internal pharyngoesophagotomy, the Dohlman
procedure) has also been used with success.
Patients with known incompetence of the lower sphincter must be
postured upright postoperatively after a cricopharyngeal myotomy
is performed that renders the upper sphincter incompetent.
Regardless of the surgical approach, recurrence is rare, and results
are excellent.

2) Epiphrenic Diverticula:
- Mildly asymptomatic patients with pouches smaller than 3 cm often
require no treatment, whereas those with progressively severe
dysphagia and chest pain or an anatomically dependent pouch
enlargement are surgical candidates.
- Surgery is performed through a left thoracotomy for resection of
the
diverticulum
and
a
long
extramucosal
thoracic
esophagomyotomy from beneath the aortic arch to the
esophagogastric junction.

47. Peripheral benign lung tumors. Clinical picture. Diagnosis. Treatment.

Clinical picture.
1. Cough but not common.
2. Hemoptysis
3. Dyspnea and wheezing
4. Fever, chills.
5. Hoarseness
6. Chest pain dull, intermittent, aching, lasts from minutes to hours.
7. Dysphagia
8. Liver metastases anorexia, epigastric pain, hepatomegaly (hard and nodular
surface), jaundice.
9. Choradal metastases blurred vision and spots before the eyes.
Diagnosis.
2.
3.

1. X-Ray
Spherical or oral configuration.
Lobulation
Irregular margins with 1 or more strands radiating into the surrounding lung.
Dumb-bell shape.
Sputum cytology
Bronchoscopy

4. Transbronchial biopsy
5. Transbronchial needle aspiration
6. Bronchoalveolar lavage
7. Endobronchial sonography and pulmonary mucovascular cytology
8. Percutaneous fine needle biopsy
9. Pleural aspiration and biopsy
10. Thoracoscopy
11. Medistinoscopy and mediastinotomy
Treatment.
1.
2.
3.
4.
5.

Lobectomy/bilobectomy
Pneumonectomy
Radical resection
Radiotherapy
Chemotherapy

48. Diaphragmal hernias. Definition. Classification. Pathophysiological changes in

the organism.
Definition.
It is the prolapse of the abdominal organs in the thoracic cavity through the congenital
gaps (certebrocostal and sternocostal trigones) or through dilated natural apertures in the
diaphragm and through traumatic opening.
Classification.

Classification of the diaphragmatic hernias:

I.
1.
2.
II.
1.
2.
3.
4.
III.
1.
2.
IV.
1.
2.
V.

by the origin:
congenital
acquired
a) traumatic
b) non traumatic
by the localization:
hernias of the aponeurotic tendon
hernias of the muscular part of the diaphragm
hernias of the musculotendinous part of the diaphragm
hernias of the gaps and natural openings.
by the presence of the hernial sack
true
false
by the clinical course
acute
chronic
by the clinical picture

1.
2.

incarcerated
non-incarcerated
a) reducible
b) irreducible
VI.
by the hernia size
1.
small
2.
medium-sized
3.
large
VII. by the quantity
1.
solitary
2.
multiple
Pathophysiological changes in the organism.
The ma in clinical s ymptoms are: gastrointestinal and cardio-respirator y.
Character, volum and the rate of the transferred organs filling and also,
sizes, for m and localization of the hernial opening influence the clinical
s ymptoms evidence.
Cardio-respirator y abnor malities depend on the rate of the heart
displace me nt and lungs compression. Transfer speed of the abdomi nal organs in
the thoracic cavit y has the big meaning, because the compensator y mechanis m
fails to develop. Thats wh y the more evident cardio-respirator y s ymptoms
appear in case of acute traumatic hernias, which s ympto ms are the full-blown
evident d yspnea, tach ycardia, c ya nosis and someti mes collaps, connected with
the lung compression and dislocation of the mediastinum.
The localization of the hernia opening pla ys the i mportant role. So, in
case of congenital or acquired pericardial hernias the migration even of the
s mall part of the bowel or omentum in the pericardial cavit y can cause the
s ymptoms of the heart compression or pericardial ta mponade.
Gastrointestinal s ymptoms intensit y depends on the organs, which
dislocate in thoracic cavit y. Stomach transfer is accompanied b y s ympto ms of
its acute or chronic torsion. Flexure of esophagus causes the d ysphag y.
O me ntum

transfer

with

the

compression

of

the

intestine

development of the chronic or acute intestinal obstruction.

leads

to

the

49. Traumatic diahragmal hernias. Causes. Clinical picture. Diagnosis. Treatment.

Causes.
-

The cause of its development is open or closed da ma ges of the

diaphragm.

Eventration of the organs through the opening in diaphragm happens in

the mo me nt of trauma or some ti me after trauma (someti mes months or
ye ars later).

Traumatic diaphragm hernias ma y be acute or chronic in case of blunt

abdominal trauma, which brings on the increase of the intra-abdominal
pressure, the diaphragm cant stand the pressure and breaks. The left part
of the diaphragm is da maged more often than the right one.

Clinical picture.
1. GIT Pain in abdomen (high epigastrium) usually occurs on eating. Inclining forward
intensifies pain, sour belching, regurgitation of food into mouth, bloody vomit.
2. Cardiorespiratory abnormalitites due to abdominal viscera moving to the thorax.
Pleuropulmonary shock, chest pain with irradiationi to left arm and neck, cyanosis, dyspnea,
tachycardia, arrythmias, dyspnea (related with meals).
3. Symptoms of the trauma itself.
Objective examination:
1. Percussion Changed to dull/tympanic.
2. Auscultation No breath sounds or weakened. Maybe liquid movement sound.
Diagnosis.
1. X-Ray:
- Main method (chest).
- Raised dome of diaphragm and limited mobility.
- Big horizontal level of fluid indicates stomach in chest.
- Shadows of air-fluid level of intestine.
- Displacement of liver upwards.
2. Barium swallow:
- shows characteristics of herniated organ.
3. Endoscopy may be used but rarely helpful.
Treatment.
All traumatic hernias must be operated. The principles are:
(i)
Moving the herniated organs back into the abdominal cavity and
(ii)
Suturing of diaphragmatic defect using lavsan not catgut.
If strangulated hernia use transthoracic approach to reduce hernia. Duplication of diaphragm
opening or allograft can be done for better reinforcement of weak area.

50. Traumatic diaphragmal hernias. Indications for surgical treatment. Plastic

methods for diaphragmatl hernias treatment. Peculiarities of post-operative period
after surgical procedures on the diaphragm.
Indications for surgical treatment.
Any traumatic diaphragmatic hernia is an indication for surgical treatment. Type I hiatal
hernias may be left untreated.
However candidates for surgery in hiatal hernia are:
1. Patients with refractory symptoms who do not wish (or cannot afford) to take
lifelong medication.
2. Patients with related problems such as esophageal stricture, ulceration, pulmonary
complications or recurrent hemorrhage.
3. Large hiatal hernia.
Plastic methods for diaphragmal hernias treatment.
- Laparoscopic or open methods can be applied.
- Laparoscopic surgery/repair requires a shorter hospital period.
- Open methods can be done using abdominal or thoracic approach. Abdominal
approach is preferred unless the hernia is large, in which case reduction would be
problematic due to thoracic adhesions.
Aims of the operation:
(i)
Reduce the hernia
(ii)
Eliminate the sac
(iii)
Repair the large opening in the hiatus.
Approximately 2/3rds of patients have reflux (gastroesophageal) requiring anti-reflux
repair. For this, a full mobilization of the hernia, reduction of the redundant anterior and
posterior hernia sacs, placement of sutures in the diaphragmatic crura posteriorly for
narrowing the hiatus and the creation of an anti-reflux fundoplication between stomach
and esophagus are carried out.
Peculiarities of post-operative period after surgical procedures on the diaphragm.
1. Dysfunction of the diaphragm can lead to respiratory difficulties and patient
death.
2. Patient must be asked to breathe deeply and oxygen can be provided for
breathing.
3. Pain control helps minimize pulmonary complications.

51. Incarcerated diaphragmal hernias. Clinical picture. Diagnosis. Treatment.

Clinical picture.
- Acute epigastric or chest pain especially after a meal due to increased pressure or
volvulus and incarceration.
- Bleeding may occur and melena or hematemesis results.
- Sudden strangulation can cause sudden death.

In addition to this, there will be symptoms of diaphragmatic hernias in anamnesis:

Fullness after meals. Gurgling or splashing noise in chest.
Early satiety.
Postprandial vomiting.
Epigastric pain

Diagnosis.
- Barium swallowing with X-ray will reveal diaphragmatic hernia.
- Plain chest X-ray will show air-fluid levels in chest.
- Endoscopy should be done to check the condition of the stomach and esophagus.
- Sudden constricting pain and signs of collapse can occur in sudden volvulus and
strangulation. In these cases, emergency surgery is required.
- Also CT scan and ultrasonography or MRI will be applied.
Treatment.
- Only surgical intervention applied.
- A thoracolaparotomy has to be done. The hernial contents must be checked for
viability. If the organs are not gangrenous, they can be pushed back into the
abdominal cavity and defect is repaired.
- If organ is not viable, they have to be resected.
52. Indications for surgical treatment and principles of surgical corrections in hiatal
hernias cases.
Hiatal hernia is the herniation of n abdominal organ, usull the stomach,
through the esophageal hiatus in the diaphragm. The diagnosis is usull
made b radiographic contrast studies demonstrating n abdominal organ
higher than the level of the diaphragm.
Hiatal hernias are classified into two major types:

Diagrammatic representation of Type I and T II

hiatal

hernias.

In

the

hernia

the

phrenoesophageal membrane is intact and there is n

true peritoneal sac extending into the thorax, In the
T II

hiatal

phrenoesophageal

hemia

there

membrane,

is

defect

permitting

in

the
free

peritoneal sac to enter the lower pressure thoracic

cavity.
Indications for surgical treatment.
- There is n indication for n medical or surgical treatment for
T 1 hiatal hernia. If symptoms of ref1ux are associated with
T 1 hiatal hernia, the diagnostic and treatment considerations are
directed toward the ref1ux, rather than the hernia. For this reason,
further discussion of this problem focuses n gastroesophageal
ref1ux.
- The presence of the T 11 hiatal hernia is n indication for
surgical therapy, because there is n effective medical treatment for
this condition.
- Operative treatment m b performed through n abdomi nal or
thoracic incision. Because of the possibility of intratho racic
adhesions from long-standing hemia, there is risk of being unbl
to reduce the hemia through n abdominal proach or of causing
injury to the hernia contents within the thoracic sac. For these

reasons, mn surgeons prefer thoracic approach for the repair of

giant T 11 hiatal hernia .
Esophagitis leads to anemia and later stricture formation.
Inhalation pneumonia from recurring reflux.
Obstruction on strangulation in large hernia due to volvulus.
Principles of surgical corrections.
1. In principle, ll that must b accomplished b the operation is
reduction of the hemia, elimination of the sacs, and repair of the
large opening in the hiatus.
2. Preoperative esophageal function tests show that proxirnately two
thirds of patients with T 11 hernia also hv abnormal reflux
as well. For this reason, n antireflux repair is usually performed as
part of the operative treatment. The operation consists of full
mobilization of the hernia, resec tion of the redundant anterior and
posterior hernia sacs if present, placement of sutures in the
diaphragmatic crura poste riorly for narrowing the hiatus, and the
creation of n antireflux fundoplication between the stomach and
esophagus for elimi nating the risk of postoperative
gastroesophageal reflux.
1. To replace eso-gastric junction below the diaphragm.
2. To reduce the size of esophageal hiatus.
3. To produce an anti-reflex mechanism should be carried out in all patients who
have a paraesophageal hernia provided they are fine. Patients who have sliding
hernia the indications are more controversial.
Patients having T 11, , or IV hiatal hernia are treated
surgically, and n anti-ref1ux repair is generally incorporated into
the correction of the hiatal hernia.
The operations rr the names of their developers, the Belsey Mark
IV operation, the Nissen fundopli cation, and the ill posterior
gastropexy and calibration of the cardia.
Belsey Mark IV operation:
1. The operation is performed nl through thoracic rh.
sixth-inter space incision is preferred.
2. The esophagus is mobilized full to the aortic arch to allow
restoration of long segment of intra-abdominal esophagus. The
cardia is completely freed from its attachments to the diaphragm.
The esophageal hiatus is nrrwd b the placement of sutures in

the crura posteriorly.

3. When eventually tied, these should permit only one finger of the
operator t pass through the narrowed hiatus. The repair is achieved
b the plication of the stomach onto approxi mately 270 degrees of
esophageal circumference, leaving the vagus nerves posteriorly.
4. The segment of the esophagus not included in the wrap is buttressed
against the narrowed hiatus.
5. Two rows of sutures are used, and three mattress sutures are placed
in each layer. The first layer imbricates the adjacent gastric fundus
onto the lower 2 m. of esophagus. second row of sutures, passing
through the edge of the tendinous portion of the diaphragm, the
fundus of the stomach, and the esophageal muscle 4 m. above the
gastroesophageal junction is then placed.
6. The esophagus is then reduced manually through the hiatus. It
should lie there with out tension before the sutures are tied.
Nissen fundoplication:
1.

Performed through either an abdominal or thoracic

rh.

In either

case, the

esophagus

is

fully

detached from the margins of the hiatus.

2.

The thoracic approach is se lected if more extensive

mobilization of the esophagus is re quired to ensure an
adequate intra-abdominal segment of esophagus.

3.

For facilitation of full 360-degree plication of gas tric

fundus around the abdominal segment of esophagus
without tension and without injury to the spleen,
several short gas tric arteries are ligated and divided.

4.

The fundus of the stomach is brought posteriorly

around the esophagus. Sutures are placed through the
anterior fundus and the wall of the esophagus, and the
fundus is brought posteriorly. 3- to 4-m segment of
intra-abdominal esophagus is wrapped b the fundus in

this manner. If the fundus is not anchored securely to

the intra-abdominal esophagus, the fundoplication m
slip down onto the body of the stomach and cause
double-chamber

stomach,

with

obstruction

to

the

proximal h, causing se vere reflux.

5.

This is serious complication that n b avoided b

adequate mobilization of the esophagus and b placing
the wrap around the esophagus above the intact
gastrohepatic liga ment and hepatic branch of the vagus
nerve.

6.

The full 360-degree plication of stomach around the

esophagus causes some what higher luminal pressure
in the abdominal segment of esophagus than does the
Mark IV repair.

7.

Although this m b mechanically more competent

anti-reflux valve, it also in troduces greater risk of
postoperative dysphagia as well as inability to belch
and vomit.

Hill posterior gastropexy:

1. The operation is done through an abdominal incision.
2. After extensive mobilization of the esophagus through the blatus,
sutures are placed in the di phragmatic crura to narrow the hiatus.
3. The gastroesophageal junction is anchored to the arcuate ligament
just cephalad to the celiac axis.
4. Sutures are placed n both the anterior and the posterior aspects of
the gastroesophageal junction for the ur pose of causing partial
plication of stomach around the en trance of the esophagus into the
stomach. The degree of nar rowing of the abdominal esophagus is
critical in this operation, intraoperative manometry is therefore
advocated as being essential to the success of this procedure.

53. Pulmonary hemorrhages. Causes. Clinical picture. Diagnosis. Treatment.

Also known as: Idiopathic Pulmonary Hemosiderosis, IPH.
Causes.
The pulmonary bleeding is a consequence of the - bronchoectatie disease ;
- abscess and phlegmon of the lungs;
- air especially with they are suppurated;
- malignant tumours ;
- infarction of the lung;
- parasitogenic disease of the lungs;
- many forms of the candidiasis of the lung;
- pneumosclerosis;
- different pneumonia,;
- traumatic destruction of the lungs.
Also the pulmonary bleeding is a cansquence of the nonpulmonary illness:
-mitrale stenosis and others illness, in accompaniment with congestion to the lesser of
the circulation;
- hypertension;
- varicose widening of the vein of the larynx , trachea ;
- anomaly of the vesels;
- anastaminosis;
- diseases of the rens ,liver , system of the blood and atherosclerosis
At the most case the pulmonary bleeding is observed to the pathological process at the
lungs and often to the casers of the tuberculosis and suppuration
Clinical picture.
Pulmonary hemorrhage may present as hemoptysis or finding blood in the nose or
airway with no evidence of upper respiratory or gastrointestinal bleeding.
The clinical presentation of a patient with pulmonary hemorrhage is usually
hemoptysis and anemia, associated with diffuse or focal patchy alveolar infiltrates
on chest x-ray diagnosis. Symptoms include:
cough, producing blood-tinged sputum
rapid breathing
wheezing, or shortness of breath
airway obstruction

 acute otitis media, or ear infection

runny nose
stomach upset, diarrhea, vomiting, and abdominal distress
failure to thrive, a condition in which the child does not gain weight and grow
normally.
cyanosis, or a blue tinge in the skin color
anemia, a low red blood cell count that causes skin pallor, or paleness
fatigue, weakness, lethargy
liver disease, such as cirrhosis

Diagnosis.
The diagnosis is based to the :
1) - finding of the anamnesis;
2) - objectivie methods;
3) - radiological investigation (with aortography);
4) - bronchologycal investigation.
In the modern time is more offen for the diagnostic of the pulmonary bleeding is used
bronchoscopy and bronchial arteriography.
Treatment.
In modern time the methods of the choice a case of treatment correlation pulmonary
bleeding is special operation.
The complex treatment of the patient with the pulmonary bleeding consist of:
1) decreasing of the preassune in the leggen of the circulation (managing hupotension
to the 5% solutio of the Pentamin);
2) increasing of coagulability of the blood - intravenous infusion the smoll dosis of the
blood, blood plasma, fibrinogen, injection Vicacoli, Dicinon;
3) endovascular oclusion to the bleeding vesel;
4) temporany bronchoscopycal oclusion to the bronch (lobar,segmental)which is
ventilat the part of the lung ,
The methods of the tratment:
1) drugs;

2) endovascular (it effective at the 92,9%);

3) surgical
54. Acute gastroduodenal bleedings. Etiology and pathogenesis. Diagnostic methods.
Assessment of blood loss volume.
Etiology and pathogenesis.
The many causes of gastrointestinal (GI) bleeding are classified into upper or lower,
depending on their location in the GI tract.

Upper GI bleeding
o Peptic ulcer disease: Peptic ulcers are localized erosions of the wall of the
digestive tract. Ulcers usually occur in the stomach or duodenum. Breakdown
of the walls results in damage to blood vessels, causing bleeding. When the
mucous membranes break down, they are unable to counteract the harsh
effects of stomach acid. Nonsteroidal anti-inflammatory drugs (NSAIDs),
aspirin, alcohol, and cigarette smoking promote gastric ulcer formation.
Helicobacter pylori are a type of bacteria that also promote formation of
ulcers.
o Gastritis: General inflammation of the stomach wall, which can result in
bleeding. Gastritis also results from an inability of the gastric lining to protect
itself from the acid it produces. NSAIDs, steroids, alcohol, burns, and trauma
can cause gastritis.
o Esophageal varices: Swellings in veins of your esophagus or stomach usually
result from liver disease. Varices most commonly result from alcoholic liver
cirrhosis. When varices bleed, the bleeding can be massive and catastrophic
and occur without warning.
o Mallory-Weiss tear: A tear in the esophageal or stomach wall, often as a result
of vomiting or retching. Tears also can occur after seizures, forceful coughing
or laughing, lifting, straining, or childbirth. Physicians often find tears in
people who have recently binged on alcohol.

Lower GI bleeding
o Diverticulosis: One of the most common causes of lower GI bleeding. Small
out-pockets, or diverticula, form on part of the wall of your colon (large
intestine), usually in a weakened area of the bowel wall. You may develop
several pockets, which are more common in people who have constipation
and strain at stool.
o Angiodysplasia: Along with diverticulosis, this is one of the most common
causes of lower GI bleeding. Angiodysplasia is a malformation in the blood

vessels in the wall of the GI tract. The sores are most common in the large
intestine and often bleed. The elderly and people with chronic kidney failure
develop the disease most often.
o Polyps: Intestinal polyps are noncancerous tumors of the GI tract, occurring
mostly in people older than 40 years. A small proportion of these polyps may
transform into cancer. Colonic polyps may bleed rapidly, or they may bleed
slowly and go undetected.
o Hemorrhoids and fissures: Hemorrhoids are swellings of veins in and around
your rectum. Repeated stretching from straining at stool causes them to bleed.
Bleeding from hemorrhoids is usually mild, intermittent, and bright red.
Massive bleeding is rare. Anal fissures, or tears in the anal wall, also may
trigger small amounts of bright red bleeding from the anus. Forceful straining
during passage of hard stool usually causes such tears, which can be very
painful.
Diagnostic methods.
Divided into clinicals, lab studies and instrumentals:
CLINICALS: Acute gastrointestinal bleeding first will appear as vomiting of blood, bloody
bowel movements, or black, tarry stools. Blood may look like "coffee grounds." Symptoms
associated with blood loss can include the following:

Fatigue

Weakness

Shortness of breath

Abdominal pain

Pale appearance

Vomiting of blood usually originates from an upper GI source. Bright red or maroon
stool can be from either a lower GI source or from brisk bleeding at an upper GI
source.

Long-term GI bleeding may go unnoticed or may cause fatigue, anemia, black stools,
or a positive test for microscopic blood.

LAB STUDIES:

The following laboratory tests are the most useful when evaluating patients with GIB.

o Hemoglobin value and type and crossmatch blood: A type and screen or type
and crossmatch should be ordered. The patient should be crossmatched for 26 units based on the rate of active bleeding. An unstable hemoglobin
level may signify ongoing hemorrhage requiring further
intervention.
o BUN-to-creatinine ratio: The BUN-to-creatinine ratio increases with GIB. A
ratio of greater than 36 in a patient without renal insufficiency is
suggestive of UGIB.
o Coagulation profile: The patient's prothrombin time (PT), activated partial
thromboplastin time, and International Normalized Ratio (INR) should be
checked to document the presence of a coagulopathy. The coagulopathy
may be consumptive and associated with a thrombocytopenia.

A platelet count of < 50 with active acute hemorrhage requires a

platelet transfusion and fresh frozen plasma in an attempt to replete
lost clotting factors.

The coagulopathy could be a marker for advanced liver disease.

Prolongation of the PT based on an INR of more than 1.5 may

indicate moderate liver impairment.

A fibrinogen level of less than 100 mg/dL also indicates advanced

liver disease with extremely poor synthetic function.

o Liver function tests(LFT): LFT are also needed to calculate the Child-Pugh
score. Elevated aminotransferase levels are a result of hepatocellular injury.
Increased levels of alkaline phosphatase and gamma-glutamyltranspeptidase
are indicative of cholestatic liver disease.
o Plasma fibrinogen level
o Serum electrolyte values
INSTRUMENTALS:
Endoscopy is often the first-line diagnostic examination and treatment option in GIB.
Angiography is often the next step if medical management or endoscopy fails to control GIB.
Usually, abdominal CT is not used in the evaluation of acute UGIB from arterial sources,
although it has been helpful in some series. Plain radiographs of the abdomen are not usually
helpful in the diagnosis of acute UGIB. The pathophysiology of acute UGIB is often mucosal
erosion with subsequent hemorrhage, which is not detected with plain radiographs.
Ultrasonography has no role in the setting of acute UGIB. It may be helpful in establishing
portal vein patency prior to TIPS placement in patients with variceal bleeding.

Assessment of blood loss volume.

Class 1

Class 2

Class 3

Class
4

Blood Loss, mL

Up to
750

7501500

15002000

>2000

Blood Loss,% blood

volume

Up to
15%

15-30%

30-40%

>40%

CLASSIFICATION OF LOSS OF BLOOD:

(according to Struchkov)
The 1st degree: ( to 500 ml)
common state of patient is satisfactory
BP, pulse normal;
RBC > 3-5 x10.12/l;
Hb - 120 g/l
Hematocrit is - 42-43%
Deficiency of circulating blood volume (CBV) not more than 5% ( about 500)
The 2nd degree:
common state of patient is hard skin is pale, vertigo, coffee-ground vomit, melena;
BP - 90 mm.Hg
Pulse - 120-140/minute;
RBC - about 2-5 3-5 10.12/l.
Hb 80 g/l;
Hematocrit is 25-35%
Deficiency of CBV is 15%.
The 3rd degree:
common state of patient is more hard, cerebral circulatory disbalance comes,
syncope, falls, "flies" behind eyes;
BP 60 mm.HG
Urine not filtered
Pulse >140
RBC 2-5 x10.12/l;

 Ht. < 25%.

Hb. 50 g/l;
Deficiency of CBV 30%
The 4th degree:
patients state is critical, unconscious.
BP and pulse absent
RBC 1-5 x10.12/l;
Ht. < 50 %
Deficiency of CBV > 30%

55. Clinical criteria of continuing gastroduodenal bleeding. Indications for surgical

treatment. Possibilities of endoscopic modes of bleeding arrest.
Clinical criteria of continuing gastroduodenal bleeding.
1. Worsening of patients condition increasing of cold extremities, deterioration of
consciousness, recurrent hematemesis/melena.
2. Increasing pulse rate.
3. Weakening of pulse.
4. Decreasing of BP.
5. Blood pic changes seen in repeated tests:
- Decreasing RBC
- Decreasing Hb
- Decreasing hematocrit
6. Decreasing urine output.
7. Appearance of chest pain.
8. US strain bleeding, unstable
Indications for surgical treatment.
1. Active ongoing bleeding characterized in previous answer.
2. Worsening of clinical picture.
3. Severe active comorbid state of GIT.
Possibilities of endoscopic modes of bleeding arrest.
1. Thermal contact using:
- heater probe
- multipolar electrocoagulation
2. Bleeding site injection:
- epinephrine injection
- sclerosing agent injection: alchohol, varicoid, trombovax
3. Laser coagulation (rarely used) but somehow still stated.
- ND VAG Laser
- Argon laser

56. Deep venous thrombosis of the lower extremities. Etiology and pathogenesis. Clinical
picture, differential diagnosis. Main principles of treatment.
Etiology & pathogenesis.
Predisposing factors :
(1) AgeMore in elderly
(2) Obesity
(3) Prolonged immobilisation/convalescence
(4) Contraceptive pills
(5) Chhildbirth
(6) Trauma-extensive surgery (abdominal/pelvic) and accidental injury
(7) Heart disease, congestive failure and cardia arrhythmia
(8) Malignant diseases.
Predisposing triad of Virchow :
A) Change in the vessel wall, namely endothetial damage by trauma or inflammation.
B) Stasis due to sluggish blood flow e.g. during or after operation, prolonged convalescence
and in debilitating conditions such as typhoid fever.
C) Hypercoagulability of blood e.g. in infection, after haemorrhage, in visceral cancer and
during pregnancy. Hypercoagulable states and deficiencies in the fibrinolytic system also
increase the clotting.
Sequence of events in DVT :
1) With any of the factors of Virchow, platelets adhere to the endothelium of venous wall and
then to each other forming platelet aggregate.
2) Initial platelet aggregates + deposition of fibrin mesh + further platelet deposition = Red
thrombus formation.
3) Subsequent behaviour of thrombus
a) ProximallyA 'tail' may extend from the clot into the larger veins (blood stream) and
may break off as an embolus which is swept onward to lodge into the lung. The process of
formation and migration of thrombi are now considered together under the term
'thromboembolism', two processes being inseparable in both their causes and treatment,
b) DistallyVarying degree of edema is followed by opening up of a venous collateral
circulation evidenced by the appearance of tortuous superficial vein.
c) Locally1) A much slower process of inflammation in and around the venous wall is
followed, by fibroblastic organization (or recanalisation) which may destroy valve cusps. So
retrograde flow may occur during exercise, 2) Infection can lead to abscess formation or
pyaemia. Infected clot in the portal vein may cause liver abscess (pylephlebitis).
Veins commonly involved :
1) Large venous sinuses in the soleus muscle where thrombosis arises in the large majority of
cases
2) Less often thrombus spreads into the tibial, popliteal, femoral, iliac and pelvic veins.
Clinical picture.
The signs and symptoms of deep vein thrombosis are:
swelling
pain
redness
dilated superficial veins
low grade pyrexia

History
Subjects with clinically predicting factors for deep vein thrombosis in lower limb like
immobility from any cause, old age, obesity, magnitude of injury or operative procedure,
myocardial infarction or heart failure, previous episodes of venous thromboembolism,
varicose veins, and drugs like estrogens etc. (2) OnsetSudden, may be spontaneous,
particularly in subjects on oral contraceptives or may follow some injury, operation or some
prolonged illness
Symptoms:
(1) Bursting pain or tightness in affected lower extremity particularly in calf, especially in
sitting, standing or walking.
(2) Swelling in the affected calf or whole leg often causing difficulty in walking.
(3) Unexplained syrexia and rapid pulse towards the end of first post-operative week.
Local features
1) Swollen leg
a) Slight edema around ankle (thrombosis confined to the calf),
b) Thigh, lower leg even the groin (iliofemoral venous thrombosis),
c) Both legs, and perhaps also the buttocks, abdominal wall and genitalia with distended
collaterals veins over the abdomen and throax even with bilateral varicocolsin inferior
vena caval obstruction.
2) Muscles e.g. calf-muscles (turgid due to thrombosed vein) are swollen, woody (induration)
and tender (Mose's sign).
3) Tenderness over involved veins (posterior tibial and peroneal veins) with venous
distension of the involved part.
4) Homan's sign : Pain in the calf on dorsiflexion of foot.
5) Finger firmly pressed on the tendo Achilles in the midline at its insertion into the
calcaneum is drawn up towards the muscles belly of the calf elicits tenderness as the site of
thrombosis is passed over (commonest site of thrombosis is usually the soleus just above its
junction with the tendo Achilles in the midline).
6) A large painful swollen and pale limb due to severe edema is called 'White Leg' or 'Milk
Leg' (occlusion of a length of deep femoral vein + associated lymphangitis) or phlegmasia
alba dolens.
(7) The large swollen congested and blue limb or 'blue leg' due to extensive deep vein
thrombosis of the iliac and pelvic veins is called phlegmasia caerulea dolens. In this
condition, either venous gangrene or areas of infarction may threaten part of or the whole of
the limb.
8) Varicosity of veins.
9) Skin changes like pigmentation, eczema etc.
Differential diagnosis.
Points
Thrombophlebitis

Phlebotfirombosis

1. Major cause Inflammation of superficial vein Stasis (noninflammatory)

as in varicose vein or in a vein
cannulated for infusion
2. Site
Any superficial vein
Deep veins (usually can vein)
3. Size of
Primary
thrombus

Larger depending upon the

Smaller
extent of invo vement of venous
segment

4.Size of Propa- Usually none, short and wellpated clot

anchored
if present
5. Clinical
Signs of acute inflammation
features
(general & local) with a painful
cord-like inflammed and tender
6. Embolism
Rare as the thrombus is adherent
to intima except in infective
cases Pvaemic

Long and often poorly attached

Silent painless and so overlooked. Unexplained
fever or tachy cardia at the end of the first Postoperativ week.
Common and massive but sterile

Pulmonary Embolism
Thrombophlebitis, Septic
Thrombophlebitis, Superficial
Other Problems to be Considered:
Achilles tendonitis
Arterial insufficiency
Arthritis
Asymmetric peripheral edema secondary to CHF, liver disease, renal failure, or nephrotic
syndrome
Cellulitis, lymphangitis
Extrinsic compression of iliac vein secondary to tumor, hematoma, or abscess
Hematoma
Lymphedema
Muscle or soft tissue injury
Neurogenic pain
Postphlebitic syndrome
Prolonged immobilization or limb paralysis
Ruptured Baker cyst
Stress fractures or other bony lesions
Superficial thrombophlebitis
Varicose veins
Peripheral vascular disease, arterial
Central venous occlusion
Main principles of treatment.
1.Conservative
1) Elevation
2) Elastic stocking
3) Massage as described under lymphodema
4) Anticoagulant therapyHeparin I.V. for 7-10 days followed by warfarin orally tor 3
months
5) Analgesics
6) Fibrinolytic therapy e.g. streptokinase or urokinase may cause serious bleeding at the site
of operation if used in about 10 days after operation.
7) If fever persists, blood culture should be performed and antibiotics given for fear of
septicaemia & pyaemia
8) Patients with extensive thrombosis are often very anaemic and urgent blood transfusion
should be considered.

OperativeWhen conservative treatment fails.

2.Operative
1) Thrombectomy: Deserves consideration if, there is evidence of venous gangrene.
2) Venous interruption may be called for extension of life-threatening thrombus.
Palma operationIliac vein obstruction is bypassed by long saphenous vein of the good
leg. The vein is rerouted across the pubis through a subcutaneous tunnel and anastomosed to
a vein below the iliac vein obstructin.
Femoral and iliac venous thrombectomy
Femoral vein ligation
The access and dissection are identical to those for iliac thrombectomy, with which ligation
may be combined. Femoral thrombus may be removed above the profunda vein by the
techniques described above, and distal thrombus is then prevented from embolizing by
ligation of the femoral vein below the confluence with the profunda vein. You may use
ligation as the sole manoeuvre if thrombus is present only below the profunda origin.
Caval clipping or plication
Carefully dissect free and snare a segment of vena cava between two pairs of lumbar veins
using a combination of sharp and blunt dissection.
2. Place a plastic Miles-DeWeese clip around the vena cava and hold it closed with a silk
ligature as shown. Alternatively pass three or four mattress sutures across the vena cava from
front to back and tie them down. Both techniques convert the vena cava into a number of
small channels which prevent large emboli from reaching the lungs.
Insertion of umbrella filter
Both the Mobin-Uddin and Greenfield-Kimway umbrella filters may be inserted into the
inferior vena cava via a venoiomy in the internal jugular vein under local anaesthesia.
57. Deep venous thrombosis of extremities antithrombotic therapy. Criterions of
efficiency.
Antithrombotic therapy.
1) pharmacies, which have
effect on thrombus lysis
2) medicines, wichstabilize thrombotic process and prevent rethrombosis (anticoagulants of
direct and indirect
action, reopoliglucin,);
3) medicines, wich reduce inflammation and prevent phlebosclerosis (antibiotics);
4) measures, wich are directed for stimulation of venous blood flow, improving of
collateral blood circulation, microcirculation and trophics in ill extremity (elastic bandege, high
position of extrimity,
The basis of conservative treatment consist of thrombolytics and
anticoagulants.
1) Elevation
2) Elastic stocking
3) Massage as described under lymphodema
4) Anticoagulant therapyHeparin I.V. for 7-10 days followed by warfarin orally tor 3 months
5) Analgesics
6) Fibrinolytic therapy e.g. streptokinase or urokinase may cause serious bleeding at the site of
operation if used in about 10 days after operation.

7) If fever persists, blood culture should be performed and antibiotics given for fear of
septicaemia & pyaemia
8) Patients with extensive thrombosis are often very anaemic and urgent blood transfusion should
be considered.
OperativeWhen conservative treatment fails.
2.Operative
1) Thrombectomy: Deserves consideration if, there is evidence of venous gangrene.
2) Venous interruption may be called for extension of life-threatening thrombus.
Palma operationIliac vein obstruction is bypassed by long saphenous vein of the good leg.
The vein is rerouted across the pubis through a subcutaneous tunnel and anastomosed to a vein
below the iliac vein obstructin.
Femoral and iliac venous thrombectomy
Femoral vein ligation
The access and dissection are identical to those for iliac thrombectomy, with which ligation may
be combined. Femoral thrombus may be removed above the profunda vein by the techniques
described above, and distal thrombus is then prevented from embolizing by ligation of the
femoral vein below the confluence with the profunda vein. You may use ligation as the sole
manoeuvre if thrombus is present only below the profunda origin.
Caval clipping or plication
. Carefully dissect free and snare a segment of vena cava between two pairs of lumbar veins using
a combination of sharp and blunt dissection.
2. Place a plastic Miles-DeWeese clip around the vena cava and hold it closed with a silk ligature
as shown. Alternatively pass three or four mattress sutures across the vena cava from front to
back and tie them down. Both techniques convert the vena cava into a number of small channels
which prevent large emboli from reaching the lungs.
Insertion of umbrella filter
Both the Mobin-Uddin and Greenfield-Kimway umbrella filters may be inserted into the inferior
vena cava via a venoiomy in the internal jugular vein under local anaesthesia
Criterions of efficiency.
1 to stop further thrombogenesis;
2 to supress inflammation;
3 to make lysis of formed thrombus;
4 to recover natural or accelerate forming of round about flood flow.

58. Gastrinoma, idea definition, diagnostic triad, clinical manifestations,

peculiarities of gastric acid analysis, instrumental investigations, treatment.
Idea definition.
A gastrinoma is a gastrin-secreting tumor that usually is located in the pancreas (40%),
duodenal wall (40%), and adjacent lymph nodes. Nearly 90% of gastrinomas arise within
the triangle surrounded by the porta hepatis, the neck of the pancreas, and the third
portion of the duodenum. Rarely, they may arise from other areas such as the parathyroid
and ovaries . Gastrinomas may be either solitary or multifocal. Two thirds of gastrinomas
are malignant and can metastasize to regional lymph nodes and the liver. One fourth of
gastrinomas are related to multiple endocrine neoplasia type 1 and are associated with
hyperparathyroidism and pituitary adenomas. The triad of nonbeta islet cell tumors of the
pancreas (gastrinomas), hypergastrinemia, and severe ulcer disease

Diagnostic triad.
1) severe gastrointestinal ulcerative disease, (2) gastric acid hypersecretion, and (3)
nonbeta islet cell tumors of the pancreas
Clinical manifestations.
The symptoms in 90-95% of patients with gastrinomas are similar to the
symptoms of common peptic ulcer disease. Usually, persistent abdominal pain
exists that is less responsive to medical treatment.
Sometimes, symptoms may relate to a complication of peptic ulcer disease, such
as bleeding (eg, melena, hematemesis), gastric outlet obstruction (eg, vomiting),
and perforation (eg, peritoneal irritation).
Other symptoms include gastroesophageal reflux, diarrhea, steatorrhea, and
weight loss, all of which are secondary to acid hypersecretion. Vitamin B-12
malabsorption also is observed.
Physical:
Epigastric tenderness is the most frequent abnormal physical finding. Depending
on the possible ulcer complications, signs may vary.
Nearly 75% of ulcers in patients with gastrinomas are present in the first portion
of the duodenum. These ulcers usually are single or multiple and are
indistinguishable from peptic ulcer disease.
Nearly 10% of patients with ZES have no demonstrable ulcer. Ulcers located in
the second, third, or fourth portion of the duodenum or jejunum should increase
the possibility of gastrinoma.
The other factors that alert one to the presence of underlying gastrinomas are the
following:
o Ulcers that are refractory to standard therapy
o Multiple ulcers
o Giant ulcers, larger than 2 cm
o Recurrent ulcers
o Ulcers with unexplained diarrhea
o Strong family history of ulcers
o Hypercalcemia
o Duodenal ulcer that is not related to Helicobacter pylori infection or
nonsteroidal anti-inflammatory drug use
Peculiarities of gastric acid analysis.
o Fasting serum gastrin test: Levels greater than 200 pg/mL are suggestive
of gastrinoma, and levels greater than 1000 pg/mL are virtually diagnostic
of gastrinoma. Serum gastrin levels are also elevated in patients with
pernicious anemia because of a lack of negative feedback from parietal
cell secretion of hydrochloric acid; thus, hypergastrinemia in the absence
of hyperchlorhydria and peptic ulcer is not attributable to a gastrinoma.
o Gastric acid analysis: Basal acid secretion at a rate higher than 15 mEq/h
or a basal-to-maximal acid output ratio that exceeds 0.6 supports the
diagnosis of gastrinoma

Secretin stimulation test: A baseline fasting serum sample is drawn, after which secretin
at 2 U/kg is administered as an intravenous bolus. Blood is drawn every 5 minutes for 30
minutes, and the serum gastrin level is determined in each sample. An increase in the
gastrin level of more than 200 pg/mL above the basal level supports the diagnosis of
gastrinoma
Instrumental investigations.
Somatostatin receptor scintigraphy is the most sensitive imaging modality for
detection of primary or metastatic lesions
CT scan can be performed to localize the tumor and is useful for evaluation for
metastatic disease.
Other imaging studies, such as magnetic resonance imaging and abdominal
ultrasound,
Endoscopic ultrasound is one of the newer methods for localizing gastrinomas. Its
sensitivity is higher for pancreatic gastrinoma (40-75%) than for duodenal
gastrinoma (50%).
Esophagogastroduodenoscopy should be performed to look for duodenal
ulcerations and hypertrophy of gastric folds. Sensitivity for hypertrophic gastric
folds is 94%. Rarely, thickened duodenal folds also may be present
Treatment.
Medical Care:.
Proton pump inhibitors (eg, omeprazole, lansoprazole)
o These are highly effective drugs and are the drugs of choice for
suppressing acid secretion. Long duration of action, fewer adverse effects,
and high potency make them superior to H2 blockers.
H2-receptor antagonists
o The dose usually is 4-8 times higher than the dose administered to patients
with peptic ulcer disease.
Chemotherapy
o This is indicated in patients with metastatic disease and in patients who are
not candidates for surgery.
o Chemotherapy reduces tumor size and improves the symptoms secondary
to metastatic effects of the tumor.
o A combination of streptozocin, 5-fluorouracil, and doxorubicin has been
used, with the response rate reported to be as high as 65%.
Surgical Care:
Surgical care is indicated for localized disease. Surgical resection of localized
disease leads to a complete cure without any recurrence in 20-25% of patients
with gastrinomas.
Patients who have an isolated lesion or patients in whom the preoperative workup
fails to localize the tumor should undergo laparotomy (by an experienced
surgeon) with the intent to resect.
Small benign lesions remote from the main pancreatic duct can be enucleated

Tumors deep in the substance of the pancreatic gland, and therefore close to the main
duct, have ill-defined capsules, and tumors larger than 2 cm in diameter should be treated
with regional pancreatectomy
Tumors in the body or tail of the pancreas can be managed with distal pancreatectomy
59. Verner-Morrison syndrome, idea definition, diagnostic triad, instrumental
investigations, treatment.
Idea definition.
Verner and Morrison described a syndrome of watery diarrhea, hypokalemia, and
achlorhydria
that was due to pancreatic tumors associated with raised plasma levels of a hormone. The
extirpated tumors from these cases were found to contain large amounts of what now is
known as vasoactive intestinal polypeptide (VIP).
VIPomas originate in amine precursor uptake and decarboxylation (APUD) cells of the
gastroenteropancreatic endocrine system and in adrenal or extra-adrenal neurogenic sites.
Neural crest cells are precursors of APUDoma and neurogenic cells.
Diagnostic triad.
watery diarrhea, hypokalemia, and achlorhydria
The onset of symptoms is insidious. Diarrhea may persist for years before the diagnosis is
made. Diarrhea typically occurs in episodes. Secretory diarrhea persists even when the
patient is restricted to nothing PO.
Fecal loss of large amounts of potassium and bicarbonate cause hypokalemia,
acidosis, and volume depletion.
Clinical diagnosis is based on a history of approximately 10 watery stools per day.
Fecal losses while fasting are at least 20 mL/kg/d but exceed 50 mL/kg/d in most
cases. Fecal osmolality is entirely accounted for by twice the sum of the
concentrations of sodium and potassium, indicating the electrolyte loss.
Patients may complain about colicky abdominal pain or pain in the upper
abdominal area radiating to the back.
Instrumental investigations.
Imaging Studies:
Localization techniques: These focus on the pancreas, where 90% of VIPomas are
located.
CT scan
o CT scan may identify primary tumor in the pancreas or retroperitoneum
and assists in excluding liver metastases.
o CT scan only visualizes tumors larger than 2-3 cm.
MRI
o MRI is used to localize VIPomas.
o VIPomas are observed best on T1-weighted, fat-suppressed images as
low-signal intensity masses.

Liver metastases may demonstrate intensive peripheral ring enhancement

on immediate postgadolinium spoiled gradient-echo images.
Somatostatin receptor scintigraphy: Use for localization of neuroendocrine
tumors, including VIPomas, may be improved in the near future by single-photon
emission computed tomography, as suggested by recent investigations.
Technetium 99m sestamibi: New reports exist of successful VIPoma localization
with technetium 99m sestamibi.
Transabdominal ultrasonography: This may be used for early screening to exclude
liver metastases, which may present as hepatic calcifications.
Endoscopic retrograde cholangiopancreatography
o Endoscopic retrograde cholangiopancreatography may demonstrate
occlusion of the major pancreatic duct.
o It also may demonstrate calcifications in the body of the pancreas.
Iodine-123 VIP receptor scintigraphy
o This has been used successfully in the localization of a VIPoma.
o The identity of the VIP binding site, analyzed by Northern blot analysis,
revealed expression of somatostatin receptor 3, which binds VIP with
higher affinity than octreotide.
o This test is currently under investigation.
Colonoscopy: This may be useful to evaluate for a possible villous adenoma as an
alternative cause of potassium-losing diarrhea.
Histologic Findings
o

Treatment.
Medical Care:
Because most patients present in a weakened clinical condition at the time of
diagnosis, initial treatment is aimed at correcting volume and electrolyte
abnormalities with potassium chloride and sodium bicarbonate.
Somatostatin is highly effective in controlling diarrhea. Short-acting and longacting depot preparations are now available.
Glucocorticoids are less effective but less expensive, reducing symptoms in
approximately 50% of patients.
Surgical Care:
Tumor resection is indicated in patients without extensive metastatic disease.
Abdominal exploration and resection are indicated in those in whom the tumor is
not localized by various imaging techniques. Intraoperative ultrasound of the
pancreas may have some use in identifying VIPomas in such situations.
o Local tumor resection is the treatment of choice. If the tumor is located in
the pancreatic tail, a pancreatic tail resection is the procedure of choice.
o Pancreatoduodenectomy is indicated when the tumor is in the pancreatic
head or processus uncinatus.
o Intraoperative sonography of the pancreas may facilitate intraoperative
tumor localization.
If metastatic disease is found at surgery, tumor debulking may reduce clinical
symptoms. Tumor debulking may not be effective in every patient.

If no tumor is found at surgery, a blind pancreatic tail resection may be

performed. A total pancreatectomy no longer is recommended.
Orthotopic liver transplantation has been successful for patients in whom
conventional symptomatic and cytostatic treatments are not tolerated or are
ineffective. At 1-year follow-up examination, 1 such patient had no evidence of
tumor recurrence

60. Insulinoma idea definition. Wipples triad. Laboratory and instrumental investigations.
Treatment.
Idea definition.
Insulinomas are insulin-secreting tumors associated with the Whipple triad. The triad includes (1)
symptoms of fasting hypoglycemia, (2) documented fasting hypoglycemia with a serum glucose level
less than 50 mg/dL, and (3) relief of hypoglycemic symptoms after glucose administration
insulinoma is a neuroendocrine tumor deriving mainly from pancreatic islet cells that produce
excessive amounts of insulin. About 90% of insulinomas are benign. In healthy individuals, insulin
and C-peptide are secreted in equimolar quantities because they derive from the same inactive
precursor, proinsulin. Normally, less than 20% of proinsulin is released directly into the circulation.
Some insulinomas secrete additional hormones, such as gastrin, 5-hydroxyindolic acid,
adrenocorticotropic hormone (ACTH), glucagon, human chorionic gonadotropin, and somatostatin.
The tumor may secrete insulin in short bursts, causing wide fluctuations in blood levels.
Wipples triad.
The triad includes (1) symptoms of fasting hypoglycemia, (2) documented fasting hypoglycemia with
a serum glucose level less than 50 mg/dL, and (3) relief of hypoglycemic symptoms after glucose
administration
Laboratory and instrumental investigations.
Lab Studies:
The presence of hypoglycemia in the face of inappropriately elevated levels of insulin is the
key to diagnosis. Considering the reference range, the fasting plasma levels of insulin, Cpeptide, and, to a lesser degree, proinsulin need not be elevated in insulinoma patients in
absolute terms.
The biochemical diagnosis is established in 95% of patients during prolonged fasting (up to
72 h) when the following parameters are found:
o Serum insulin levels of 10 mU/mL or more (normal <6 mU/mL)
o Glucose levels of less than 40 mg/dL
o C-peptide levels exceeding 2.5 ng/mL (normal <2 ng/mL)
o Proinsulin levels greater than 25% (or up to 90%) that of immunoreactive insulin
o Screening for sulfonylurea negative
Stimulation intravenous application of tolbutamide, glucagon, or calcium
Failure of endogenous insulin secretion to be suppressed in the presence of hypoglycemia is
the hallmark of an insulinoma.
Prolonged (ie, 72 h) supervised fast in hospitalized patients provides the most reliable results.
o The calculation of ratios of insulin (mU/mL) to plasma glucose (mg/dL) is
diagnostic.
o Healthy patients maintain a rate of less than 0.25. Obese patients may have a slightly
higher rate.
o In patients with insulinoma, the ratio rises during fasting.
The presence of MEN 1 must be evaluated by excluding the following:

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Hyperprolactinemia due to a pituitary adenoma

Hyperparathyroidism due to parathyroid hyperplasia
Hypergastrinemia due to a gastrinoma

Imaging Studies:
Start imaging studies only after the diagnosis has been confirmed biochemically, because
80% of insulinomas are less than 2 cm in size and may not be visible by CT scan or
transabdominal ultrasonography.
CT scan has 24% sensitivity.
When performed with gadolinium, MRI has 40% sensitivity.
The accuracy of selective arteriography is 47%,
Arteriography with catheterization of small arterial branches of the celiac system combined
with calcium injections (which stimulate insulin release from neoplastic tissue but not from
normal islets), and simultaneous measurements of hepatic vein insulin during each selective
calcium injection localizes tumors in 47% of patients.
The sensitivity of somatostatin receptor scintigraphy is 60%, although many insulinomas lack
somatostatin receptor subtype 2 for successful identification.
Endoscopic ultrasonography detects 77% of insulinomas in the pancreas.
Real-time transabdominal high-resolution ultrasonography has 50% sensitivity.
Intraoperative transabdominal high-resolution ultrasonography with the transducer wrapped
in a sterile rubber glove and passed over the exposed pancreatic surface detects more than
90% of insulinomas.
Other Tests:
Preoperative portal venous sampling is obsolete as a routine investigation because of a high
complication rate (10%), but it may be employed when all other imaging procedures fail and
surgical exploration findings are negative.
Localization with anti-insulin labeled with iodine 131 was achieved in 50% of patients, with a
37.5% false-positive rate. Therefore, it is not recommended.
Recently, endoscopic ultrasound-guided fine-needle aspiration biopsy has been described in
an insulinoma. It is a technique combining endoscopic ultrasonography with local tumor
biopsy and may be indicated when the tissue diagnosis must be established preoperatively.
Laparoscopic ultrasound with eventual tumor biopsy may be used in rare cases when other
localization techniques failed.
Histologic Findings
Treatment.
Medical therapy is indicated in patients with malignant insulinomas and in those who will not or
cannot undergo surgery. These measures are designed to prevent hypoglycemia and, in patients with
malignant tumors, to reduce the tumor burden.
Diazoxide is related to the thiazide diuretics and reduces insulin secretion
Prescribe hydrochlorothiazide to counteract the edema and hyperkalemia secondary to
diazoxide and to potentate its hyperglycemic effect.
Surgical Care: Because insulinoma resection achieves cure in 90% of patients, it is currently the
therapy of choice.
Successful tumor location
o Fully expose the pancreas, including a wide Kocher maneuver to allow complete
bimanual palpation.
o Laparoscopic enucleation techniques, also in combination with preservation of the
spleen for distal pancreatic tumors, have been described recently.
o Simple enucleation is the procedure of choice in insulinomas in the pancreatic head.

Avoid total pancreatectomy because of its high morbidity and mortality rates.
Major resections, such as the Whipple procedure, may become necessary when the
tumor is found in the pancreatic head and local excision is not possible.
o Resect all gross disease when multiple tumors or metastases are present.
o If insulinoma is associated with MEN 1, the management strategy is modified
because tumors are often multiple, diffusely spread in the pancreas, and of small size.
Definite cure by surgery is rare.
o Subtotal pancreatectomy with enucleation of tumors from the pancreatic head and
uncinate processus often is recommended over simple enucleation because of
frequent multiple tumors in MEN 1.
Tumor not localized at surgery (10% of patients)
o If the patient is responsive to diazoxide, continue it, while more invasive imaging
studies are performed before repetitive surgery is considered.
o If the patient is not responsive (5-10%) or if drug intolerance is present and ectopic
disease is excluded, a blind distal two-thirds pancreatectomy may be performed.
(This procedure has only a 25% success rate.)
o Most authorities recommend serial sectioning during resection.
o Tumors that are not found at surgery normally are located in the pancreatic head
(54%), body (20%), and tail (14%).
Metastatic disease found
o Even when metastases are found, surgical excision is often feasible before any
medical, chemotherapeutic, or other interventional therapy is considered.
o Resect all gross disease, including wedge resections of hepatic metastases.
o Avoid ligation of the hepatic artery in case further regional infusion therapy becomes
necessary.
Intraoperative serum insulin measurements recently have been employed to assure complete
tumor removal. This may be important, particularly in patients with MEN 1 who harbor
multiple insulinomas.
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